essay on acute heart failure

Internet Book of Critical Care (IBCC)

Online Medical Education on Emergency Department (ED) Critical Care, Trauma, and Resuscitation

Acute decompensated heart failure (including cardiogenic shock)

March 5, 2024 by Josh Farkas

core considerations for every patient

• Bedside hemodynamic assessment
• Why is this patient presenting with heart failure?
• [Rx 1] Fix the lungs
• [Rx 2] Optimize the MAP/afterload
• [Rx 3] Optimize volume status
• [Rx 4] Consider inotrope for HFrEF (including digoxin)
• [Rx 5] Treat underlying etiology
• [Rx 6] Mechanical circulatory support
• [Rx 7] Things to avoid

related topics & background

• More on hemodynamic assessment & risk stratification
• Pulmonary artery catheter
• Usual CT scan findings in heart failure
• SCAPE (sympathetic crashing acute pulmonary edema)
• Asymmetric pulmonary edema
• Radiological differential diagnosis

(back to contents)

Basic hemodynamic assessment involves assessment of three variables: cardiac output, PCWP (pulmonary capillary wedge pressure) and CVP (central venous pressure). 

[a] signs of inadequate cardiac output: 

• [1] Cool extremities.
• [2] Delayed capillary refill.
• [3] Mottling (look at the knees ).
• [4] Narrow pulse pressure (<25% SBP suggests poor cardiac output).
• Only accurate in the presence of sinus rhythm without negative chronotropes.
• Acute kidney injury.
• Shock liver (markedly elevated AST/ALT).
• Lactate elevation.
• Delirium, poor mentation (but this is a very late indicator of cardiogenic shock).

[b] signs of PCWP elevation: 

• Dyspnea, tachypnea.
• Lung POCUS shows B-lines (outstanding performance).
• CXR/CT shows pulmonary edema.

[c] signs of CVP elevation: 

• Peripheral edema.
• Weight gain.
• JVP elevation.
• IVC distended & lacking respirophasic variation.

reminder of things to look for at the bedside:

• Skin temperature.
• Capillary refill.
• Knee mottling.
• Cardiac exam.
• Lung exam (B lines vs. A lines).

causes of heart failure presentation

Acute drop in lv ejection fraction.

• Acute MI (the cause of ~75% of cardiogenic shock). ( 31262417 )
• Takotsubo cardiomyopathy 📖 , post-cardiac arrest stunning.
• Peripartum cardiomyopathy.
• Myocarditis (e.g., viral, SLE, giant-cell, eosinophilic, checkpoint inhibitors).
• Tachymyopathy.

volume alteration

• Acute volume overload (e.g., diuretic nonadherence, dietary indiscretion, iatrogenic volume administration).
• Acute hypovolemia (e.g., over-diuresis, reduced oral intake, gastroenteritis).
• Renal failure causing volume retention.
• Bradyarrhythmia.
• Tachyarrhythmia (most often new-onset atrial fibrillation).
• Decreased cardiac resynchronization therapy (CRT) pacing. (Irwin & Rippe, 9th ed.)
• Increased isolated right ventricle pacing. (Irwin & Rippe, 9th ed.)

valvular dysfunction

• LV outflow tract obstruction (LVOTO). 📖
• Prosthetic valve dysfunction (e.g., thrombosis).
• Native valve dysfunction (e.g., endocarditis, ruptured papillary muscle 📖 ).

medications/substances

• Nonadherence with heart failure therapies.
• Negative inotropy due to excess beta-blocker, diltiazem, Class I antiarrhythmics, and some Class III antiarrhythmics (including dronedarone and sotalol). (Griffin 2021)
• Volume overload may be promoted by NSAIDs, steroid, or pioglitazone.
• Digoxin toxicity.
• Cardiotoxic chemotherapy.
• Sympathomimetic abuse.
• Uncontrolled hypertension.
• Uncontrolled sleep-disordered breathing.
• Hypophosphatemia.
• Iron deficiency (with or without anemia).
• Thyroid disease (hypothyroidism or hyperthyroidism).
• Infection/sepsis.

evaluation of the patient presenting with heart failure 

Laboratory studies.

• CBC (consider transfusion for HgB <7-8 mg/dL).
• Electrolytes including Ca/Mg/Phos.
• Liver function tests.
• Lactate, if shock is suspected.
• TSH (thyroid stimulating hormone).
• Digoxin level.
• Ferritin and transferrin saturation.
• BNP/proBNP (may be falsely low in obesity, HFpEF, or predominant RV failure). (Gaggin 2021)

imaging studies

• Formal echocardiogram.
• Chest radiography (for respiratory failure; exclude other causes).

BiPAP (noninvasive ventilation)

• BiPAP has been shown to reduce intubation and mortality.
• BiPAP reduces cardiac preload and afterload (physiologic effects similar to an ACE inhibitor).
• It's not merely enough to place the patient on BiPAP – for maximal benefit the pressures should be up-titrated as tolerated (figure below). The most important parameter is the expiratory pressure, which should be ramped up rapidly if possible. An alternative and equally effective strategy is simply to use CPAP. 📖
• 🛑 Ongoing use of BiPAP is generally not advisable in patients with true cardiogenic shock and multiorgan failure (e.g., delirium, renal failure).
• Often needed for frank cardiogenic shock (especially patients with delirium due to brain hypoperfusion).
• Provides full support for the work of breathing, which may allow shunting of blood away from the diaphragm and towards vital organs.
• Stabilizes patients for procedures that require lying flat (e.g. cardiac catheterization)
• Disadvantage: intubation in cardiogenic shock carries risks of hypotension/arrest, so be careful.
• When in doubt about the need for intubation: start BiPAP and optimize other factors as rapidly as possible. Then re-evaluate the patient's trajectory and need for BiPAP.

drainage of large effusions

• (Note that even if the effusion is drained, the underlying heart failure must still be optimized. If the effusion is drained without management of the underlying heart failure, it will soon recur. Draining the effusion doesn’t fix the heart failure, it just temporarily stabilizes respiratory function.)

HFrEF + (MAP >~75 mm) = consider afterload reduction 

• Afterload reduction is greater for patients with HFrEF and sufficient blood pressure to tolerate it. Afterload reduction may improve cardiac output, decongest the lungs, and reduce the myocardial workload.
• ⚠️ Unfortunately, patients with preserved ejection fraction may benefit less from afterload reduction (with a higher risk of hypotension). ( 22281246 ) However, vasodilators may remain useful in such patients with the context of hypertensive emergency (i.e., SCAPE 📖 ). 
• [a] High-dose nitroglycerine infusion 📖 (especially for SCAPE).
• [b] Nitroprusside infusion. 📖
• [c] Dobutamine infusion (discussed further below ⚡️ ).
• [d] Oral hydralazine/isosorbide dinitrate (similar to ACE-i without nephrotoxicity). 📖 ( 3520315 )
• [e] ACE-i/ARB (risk of renal failure; avoid in shocky patients or with aggressive diuresis).

hypotension (severe or with organ dysfunction): consider inopressor

• Norepinephrine is widely recommended as a front-line agent for cardiogenic shock. Norepinephrine will improve the blood pressure, but there is a risk that excessive afterload could drop the cardiac output.
• At very low doses, it seems that the epinephrine causes some vasodilation by acting on beta-2 receptors, but also some vasoconstriction by acting on alpha-receptors. The net effect on systemic vascular resistance seems to be relatively neutral. The net effect of low-dose epinephrine is often an improvement in blood pressure and cardiac output, without affecting systemic vascular resistance much.
• Epinephrine may be especially helpful in patients with bradycardia or inappropriately normal heart rates.

fluid administration

• [1] There is insufficient end-organ perfusion (e.g., acute kidney injury).
• [2] No evidence of pulmonary congestion (e.g., no B-lines on lung ultrasonography).
• [3] Overall assessment suggests true hypovolemia (e.g., no systemic congestion).
• Monitor the effect of fluid administration carefully. If fluid isn't causing clinical improvement, don't give more.
• Be careful – static hemodynamic parameters (e.g., CVP, pulmonary capillary wedge pressure) do not predict fluid-responsiveness and should not be used as the primary determinant of fluid administration. ( 24286266 )

fluid removal

• (1) There is significant pulmonary and/or systemic congestion.
• (2) Overall assessment suggests total body fluid overload.
• For patients who aren't responding adequately to furosemide, consider adding a thiazide diuretic (e.g., metolazone 5 mg q12hr-q24hr). This may enhance sodium excretion, with improved clearance of extravascular edema fluid. ( 23131078 , 26948252 , 31838029 ). Patients with severe systemic congestion may have reduced absorption of some diuretics, so they may require IV diuretics (e.g., IV furosemide plus IV chlorothiazide). More on diuresis: 📖 .
• Patients with substantially elevated central venous pressure can experience an improvement in renal function with diuresis, because decreasing venous congestion will increase blood flow through the kidney. The driving pressure through the kidneys is equal to the MAP minus the CVP, so lowering the CVP may increase renal perfusion.

avoid catecholamine inotropes when possible

• Inotropes will cause a short-term improvement in hemodynamics. Unfortunately, available evidence indicates that inotrope use associates with worse outcomes. ( 28602370 ) Available prospective RCT data is scanty, but it likewise suggests that inotropes may be harmful. ( 11911756 )
• Hypoperfusion with low-normal blood pressure (e.g. acute kidney injury with poor urine output despite #1-3 above).
• Refractory cardiogenic pulmonary edema : Front-line therapies for cardiogenic pulmonary edema include #1-3 above: BiPAP, nitroglycerine (if blood pressure is adequate), and diuresis (if there is evidence of volume overload). Some patients will fail to respond to these treatments, especially hypotensive patients in whom nitroglycerine or diuresis are contraindicated. In such patients inotropes may be used with a goal of reducing the pulmonary capillary wedge pressure and decongesting the lungs.

dobutamine vs milrinone?

• An RCT comparing dobutamine vs. milrinone in patients with cardiogenic shock found no difference between the two agents. ( 34347952 ) Dobutamine has a shorter half-life which makes it more easily titratable, which arguably makes it the preferred agent. Alternatively, milrinone is renally cleared so it may exhibit erratic pharmacokinetics in shocked patients (e.g., accumulating unexpectedly if there is a reduction in renal function). Even with normal renal function, the half-life of milrinone is long (2.3 hours) – making rapid titration impossible.
• Both agents may cause hypotension, so they shouldn't be used in profoundly hypotensive patients. Thus, it's generally preferable to start with blood pressure control (step #2 above).
• Home inotropic therapy may be beneficial for patients with severe heart failure symptoms who aren't candidates for mechanical support devices. (Sadu 2023)
• Digoxin is the only positive inotropic agent whose use doesn't correlate with increased mortality. Digoxin isn't a particularly powerful inotrope, but it might be the safest (with close monitoring of digoxin levels).
• Digoxin can be considered for patients with long-standing atrial fibrillation and systolic heart failure . (Patients with new-onset atrial fibrillation might benefit from cardioversion to sinus rhythm instead of digoxin.)  Further discussion regarding which patients are optimal candidates for digitization is here: 💉

arrhythmia treatment

• If shock is caused by new-onset tachyarrhythmia (e.g. atrial fibrillation), then reversion to sinus rhythm may be beneficial. However, if the heart rate isn't very high then be careful – slowing down the heart rate may actually aggravate matters.
• If shock is caused or aggravated by bradycardia , this should be treated accordingly. 📖

cardiogenic shock due to MI

• Treat with medical therapies for type-I MI (e.g. aspirin, P2Y12 inhibitor, anticoagulation).
• Revascularization is essential. This is beneficial even at delayed time points. ( 10460813 ) Thrombolysis works poorly in cardiogenic shock, so PCI or CABG is generally necessary.
• Although heart failure patients are often anemic, this usually isn't the cause of their decompensation. As a general rule, treatment of the dyspneic patient with blood transfusion in the expectation that this will improve pulmonary status is disappointing.
• Patients should be transfused to standard transfusion targets (>7 mg/dL, or >8 mg/dL if there is evidence of active myocardial ischemia).

Mechanical support is indicated for patients refractory to #1-5 above. Perhaps the most important end-organ to support is the kidneys. If the patient develops severe renal failure, this aggravates matters greatly. Commonly utilized options include:

IABP (intra-aortic balloon pump)

• Intra-aortic balloon pumps may augment cardiac output by 0.3-0.5 liters/minute. ( 31374209 )  However, RCTs consistently fail to show improvement in patient-centered outcomes with IABP therapy. ( 22920912 , 21878431 ) 
• Less effective in the context of tachycardia or irregular rhythms. ( 32469155 )
• Severe peripheral artery disease.
• Moderate-to-severe aortic regurgitation.
• Aortic disease (e.g., aortic dissection).
• Evidentiary basis: DanGer Shock trial demonstrated improved outcomes among patients with infarct-related cardiogenic shock. 🌊
• Aortic valve pathologies including: mechanical aortic valve, severe aortic stenosis, moderate-to-severe aortic regurgitation.
• LV thrombus.
• Severe peripheral arterial disease.
• Inability to tolerate anticoagulation.
• Ventricular septal defect (VSD).
• VA-ECMO reflects the greatest level of support for the sickest patients (e.g., patients with respiratory failure and/or biventricular heart failure). ( 29655828 )
• Candidacy for VA-ECMO is discussed here: 📖
• Nephrotoxic medications (e.g. NSAIDs, ACEi/ARB) 📖 .
• Don't try to suppress a sinus tachycardia. This is often a compensatory mechanism that may be keeping the patient alive.
• Avoid using diltiazem for rate control in AF patients with decompensated heart failure and reduced ejection fraction (the negative inotropic effects may be problematic). 📖
• Don't treat mild, stable hyponatremia with an infusion of 3% saline or salt tablets. Patients with heart failure commonly have mild hyponatremia. This will generally tend to resolve with treatment of the underlying heart failure (e.g. diuresis with furosemide).
• Fluid and sodium restriction haven't shown benefit in RCTs. ( 23689381 , 17395053 ) Hospital food often isn't great, so the must humane thing is probably to provide a regular diet. Follow fluid balance and use diuretics if needed.

be very careful with beta blockers in decompensated heart failure

• Beta-blockers are fantastic for chronic, compensated heart failure, but potentially dangerous in decompensated heart failure (negative inotropy may further impair cardiac function).
• Beta-blockers shouldn't be started in the context of decompensated heart failure.
• Beta-blockers should be held in patients with cardiogenic shock.
• For patients who aren't in shock, beta-blockers may be continued (perhaps at a reduced dose initially).
• Please note that a beta-blocker is the opposite to giving an inotrope. So any enthusiasm for using dobutamine in heart failure should translate into an equal and opposite aversion towards beta-blockers.

Forrester classifications

• Based on the pulmonary capillary wedge pressure and the cardiac index, patients may be categorized as shown above. These categorizations have direct implications for prognosis and treatment. ( 790191 )
• Green curve: normal cardiac output function
• Orange curve: moderate heart failure
• Red curve: severe heart failure
• Patients who are warm/wet may often be managed with volume removal and/or vasodilation to reduce their afterload (vasodilation shifts fluid out of the lungs without affecting the total body volume).
• Patients who are cold/dry may often be managed by fluid administration:

classic presentation of cardiogenic shock: patients who are cold & wet

• (1) Systemic hypoperfusion due to low cardiac output (cold).
• (2) Filling pressures are elevated (wet).
• Giving volume will worsen their pulmonary congestion (making them wetter).
• Removing volume will worsen their systemic hypoperfusion (making them colder).
• Management of cardiogenic shock usually requires interventions to improve cardiac function (e.g., inotropic medications, revascularization, or a mechanical support).
• Early recognition facilitates appropriate ICU management.
• The patient with unrecognized cardiogenic shock will generally fail to respond to non-intensive therapy, running in circles (typically the patient is initially diuresed, then develops worsening renal failure, then is given fluid back, then develops pulmonary edema, then transferred to ICU).

vasodilated cardiogenic shock

• To make things confusing, cardiogenic shock may trigger a systemic inflammatory response with elevated cytokine levels and reduced systemic vascular resistance . This may occur later in the course of cardiogenic shock, possibly due to ischemic tissue damage. This condition will mimic septic shock. ( 28923988 )
• This may represent a final common pathway of the dying patient.

HFpEF vs. HFrEF

• Heart failure patients may be classified as heart failure with reduced ejection fraction (<40%, HF r EF, a.k.a “systolic failure”) vs. heart failure with preserved ejection fraction (HF p EF, a.k.a. “diastolic dysfunction”).
• HFrEF: reduced ejection fraction.
• HFpEF: preserved ejection fraction. Presence of heart failure is suggested by dilated left atrium, left ventricular hypertrophy, and pulmonary congestion (B-lines on lung ultrasonography). Doppler measurements can also be used to diagnose diastolic dysfunction (E/E’, etc). In most cases, however, the diagnosis of diastolic HF can be made based on history, physical exam, EKG, CXR, and basic 2-dimensional ultrasonography of the heart and lungs.
• HFpEF patients shouldn't be treated with inotropes.
• HFpEF patients may be more preload-dependent, thus at higher risk for hypotension following diuresis.

interpretation of PA catheter data 

⚠️ beware of the normalization fallacy .

• Some patients with chronic heart failure adapt to having a low cardiac output, allowing them to avoid shock despite having a cardiac output below “normal” values.
• There is no specific cardiac output that should necessarily be targeted.
• When approaching hemodynamic data, beware of the normalization fallacy (the incorrect belief that any values should be adjusted towards normal). For example, a patient with chronic compensated heart failure may be doing well clinically with an elevated systemic vascular resistance (SVR). The elevated systemic vascular resistance functions here as a compensatory mechanism, allowing maintenance of an adequate blood pressure. Aggressive intervention to “normalize” the systemic vascular resistance could destabilize the patient by causing hypotension.

PA catheter normative data

• CVP (central venous pressure): 2-6 cm.
• 15-30 mm / 4-12 mm.
• mPAP 8-20 mm (>20 defines PH).
• PCWP (pulmonary capillary wedge pressure): <15 mm
• CO (cardiac output): 4-8 L/min.
• CI = CO/Body Surface Area
• Normal range: 2.5-4 L/min/m2.
• SVR = (MAP-CVP)/(CO*80)
• Normal range: 800-1200 dyne-s/cm5
• SVRi = (MAP-CVP)/(CI*80)
• Normal range: 1900-2400 dyne-s/cm5
• PVR = 80(mPAP-PCWP)/(CO)
• Normal range: 24-160 dyne-sec/cm5
• Normal range: 0.3-2.0 Wood Units (=PVR/80)
• PVRi = 80(mPAP-PCWP)/(CI)
• Normal range: 240-280 dyne-s/cm5
• Normal range: 3-3.5 Wood Units (=PVRi/80)
• PAPi = (PA pulse pressure)/CVP
• Normal range: >0.9
• CPO = (MAP*CO)/451
• Normal CPO: ~0.8-1.1 Watts
• CPOi = (MAP*CI)/451
• Normal CPOi: ~0.5-0.7 Watts/m2
• SV (stroke volume): 60-100 ml
• SVi (stroke volume index): 33-47 ml/m2

mixed venous oxygen saturation

• The mixed venous oxygen saturation is potentially the most accurate way to assess the cardiac output. This is particularly true in patients in whom PA catheter thermodilution measurements may be limited (e.g., due to tricuspid regurgitation). 🌊
• The Fick Equation 🧮 allows for estimation of the cardiac output using the mixed venous oxygen saturation. This is reasonably accurate for most cardiac patients, but it does require estimations regarding the metabolic rate. For patients with unusual metabolic rates (e.g., due to hypothermia or systemic inflammation), the estimated cardiac output may be inaccurate.
• Note that there are numerous factors which affect the mixed venous oxygen saturation. Random flux in these factors may cause the mixed venous oxygen saturation to vary over time. Avoid assuming that changes in the mixed venous oxygen saturation necessarily reflects an improvement or decrement in the cardiac output. 🌊
• A normal mixed venous oxygen saturation might be ~65-80%.

decision to insert a PA catheter 

Is a pulmonary artery catheter (pac) helpful.

• Hemodynamic assessment can generally be made non-invasively as described above. Furthermore, high-quality echocardiographic images with doppler can provide substantial hemodynamic information (e.g. cardiac output based on the velocity-time integral). ( 28595621 )
• [1] PA catheterization is an invasive procedure which carries risk of pneumothorax, line infection, arrhythmia, pulmonary artery perforation, and heart block.
• [2] PA catheterization will always reveal abnormal numbers, but it's unknown what we should do with this data. ( 7555127 ) Specifically, there is no defined goal for cardiac output or systemic vascular resistance. A cardiac index which may be adequate for one patient will leave another patient in cardiogenic shock.
• [3] PA catheterization encourages fluid management based on static filling pressures. Unfortunately, these pressures don't not predict fluid-responsiveness . ( 24286266 )
• [4] Numerous studies have failed to show benefit from Swan-Ganz catheterization both in critically ill patients overall and also specifically in heart failure patients. ( 14645314 , 12510037 , 16714768 , 16084255 ) The ESCAPE trial, a multicenter RCT in heart failure, showed that Swan-Ganz catheterization increased adverse events without offering benefit. ( 16204662 )
• [5] Over time, there has been steady improvement in echocardiography. Meanwhile, physicians and nurses are becoming less skilled at insertion and troubleshooting of PA catheters. Altogether, this means that the added value of PA catheter beyond echocardiography is continuously declining. Given that the Swan-Ganz catheter had dubious value in its heyday (the 1990s), it's even less beneficial currently.
• [1] Documentation of hemodynamics to determine candidacy for cardiac transplantation or ventricular assist device.
• [2] Uncertain nature of shock with no alternative source of hemodynamic information (e.g., poor transthoracic echocardiographic windows and inability to perform a transesophageal echocardiogram).

contraindications to PA catheter insertion include :

• Bundle branch block (especially left bundle branch block), since PA catheterization may cause right bundle branch block. ( 30947630 )
• Arrhythmia or hyperkalemia (insertion may trigger arrhythmias).
• Risk of displacing other devices (e.g., transvenous pacemaker, pacemaker inserted within <1 month). ( 36017548 )
• Mechanical right heart valve, or status post tricuspid valve clip (TriClip).
• Significant stenosis of the tricuspid or pulmonic valves.
• Known thrombus or tumor in the RV or RA.

CT scan isn't generally used as a diagnostic test for heart failure. Consequently, we often don't think much about what heart failure looks like on CT scan. However, this becomes important, because heart failure may mimic a variety of other disorders on CT scan.

#1/3: CT scan findings in heart failure

Direct findings reflective of hydrostatic pulmonary edema .

• Kerley B-lines.
• Thickening of the interlobar fissures (may be more easily discernible on chest X-ray).
• Initially: GGO (ground glass opacities).
• Severe edema may eventually cause bilateral consolidation .
• Central (“batwing”) distribution tends to occur in acute left ventricular failure, or renal failure. (Muller 2019)
• The presence of bilateral effusions may be especially suggestive of heart failure.

indirect findings which may be seen (depending on the etiology):

• Left ventricular dilation suggests chronic systolic heart failure.
• Left atrial dilation may occur with various etiologies of chronic left ventricular failure (including systolic or diastolic dysfunction).
• Engorgement of the inferior vena cava.

#2/3: radiologic findings in sympathetic crashing acute pulmonary edema (SCAPE) 

• Normally, interstitial pulmonary edema (i.e., septal thickening) occurs early and precedes the development of alveolar edema (i.e., ground glass opacities). Thus, ground glass opacities should be accompanied by septal thickening.
• Very abrupt pulmonary edema may produce ground glass opacities without septal thickening . This occurs if alveolar filling rapidly occurs, before enough time has passed for interstitial edema to develop. (Fishman 2023)

#3/3: asymmetric pulmonary edema 

causes of asymmetric pulmonary edema

• (1) Patient sleeps on their side, creating a gravitational gradient.
• (2) Underlying parenchymal lung disease (e.g., due to asymmetric COPD or sarcoidosis).
• Usually right-sided (may involve upper right, middle/lower right, or entire right side).
• Rarely, left-sided pulmonary edema can occur. ( 36566029 )
• Pulmonary vein stenosis following AF ablation.
• Compression by aortic dissection, tumor, or granulomatous infection. ( 36566029 )

radiological differential diagnosis

Causes of hydrostatic pulmonary edema include:.

• Systolic or diastolic dysfunction.
• Valvular heart disease.
• Iatrogenic fluid administration.
• Renal failure (often in combination with heart failure).
• Fibrosing mediastinitis.
• Status post AF ablation.
• Pulmonary vein compression by malignancy.
• Pulmonary veno-occlusive disease (PVOD).
• Neurogenic pulmonary edema . 📖

heart failure mimics on CT scan 

• (1) Findings suggestive of heart failure (e.g., septal thickening, pleural effusions, ground glass opacities).
• Normal left atrial size. 📖
• Age and/or clinical context inconsistent with heart failure.
• Acute heart failure (left atrium has not yet dilated, for example due to acute valvular regurgitation).
• Hantavirus.
• Pneumocystis jirovecii pneumonia.
• AEP (acute eosinophilic pneumonia).
• Pulmonary veno-occlusive disease (suggested by findings of pulmonary hypertension).
• Pulmonary vein stenosis s/p atrial fibrillation ablation.
• Lymphangitic carcinomatosis.
• Full differential diagnosis of septal thickening: 📖
• Other causes of hydrostatic pulmonary edema are listed above ☝️.

Follow us on iTunes

The podcast episode.

Want to Download the Episode? Right Click Here and Choose Save-As

To keep this page small and fast, questions & discussion about this post can be found on another page here .

• Failure to identify a patient who is cold and wet (Forrester class IV). These patients may not look terrible, but they have cardiogenic shock and generally require ICU admission.
• Treatment plan that focuses on a single intervention (e.g. diuresis), without optimizing other aspects of the patient (e.g. afterload reduction).
• Delayed management of respiratory distress (e.g. with BiPAP, effusion drainage, or intubation).
• Application of an outpatient-style management (e.g. beta-blocker and ACEi/ARB initiation) in a critically ill patient with cardiogenic shock.

Guide to emoji hyperlinks

• 00790191 Forrester JS, Diamond G, Chatterjee K, Swan HJ. Medical therapy of acute myocardial infarction by application of hemodynamic subsets (first of two parts). N Engl J Med. 1976 Dec 9;295(24):1356-62. doi: 10.1056/NEJM197612092952406 [ PubMed ]
• 03520315 Cohn JN, Archibald DG, Ziesche S, Franciosa JA, Harston WE, Tristani FE, Dunkman WB, Jacobs W, Francis GS, Flohr KH, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study. N Engl J Med. 1986 Jun 12;314(24):1547-52. doi: 10.1056/NEJM198606123142404 [ PubMed ]
• 07555127 Bartlett RH. Alice in intensiveland. Being an essay on nonsense and common sense in the ICU, after the manner of Lewis Carroll. Chest. 1995 Oct;108(4):1129-39. doi: 10.1378/chest.108.4.1129 [ PubMed ]
• 10460813 Hochman JS, Sleeper LA, Webb JG, Sanborn TA, White HD, Talley JD, Buller CE, Jacobs AK, Slater JN, Col J, McKinlay SM, LeJemtel TH. Early revascularization in acute myocardial infarction complicated by cardiogenic shock. SHOCK Investigators. Should We Emergently Revascularize Occluded Coronaries for Cardiogenic Shock. N Engl J Med. 1999 Aug 26;341(9):625-34. doi: 10.1056/NEJM199908263410901 [ PubMed ]
• 11911756 Cuffe MS, Califf RM, Adams KF Jr, Benza R, Bourge R, Colucci WS, Massie BM, O'Connor CM, Pina I, Quigg R, Silver MA, Gheorghiade M; Outcomes of a Prospective Trial of Intravenous Milrinone for Exacerbations of Chronic Heart Failure (OPTIME-CHF) Investigators. Short-term intravenous milrinone for acute exacerbation of chronic heart failure: a randomized controlled trial. JAMA. 2002 Mar 27;287(12):1541-7. doi: 10.1001/jama.287.12.1541 [ PubMed ]
• 12510037 Sandham JD, Hull RD, Brant RF, Knox L, Pineo GF, Doig CJ, Laporta DP, Viner S, Passerini L, Devitt H, Kirby A, Jacka M; Canadian Critical Care Clinical Trials Group. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med. 2003 Jan 2;348(1):5-14. doi: 10.1056/NEJMoa021108 [ PubMed ]
• 14645314 Richard C, Warszawski J, Anguel N, Deye N, Combes A, Barnoud D, Boulain T, Lefort Y, Fartoukh M, Baud F, Boyer A, Brochard L, Teboul JL; French Pulmonary Artery Catheter Study Group. Early use of the pulmonary artery catheter and outcomes in patients with shock and acute respiratory distress syndrome: a randomized controlled trial. JAMA. 2003 Nov 26;290(20):2713-20. doi: 10.1001/jama.290.20.2713 [ PubMed ]
• 16084255 Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D, Brampton W, Williams D, Young D, Rowan K; PAC-Man study collaboration. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet. 2005 Aug 6-12;366(9484):472-7. doi: 10.1016/S0140-6736(05)67061-4 [ PubMed ]
• 16204662 Binanay C, Califf RM, Hasselblad V, O'Connor CM, Shah MR, Sopko G, Stevenson LW, Francis GS, Leier CV, Miller LW; ESCAPE Investigators and ESCAPE Study Coordinators. Evaluation study of congestive heart failure and pulmonary artery catheterization effectiveness: the ESCAPE trial. JAMA. 2005 Oct 5;294(13):1625-33. doi: 10.1001/jama.294.13.1625 [ PubMed ]
• 16714768 National Heart, Lung, and Blood Institute Acute Respiratory Distress Syndrome (ARDS) Clinical Trials Network, Wheeler AP, Bernard GR, Thompson BT, Schoenfeld D, Wiedemann HP, deBoisblanc B, Connors AF Jr, Hite RD, Harabin AL. Pulmonary-artery versus central venous catheter to guide treatment of acute lung injury. N Engl J Med. 2006 May 25;354(21):2213-24. doi: 10.1056/NEJMoa061895 [ PubMed ]
• 17395053 Travers B, O'Loughlin C, Murphy NF, Ryder M, Conlon C, Ledwidge M, McDonald K. Fluid restriction in the management of decompensated heart failure: no impact on time to clinical stability. J Card Fail. 2007 Mar;13(2):128-32. doi: 10.1016/j.cardfail.2006.10.012 [ PubMed ]
• 17447137 Hollenberg SM. Vasodilators in acute heart failure. Heart Fail Rev. 2007 Jun;12(2):143-7. doi: 10.1007/s10741-007-9017-2 [ PubMed ]
• 18158484 Elkayam U, Janmohamed M, Habib M, Hatamizadeh P. Vasodilators in the management of acute heart failure. Crit Care Med. 2008 Jan;36(1 Suppl):S95-105. doi: 10.1097/01.CCM.0000297161.41559.93 [ PubMed ]
• 19723460 Opasich C, Cioffi G, Gualco A. Nitroprusside in decompensated heart failure: what should a clinician really know? Curr Heart Fail Rep. 2009 Sep;6(3):182-90. doi: 10.1007/s11897-009-0026-4 [ PubMed ]
• 20200382 De Backer D, Biston P, Devriendt J, Madl C, Chochrad D, Aldecoa C, Brasseur A, Defrance P, Gottignies P, Vincent JL; SOAP II Investigators. Comparison of dopamine and norepinephrine in the treatment of shock. N Engl J Med. 2010 Mar 4;362(9):779-89. doi: 10.1056/NEJMoa0907118 [ PubMed ]
• 21878431 Patel MR, Smalling RW, Thiele H, Barnhart HX, Zhou Y, Chandra P, Chew D, Cohen M, French J, Perera D, Ohman EM. Intra-aortic balloon counterpulsation and infarct size in patients with acute anterior myocardial infarction without shock: the CRISP AMI randomized trial. JAMA. 2011 Sep 28;306(12):1329-37. doi: 10.1001/jama.2011.1280 [ PubMed ]
• 22920912 Thiele H, Zeymer U, Neumann FJ, Ferenc M, Olbrich HG, Hausleiter J, Richardt G, Hennersdorf M, Empen K, Fuernau G, Desch S, Eitel I, Hambrecht R, Fuhrmann J, Böhm M, Ebelt H, Schneider S, Schuler G, Werdan K; IABP-SHOCK II Trial Investigators. Intraaortic balloon support for myocardial infarction with cardiogenic shock. N Engl J Med. 2012 Oct 4;367(14):1287-96. doi: 10.1056/NEJMoa1208410 [ PubMed ]
• 23131078 Bart BA, Goldsmith SR, Lee KL, Givertz MM, O'Connor CM, Bull DA, Redfield MM, Deswal A, Rouleau JL, LeWinter MM, Ofili EO, Stevenson LW, Semigran MJ, Felker GM, Chen HH, Hernandez AF, Anstrom KJ, McNulty SE, Velazquez EJ, Ibarra JC, Mascette AM, Braunwald E; Heart Failure Clinical Research Network. Ultrafiltration in decompensated heart failure with cardiorenal syndrome. N Engl J Med. 2012 Dec 13;367(24):2296-304. doi: 10.1056/NEJMoa1210357 [ PubMed ]
• 23689381 Aliti GB, Rabelo ER, Clausell N, Rohde LE, Biolo A, Beck-da-Silva L. Aggressive fluid and sodium restriction in acute decompensated heart failure: a randomized clinical trial. JAMA Intern Med. 2013 Jun 24;173(12):1058-64. doi: 10.1001/jamainternmed.2013.552 [ PubMed ]
• 24286266 Marik PE. Obituary: pulmonary artery catheter 1970 to 2013. Ann Intensive Care. 2013 Nov 28;3(1):38. doi: 10.1186/2110-5820-3-38 [ PubMed ]
• 26948252 Bihari S, Holt AW, Prakash S, Bersten AD. Addition of indapamide to frusemide increases natriuresis and creatinine clearance, but not diuresis, in fluid overloaded ICU patients. J Crit Care. 2016 Jun;33:200-6. doi: 10.1016/j.jcrc.2016.01.017 [ PubMed ]
• 27810347 Ouweneel DM, Eriksen E, Sjauw KD, van Dongen IM, Hirsch A, Packer EJ, Vis MM, Wykrzykowska JJ, Koch KT, Baan J, de Winter RJ, Piek JJ, Lagrand WK, de Mol BA, Tijssen JG, Henriques JP. Percutaneous Mechanical Circulatory Support Versus Intra-Aortic Balloon Pump in Cardiogenic Shock After Acute Myocardial Infarction. J Am Coll Cardiol. 2017 Jan 24;69(3):278-287. doi: 10.1016/j.jacc.2016.10.022 [ PubMed ]
• 28595621 Mercado P, Maizel J, Beyls C, Titeca-Beauport D, Joris M, Kontar L, Riviere A, Bonef O, Soupison T, Tribouilloy C, de Cagny B, Slama M. Transthoracic echocardiography: an accurate and precise method for estimating cardiac output in the critically ill patient. Crit Care. 2017 Jun 9;21(1):136. doi: 10.1186/s13054-017-1737-7 [ PubMed ]
• 28602370 Dooley DJ, Lam PH, Ahmed A, Aronow WS. The Role of Positive Inotropic Drugs in the Treatment of Older Adults with Heart Failure and Reduced Ejection Fraction. Heart Fail Clin. 2017 Jul;13(3):527-534. doi: 10.1016/j.hfc.2017.02.008 [ PubMed ]
• 28923988 van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, Kilic A, Menon V, Ohman EM, Sweitzer NK, Thiele H, Washam JB, Cohen MG; American Heart Association Council on Clinical Cardiology; Council on Cardiovascular and Stroke Nursing; Council on Quality of Care and Outcomes Research; and Mission: Lifeline. Contemporary Management of Cardiogenic Shock: A Scientific Statement From the American Heart Association. Circulation. 2017 Oct 17;136(16):e232-e268. doi: 10.1161/CIR.0000000000000525 [ PubMed ]
• 29478105 Patel H, Nazeer H, Yager N, Schulman-Marcus J. Cardiogenic Shock: Recent Developments and Significant Knowledge Gaps. Curr Treat Options Cardiovasc Med. 2018 Feb 24;20(2):15. doi: 10.1007/s11936-018-0606-2 [ PubMed ]
• 29655828 Keebler ME, Haddad EV, Choi CW, McGrane S, Zalawadiya S, Schlendorf KH, Brinkley DM, Danter MR, Wigger M, Menachem JN, Shah A, Lindenfeld J. Venoarterial Extracorporeal Membrane Oxygenation in Cardiogenic Shock. JACC Heart Fail. 2018 Jun;6(6):503-516. doi: 10.1016/j.jchf.2017.11.017 [ PubMed ]
• 29796916 Teboul JL, Cecconi M, Scheeren TWL. Is there still a place for the Swan-Ganz catheter? No. Intensive Care Med. 2018 Jun;44(6):957-959. doi: 10.1007/s00134-018-5110-3 [ PubMed ]
• 29806100 Crespo-Leiro MG, Metra M, Lund LH, Milicic D, Costanzo MR, Filippatos G, Gustafsson F, Tsui S, Barge-Caballero E, De Jonge N, Frigerio M, Hamdan R, Hasin T, Hülsmann M, Nalbantgil S, Potena L, Bauersachs J, Gkouziouta A, Ruhparwar A, Ristic AD, Straburzynska-Migaj E, McDonagh T, Seferovic P, Ruschitzka F. Advanced heart failure: a position statement of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2018 Nov;20(11):1505-1535. doi: 10.1002/ejhf.1236 [ PubMed ]
• 29907274 Chakravarthy M, Tsukashita M, Murali S. A Targeted Management Approach to Cardiogenic Shock. Crit Care Clin. 2018 Jul;34(3):423-437. doi: 10.1016/j.ccc.2018.03.009 [ PubMed ]
• 30072134 Bellumkonda L, Gul B, Masri SC. Evolving Concepts in Diagnosis and Management of Cardiogenic Shock. Am J Cardiol. 2018 Sep 15;122(6):1104-1110. doi: 10.1016/j.amjcard.2018.05.040 [ PubMed ]
• 30586755 Schrage B, Ibrahim K, Loehn T, Werner N, Sinning JM, Pappalardo F, Pieri M, Skurk C, Lauten A, Landmesser U, Westenfeld R, Horn P, Pauschinger M, Eckner D, Twerenbold R, Nordbeck P, Salinger T, Abel P, Empen K, Busch MC, Felix SB, Sieweke JT, Møller JE, Pareek N, Hill J, MacCarthy P, Bergmann MW, Henriques JPS, Möbius-Winkler S, Schulze PC, Ouarrak T, Zeymer U, Schneider S, Blankenberg S, Thiele H, Schäfer A, Westermann D. Impella Support for Acute Myocardial Infarction Complicated by Cardiogenic Shock. Circulation. 2019 Mar 5;139(10):1249-1258. doi: 10.1161/CIRCULATIONAHA.118.036614 [ PubMed ]
• 30947630 Vahdatpour C, Collins D, Goldberg S. Cardiogenic Shock. J Am Heart Assoc. 2019 Apr 16;8(8):e011991. doi: 10.1161/JAHA.119.011991 [ PubMed ]
• 31262417 Wilcox SR. Nonischemic Causes of Cardiogenic Shock. Emerg Med Clin North Am. 2019 Aug;37(3):493-509. doi: 10.1016/j.emc.2019.03.007 [ PubMed ]
• 31374209 Fryer ML, Balsam LB. Mechanical Circulatory Support for Cardiogenic Shock in the Critically Ill. Chest. 2019 Nov;156(5):1008-1021. doi: 10.1016/j.chest.2019.07.009 [ PubMed ]
• 31838029 Cox ZL, Hung R, Lenihan DJ, Testani JM. Diuretic Strategies for Loop Diuretic Resistance in Acute Heart Failure: The 3T Trial. JACC Heart Fail. 2020 Mar;8(3):157-168. doi: 10.1016/j.jchf.2019.09.012 [ PubMed ]
• 32280416 Kim JH, Sunkara A, Varnado S. Management of Cardiogenic Shock in a Cardiac Intensive Care Unit. Methodist Debakey Cardiovasc J. 2020 Jan-Mar;16(1):36-42. doi: 10.14797/mdcj-16-1-36 [ PubMed ]
• 32469155 Chioncel O, Parissis J, Mebazaa A, Thiele H, Desch S, Bauersachs J, Harjola VP, Antohi EL, Arrigo M, Gal TB, Celutkiene J, Collins SP, DeBacker D, Iliescu VA, Jankowska E, Jaarsma T, Keramida K, Lainscak M, Lund LH, Lyon AR, Masip J, Metra M, Miro O, Mortara A, Mueller C, Mullens W, Nikolaou M, Piepoli M, Price S, Rosano G, Vieillard-Baron A, Weinstein JM, Anker SD, Filippatos G, Ruschitzka F, Coats AJS, Seferovic P. Epidemiology, pathophysiology and contemporary management of cardiogenic shock – a position statement from the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2020 Aug;22(8):1315-1341. doi: 10.1002/ejhf.1922 [ PubMed ]
• 33967208 Jentzer JC, Tabi M, Burstein B. Managing the first 120 min of cardiogenic shock: from resuscitation to diagnosis. Curr Opin Crit Care. 2021 Aug 1;27(4):416-425. doi: 10.1097/MCC.0000000000000839 [ PubMed ]
• 34347952 Mathew R, Di Santo P, Jung RG, Marbach JA, Hutson J, Simard T, Ramirez FD, Harnett DT, Merdad A, Almufleh A, Weng W, Abdel-Razek O, Fernando SM, Kyeremanteng K, Bernick J, Wells GA, Chan V, Froeschl M, Labinaz M, Le May MR, Russo JJ, Hibbert B. Milrinone as Compared with Dobutamine in the Treatment of Cardiogenic Shock. N Engl J Med. 2021 Aug 5;385(6):516-525. doi: 10.1056/NEJMoa2026845 [ PubMed ]

The Internet Book of Critical Care is an online textbook written by Josh Farkas ( @PulmCrit ), an associate professor of Pulmonary and Critical Care Medicine at the University of Vermont.

We are the EMCrit Project , a team of independent medical bloggers and podcasters joined together by our common love of cutting-edge care, iconoclastic ramblings, and FOAM.

Resus Leadership Academy

Subscribe by Email

Insert/edit link.

Enter the destination URL

Or link to existing content

• Search Menu
• Sign in through your institution
• Advance Articles
• Editor's Choice
• Braunwald's Corner
• ESC Guidelines
• EHJ Dialogues
• Issue @ a Glance Podcasts
• CardioPulse
• Weekly Journal Scan
• European Heart Journal Supplements
• Year in Cardiovascular Medicine
• Asia in EHJ
• Most Cited Articles
• ESC Content Collections
• Author Guidelines
• Submission Site
• Why publish with EHJ?
• Open Access Options
• Submit from medRxiv or bioRxiv
• Author Resources
• Self-Archiving Policy
• Read & Publish
• Advertising and Corporate Services
• Advertising
• Reprints and ePrints
• Sponsored Supplements
• Journals Career Network
• About European Heart Journal
• Editorial Board
• About the European Society of Cardiology
• ESC Publications
• War in Ukraine
• ESC Membership
• ESC Journals App
• Developing Countries Initiative
• Dispatch Dates
• Terms and Conditions
• Journals on Oxford Academic
• Books on Oxford Academic

Article Contents

Introduction, therapeutic management and treatments of acute heart failure, future directions for research on acute heart failure pharmacological treatments, supplementary data, declarations, data availability.

• < Previous

Acute heart failure: current pharmacological treatment and perspectives

• Article contents
• Figures & tables
• Supplementary Data

Benjamin Deniau, Maria Rosa Costanzo, Karen Sliwa, Ayu Asakage, Wilfried Mullens, Alexandre Mebazaa, Acute heart failure: current pharmacological treatment and perspectives, European Heart Journal , Volume 44, Issue 44, 21 November 2023, Pages 4634–4649, https://doi.org/10.1093/eurheartj/ehad617

• Permissions Icon Permissions

Acute heart failure (AHF) represents the most frequent cause of unplanned hospital admission in patients older than 65 years. Symptoms and clinical signs of AHF (e.g. dyspnoea, orthopnoea, oedema, jugular vein distension, and variation of body weight) are mostly related to systemic venous congestion secondary to various mechanisms including extracellular fluids, increased ventricular filling pressures, and/or auto-transfusion of blood from the splanchnic into the pulmonary circulation. Thus, the initial management of AHF patients should be mostly based on decongestive therapies on admission followed, before discharge, by rapid implementation of guideline-directed oral medical therapies for heart failure. The therapeutic management of AHF requires the identification and rapid diagnosis of the disease, the diagnosis of the cause (or triggering factor), the evaluation of severity, the presence of comorbidities, and, finally, the initiation of a rapid treatment. The most recent guidelines from ESC and ACC/AHA/HFSA have provided updated recommendations on AHF management. Recommended pharmacological treatment for AHF includes diuretic therapy aiming to relieve congestion and achieve optimal fluid status, early and rapid initiation of oral therapies before discharge combined with a close follow-up. Non-pharmacological AHF management requires risk stratification in the emergency department and non-invasive ventilation in case of respiratory failure. Vasodilators should be considered as initial therapy in AHF precipitated by hypertension. On the background of recent large randomized clinical trials and international guidelines, this state-of-the-art review describes current pharmacological treatments and potential directions for future research in AHF.

Schematic representation of management of acute heart failure (AHF) patients from hospital admission to post-discharge period. Assessment of congestion includes clinical signs and symptoms (fatigue, dyspnoea, orthopnoea, oedema, and body weight), ultrasound assessment (lung, pleura, inferior vena cava, and ascites), and biology (natriuretic peptides and haematocrit). i.v., intravenous.

Acute heart failure (AHF), defined as the new onset or recurrence of signs of heart failure (HF), represents the most frequent cause of unplanned hospital admission, worldwide, in patients older than 65. 1 Acute heart failure symptoms include dyspnoea, fatigue, pulmonary rales, peripheral oedema, and distended jugular veins at physical examination. Two clinical situations are described in AHF patients as follows: (i) the very frequent ‘acutely decompensated HF’, where symptoms of congestion appear and/or worsen in patients with known history of HF, and (ii) de novo AHF characterized by the occurrence of symptoms of congestion in patients without history of HF. 2 , 3 Symptoms and clinical signs of AHF are mostly related to systemic venous congestion secondary to various mechanisms including accumulation of extracellular fluids, increased ventricular filling pressures, and/or auto-transfusion of blood from the splanchnic into the pulmonary circulation. 4 Thus, the initial management of AHF patients is mostly based on decongestive therapies on admission which should be followed, before discharge, by rapid implementation of guideline-directed oral medical therapies for HF. 5 Despite significant scientific and clinical progress occurring in recent years, AHF remains associated with poor outcomes, including very high readmission rates and/or high mortality.

This state-of-the-art review describes current pharmacological treatments and perspectives in AHF. It will however not cover cardiogenic shock, the less frequent but most severe form of AHF, defined as low blood pressure associated with low cardiac output, altered end-organ perfusion, which requires specific treatment 6 , 7 and is outside the scope of the present work.

Epidemiology and prevalence

Acute heart failure is a major and global public health issue, and the pathophysiologic abnormalities occurring with HF significantly impact patient’s quality of life. The epidemiology of HF has been the subject of large epidemiological studies (with cardiac measurements largely derived from Caucasian populations) and pivotal clinical trials [e.g. the Prospective Comparison of ARNI with ACEI to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial 8 ]. Even if a comprehensive picture of acute and chronic HF occurring globally cannot be achieved, it is important to note the enormous burden the syndrome imposes on the patients, their families, and the health care systems. Global data on AHF are limited, mainly due to the differential coding of the syndrome precluding an exact estimation of the prevalence and comparison between regions. Each year, in USA and Europe, 1 million patients in both continents are hospitalized with the diagnosis of AHF. 2 , 3 The prevalence of AHF appears to be heterogeneous across the world, and it may be higher in countries where chronic HF is more prevalent. 2 , 3 Despite the differences in diagnostic criteria, most studies estimated that over half of all HF patients in the general population have a preserved left ventricular ejection fraction (LVEF) and that the proportion of this HF phenotype is increasing due to the aging of the population and the increasing prevalence of cardiometabolic disorders. 9 In-hospital mortality of AHF reaches 4%, and rises to 10% within 60 to 90 days after hospital discharge and further increases to 25%–30% at 1 year. 10–14 A recent large meta-analysis demonstrated a steady decrease in mortality related to AHF over the last three decades while readmissions remain unacceptably high (10%–30% at 30 days and 46% at 1 year) with similar results in surveys and in trials. 15 Notably, Kimmoun et al. 15 showed that HF readmissions remain high in the USA and Asia but continue to decrease in Europe.

Congestion in acute heart failure

Systemic venous congestion is the central feature of AHF and due to redistribution of blood from the splanchnic to the pulmonary circulation and/or to abnormal intravascular and interstitial fluid accumulation. 16 , 17 Systemic venous congestion may be associated with hypoperfusion due to poor cardiac function but can also occur in many patients with preserved cardiac output and/or LVEF. Systemic congestion is the pathophysiological cornerstone of AHF leading to organ dysfunction, including the kidneys, liver, lungs, and gut. Organ dysfunction during AHF is associated with an increased risk of death. 18 Impairment of renal function in AHF is often secondary to increased central venous pressure leading to renal venous hypertension and higher renal interstitial pressure resulting in decreased glomerular filtration rate and oliguria. Increased central venous pressure also contributes to liver congestion which must be suspected in case of abdominal pain, elevation of alkaline phosphatase, bilirubin, and/or γ-glutamyl transferase. 19 Hypoxic hepatitis can be observed in the most severe form of AHF, particularly in the setting of cardiogenic shock. Elevation of ventricular filling pressures leads to increased ventricular wall tension, myocardial stretch, and progressive worsening in cardiac contractility. 1 Elevation of the filling pressure in the left atrium increases the hydrostatic pressure in the upstream pulmonary capillaries increasing fluid filtration rate to the pulmonary interstitium to the alveoli. Finally, the drainage capacities of the lymphatic system of the pleural cavities are rapidly exceeded by the elevation of the venous pressure, causing fluid shifts to the pleural cavities which manifest as pleural effusions. Finally, high venous central pressure leads to increased abdominal pressure and to splanchnic congestion with the direct consequence of alteration of intestinal permeability, impaired nutrient absorption and malnutrition, increased oxygen gradient from the base to the apex of the villi causing epithelial injury, which results in extravasation of endotoxins which enhance inflammatory milieu and the progression to end-organ dysfunction. 20 , 21

Clinical tools

A universally accepted diagnostic algorithm for quantification of congestion and identification of precise therapeutic targets is lacking. However, it is known that unresolved congestion, occurring in 40% of patients at hospital discharge, is an independent predictor of poor outcomes. 22   Figure 1 proposes a contemporary way to assess congestion measured by clinical variables, biomarkers, and imaging. Signs and symptoms of congestion are late manifestations of increased cardiac filling pressures. 23

Assessment of congestion (clinical, biology, and ultrasonography). Lung ultrasound and quantification of inferior vena cava diameters through respiratory cycles. ( A and B ) Two techniques for quantifying pulmonary congestion using lung ultrasound (LUS). With the 28 scanning-site LUS technique, a precise quantification of extravascular lung water can be achieved; 16 to 30 comets (also called B-lines) detected in the entire lung are evocative of moderate pulmonary congestion, and >30 comets are evocative of severe pulmonary congestion. The eight-region LUS technique is a semiquantitative technique. A positive region is defined by the presence of ≥3 B-lines in a longitudinal plane between two ribs and ≥2 positive regions on each lung, which suggest significant pulmonary congestion. Lung ultrasound lasts <5 min using both techniques. ( C ) Upper images: normally aerated lung and regular interstitium, the only image that can be visualized below the pleural line is the reflection of the chest wall from the probe to the parietal pleura (A lines), or a few vertical artefacts can be detected (images with one and two lung comets). ( C ) Bottom images: progressive extravascular lung water accumulation as shown by the increasing number of lung comets. Right panels: right atrial pressures can be assessed with IVC diameters as shown in the upper and lower right panels. Reproduced with permission from Girerd et al. 16

The use of natriuretic peptides (NPs) to assess volume status and guide decongestive therapies is useful, though fluid overload may not the sole cause of increased levels of these biomarkers, 24 , 25 particularly in patients with impaired renal function. Fluid removal is often associated with reduction of plasma NP levels with a decrease >30% at Day 5 being a good prognostic marker. 26 Serum creatinine (sCr) is the most widely used biomarker to guide fluid removal due to the belief that its level reflects both renal filtration function and tubular status. 27 , 28 Of note, sCr may be altered in the days and weeks following hospitalization for AHF due to many mechanisms including diuretic therapies; it often returns eventually to baseline values and should not be considered as an indicator of poor prognosis. 29–32 Therefore, some suggest to use the term of ‘permissive hypercreatininemia’ in HF. 33 Therefore, the terms worsening renal function, acute kidney injury, and increased sCr cannot be used interchangeably.

Contemporary indices of congestion

In daily practice, congestion may be assessed by clinical signs and symptoms, imaging, and biological markers. 34 Few additional tools to assess congestion and guide the use of ‘decongestive’ therapies are yet available. A comprehensive echocardiogram is the gold standard for evaluating volume status and left ventricular (LV) filling pressures at baseline and before discharge. The analysis of LV filling pressure by transmitral flow and early diastolic tissue wave (E/eʹ) ratio provides useful details on LV pressure and volume overload. The diameter of the inferior vena cava (IVC) is typically measured from the long-axis subxiphoid view between 5 and 30 mm from the IVC and right atrial junction during end-expiration and after sniff ( Figure 1 ). Inferior vena cava diameter and per cent change during inspiration are correlated with right atrial pressure. 35 The accuracy of IVC measurements is influenced by the presence of a prominent Eustachian valve, patient’s position, and operator’s experience ( Figure 1 ). Despite its limitations, echocardiography outperforms congestion scores for the prediction of short- and medium-term readmissions. 36 , 37

Direct blood volume (BV) analysis can be done using the indicator-dilution method via the standardized technique using intravenous injection of a known dose of I-131 labelled albumin. 38 The unknown variable (BV) can then be measured using a known concentration of the injectate in a known volume and the concentration of the injectate in the unknown volume to be calculated. 39 A nuclear medicine technique that can accurately measure a radioisotope tracer concentration in fluid samples using the indicator-dilution technique was approved by the Food and Drug Administration (FDA) in 1998 and can provide BV results in ≤90 min (BVA-100 blood volume analyzer; Daxor Corporation Inc., New York, NY). Multiple studies have confirmed that the BVA-100 can assess BV and determine the causes of its abnormalities. 40–42 Although BVA is user-friendly and can be repeated, independent validation in randomized controlled trials to demonstrate incremental benefit and favourable cost–benefit ratio is needed.

Extravascular lung water (ELW) reflects the water content of the lung interstitium, determined by lung permeability and cardiac filling pressures. Lung ultrasound (LUS) is increasingly used for ELW assessment through the analysis of B-line artefacts ( Figure 1 ). 43 According to a recent meta-analysis, three or more B-lines in two or more bilateral lung zones can be considered diagnostic for pulmonary oedema (sensitivity, 94%; specificity, 92%). 44 A B-line score cut-off ≥ 15 is significantly correlated with clinical congestion scores, E/Eʹ ratio, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels, increased LV filling pressure, larger LV volumes, LV mass index, left atrial volume index, tricuspid regurgitation velocity, and estimated systolic pulmonary artery pressure (PAP). 45

The CardioMEMS™ PAP sensor was tested in the CHAMPION trial (CardioMEMS™ Heart Sensor Allows Monitoring of Pressure to Improve Outcomes in Class III Heart Failure). 46 The PAP-guided HF management was associated with a 28% and 37% fewer HF hospitalization after 6 and 15 months, respectively, compared to clinically-driven therapy. 46 The benefits of PAP-guided therapy occurred regardless of LVEF and have been replicated in clinical practice. 47–49 In patients implanted with the CardioMEMS device, PAP can be measured at least daily in both outpatient and hospital settings. The pre-COVID-19 impact analysis of the Hemodynamic-GUIDEd Management of Heart Failure (GUIDE-HF), a multicentre, prospective, single-blind study where 1000 New York Heart Association (NYHA) class II–IV HF patients with either elevated NT-proBNP [or B-type natriuretic peptide (BNP)] and/or a prior HF hospitalization were randomized to either PAP-based HF therapy or standard care, indicated a benefit of PAP-guided management on the primary outcome, primarily driven by lower HF hospitalization rates. 44

In HF patients with cardiac implantable electronic devices (CIEDs) from the manufacturer Boston Scientific (Boston, MA, USA), the MultiSENSE (Multisensor Chronic Evaluation in Ambulatory Heart Failure Patients) study showed that the HeartLogic multiparameter index, combining heart sounds (S1 and S3), thoracic impedance, respiration, heart rate, and activity, emerged as a timely predictor of impending HF decompensation 50 with a warning time of ∼34 days. In addition to MultiSENSE, other studies have been conducted for risk stratification of HF patients based on combinations of data obtainable from CIEDs. 51 However, limitations of the HeartLogic algorithm include inability to stratify the risk of HF patients with preserved LVEF and of those lacking an indication for CIEDs. Ongoing research efforts are focused on the development of wearable devices that can detect non-invasive parameters similar to those collected by the CIEDs to enable the timely implementation of therapies that can effectively prevent HF decompensation.

In general, the therapeutic management of AHF is based on the identification and rapid diagnosis of the disease, the diagnosis of the cause (or triggering factor), the evaluation of the severity, the existence of comorbidities and finally, the initiation of a rapid treatment. Latest guidelines from ESC and ACC/AHA/HFSA have provided updated recommendations on AHF management, summarized in Table 1 . 49 , 52

Head to head comparison between recommendations for the initial treatment of acute heart failure recommended by ESC 52 and ACC/AHA/HFSA 53 with class (green: is recommended or is indicated, orange: should be considered, red: is not recommended) and level (A: data derived from multiple randomized clinical trials or meta-analyses, B: data derived from a single randomized clinical trial or large non-randomized studies, C: consensus of opinion of the experts and/or small studies, retrospective studies, registries) of recommendations

AHF, acute heart failure; B-NR, level B non-randomised; B-R, level B randomised; COR, class of recommendation; HF, heart failure; LOE, level of evidence; LMWH, low-molecular-weight heparin; SBP, systolic blood pressure; VTE, venous thromboembolism.

Treatment according to aetiology of acute heart failure

Management of AHF differs according to the conditions which have triggered it. As recommended by the 2021 ESC HF guidelines, an initial step of the management of AHF patients is to search for specific causes summarized under the CHAMPIT acronym as follows: acute coronary syndrome, hypertensive emergency, rapid arrhythmias or severe bradycardia/conduction disturbance, acute mechanical causes (e.g. pulmonary embolism), infection (e.g. myocarditis and endocarditis), and tamponade. 52 Other aetiologies, less frequent, include valvular disease, peri-partum cardiomyopathy, hypertensive disorders, and thyroid disease. Thus, specific aetiological therapies should be implemented as early as possible.

Decongestive therapies

The goal of decongestive therapies is to treat fluid overload and hopefully achieve optimal fluid status. Currently, diuretics are the mainstay of decongestive therapies. However, determination of the optimal diuretic strategy remains challenging especially when worsening renal function, diuretic resistance, and electrolyte disturbances occur. Thorough knowledge of the pharmacokinetics and—dynamics of diuretics are mandatory to use them effectively. 54 The site of action and cellular mechanisms of different diuretics are listed in Figure 2 .

Local and systemic action of diuretics. Reproduced with permission from Mullens et al. 54 HF, heart failure

Despite the use of intravenous loop diuretics, many patients are discharged with residual clinical signs of volume overload, a strong predictor of poor outcome. 1 , 55 Although sequential nephronal blockade has been suggested as a more effective decongestive strategy which can attenuate tubular adaptation to loop diuretics, convincing evidence of the optimal diuretic agents, dosing schedule, and route of administration is lacking. 52–54   Figure 3 shows the contemporary management and recommendations of 2022 AHA/ACC/HFSA guidelines on the use of diuretics as decongestive therapy in AHF. 53

Acute heart failure: ( A ) management and ( B ) recommendations for decongestive therapy to manage hyponatraemia. AVP, arginine vasopressin. Adapted from Verbrugge et al. 56 HF, heart failure

Diuretic response

Decrease in body weight, net fluid total loss, or total urinary output following administration of loop diuretics is defined as a favourable response to the diuretic and natriuretic effect of these medications. Diuretic resistance is defined as a failure to increase diuresis and natriuresis output to relieve volume overload, oedema, or congestion despite optimal doses of a loop diuretic. 57 , 58 Qualitatively, pathologic diuretic resistance can be defined as an unsatisfactory rate of diuresis/natriuresis despite an adequate diuretic regimen in a hypervolaemic patient. 59

Furthermore, diuretic response should always be interpreted considering the dose and type of the diuretic agent administered as well as the degree of volume overload and kidney function. Currently, net fluid output and changes in body weight are frequently used, though they only capture changes in total body water and not in extracellular sodium accumulation. Furthermore, body weight data are misleading as measurements are performed by different people, on different scales at variable time-points. Fluctuations in weight might also not represent changes in volume redistribution. 60

As the objective of diuretic therapy is to eliminate excessive sodium (and accompanying water), the measurement of urinary sodium content has experienced a renewed interest as a better indicator for diuretic response. 61–64 In addition to measuring sodium in a continuous urinary collection, a spot urine sample 1–2 h following loop diuretic administration has been shown to have an excellent correlation with total urine sodium output in a 6 h urine collection. 65 Therefore, this strategy might allow the clinician to determine loop diuretic response in a timely fashion, allowing for faster and more frequent adjustments in therapy. Despite persistent increased urinary volume output (diuresis), renal sodium output (natriuresis) diminishes over time, due to increased renal sodium reabsorption while facing low sodium intake. Therefore, increasingly hypotonic urine is produced during consecutive days of loop diuretic therapy, depending upon altered renal haemodynamics, differential substrate delivery (sodium and/or diuretics), neurohormonal factors, and structural kidney abnormalities, including arginine vasopressin action. The use of urinary sodium following a first administration of loop diuretics to guide diuretic therapy has now been incorporated in the European guidelines for the diagnosis and treatment of HF. 52

Diuretic utilization

Guidelines recommend the use of intravenous loop diuretics in AHF, as the gastrointestinal absorption of oral diuretics will be diminished in AHF due to bowel oedema. 52 , 54 Optimal dosing and timing of intravenous loop diuretics are of pivotal importance. Loop diuretics must achieve a threshold concentration at their renal site of action to induce effective natriuresis. 57 Over 95% of the loop diuretics are bound to albumin, do not undergo glomerular filtration, and reach their target site by active secretion from the blood into the urine by the organic acid transporters present in the proximal tubules. 66 Hypoalbuminaemia leads to a decreased secretion of loop diuretics into the tubules and reduces their diuretic effect. Afterwards, a log-linear increase in the dose is necessary to achieve the ceiling of urinary sodium excretion. Similarly, multiple administrations can cause additional natriuresis, as this increases the duration of time above a natriuretic threshold. These pharmacologic characteristics lead to the following recommendation in the ESC guidelines for the treatment of AHF 52 : (i) diuretic naïve patients with AHF should receive a dose of intravenous furosemide of at least 20–40 mg furosemide equivalent; (ii) higher doses should be considered in patient with pre-existing kidney dysfunction which is associated with a downward and rightward shift in the dose–response curve; and (iii) patients previously treated with oral diuretics are likely to require higher initial intravenous loop diuretic doses. An intravenous dose ranging between 400 and 600 mg furosemide vs. 10–15 mg bumetanide is generally considered as the maximal total daily dose as the diuretic ceiling effect is reached. 54 , 59 Generally, loop diuretics are given in multiple doses (two to three times daily). Intravenous loop diuretics should be administered as early as possible, since early institution of intravenous loop diuretic therapy could be associated with lower in-hospital mortality. 67 In the DOSE-AHF trial, no difference in improved global assessment of dyspnoea was seen between continuous infusion vs. bolus injection. 57 If bolus injections are given, these should be administered at least at 6 h intervals, to maximize the time the diuretic tubular concentration is adequate to trigger a natriuretic response.

A satisfactory diuretic response can be defined as a urine sodium content > 50–70 mEq/L at 2 h and/or by a urine output > 100–150 mL/h during the first 6 h 52 , 54 after administration. If there is an insufficient diuretic response, the loop diuretic dose should be doubled, with a repeated assessment of diuretic response. This strategy, based on early and frequent assessment of diuretic response, is currently being tested in two prospective randomized clinical trials. 68 , 69 Finally, a transient increased in sCr after initiation of decongestive therapy can be observed, which may not represent acute kidney injury but rather a haemodynamically-driven event that should not prompt discontinuation of diuretics or other life-saving therapies. 70

If the diuretic response remains inadequate, e.g. <100 mL hourly diuresis despite doubling loop diuretic dose and reaching the maximal amount of loop diuretics (200 mg intravenous furosemide equivalents three times a day), concomitant administration of other diuretics with different tubular sites of action, such as thiazides or acetazolamide, may be considered. It was recently shown that increased natriuresis is strongly related to successful decongestion with the combination of furosemide and acetazolamide in AHF. 71 However, this combination requires careful monitoring of serum electrolytes and renal function. A multicentre, randomized, double-blind, phase IV clinical trial of the diuretic effects of Acetazolamide in Decompensated heart failure with Volume OveRload (ADVOR) investigated if combination therapy with intravenous acetazolamide improves loop diuretic response in decompensated heart failure patients. 72 ADVOR showed that the addition of intravenous acetazolamide to loop diuretic in patients admitted for AHF was associated with a greater incidence of successful decongestion defined as the absence of signs of volume overload (i.e. no more than trace oedemas, no residual pleural effusion, and no residual ascites), within 3 days after initiation of decongestive therapy and at discharge; benefits were seen in all AHF regardless of LVEF. 71 , 73 Furthermore, addition of intravenous acetazolamide to loop diuretics was safe and associated with a reduced hospital stay though not associated with change in death from any cause or rehospitalization for HF during 3 months of follow-up. 73 New diuretic agents to treat congestion and to improve quality of life and survival are needed in AHF.

Recently, the multicentre placebo controlled randomized CLOROTIC trial (Combining Loop with Thiazide Diuretics for Decompensated Heart Failure) evaluated if the addition of hydrochlorothiazide (HCTZ) to loop diuretics in patients with AHF leads to improved decongestion. 74 Co-primary endpoints were weight loss and dyspnoea improvement at 72 h. There was a beneficial effect on weight loss, with no changes in patient-reported dyspnoea 72 h after randomization. 74 Additionally, there were no differences in mortality or rehospitalizations. 74 Concerning side effects, hypokalaemia was more frequent in the intervention group. In 2020, the Comparison of Oral or Intravenous Thiazides vs. Tolvaptan in Diuretic Resistant Decompensated Heart Failure (the 3T trial) showed that combination of high-dose of intravenous furosemide with oral metolazone, or intravenous chlorothiazide or tolvaptan in AHF patients with diuretic resistance, resulted in improved diuretic efficacy as defined by more greater weight loss at 48 h without detectable between-group difference. 75 Finally, recently, Mentz et al. 76 in a pragmatic trial entitled the Torsemide Comparison with Furosemide for Management of Heart Failure (TRANSFORM-HF) that aimed to overcome traditional HF trial challenges and to compare the effect of torsemide (loop diuretic with beneficial effects on cardiac fibrosis, aldosterone production, sympathetic activation, ventricular remodelling, and NP) vs. furosemide after discharge on all-cause mortality in patients with HF. In this randomized clinical trial, torsemide compared with furosemide did not result in a difference in all-cause mortality 1 year after an episode of AHF. However, results must be interpreted with great caution given loss of follow-up, participant crossover, and non-adherence.

Vasopressin receptor antagonists

Tolvaptan is an oral selective arginine V2 receptor antagonist preventing the activation of the aquaporin system and impairing the ability of AVP-mediated reabsorption of free water in the kidney to reabsorb water. 77 Randomized controlled clinical trials have failed to demonstrate benefit of tolvaptan on HF hospitalizations and mortality at 60 days after discharge. 77–79 Tolvaptan does not have an indication for hyponatraemia specifically in the setting of HF in the USA and Europe. 52 , 53

Vasodilators

Despite clinical evidence suggesting haemodynamic and clinical improvement, there have been limited data on the benefits of intravenous infusion of vasodilators on long-term outcomes. Drugs with a dual arteriolar and venous effects like sodium nitroprusside (SNP) appear to contribute to the immediate haemodynamic response of the drug. 80 Dilatation of the arterial resistance vessels as well as direct reduction in wall stress reduce LV afterload and allow the severely compromised LV to eject more blood. Importantly, these agents work preferentially in advanced HF with reduced ejection fraction (HFrEF) with dilated ventricles [i.e. highest wall tension = (pressure × radius)/(2 × wall thickness)]. The venodilator effect increases venous capacitance and reduces congestion. Both effects lead to an increase in cardiac output in patients with HF and often reduce the basal tachycardia (see Supplementary data online , Figure S1 ).

In case of advanced HF, SNP maybe administered in critical care settings with careful invasive haemodynamic monitoring due to the risk of inducing hypotension. A large retrospective, non-randomized case–control series showed that SNP can be safely administered to achieve haemodynamic improvement in patients presenting with advanced low-output HF. 81 The use of SNP according to a clinical protocol based on achieving a target mean arterial pressure is associated with more haemodynamic improvement that may facilitate the institution of a more aggressive oral vasodilator regimen beyond standard neurohormonal antagonists at the time of discharge. 82 , 83 Taken together, the use of SNP was associated with significantly lower all-cause mortality and fewer clinical adverse events at long-term follow-up, irrespective of the use of inotropic therapy or underlying renal function. 81 However, two recent large randomized clinical trials failed to demonstrate benefit of vasodilators in AHF patients on mortality and readmission rate. 84 , 85 An important issue with SNP is that prolonged use beyond 72 h can lead to cyanide poisoning, particularly in patients with impaired renal function. 86

In the Early and Comprehensive Care Bundle in Elderly for Acute Heart Failure: A Stepped Wedge Cluster Randomized Trial (ELISABETH), among older patients admitted to the emergency department (ED) for AHF, the use of a guideline-based comprehensive care bundle, including early intravenous nitrate boluses and management of precipitating factors, such as acute coronary syndrome, infection, or atrial fibrillation did not result in a reduced number of days alive at 30 days compared to usual care. 85 In the Goal-directed Afterload Reduction in Acute Congestive Cardiac Decompensation (GALACTIC) randomized clinical trial in patients hospitalized for AHF with dyspnoea, a strategy of early intensive vasodilation (including sublingual and transdermal glyceryl trinitrate) did not improve all-cause mortality and AHF rehospitalization at 180 days. Taken together, these results suggest that in the absence of hypertension, the use of vasodilators in AHF patients was not associated with better outcomes when compared to loop diuretic therapy alone. 52 Recent ESC HF guidelines indicated that titrated intravenous vasodilators can be considered in case of high systolic blood pressure in AHF patients. Care should be taken to avoid hypotension. 52

Other therapeutic measures

Hyponatraemia is a frequent therapeutic challenge in AHF ( Figure 3 ). Of note, a pseudo-hyponatraemia may occur in hyperglycaemia. In case of true hyponatraemia, physicians should first measure osmolarity to assess that it is reduced to confirm the true dilutional hyponatraemia, the most common type of low serum sodium levels in HF. ‘Depletional hyponatraemia’ (=deficit in Na + ) is due to various mechanisms including diuretic agents that enhance sodium excretion, associated with potassium/magnesium losses, malnutrition, diarrhoea, vomiting. Hence, hyponatraemia is common, for instance, with use of thiazides, begins soon after initiation of thiazides, may be severe, and is more likely to occur in elderly females. Isotonic saline with potassium/magnesium may often restore normal serum sodium levels. In contrast, ‘dilutional hyponatraemia’ is related to increased water retention due to increased osmotic and non-osmotic release of arginine vasopressin (AVP) and insufficient tubular flow through diluting (distal) segments of the nephron. Hyponatraemia may be corrected by improving distal nephron flow (loop diuretics with or without hypertonic saline, acetazolamide, renin-angiotensin system blockers, inotropes, or vasodilator therapy) or by administration of a vasopressin antagonist. Regardless of the mechanisms, distally working diuretics (thiazide-type, amiloride, mineralocorticoid receptor antagonists) should be stopped and plasma K + and Mg ++ restored. 56

Non-invasive ventilation

Application of a positive airway pressure by three modalities (continuous positive airway pressure, non-invasive pressure support ventilation, or high-flow nasal cannula) in conscious AHF patients can reduce the need for endotracheal intubation and decreases the risk of ventilator-associated pneumonia. 87 The latest ESC guidelines recommended non-invasive ventilation as Class IIa recommendations with a level of evidence B in AHF patients with respiratory distress (defined as respiratory rate > 25/min and/or SpO 2 < 90%). 52

Morphine and anxiolytic treatments

Acute heart failure is a stressful situation for patients due to the progressive respiratory failure frequently induced. To reduce anxiety and dyspnoea and to improve vasoconstriction accompanying hypertensives crises, morphine and short half-life benzodiazepines (e.g. midazolam) have been tested. In the multicentre, open-label, and randomized controlled Midazolam versus Morphine (MIMO) trial, the authors compared efficacy and safety of both molecules in AHF patients admitted to the ED. 88 Although the number of randomized patients was too small to make definitive conclusions, mortality was similar in both groups, and serious adverse events were more common in the morphine group, confirming results of previous studies. 89–91 Routine use of opiates in AHF patients is currently not recommended. 52

Risk stratification and early follow-up after discharge

Surprisingly, 30-day risk of readmission has not decreased over time in AHF patients 92 , 93 underscoring the need for new approaches to improve outcomes. The decision to admit or discharge an AHF patient presenting to the ED is mainly based on clinical judgement, with a risk of inaccuracy in prognostication leading to low-risk patients being hospitalized and high-risk patients being discharged. 94 Risk stratification could help ED physicians to improve clinical decision making in AHF patients’. 94 By combining a validated point-of-care tool for risk stratification in the ED to support clinicians’ decisions about admissions or discharge of AHF patients, with the provision of standardized transitional care, Lee et al. 95 observed a reduction of 12% in the risk of death from any cause or hospitalization for cardiovascular causes within 30 days after an AHF episode. This risk remained lower at 20 months after the AHF episode.

Post-discharge therapies and implementation of oral therapies

The latest North American and European guidelines for chronic HF recommended that guideline-directed medical therapy (GDMT) for HF includes beta-blocker, renin-angiotensin system inhibitors and mineralocorticoid receptor antagonists for HFrEF, and sodium-glucose cotransporter 2 inhibitors for all HF patients regardless of LVEF, with the aim of improving survival and preventing recurrent HF hospitalizations. 96 Concerning AHF, after the initial phase when patients recover from severe congestion, hypoxaemia, and/or organ dysfunction, the next step is to organize a seamless transition from hospital to home. Indeed, discharge to home is associated with high rates of early readmission and death, the ‘vulnerable’ post-discharge phase. 97 To improve this critically important issue, guidelines recommend the continuation of the home HF medications provided that haemodynamic instability is absent. Furthermore, implementation of oral GDMT as soon as possible is highly recommended. Recently, four studies improved our understanding on how to optimally implement GDMT for HF before and after discharge ( Table 2 ). 5 , 98–101 The multinational randomized trial Empagliflozin in Patients Hospitalized With Acute Heart Failure Who Have Been Stabilized (EMPULSE) trial showed that initiation of empagliflozin (at a dose of 10 mg orally daily) in patients hospitalized for AHF was associated with improved symptoms, physical limitations, and quality of life soon after discharge. 98 , 99 The Effect of Sotagliflozin ion Cardiovascular Events in Patients with Type 2 Diabetes Post Worsening Heart Failure trial (SOLOIST-WHF), a double-blind trial including type 2 diabetes mellitus patients admitted for worsening HF, found that sotagliflozin therapy initiated before or shortly after discharge resulted with better outcomes at 18 months, including deaths from cardiovascular causes, hospitalizations, and urgent visits for AHF. 100 The Comparison of Sacubitril-Valsartan versus Enalapril on Effect on NT-proBNP in Patients Stabilized from an Acute Decompensated Heart Failure Episode (PIONEER-HF) showed that initiation of sacubitril/valsartan therapy in patients stabilized after treatment of AHF was associated with a greater reduction in the NT-proBNP concentration and of the risk of cardiovascular death or HF readmission when compared to enalapril therapy. 101 Death and rehospitalization rates between groups were similar. Finally, the Safety, Tolerability and Efficacy of Rapid Optimization, Helped by NT-proBNP Testing, of Heart Failure Therapies (STRONG-HF), a multinational open-label randomized trial, recently showed that an early and intensive treatment strategy consisting of rapid GDMT establishment and up-titration 2 days before discharge from an episode of AHF, was safe and beneficial with reduced 180-day HF readmission and/or all-cause death. 5 The close follow-up with clinical exam and biological tests including plasma NT-proBNP, at each visit, allowed safe rapid up-titration of oral HF medications with almost no side effects. 5

Trials showing benefits of heart failure medications at and after discharge of acute heart failure

CI, confidence interval; HR, hazard ratio; NT-proBNP, N-terminal pro-B-type natriuretic peptide; HF, heart failure; HFrEF, heart failure with reduced ejection fraction.

Implementation of iron supplementation therapies

Iron deficiency is common in AHF patients and is associated with poor outcomes. 102 , 103 Therefore, diagnosis and treatment of iron deficiency after an AHF episode are highly recommended. 52 The A Randomised, Double-blind Placebo Controlled Trial Comparing the Effect of Intravenous Ferric Carboxymaltose on Hospitalisations and Mortality in Iron Deficient Subjects Admitted for Acute Heart Failure (AFFIRM-HF) trial was designed to evaluate the effect of carboxymaltose compared with placebo on outcomes in patients with iron deficiency with a reduced LVEF (<50%) after an episode of AHF. 104 The authors observed that treatment with ferric carboxymaltose was safe and reduced the risk of HF hospitalizations, with no apparent effect on the risk of cardiovascular death. A new trial, Effectiveness of Intravenous Iron Treatment versus Standard Care in Patients with Heart Failure and Iron Deficiency (IRONMAN) confirmed, on a COVID-19 pre-specified analysis, a reduction in the risk of the primary endpoint with ferric derisomaltose vs. control and a greater improvement of the overall Minnesota Living with Heart Failure Questionnaire at 4-month follow-up. 105

The Graphical Abstract summarizes main principles of the therapeutic management of AHF patients, from pre-admission to post-discharge period, based on the most recent guidelines and important trials. Of note, post-discharge management of congestion remains a difficult task for physicians. To improve clinical outcomes, a wide range of monitoring strategies (invasive and non-invasive) to prevent HF decompensation and to guide decongestion are available. Recently, a systematic review and meta-analysis, including randomized controlled trials, found that, compared to standard therapy, a device-based remote monitoring strategy for haemodynamic-guided management of patients with chronic HF is associated with a reduction of all-cause death and HF hospitalizations. 106 Thus, future studies will determine the best strategy and monitoring in guiding the long-term management of patients with HF.

Several clinical trials around the world are currently underway in AHF. Main molecules being studied are sodium-glucose cotransporter inhibitors, which are associated with a decreased risk of worsening HF events, cardiovascular deaths, and improved symptoms when used in HFrEF 107–109 regardless of the existence of diabetes, raising expectations for the future of AHF patients. Main clinical studies (randomized and open-label studies) are summarized in Table 3 . As described above, congestion is still present in many patients discharged home from an AHF episode and congestion is the main reason of unscheduled readmission in outpatient HF clinics and ED in the following weeks. As intravenous diuretics showed limited benefits in preventing HF readmission, research should therefore focus on developing enteral or parenteral novel therapies that may markedly reduce congestion and prevent episodes of short-term readmission. Those therapies should be tested in worsening HF episodes seen at outpatient centre or in hospital. In addition, AHF with preserved LVEF is highly present in old patients and patients with metabolic disorders; novel therapies should also be assessed on those patients. Furthermore, research should focus on the best way to combine agents that will reduce and prevent congestion with guideline-directed HF medications to cure HF and have patients back to ‘normal’ uneventful life.

Drugs being tested in ongoing trials in acute heart failure

RCT, randomized clinical trial.

To conclude, AHF is a worldwide and frequent syndrome associated with poor outcomes. Signs and symptoms are related to systemic venous congestion due to the accumulation of extracellular fluids related to increased ventricular filling pressures. Intravenous diuretics are considered as the cornerstone of therapeutic management of AHF associated with non-invasive ventilation if needed. The 2023 focused update of those guidelines yet recommends an intensive strategy of initiation and rapid up-titration of evidence-based treatment before discharge and during frequent and careful follow-up visits in the first 6 weeks following a HF hospitalization is recommended to reduce the risk of HF rehospitalization or death. 110

Supplementary data are available at European Heart Journal online.

Disclosure of Interest

B.D. declares no conflict of interest. M.R.C. declares grants for Novartis, Bayer, and V-Wave, and consulting fees for Nuwellis and Boehringer Ingelheim. M.R.C. declares participation of advisory committee and national leader VICTOR HF study. K.S. declares participation of advisory committee and national leader VICTOR HF study, board member of Heart Failure Society of South Africa, and board member of Pan African Society of Cardiology. A.A. declares no conflict of interest. W.M. declares honoraria from Medtronic, Abott, Vifor Pharma, Astra Zeneca, Boehringer Ingelheim, and Pfizer. A.M. declares consulting fees from Novartis, Orion, Roche, Servier, Sanofi, Adrenomed, 4TEEN4, and Philips.

No data were generated or analysed for this manuscript.

All authors declare no funding for this contribution.

Arrigo   M , Jessup   M , Mullens   W , Reza   N , Shah   AM , Sliwa   K , et al.    Acute heart failure . Nat Rev Dis Primers   2020 ; 6 : 16 . https://doi.org/10.1038/s41572-020-0151-7

Google Scholar

Ambrosy   AP , Fonarow   GC , Butler   J , Chioncel   O , Greene   SJ , Vaduganathan   M , et al.    The global health and economic burden of hospitalizations for heart failure . J Am Coll Cardiol   2014 ; 63 : 1123 – 33 . https://doi.org/10.1016/j.jacc.2013.11.053

Crespo-Leiro   MG , Anker   SD , Maggioni   AP , Coats   AJ , Filippatos   G , Ruschitzka   F , et al.    European Society of Cardiology Heart Failure Long-Term Registry (ESC-HF-LT): 1-year follow-up outcomes and differences across regions . Eur J Heart Fail   2016 ; 18 : 613 – 25 . https://doi.org/10.1002/ejhf.566

Fudim   M , Khan   MS , Paracha   AA , Sunagawa   K , Burkhoff   D . Targeting preload in heart failure: splanchnic nerve blockade and beyond . Circ Heart Fail   2022 ; 15 : e009340 . https://doi.org/10.1161/CIRCHEARTFAILURE.121.009340

Mebazaa   A , Davison   B , Chioncel   O , Cohen-Solal   A , Diaz   R , Filippatos   G , et al.    Safety, tolerability and efficacy of up-titration of guideline-directed medical therapies for acute heart failure (STRONG-HF): a multinational, open-label, randomised, trial . Lancet   2022 ; 400 : 1952 . https://doi.org/10.1016/S0140-6736(22)02076-1

Mebazaa   A , Combes   A , van Diepen   S , Hollinger   A , Katz   JN , Landoni   G , et al.    Management of cardiogenic shock complicating myocardial infarction . Intensive Care Med   2018 ; 44 : 760 – 73 . https://doi.org/10.1007/s00134-018-5214-9

van Diepen   S , Katz   JN , Albert   NM , Henry   TD , Jacobs   AK , Kapur   NK , et al.    Contemporary management of cardiogenic shock: a scientific statement from the American Heart Association . Circulation   2017 ; 136 : e232 – 68 . https://doi.org/10.1161/CIR.0000000000000525

McMurray   JJV , Packer   M , Desai   AS , Gong   J , Lefkowitz   M , Rizkala   AR , et al.    Baseline characteristics and treatment of patients in prospective comparison of ARNI with ACEI to determine impact on global mortality and morbidity in heart failure trial (PARADIGM-HF) . Eur J Heart Fail   2014 ; 16 : 817 – 25 . https://doi.org/10.1002/ejhf.115

Triposkiadis   F , Butler   J , Abboud   FM , Armstrong   PW , Adamopoulos   S , Atherton   JJ , et al.    The continuous heart failure spectrum: moving beyond an ejection fraction classification . Eur Heart J   2019 ; 40 : 2155 – 63 . https://doi.org/10.1093/eurheartj/ehz158

Filippatos   G , Khan   SS , Ambrosy   AP , Cleland   JGF , Collins   SP , Lam   CSP , et al.    International REgistry to assess medical Practice with lOngitudinal obseRvation for Treatment of Heart Failure (REPORT-HF): rationale for and design of a global registry . Eur J Heart Fail   2015 ; 17 : 527 – 33 . https://doi.org/10.1002/ejhf.262

Gheorghiade   M , Zannad   F , Sopko   G , Klein   L , Piña   IL , Konstam   MA , et al.    Acute heart failure syndromes: current state and framework for future research . Circulation   2005 ; 112 : 3958 – 68 . https://doi.org/10.1161/CIRCULATIONAHA.105.590091

Cleland   JGF , Swedberg   K , Follath   F , Komajda   M , Cohen-Solal   A , Aguilar   JC , et al.    The EuroHeart Failure survey programme—a survey on the quality of care among patients with heart failure in Europe. Part 1: patient characteristics and diagnosis . Eur Heart J   2003 ; 24 : 442 – 63 . https://doi.org/10.1016/S0195-668X(02)00823-0

Sliwa   K , Davison   BA , Mayosi   BM , Damasceno   A , Sani   M , Ogah   OS , et al.    Readmission and death after an acute heart failure event: predictors and outcomes in sub-Saharan Africa: results from the THESUS-HF registry . Eur Heart J   2013 ; 34 : 3151 – 9 . https://doi.org/10.1093/eurheartj/eht393

Abraham   WT , Fonarow   GC , Albert   NM , Stough   WG , Gheorghiade   M , Greenberg   BH , et al.    Predictors of in-hospital mortality in patients hospitalized for heart failure: insights from the Organized Program to Initiate Lifesaving Treatment in Hospitalized Patients with Heart Failure (OPTIMIZE-HF) . J Am Coll Cardiol   2008 ; 52 : 347 – 56 . https://doi.org/10.1016/j.jacc.2008.04.028

Kimmoun   A , Takagi   K , Gall   E , Ishihara   S , Hammoum   P , El Bèze   N , et al.    Temporal trends in mortality and readmission after acute heart failure: a systematic review and meta-regression in the past four decades . Eur J Heart Fail   2021 ; 23 : 420 – 31 . https://doi.org/10.1002/ejhf.2103

Girerd   N , Seronde   MF , Coiro   S , Chouihed   T , Bilbault   P , Braun   F , et al.    Integrative assessment of congestion in heart failure throughout the patient journey . JACC Heart Fail   2018 ; 6 : 273 – 85 . https://doi.org/10.1016/j.jchf.2017.09.023

Fudim   M , Kaye   DM , Borlaug   BA , Shah   SJ , Rich   S , Kapur   NK , et al.    Venous tone and stressed blood volume in heart failure: JACC review topic of the week . J Am Coll Cardiol   2022 ; 79 : 1858 – 69 . https://doi.org/10.1016/j.jacc.2022.02.050

Mentz   RJ , O’Connor   CM . Pathophysiology and clinical evaluation of acute heart failure . Nat Rev Cardiol   2016 ; 13 : 28 – 35 . https://doi.org/10.1038/nrcardio.2015.134

Nikolaou   M , Parissis   J , Yilmaz   MB , Seronde   MF , Kivikko   M , Laribi   S , et al.    Liver function abnormalities, clinical profile, and outcome in acute decompensated heart failure . Eur Heart J   2013 ; 34 : 742 – 9 . https://doi.org/10.1093/eurheartj/ehs332

Verbrugge   F , Dupont   M , Steels   P , Lars   G , Malbrain   M , Tang   W , et al.    Abdominal contributions to cardiorenal dysfunction in congestive heart failure . J Am Coll Cardiol   2013 ; 62 : 485 – 95 . https://doi.org/10.1016/j.jacc.2013.04.070

Singhal   R , Shah   YM . Oxygen battle in the gut: hypoxia and hypoxia-inducible factors in metabolic and inflammatory responses in the intestine . J Biol Chem   2020 ; 295 : 10493 – 505 . https://doi.org/10.1074/jbc.REV120.011188

Ambrosy   AP , Pang   PS , Khan   S , Konstam   MA , Fonarow   GC , Traver   B , et al.    Clinical course and predictive value of congestion during hospitalization in patients admitted for worsening signs and symptoms of heart failure with reduced ejection fraction: findings from the EVEREST trial . Eur Heart J   2013 ; 34 : 835 – 43 . https://doi.org/10.1093/eurheartj/ehs444

Abraham   WT , Adamson   PB , Hasan   A , Bourge   RC , Pamboukian   SV , Aaron   MF , et al.    Safety and accuracy of a wireless pulmonary artery pressure monitoring system in patients with heart failure . Am Heart J   2011 ; 161 : 558 – 66 . https://doi.org/10.1016/j.ahj.2010.10.041

Bayes-Genis   A , Lupón   J , Jaffe   AS . Can natriuretic peptides be used to guide therapy?   EJIFCC   2016 ; 27 : 208 – 16 .

Felker   GM , Ahmad   T , Anstrom   KJ , Adams   KF , Cooper   LS , Ezekowitz   JA , et al.    Rationale and design of the GUIDE-IT study: guiding evidence based therapy using biomarker intensified treatment in heart failure . JACC Heart Fail   2014 ; 2 : 457 – 65 . https://doi.org/10.1016/j.jchf.2014.05.007

Cohen-Solal   A , Logeart   D , Huang   B , Cai   D , Nieminen   MS , Mebazaa   A . Lowered B-type natriuretic peptide in response to levosimendan or dobutamine treatment is associated with improved survival in patients with severe acutely decompensated heart failure . J Am Coll Cardiol   2009 ; 53 : 2343 – 8 . https://doi.org/10.1016/j.jacc.2009.02.058

Levey   AS , Inker   LA . Assessment of glomerular filtration rate in health and disease: a state of the art review . Clin Pharmacol Ther   2017 ; 102 : 405 – 19 . https://doi.org/10.1002/cpt.729

Bragadottir   G , Redfors   B , Ricksten   SE . Assessing glomerular filtration rate (GFR) in critically ill patients with acute kidney injury—true GFR versus urinary creatinine clearance and estimating equations . Crit Care   2013 ; 17 : R108 . https://doi.org/10.1186/cc12777

Waikar   SS , Betensky   RA , Emerson   SC , Bonventre   JV . Imperfect gold standards for kidney injury biomarker evaluation . J Am Soc Nephrol   2012 ; 23 : 13 – 21 . https://doi.org/10.1681/ASN.2010111124

Costanzo   MR . Verdict in: congestion guilty! . JACC Heart Fail   2015 ; 3 : 762 – 4 . https://doi.org/10.1016/j.jchf.2015.06.004

Brisco   MA , Zile   MR , Hanberg   JS , Wilson   FP , Parikh   CR , Coca   SG , et al.    Relevance of changes in serum creatinine during a heart failure trial of decongestive strategies: insights from the DOSE trial . J Card Fail   2016 ; 22 : 753 – 60 . https://doi.org/10.1016/j.cardfail.2016.06.423

Costanzo   MR , Barasch   J . Creatinine and cystatin C: not the troponin of the kidney . Circulation   2018 ; 137 : 2029 – 31 . https://doi.org/10.1161/CIRCULATIONAHA.118.033343

Parikh   CR , Coca   SG . “Permissive AKI” with treatment of heart failure . Kidney Int   2019 ; 96 : 1066 – 8 . https://doi.org/10.1016/j.kint.2019.07.003

Mebazaa   A , Solal   AC , Colombo   PC . Assessing and treating congestion in acute decompensated heart failure: are we seeing the light at the end of the tunnel?   Eur Heart J   2023 ; 44 : 51 – 3 . https://doi.org/10.1093/eurheartj/ehac680

Tsutsui   RS , Borowski   A , Tang   WHW , Thomas   JD , Popović   ZB . Precision of echocardiographic estimates of right atrial pressure in patients with acute decompensated heart failure . J Am Soc Echocardiogr   2014 ; 27 : 1072 – 1078.e2 . https://doi.org/10.1016/j.echo.2014.06.002

Palazzuoli   A , Evangelista   I , Nuti   R . Congestion occurrence and evaluation in acute heart failure scenario: time to reconsider different pathways of volume overload . Heart Fail Rev   2020 ; 25 : 119 – 31 . https://doi.org/10.1007/s10741-019-09868-0

Fitzsimons   S , Doughty   RN . Role of transthoracic echocardiogram in acute heart failure . Rev Cardiovasc Med   2021 ; 22 : 741 – 54 . https://doi.org/10.31083/j.rcm2203081

Rao   VN , Andrews   J , Applefeld   WN , Gray   JM , Molinger   J , Felker   GM , et al.    Quantitative blood volume analysis and hemodynamic measures of vascular compliance in patients with worsening heart failure . J Card Fail   2022 ; 28 : 1469 – 74 . https://doi.org/10.1016/j.cardfail.2022.04.004

Manzone   TA , Dam   HQ , Soltis   D , Sagar   VV . Blood volume analysis: a new technique and new clinical interest reinvigorate a classic study . J Nucl Med Technol   2007 ; 35 : 55 – 63 ; quiz 77, 79 . https://doi.org/10.2967/jnmt.106.035972

Hong   N , Youn   JC , Oh   J , Lee   HS , Park   S , Choi   D , et al.    Prognostic value of new-onset anemia as a marker of hemodilution in patients with acute decompensated heart failure and severe renal dysfunction . J Cardiol   2014 ; 64 : 43 – 8 . https://doi.org/10.1016/j.jjcc.2013.11.007

Mancini   DM , Katz   SD , Lang   CC , LaManca   J , Hudaihed   A , Androne   AS . Effect of erythropoietin on exercise capacity in patients with moderate to severe chronic heart failure . Circulation   2003 ; 107 : 294 – 9 . https://doi.org/10.1161/01.CIR.0000044914.42696.6A

Shevde   K , Pagala   M , Tyagaraj   C , Udeh   C , Punjala   M , Arora   S , et al.    Preoperative blood volume deficit influences blood transfusion requirements in females and males undergoing coronary bypass graft surgery . J Clin Anesth   2002 ; 14 : 512 – 7 . https://doi.org/10.1016/S0952-8180(02)00423-3

Price   S , Platz   E , Cullen   L , Tavazzi   G , Christ   M , Cowie   MR , et al.    Expert consensus document: echocardiography and lung ultrasonography for the assessment and management of acute heart failure . Nat Rev Cardiol   2017 ; 14 : 427 – 40 . https://doi.org/10.1038/nrcardio.2017.56

Martindale   JL , Wakai   A , Collins   SP , Levy   PD , Diercks   D , Hiestand   BC , et al.    Diagnosing acute heart failure in the emergency department: a systematic review and meta-analysis . Acad Emerg Med   2016 ; 23 : 223 – 42 . https://doi.org/10.1111/acem.12878

Miglioranza   MH , Gargani   L , Sant’Anna   RT , Rover   MM , Martins   VM , Mantovani   A , et al.    Lung ultrasound for the evaluation of pulmonary congestion in outpatients: a comparison with clinical assessment, natriuretic peptides, and echocardiography . JACC Cardiovasc Imaging   2013 ; 6 : 1141 – 51 . https://doi.org/10.1016/j.jcmg.2013.08.004

Abraham   WT , Adamson   PB , Bourge   RC , Aaron   MF , Costanzo   MR , Stevenson   LW , et al.    Wireless pulmonary artery haemodynamic monitoring in chronic heart failure: a randomised controlled trial . Lancet   2011 ; 377 : 658 – 66 . https://doi.org/10.1016/S0140-6736(11)60101-3

Adamson   PB , Abraham   WT , Bourge   RC , Costanzo   MR , Hasan   A , Yadav   C , et al.    Wireless pulmonary artery pressure monitoring guides management to reduce decompensation in heart failure with preserved ejection fraction . Circ Heart Fail   2014 ; 7 : 935 – 44 . https://doi.org/10.1161/CIRCHEARTFAILURE.113.001229

Heywood   JT , Jermyn   R , Shavelle   D , Abraham   WT , Bhimaraj   A , Bhatt   K , et al.    Impact of practice-based management of pulmonary artery pressures in 2000 patients implanted with the CardioMEMS sensor . Circulation   2017 ; 135 : 1509 – 17 . https://doi.org/10.1161/CIRCULATIONAHA.116.026184

Desai   AS , Bhimaraj   A , Bharmi   R , Jermyn   R , Bhatt   K , Shavelle   D , et al.    Ambulatory hemodynamic monitoring reduces heart failure hospitalizations in “Real-World” clinical practice . J Am Coll Cardiol   2017 ; 69 : 2357 – 65 . https://doi.org/10.1016/j.jacc.2017.03.009

Boehmer   JP , Hariharan   R , Devecchi   FG , Smith   AL , Molon   G , Capucci   A , et al.    A multisensor algorithm predicts heart failure events in patients with implanted devices: results from the MultiSENSE study . JACC Heart Fail   2017 ; 5 : 216 – 25 . https://doi.org/10.1016/j.jchf.2016.12.011

Costanzo   MR . The luck of having a cardiac implantable electronic device . Circ Heart Fail   2018 ; 11 : e004894 . https://doi.org/10.1161/CIRCHEARTFAILURE.118.004894

McDonagh   TA , Metra   M , Adamo   M , Gardner   RS , Baumbach   A , Böhm   M , et al.    2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure . Eur Heart J   2021 ; 42 : 3599 – 726 . https://doi.org/10.1093/eurheartj/ehab368

Heidenreich   PA , Bozkurt   B , Aguilar   D , Allen   LA , Byun   JJ , Colvin   MM , et al.    2022 AHA/ACC/HFSA guideline for the management of heart failure: executive summary: a report of the American College of Cardiology/American Heart Association joint committee on clinical practice guidelines . J Am Coll Cardiol   2022 ; 79 : 1757 – 80 . https://doi.org/10.1016/j.jacc.2021.12.011

Mullens   W , Damman   K , Harjola   VP , Mebazaa   A , Brunner-La Rocca   HP , Martens   P , et al.    The use of diuretics in heart failure with congestion—a position statement from the Heart Failure Association of the European Society of Cardiology . Eur J Heart Fail   2019 ; 21 : 137 – 55 . https://doi.org/10.1002/ejhf.1369

Metra   M , Davison   B , Bettari   L , Sun   H , Edwards   C , Lazzarini   V , et al.    Is worsening renal function an ominous prognostic sign in patients with acute heart failure? The role of congestion and its interaction with renal function . Circ Heart Fail   2012 ; 5 : 54 – 62 . https://doi.org/10.1161/CIRCHEARTFAILURE.111.963413

Verbrugge   FH , Steels   P , Grieten   L , Nijst   P , Tang   WHW , Mullens   W . Hyponatremia in acute decompensated heart failure: depletion versus dilution . J Am Coll Cardiol   2015 ; 65 : 480 – 92 . https://doi.org/10.1016/j.jacc.2014.12.010

Felker   GM , Lee   KL , Bull   DA , Redfield   MM , Stevenson   LW , Goldsmith   SR , et al.    Diuretic strategies in patients with acute decompensated heart failure . N Engl J Med   2011 ; 364 : 797 – 805 . https://doi.org/10.1056/NEJMoa1005419

Ellison   DH . Diuretic therapy and resistance in congestive heart failure . Cardiology   2001 ; 96 : 132 – 43 . https://doi.org/10.1159/000047397

Cox   ZL , Rao   VS , Testani   JM . Classic and novel mechanisms of diuretic resistance in cardiorenal syndrome . Kidney360   2022 ; 3 : 954 – 67 . https://doi.org/10.34067/KID.0006372021

Testani   JM , Brisco   MA , Kociol   RD , Jacoby   D , Bellumkonda   L , Parikh   CR , et al.    Substantial discrepancy between fluid and weight loss during acute decompensated heart failure treatment . Am J Med   2015 ; 128 : 776 – 783.e4 . https://doi.org/10.1016/j.amjmed.2014.12.020

Verbrugge   FH , Nijst   P , Dupont   M , Reynders   C , Penders   J , Tang   WHW , et al.    Prognostic value of glomerular filtration changes versus natriuretic response in decompensated heart failure with reduced ejection . J Card Fail   2014 ; 20 : 817 – 24 . https://doi.org/10.1016/j.cardfail.2014.08.002

Ferreira   JP , Girerd   N , Bettencourt Medeiros   P , Bento Ricardo   M , Almeida   T , Rola   A , et al.    Lack of diuretic efficiency (but not low diuresis) early in an acutely decompensated heart failure episode is associated with increased 180-day mortality . Cardiorenal Med   2017 ; 7 : 137 – 49 . https://doi.org/10.1159/000455903

Brinkley   DM , Burpee   LJ , Chaudhry   SP , Smallwood   JA , Lindenfeld   J , Lakdawala   NK , et al.    Spot urine sodium as triage for effective diuretic infusion in an ambulatory heart failure unit . J Card Fail   2018 ; 24 : 349 – 54 . https://doi.org/10.1016/j.cardfail.2018.01.009

Singh   D , Shrestha   K , Testani   JM , Verbrugge   FH , Dupont   M , Mullens   W , et al.    Insufficient natriuretic response to continuous intravenous furosemide is associated with poor long-term outcomes in acute decompensated heart failure . J Card Fail   2014 ; 20 : 392 – 9 . https://doi.org/10.1016/j.cardfail.2014.03.006

Testani   JM , Hanberg   JS , Cheng   S , Rao   V , Onyebeke   C , Laur   O , et al.    Rapid and highly accurate prediction of poor loop diuretic natriuretic response in patients with heart failure . Circ Heart Fail   2016 ; 9 : e002370 . https://doi.org/10.1161/CIRCHEARTFAILURE.115.002370

Pichette   V , Geadah   D , du Souich   P . Role of plasma protein binding on renal metabolism and dynamics of furosemide in the rabbit . Drug Metab Dispos   1999 ; 27 : 81 – 5 .

Matsue   Y , Damman   K , Voors   AA , Kagiyama   N , Yamaguchi   T , Kuroda   S , et al.    Time-to-furosemide treatment and mortality in patients hospitalized with acute heart failure . J Am Coll Cardiol   2017 ; 69 : 3042 – 51 . https://doi.org/10.1016/j.jacc.2017.04.042

Dauw   J , Lelonek   M , Zegri-Reiriz   I , Paredes-Paucar   CP , Zara   C , George   V , et al.    Rationale and design of the efficacy of a standardized diuretic protocol in acute heart failure study . ESC Heart Fail   2021 ; 8 : 4685 – 92 . https://doi.org/10.1002/ehf2.13666

ter Maaten   JM , Beldhuis   IE , van der Meer   P , Krikken   JA , Coster   JE , Nieuwland   W , et al.    Natriuresis-guided therapy in acute heart failure: rationale and design of the Pragmatic Urinary Sodium-based treatment algoritHm in Acute Heart Failure (PUSH-AHF) trial . Eur J Heart Fail   2022 ; 24 : 385 – 92 . https://doi.org/10.1002/ejhf.2385

Goldsmith   SR , Bart   BA , Burnett   J . Decongestive therapy and renal function in acute heart failure . Circ Heart Fail   2014 ; 7 : 531 – 5 . https://doi.org/10.1161/CIRCHEARTFAILURE.113.000828

Martens   P , Dauw   J , Verbrugge   FH , Nijst   P , Meekers   E , Augusto   SN , et al.    Decongestion with acetazolamide in acute decompensated heart failure across the spectrum of left ventricular ejection fraction: a prespecified analysis from the ADVOR trial . Circulation   2023 ; 147 : 201 – 11 . https://doi.org/10.1161/CIRCULATIONAHA.122.062486

Mullens   W , Verbrugge   FH , Nijst   P , Martens   P , Tartaglia   K , Theunissen   E , et al.    Rationale and design of the ADVOR (Acetazolamide in Decompensated Heart Failure with Volume Overload) trial . Eur J Heart Fail   2018 ; 20 : 1591 – 600 . https://doi.org/10.1002/ejhf.1307

Mullens   W , Dauw   J , Martens   P , Meekers   E , Nijst   P , Verbrugge   FH , et al.    Acetazolamide In Decompensated Heart Failure with Volume Overload trial (ADVOR): baseline characteristics . Eur J Heart Fail   2022 ; 24 : 1601 – 10 . https://doi.org/10.1002/ejhf.2587

Trullàs   JC , Morales-Rull   JL , Casado   J , Carrera-Izquierdo   M , Sánchez-Marteles   M , Conde-Martel   A , et al.    Combining loop with thiazide diuretics for decompensated heart failure: the CLOROTIC trial . Eur Heart J   2023 : 44 : 411 – 21 . https://doi.org/10.1093/eurheartj/ehac689

Cox   ZL , Hung   R , Lenihan   DJ , Testani   JM . Diuretic strategies for loop diuretic resistance in acute heart failure: the 3T trial . JACC Heart Fail   2020 ; 8 : 157 – 68 . https://doi.org/10.1016/j.jchf.2019.09.012

Mentz   RJ , Anstrom   KJ , Eisenstein   EL , Sapp   S , Greene   SJ , Morgan   S , et al.    Effect of torsemide vs furosemide after discharge on all-cause mortality in patients hospitalized with heart failure: the TRANSFORM-HF randomized clinical trial . JAMA   2023 ; 329 : 214 – 23 . https://doi.org/10.1001/jama.2022.23924

Matsue   Y , Ter Maaten   JM , Suzuki   M , Torii   S , Yamaguchi   S , Fukamizu   S , et al.    Early treatment with tolvaptan improves diuretic response in acute heart failure with renal dysfunction . Clin Res Cardiol   2017 ; 106 : 802 – 12 . https://doi.org/10.1007/s00392-017-1122-1

Felker   GM , Mentz   RJ , Cole   RT , Adams   KF , Egnaczyk   GF , Fiuzat   M , et al.    Efficacy and safety of tolvaptan in patients hospitalized with acute heart failure . J Am Coll Cardiol   2017 ; 69 : 1399 – 406 . https://doi.org/10.1016/j.jacc.2016.09.004

Konstam   MA , Kiernan   M , Chandler   A , Dhingra   R , Mody   FV , Eisen   H , et al.    Short-term effects of tolvaptan in patients with acute heart failure and volume overload . J Am Coll Cardiol   2017 ; 69 : 1409 – 19 . https://doi.org/10.1016/j.jacc.2016.12.035

Cohn   JN , Archibald   DG , Ziesche   S , Franciosa   JA , Harston   WE , Tristani   FE , et al.    Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study . N Engl J Med   1986 ; 314 : 1547 – 52 . https://doi.org/10.1056/NEJM198606123142404

Mullens   W , Abrahams   Z , Francis   GS , Skouri   HN , Starling   RC , Young   JB , et al.    Sodium nitroprusside for advanced low-output heart failure . J Am Coll Cardiol   2008 ; 52 : 200 – 7 . https://doi.org/10.1016/j.jacc.2008.02.083

Mullens   W , Abrahams   Z , Francis   GS , Sokos   G , Starling   RC , Young   JB , et al.    Usefulness of isosorbide dinitrate and hydralazine as add-on therapy in patients discharged for advanced decompensated heart failure . Am J Cardiol   2009 ; 103 : 1113 – 9 . https://doi.org/10.1016/j.amjcard.2008.12.028

Martyn   T , Faulkenberg   KD , Albert   CL , Il’giovine   ZJ , Randhawa   VK , Donnellan   E , et al.    Acute hemodynamic effects of sacubitril–valsartan in heart failure patients receiving intravenous vasodilator and inotropic therapy . J Card Fail   2021 ; 27 : 368 – 72 . https://doi.org/10.1016/j.cardfail.2020.12.013

Kozhuharov   N , Goudev   A , Flores   D , Maeder   MT , Walter   J , Shrestha   S , et al.    Effect of a strategy of comprehensive vasodilation vs usual care on mortality and heart failure rehospitalization among patients with acute heart failure: the GALACTIC randomized clinical trial . JAMA   2019 ; 322 : 2292 – 302 . https://doi.org/10.1001/jama.2019.18598

Freund   Y , Cachanado   M , Delannoy   Q , Laribi   S , Yordanov   Y , Gorlicki   J , et al.    Effect of an emergency department care bundle on 30-day hospital discharge and survival among elderly patients with acute heart failure: the ELISABETH randomized clinical trial . JAMA   2020 ; 324 : 1948 – 56 . https://doi.org/10.1001/jama.2020.19378

Hall   VA , Guest   JM . Sodium nitroprusside-induced cyanide intoxication and prevention with sodium thiosulfate prophylaxis . Am J Crit Care   1992 ; 1 : 19 – 25 ; quiz 26–7 . https://doi.org/10.4037/ajcc1992.1.2.19

Girou   E , Brun-Buisson   C , Taillé   S , Lemaire   F , Brochard   L . Secular trends in nosocomial infections and mortality associated with noninvasive ventilation in patients with exacerbation of COPD and pulmonary edema . JAMA   2003 ; 290 : 2985 – 91 . https://doi.org/10.1001/jama.290.22.2985

Domínguez-Rodríguez   A , Suero-Mendez   C , Burillo-Putze   G , Gil   V , Calvo-Rodriguez   R , Piñera-Salmeron   P , et al.    Midazolam versus morphine in acute cardiogenic pulmonary oedema: results of a multicentre, open-label, randomized controlled trial . Eur J Heart Fail   2022 ; 24 : 1953 – 62 . https://doi.org/10.1002/ejhf.2602

Iakobishvili   Z , Cohen   E , Garty   M , Behar   S , Shotan   A , Sandach   A , et al.    Use of intravenous morphine for acute decompensated heart failure in patients with and without acute coronary syndromes . Acute Card Care   2011 ; 13 : 76 – 80 . https://doi.org/10.3109/17482941.2011.575165

Miró   Ò , Gil   V , Martín-Sánchez   FJ , Herrero-Puente   P , Jacob   J , Mebazaa   A , et al.    Morphine use in the ED and outcomes of patients with acute heart failure: a propensity score-matching analysis based on the EAHFE registry . Chest   2017 ; 152 : 821 – 32 . https://doi.org/10.1016/j.chest.2017.03.037

Caspi   O , Naami   R , Halfin   E , Aronson   D . Adverse dose-dependent effects of morphine therapy in acute heart failure . Int J Cardiol   2019 ; 293 : 131 – 6 . https://doi.org/10.1016/j.ijcard.2019.06.015

Khera   R , Dharmarajan   K , Wang   Y , Lin   Z , Bernheim   SM , Wang   Y , et al.    Association of the hospital readmissions reduction program with mortality during and after hospitalization for acute myocardial infarction, heart failure, and pneumonia . JAMA Netw Open   2018 ; 1 : e182777 . https://doi.org/10.1001/jama.2012.21

Ko   DT , Khera   R , Lau   G , Qiu   F , Wang   Y , Austin   PC , et al.    Readmission and mortality after hospitalization for myocardial infarction and heart failure . J Am Coll Cardiol   2020 ; 75 : 736 – 46 . https://doi.org/10.1016/j.jacc.2019.12.026

Lee   DS , Lee   JS , Schull   MJ , Borgundvaag   B , Edmonds   ML , Ivankovic   M , et al.    Prospective validation of the emergency heart failure mortality risk grade for acute heart failure . Circulation   2019 ; 139 : 1146 – 56 . https://doi.org/10.1161/CIRCULATIONAHA.118.035509

Lee   DS , Straus   SE , Farkouh   ME , Austin   PC , Taljaard   M , Chong   A , et al.    Trial of an intervention to improve acute heart failure outcomes . N Engl J Med   2023 ; 388 : 22 – 32 . https://doi.org/10.1056/NEJMoa2211680

Tsao   CW , Lyass   A , Enserro   D , Larson   MG , Ho   JE , Kizer   JR , et al.    Temporal trends in the incidence of and mortality associated with heart failure with preserved and reduced ejection fraction . JACC Heart Fail   2018 ; 6 : 678 – 85 . https://doi.org/10.1016/j.jchf.2018.03.006

Greene   SJ , Fonarow   GC , Vaduganathan   M , Khan   SS , Butler   J , Gheorghiade   M . The vulnerable phase after hospitalization for heart failure . Nat Rev Cardiol   2015 ; 12 : 220 – 9 . https://doi.org/10.1038/nrcardio.2015.14

Kosiborod   MN , Angermann   CE , Collins   SP , Teerlink   JR , Ponikowski   P , Biegus   J , et al.    Effects of empagliflozin on symptoms, physical limitations, and quality of life in patients hospitalized for acute heart failure: results from the EMPULSE trial . Circulation   2022 ; 146 : 279 – 88 . https://doi.org/10.1161/CIRCULATIONAHA.122.059725

Voors   AA , Angermann   CE , Teerlink   JR , Collins   SP , Kosiborod   M , Biegus   J , et al.    The SGLT2 inhibitor empagliflozin in patients hospitalized for acute heart failure: a multinational randomized trial . Nat Med   2022 ; 28 : 568 – 74 . https://doi.org/10.1038/s41591-021-01659-1

Bhatt   DL , Szarek   M , Steg   PG , Cannon   CP , Leiter   LA , McGuire   DK , et al.    Sotagliflozin in patients with diabetes and recent worsening heart failure . N Engl J Med   2021 ; 384 : 117 – 28 . https://doi.org/10.1056/NEJMoa2030183

Velazquez   EJ , Morrow   DA , DeVore   AD , Duffy   CI , Ambrosy   AP , McCague   K , et al.    Angiotensin–neprilysin inhibition in acute decompensated heart failure . N Engl J Med   2019 ; 380 : 539 – 48 . https://doi.org/10.1056/NEJMoa1812851

Jankowska   EA , Kasztura   M , Sokolski   M , Bronisz   M , Nawrocka   S , Oleśkowska-Florek   W , et al.    Iron deficiency defined as depleted iron stores accompanied by unmet cellular iron requirements identifies patients at the highest risk of death after an episode of acute heart failure . Eur Heart J   2014 ; 35 : 2468 – 76 . https://doi.org/10.1093/eurheartj/ehu235

Núñez   J , Comín-Colet   J , Miñana   G , Núñez   E , Santas   E , Mollar   A , et al.    Iron deficiency and risk of early readmission following a hospitalization for acute heart failure . Eur J Heart Fail   2016 ; 18 : 798 – 802 . https://doi.org/10.1002/ejhf.513

Ponikowski   P , Kirwan   BA , Anker   SD , McDonagh   T , Dorobantu   M , Drozdz   J , et al.    Ferric carboxymaltose for iron deficiency at discharge after acute heart failure: a multicentre, double-blind, randomised, controlled trial . Lancet   2020 ; 396 : 1895 – 904 . https://doi.org/10.1016/S0140-6736(20)32339-4

Kalra   PR , Cleland   JGF , Petrie   MC , Thomson   EA , Kalra   PA , Squire   IB , et al.    Intravenous ferric derisomaltose in patients with heart failure and iron deficiency in the UK (IRONMAN): an investigator-initiated, prospective, randomised, open-label, blinded-endpoint trial . Lancet   2022 ; 400 : 2199 – 209 . https://doi.org/10.1016/S0140-6736(22)02083-9

Zito   A , Princi   G , Romiti   GF , Galli   M , Basili   S , Liuzzo   G , et al.    Device-based remote monitoring strategies for congestion-guided management of patients with heart failure: a systematic review and meta-analysis . Eur J Heart Fail   2022 ; 24 : 2333 – 41 . https://doi.org/10.1002/ejhf.2655

McMurray   JJV , Solomon   SD , Inzucchi   SE , Køber   L , Kosiborod   MN , Martinez   FA , et al.    Dapagliflozin in patients with heart failure and reduced ejection fraction . N Engl J Med   2019 ; 381 : 1995 – 2008 . https://doi.org/10.1056/NEJMoa1911303

Petrie   MC , Verma   S , Docherty   KF , Inzucchi   SE , Anand   I , Belohlávek   J , et al.    Effect of dapagliflozin on worsening heart failure and cardiovascular death in patients with heart failure with and without diabetes . JAMA   2020 ; 323 : 1353 – 68 . https://doi.org/10.1001/jama.2020.1906

McMurray   JJV , DeMets   DL , Inzucchi   SE , Køber   L , Kosiborod   MN , Langkilde   AM , et al.    A trial to evaluate the effect of the sodium-glucose co-transporter 2 inhibitor dapagliflozin on morbidity and mortality in patients with heart failure and reduced left ventricular ejection fraction (DAPA-HF) . Eur J Heart Fail   2019 ; 21 : 665 – 75 . https://doi.org/10.1002/ejhf.1432

McDonagh   TA , Metra   M , Adamo   M , Gardner   RS , Baumbach   A , Böhm   M , et al.    2023 Focused Update of the 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure: developed by the task force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) With the special contribution of the Heart Failure Association (HFA) of the ESC . Eur Heart J   2023 ; 44 : 3627 – 39 . https://doi.org/10.1093/eurheartj/ehad195

• heart failure, acute
• pharmacotherapy
• heart failure
• vasodilators
• noninvasive ventilation
• medical management

Email alerts

More on this topic, related articles in pubmed, citing articles via, looking for your next opportunity, affiliations.

• Online ISSN 1522-9645
• Print ISSN 0195-668X
• Copyright © 2024 European Society of Cardiology
• About Oxford Academic
• Publish journals with us
• University press partners
• What we publish
• New features  
• Open access
• Institutional account management
• Rights and permissions
• Get help with access
• Accessibility
• Media enquiries
• Oxford University Press
• Oxford Languages
• University of Oxford

Oxford University Press is a department of the University of Oxford. It furthers the University's objective of excellence in research, scholarship, and education by publishing worldwide

• Copyright © 2024 Oxford University Press
• Cookie settings
• Cookie policy
• Privacy policy
• Legal notice

This Feature Is Available To Subscribers Only

Sign In or Create an Account

This PDF is available to Subscribers Only

For full access to this pdf, sign in to an existing account, or purchase an annual subscription.

Heart Failure (CHF): Nursing Diagnoses, Care Plans, Assessment & Interventions

Heart failure (HF) , sometimes referred to as Congestive Heart Failure (CHF) , occurs when the heart can’t supply blood effectively to the rest of the body . The left ventricle of the heart is larger and is responsible for most of the pumping action. In left-sided HF , the left ventricle either loses its contractility, so it can’t pump normally, or the ventricle becomes stiff and cannot relax and fill with blood properly between each beat.

Left-sided HF often leads to right-sided heart failure. In right-sided HF , if the right ventricle can’t pump properly, blood backs up in the veins, which leads to congestive heart failure (CHF). If the heart isn’t pumping blood effectively to the body, all organ systems will suffer.

In this article:

• Nursing Process
• Review of Health History
• Physical Assessment
• Diagnostic Procedures
• Nursing Interventions
• Activity Intolerance
• Decreased Cardiac Output
• Decreased Cardiac Tissue Perfusion
• Excess Fluid Volume
• Impaired Gas Exchange
• Ineffective Health Maintenance
• Risk for Unstable Blood Pressure

Nurses play a pivotal role not only in treating patients with heart failure but educating them on lifestyle modifications to prevent disease progression or complications.

The nurse must understand the mechanism of the heart and the pathophysiology of HF in order to effectively treat patients, monitor for impending changes, and prevent worsening effects on other body systems.

Nursing Assessment

The first step of nursing care is the nursing assessment, during which the nurse will gather physical, psychosocial, emotional, and diagnostic data. In this section we will cover subjective and objective data related to heart failure.

1. Assess the patient’s general symptoms. Record the patient’s complaints and general symptoms, such as:

• Dyspnea on exertion  
• Orthopnea  
• Fatigue /weakness 
• Edema in lower extremities  
• Tachycardia   
• Irregular heartbeat  
• Exercise intolerance 
• Persistent cough  
• Wheezing  
• Abdominal swelling 
• Rapid weight gain  
• Lack of appetite  
• Decreased alertness  

2. Investigate the underlying cause. Heart failure typically occurs due to something else (i.e., another condition/disease or possibly a medication) causing damage to the heart muscle. Conditions that could potentially damage the heart and lead to heart failure include: 

• Coronary artery disease
• Myocardial infarction
• Hypertension
• Heart valve disease
• Myocarditis
• Congenital heart defects
• Cardiac arrhythmias
• Other long-term, chronic conditions that are poorly managed (such as diabetes mellitus , HIV , hyperthyroidism, or hypothyroidism )

3. Identify the stage of heart failure. Heart failure classification is used to denote the severity of symptoms.

Stages of Heart Failure:

• Class I: No limitation to physical activity.
• Class II: Activities of daily living can be completed without difficulty; however, exertion causes shortness of breath and some fatigue.
• Class III: Difficulty completing activities of daily living without fatigue, palpitations, or dyspnea.
• Class IV: Shortness of breath occurs at rest.

4. Know the patient’s risk.

Non-modifiable risk factors:

• Age: The heart can become stiff and frail with advanced age. The risk of heart failure is increased in people over 65. Elderly patients are also more prone to various health issues that cause heart failure.
• Gender: Heart failure is twice as likely to occur in men.
• Family history of ischemic heart disease: There is a high risk if a close female relative (mother or sister) had heart disease before age 65 or if a close male relative (father or brother) had it before age 55.
• Race/ethnicity: Heart failure is more common in African-Americans and Latinos than in Caucasian people.

Modifiable risk factors:

• Hypertension: Uncontrolled high blood pressure can result in stiffening and rigid arteries. Coronary artery constriction may impair blood flow.
• Hyperlipidemia/hypercholesterolemia/coronary artery disease: Increased levels of low-density lipoprotein (LDL) or decreasing levels of high-density lipoprotein (HDL) in the blood can increase the risk of atherosclerosis, narrowing the blood vessels.
• Diabetes or insulin resistance: Hardening of the blood arteries and accumulating fatty plaque are effects of diabetes or insulin resistance.
• Heart valve disease: If the heart valves are impaired, the heart must work harder to pump blood throughout the body, which can lead to heart failure.
• Tobacco use: Smoking accelerates the buildup of plaque in blood vessels. Smokers experience heart failure at a rate twice that of non-smokers.
• Obesity: Obesity increases the risk of high blood pressure, raised blood cholesterol, and diabetes. All are risk factors for heart failure.
• Physical inactivity: Those who are physically inactive are almost two times more likely to acquire heart disease than those who are active.
• Diet: A diet high in fatty, processed foods, high-sodium, or sugary foods increases the risk of obesity and chronic diseases that can lead to heart failure.  
• Stress: Blood vessels constrict as inflammatory levels rise under stress. Excessive stress hormones secreted can lead to heart failure.
• Alcohol use: Alcohol impairs the heart muscle and alters blood clot formation, resulting in the occlusion of blood vessels.
• Lack of sleep: Stress levels rise with insufficient sleep and cause blood vessels to constrict.
• Urinary tract infections
• Endocarditis

5. Review the patient’s treatment record. Medications and past vascular surgery compromise artery integrity. These medications include:

• Nonsteroidal anti-inflammatory drugs (NSAIDs)
• Diabetes medications rosiglitazone (Avandia) and pioglitazone (Actos) 
• Antihypertensive medications
• Blood disorders
• Irregular or abnormal heartbeats
• Nervous system disorders
• Mental health issues
• Lung and urinary issues
• Inflammatory diseases

1. Assess the vital signs. Vital indicators, particularly pulse rate and blood pressure, are anticipated to rise or change due to the heart’s reduced oxygenated blood supply. Monitor Spo2 for changes in oxygen saturation that signal deteriorating perfusion.

2. Systemic assessment approach:

• Neck: distended jugular veins 
• CNS: decreased alertness
• Cardiovascular: tachycardia, chest pain, abnormal heart sounds (pathological S3) upon auscultation, arrhythmias
• Circulatory: decreased peripheral pulses, narrow pulse pressure (less than 25 mmHg caused by reduced cardiac output)
• Respiratory: dyspnea on exertion or at rest, tachypnea, orthopnea, persistent or nocturnal cough, crackles or rhonchi in the lung bases upon auscultation
• Gastrointestinal: nausea and vomiting, lack of appetite, abdominal swelling from hepatic congestion and ascites
• Lymphatic: edema in the lower extremities
• Musculoskeletal: neck, arm, back, jaw, and upper body pain, fatigue, muscle weakness, activity intolerance, rapid weight gain from fluid
• Integumentary: cyanotic and pale skin and excessive sweating

1. Obtain ECG. ECG findings in heart failure are characterized by P wave changes resulting in left atrial hypertrophy (enlargement).

2. Analyze BNP lab results. As heart failure occurs, the heart releases B-type natriuretic peptide (BNP) in the blood, causing an elevation in the blood test. 

3. Investigate other blood tests.

• Complete blood count with differential indicates the presence of infection (WBC), blood coagulation (platelets), and anemia (low RBC levels).
• Cholesterol levels show a risk for coronary artery disease (a risk factor for heart failure).
• Thyroid levels reflect disturbed thyroid hormones that can cause arrhythmias.

4. Review chest X-ray results. Chest X-ray shows any changes in the size of the heart. It also reflects fluid accumulation around the heart and lungs.

5. Prepare the patient for an echocardiogram. An echocardiogram assesses the heart’s structure. This test is used to identify ejection fraction (EF) , a percentage that measures how well the ventricles pump blood. 

• An EF of 55-70% is normal
• 40-54% is slightly below normal and may not produce symptoms
• 35-39% is considered mild heart failure
• EF less than 35% is moderate to severe heart failure

6. Investigate further.

• Exercise treadmill test benefits a patient who is physically capable of exercising and has a normal resting ECG.
• Nuclear stress test shows images of blood flow to the heart muscle using an IV radioactive tracer dye. This is combined with exercise or medication to stimulate the heart rate.
• Stress imaging is for patients who had revascularization, with challenging ECGs to read, or are physically unable to exercise.
• Cardiac CT scan displays calcium deposits and cardiac artery blockages.
• Cardiac catheterization reveals any obstructed cardiac arteries or the presence of coronary artery disease.
• CT coronary angiogram is comparable to a cardiac CT scan but creates a more detailed image using dye (contrast).
• Myocardial biopsy investigates other heart diseases that can cause heart failure.

Nursing interventions and care are essential for the patients recovery. In the following section you’ll learn more about possible nursing interventions for a patient with heart failure.

Promote Perfusion

1. Relax the blood vessels. Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (ARBs) improve blood flow by relaxing the blood vessels. It also lowers blood pressure and cardiac muscle strain.

2. Lower the heart rate and pressure. Administer beta-blockers to reduce the heart rate and blood pressure, which can improve heart function.

3. Induce diuresis. Diuretics cause an increase in urination to remove excess fluid from the body.

4. Consider potassium-sparing diuretics. Aldosterone antagonists are potassium-sparing diuretics that help treat systolic heart failure. It removes the excess fluid in the heart and body.

5. Strengthen the heart contraction.

• Inotropes are typically given IV while hospitalized. These are designed to increase the effectiveness of the heart pumping and maintain blood pressure.
• Digoxin increases the strength of the heart’s contractions. Monitor closely for digoxin toxicity through lab testing.

6. Treat the underlying condition.

• Coronary artery bypass graft surgery (CABG) builds an additional pathway for blood in the heart. The blocked or constricted coronary artery is bypassed using an artery from another part of the body, such as the leg.
• Heart valve repair or replacement fixes or replaces the defective heart valve causing heart failure. 
• Cardiac resynchronization therapy (CRT) uses a biventricular pacemaker to correct electrical signals in the heart that causes arrhythmias.
• Ventricular assist devices (VADs) are mechanical pumps that improve heart contraction and pumping in heart failure.
• Heart transplant is recommended for patients with severe heart failure when treatments are no longer effective.

Cardiac Rehabilitation

1. Collaborate with the team. Patients will work with cardiologists, cardiac rehab nurse specialists, dieticians, social workers, and physical and occupational therapists to meet their health needs.

2. Improve activity tolerance. Following surgery or a procedure for heart failure, recovery will take time. Cardiac rehab will slowly introduce exercises to strengthen the heart.

3. Strengthen the patient’s health. Cardiac rehab enhances the patient’s health and quality of life by supporting the patient in restoring strength and preventing HF recurrence and complications.

Reduce the Risk of Complications

1. Regulate the heart rhythm. Implantable cardioverter-defibrillators (ICDs) are devices that prevent heart failure complications. ICD tracks the heart rhythm and keeps the heart rate regular if an arrhythmia occurs.

2. Repeat the importance of lifestyle modifications.  Adopting lifestyle adjustments can reduce heart failure symptoms and keep the condition from getting worse.

• Regular exercise
• Heart-healthy diets
• Smoking cessation
• Avoiding secondhand smoke
• Stress management
• Vaccinations
• Limiting alcohol consumption
• Restful sleep

3. Advise on activity.  Aerobic exercise regularly improves heart function in persons with heart disease. Physical activity may be difficult or impossible for patients with severe HF. Advise the patient to go for five to ten minutes at a moderate pace and aim to add one or two minutes daily as they can. 

4. Keep a healthy weight. Being overweight can cause fatty deposits to build up in the arteries. Advise the patient to limit saturated or trans fat. Blood pressure, cholesterol, and metabolic activity all improve with weight loss. 

5. Promote patient adherence to treatment. Treatment adherence promotes continuity of care and patient-centered care. Increased patient adherence leads to more efficient HF treatment and prevention of complications.

6. Decrease stress. Stress raises blood pressure and heart rate. Because the inflammatory response is activated, blood vessels constrict, increasing the risk of HF. Guided imagery, yoga, deep breathing exercises, muscle relaxation, meditation, and getting adequate sleep are examples of stress reduction techniques.

7. Prevent fluid accumulation. Monitor for any swelling in the lower extremities, which may indicate the presence of edema or fluid accumulation. Instruct on contacting their healthcare team if weight gain of more than 2.5 lbs overnight or 5 lbs in a week is observed. Also, limit sodium (salt) intake to prevent water retention. Fluid accumulation can increase the heart’s workload. 

8. Teach the patient when to seek medical attention. HF signs and symptoms that are a cause for concern are:

• Sudden weight gain
• Fainting (syncope)
• Sudden productive cough with white or pink, foamy secretions

9. Follow up with the cardiologist. Visits to a cardiologist and regular examinations, such as blood tests and echocardiograms, will aid in monitoring the disease process. Patients with HF are advised to visit their cardiologist every three-six months or as recommended.

10. Emphasize the use of medical identification. The emergency responders can be alerted about the patient’s history of HF by a medical identity bracelet, necklace, or ID tag. This can be helpful, especially for patients who are living alone.

Nursing Care Plans

Once the nurse identifies nursing diagnoses for heart failure, nursing care plans help prioritize assessments and interventions for both short and long-term goals of care. In the following section you will find nursing care plan examples for heart failure.

Activity intolerance is a common manifestation and nursing diagnosis related to HF that can lead to worsening health conditions and physical deconditioning.

Nursing Diagnosis: Activity Intolerance

Related to:

• Imbalance between oxygen supply and demand 
• Weakness/deconditioning 
• Sedentary lifestyle 

As evidenced by:

• Fatigue 
• Dyspnea 
• Immobility  
• Vital sign changes in response to activity 
• Chest pain on exertion 
• Diaphoresis 

Expected outcomes:

• Patient will perform activities within their limitations so as not to stress cardiac workload.
• Patient will alternate between work and rest periods to complete ADLs.
• Patient will demonstrate vital signs and heart rhythm within normal limits during activity.

Assessment:

1. Observe cardiopulmonary response to activity. The nurse can monitor the patient’s heart rate, oxygen saturation, and cardiac rhythm during activity. A rise or drop in blood pressure, tachycardia, or EKG changes can signify overexertion and help plan appropriate interventions.

2. Assess the patient’s perspective. Assess the patient’s understanding of their condition and their perceived activity limitations. The goal is to ensure the patient is not overexerting themselves but also feels motivated to make progress with their activity tolerance and maintain independence.

3. Assess the degree of debility. Interventions can be tailored to the severity of the patient’s symptoms. Assess the level of fatigue, weakness, and dyspnea in relation to activity and length of exertion. The nurse may need to assist with ADLs or adjust the activities the patient can undertake for their safety .

Interventions:

1. Provide a calm environment. Dyspnea from HF can result in anxiety and restlessness. Provide the patient with a cool, dimly lit space free from clutter and stimulation. Assist the patient in taking slow, controlled breaths and provide emotional support so they feel in control.

2. Encourage participation. Even a patient with chronic HF and severe activity intolerance can assist with care to some extent. Provide toiletries at the bedside so the patient can brush their teeth or comb their hair. Have the patient assist with turning themselves in bed. A patient who becomes immobile from a sedentary lifestyle is at an increased risk for other complications such as skin breakdown, deep vein thrombosis (DVT) , and pneumonia.

3. Teach methods to conserve energy. Group tasks together, sit when possible when performing ADLs, plan rest periods, promote restful sleep, do not rush activities, and avoid activities in hot or cold temperatures.

4. Recommend cardiac rehabilitation. This is a medically supervised outpatient program that teaches a patient with a cardiac history how to reduce their risk of heart problems through exercise, heart-healthy diets, stress reduction , and management of chronic conditions. This is a team-based approach working with providers, nurses who specialize in cardiac care, PT and OT, and dieticians.

A decline in stroke volume from a loss of cardiac contractility or muscle compliance results in reduced filling or ejection of the ventricles. This reduced output decreases blood flow to other organs.

Nursing Diagnosis: Decreased Cardiac Output

• Altered heart rate/rhythm 
• Altered contractility 
• Structural changes (aneurysm, rupture) 
• Increased heart rate (palpitations) 
• Dysrhythmias 
• Shortness of breath 
• Anxiety  
• Orthopnea 
• Jugular vein distention; edema 
• Central venous pressure changes 
• Murmurs 
• Decreased peripheral pulses 
• Decreased urine output 
• Skin pallor, mottling, or cyanosis 
• Patient will display hemodynamic stability with vital signs, cardiac output, and renal perfusion within normal limits.
• Patient will participate in activities that reduce the workload of the heart.
• Patient will report an absence of chest pain or shortness of breath.

1. Assess vital signs, cardiac rhythm, and hemodynamic measurements. HF patients benefit from continuous cardiac monitoring via telemetry. The nurse can then act quickly if a dysrhythmia is observed. Blood pressure, pulse rate, and oxygen saturation should also be assessed regularly for changes. Unstable patients may need hemodynamic monitoring to maintain adequate perfusion.

2. Monitor skin and pulses. Poor cardiac output will result in decreased tissue perfusion . The nurse may observe skin mottling, pallor, or cyanosis. The skin may also feel cool or clammy. Along with these outward changes, peripheral pulses may be weak or irregular due to the lack of circulating blood volume.

3. Monitor mental status changes. HF can have long-term mental effects on the brain leading to poor memory and impaired cognition. The nurse can monitor for subtle changes or a decline in baseline presentation such as acute confusion or altered alertness.

1. Apply oxygen. Patients with low oxygen saturation may need supplemental oxygen due to the heart’s inability to pump oxygen-rich blood to the body. Patients with chronic HF may require oxygen therapy at home.

2. Administer medications. Vasodilators open arteries and veins to allow for decreased vascular resistance, increasing cardiac output and reducing ventricular workload. Morphine and anti-anxiety medications help with relaxing and calming the patient which can reduce cardiac workload. Angiotensin receptor blockers (ARBs) lower blood pressure and make pumping blood easier for the heart.

3. Instruct on ways to reduce the workload of the heart. Depending on the severity of the patient’s HF, they may need to modify daily activities. They may need assistance with ADLs, plenty of rest periods, and reduced exercise regimens.

4. Educate on risk factors and lifestyle modifications. Patients who are not yet diagnosed with HF or only have mild HF should be educated on prevention. Educate patients on risk factors such as hypertension, diabetes, atherosclerosis, and myocardial infarction that increase the risk of developing heart failure. Modifiable risk factors like smoking, obesity , sedentary lifestyle, and diets high in fat also increase the risk.

Decreased cardiac tissue perfusion associated with heart failure can be caused by insufficient blood flow resulting from impaired cardiac function.

Nursing Diagnosis: Decreased Cardiac Tissue Perfusion

• Structural impairment of the heart
• Malfunctions of the heart structures
• Difficulty of the heart muscle to pump
• Increased exertion in workload
• Inadequate blood supply to the heart
• Inability to contract and relax effectively
• Erratic signals causing chaotic or irregular heart contraction
• Decreased cardiac output
• Decreased blood pressure (hypotension)
• Decreased peripheral pulses
• Increased central venous pressure (CVP)
• Increased pulmonary artery pressure (PAP)
• Tachycardia
• Dysrhythmias
• Ejection fraction less than 40%
• Decreased oxygen saturation
• Presence of abnormal S3 and S4 heart sounds upon auscultation
• Patient will manifest pulse rate and rhythm within normal limits.
• Patient will demonstrate ejection fraction >40%.
• Patient will maintain palpable peripheral pulses.

1. Auscultate the apex of the heart. Determine if an abnormal heart sound S3 or S4 can be detected by auscultating the left lower sternal border. Children and athletes may naturally produce an S3 heart sound, but it is an abnormal finding in older adults and those with heart failure. Blood ejecting into a rigid ventricle causes the S4 heart sound.

2. Assist in myocardial perfusion test. Myocardial perfusion imaging (nuclear stress test) demonstrates how efficiently blood flows through the heart muscle. Additionally, it displays how efficiently the heart is pumping.

3. Check the BNP or NT-proBNP. B-type natriuretic peptide (BNP) or N-terminal pro-B-type natriuretic peptide (NT-proBNP) diagnoses heart failure (HF). It also supports the diagnosis of acutely decompensated HF in hospitalized patients or those treated in emergency rooms.

4. Obtain EKG. EKG can help rule out HF with a high sensitivity but low specificity. It can reveal the cause (such as a history of previous MI) and offer therapeutic indications (such as anticoagulation for atrial fibrillation).

5. Assist in TEE. Transthoracic echocardiography (TEE) can be useful in determining ejection fraction, left-atrial pressure, and cardiac output.

6. Prepare for a left heart catheterization or coronary angiography. Left-heart catheterization or coronary angiography is done to identify blockages or abnormalities with blood vessels in the heart to guide interventions.

1. Set the goal with the patient. Therapy aims to increase survival and symptoms, shorten hospital stays and avoid HF readmission, minimize morbidity, prevent HF-related organ damage, and suppress symptoms in patients with asymptomatic heart failure.

2. Administer medications as ordered. The following medications are included in the pharmacologic treatment of HF:

• Angiotensin system blockers (ACE inhibitors, ARBs, or ARNIs)
• Hydralazine with nitrate as an alternative if angiotensin system blockers are not tolerable
• Beta-blockers

3. Instruct on lifestyle modifications. Behavioral and lifestyle modifications include the following:

• Dietary and nutritional consultation
• Limit sodium to 2 to 3 g/day
• Fluid restriction to 2 L/day 
• Weight monitoring
• Aerobic exercise training 
• Control of existing risk factors (such as DM and lipid disorders)
• Smoking/alcohol/ illicit drug use cessation

4. Consider device therapy. Device therapies include cardiac resynchronization treatment (CRT) and implanted cardioverter-defibrillators (ICD). Patients should receive ACE inhibitors/ARB plus beta-blockers for at least three months prior to surgery. 

5. Anticipate the possibility of surgery. Heart transplantation, heart valve replacement, catheter ablation, and more are procedures to remodel, repair, or replace all or part of the heart’s function in treating HF. Surgery is often considered when medications aren’t effective.

Heart failure results in poor perfusion of the kidneys. If the kidneys cannot excrete sodium, water retention will occur and accumulate in tissues leading to fluid overload.

Nursing Diagnosis: Excess Fluid Volume

• Fluid intake or sodium intake 
• Reduced glomerular filtration rate  
• Increased secretion of antidiuretic hormone 
• Weight gain 
• Edema in extremities 
• Jugular vein distention 
• Adventitious breath sounds (crackles, rales) 
• High blood pressure 
• Oliguria 
• Tachycardia 
• Pulmonary congestion 
• Cough 
• S3 heart sound 
• Patient will demonstrate stable fluid volume through balanced intake and output, normal baseline weight, and no peripheral edema.
• Patient will verbalize signs and symptoms of fluid overload and when to seek help.
• Patient will verbalize dietary recommendations and fluid restrictions to maintain.

1. Assess for peripheral edema, anasarca, and JVD. Signs of fluid retention include edema in the lower legs and feet which is often pitting or generalized edema to the entire body known as anasarca. The most reliable sign indicating fluid overload is jugular vein distention (JVD).

2. Monitor breath and heart sounds. Patients with congestive heart failure (CHF) will present with shortness of breath and may have a cough with blood-tinged sputum due to pulmonary congestion. Upon assessment, the nurse will likely hear “wet” breath sounds (crackles). An S3 gallop signifies significant heart failure.

3. Monitor urine output and strict I&Os. Strict documentation of intake and output is required to monitor hydration and prevent worsening fluid overload. The nurse should record intake from oral and IV sources, maintain adherence to fluid restrictions, and assess urine output and characteristics. This is especially important if the patient is on diuretic therapy.

1. Maintain upright position. Semi-Fowlers or Fowler’s positioning will help the patient breathe easier and maintain comfort. They may require extra pillows or need to sleep in a reclining chair at home.

2. Administer diuretics. Diuretics are often prescribed as they rid the body of excess fluid which will decrease edema and dyspnea. Diuretics can be given by mouth or IV and must be monitored closely as they increase urination, decrease blood pressure, and decrease potassium.

3. Instruct on sodium and fluid restrictions. Diet education may include decreasing sodium and restricting fluids and will be directed by a provider. Patients should not use table salt or add salt to foods and should be aware of sodium contents in frozen or canned food. If a fluid restriction is ordered, the patient can track this by using a large pitcher that is their daily amount of fluid and drinking from it throughout the day. Ensure the patient understands their restriction includes all sources of fluid: soups, jello, and ice cream.

4. Teach how to monitor for fluid volume overload. Educate patients at discharge on signs of fluid retention. They should weigh themselves daily, using the same scale and at the same time each day. If a weight gain of 2 lbs in 24 hours or 5 lbs in a week is observed, they should call their doctor. Observed swelling to ankles or feet as well as an increase in dyspnea also requires assessment.

Inadequate blood flow results in decreased oxygenation and perfusion to tissues and organs. Heart failure itself is a related factor, but complications such as excess fluid can further impair gas exchange.

Nursing Diagnosis: Impaired Gas Exchange

• Ventilation perfusion imbalance related to altered blood flow 
• Changes to the alveolar-capillary membrane 
• Pulmonary congestion due to fluid retention 
• Changes in mental status 
• Restlessness 
• Anxiety 
• Abnormal ABGs 
• Changes in respiratory rate, depth, or rhythm 
• Patient will maintain ventilation and perfusion as evidenced by ABGs within normal limits.
• Patient will display improvement in ventilation by oxygen saturation above 95%.
• Patient will participate in ambulation and ADLs as allowed by respiratory ability.

1. Auscultate breath sounds. The patient may experience crackles, wheezes, or diminished breath sounds related to excess fluid in the lungs. Monitor closely for acute respiratory changes.

2. Monitor pulse oximetry. Abnormal oxygen saturation levels are a sign of hypoxemia, a lack of oxygen in the blood. This requires oxygen therapy and the underlying cause should be investigated and treated.

3. Monitor arterial blood gases (ABGs). ABGs measure the amount of oxygen and carbon dioxide in the blood. Abnormal or worsening ABGs indicate that the lungs are not ventilating or removing CO2 adequately.

1. Educate on coughing and deep breathing exercises. Clearing the airway and expanding the lungs will assist in promoting oxygenation.

2. Change positions frequently. Movement also assists with the drainage of secretions which can decrease the risk of complications such as atelectasis and/or pneumonia. If the patient is able to ambulate, this should be encouraged multiple times per day.

3. Maintain semi-Fowler’s position. Keeping the head of the bed elevated maintains an open airway. This can also be based on the patient’s comfort as some cannot tolerate high-Fowler’s positioning. If the patient is able to sit in a chair this is recommended.

4. Administer supplemental oxygen as needed. Apply oxygen per provider orders and to maintain the oxygenation of the patient. Patients may need oxygen titrated up or down or may require more significant interventions such as BiPap or mechanical ventilation.

5. Administer medications as ordered. If the impaired gas exchange is in relation to excess fluid volume, medications such as diuretics may be required to treat the underlying cause.

Poor patient understanding or management of their condition can result in worsening symptoms and outcomes.

Nursing Diagnosis: Ineffective Health Maintenance

• Lack of understanding of heart failure and prognosis 
• Difficulty in following recommended treatment plan 
• Poor motivation to make lifestyle changes 
• Insufficient resources (access to cardiologist, finances) 
• Lack of support from family to encourage or monitor condition 
• Demonstrates a lack of knowledge of heart failure 
• Continues with inappropriate diet or behaviors despite education 
• Inconsistent with keeping appointments, taking medications, etc. 
• Patient will seek out information to prevent worsening heart failure.
• Patient will identify (3) lifestyle modifications to improve heart failure.
• Patient will take responsibility for their health outcomes by identifying areas for improvement.

1. Assess the level of understanding of the disease process. Determine the patient’s present knowledge of risk factors, symptoms, treatments, and goals in order to tailor teaching to meet their needs.

2. Assess support system. Management of chronic conditions can be very challenging for patients and having a strong support system can assist in better adherence to the treatment plan.

1. Educate on normal heart function compared to the patient’s current heart function. Understanding the disease process can help the patient understand the goals of treatment and improve adherence. Explaining results of testing, such as the EF, or reviewing the HF classification system helps them feel more involved in their care.

2. Reinforce the rationale of treatments. Furthermore, patients may not grasp the reasoning for certain treatments such as fluid restrictions, weighing themselves daily, or the importance of medications. Explain in simple terms and provide written education if appropriate.

3. Educate on the importance and benefits of regular exercise. This will assist with maintaining muscle strength and organ function to strengthen the heart. Ensure exercise programs are safe for the patient and cleared by their provider.

4. Review medications. Thorough medication reconciliation and review is required before discharge or after each provider visit. The nurse should review changes and instruct on frequencies, side effects, and any considerations with each medication.

Risk for unstable blood pressure (BP) associated with heart failure can be caused by impaired structure and function of the heart muscle to pump blood effectively throughout the body.

Nursing Diagnosis: Risk for Unstable Blood Pressure

• Conditions that compromise the blood supply

A risk diagnosis is not evidenced by signs and symptoms as the problem has not yet occurred and the goal of nursing interventions is aimed at prevention.

• Patient will maintain blood pressure within normal limits.
• Patient will not experience hypotension with activity.
• Patient will maintain strict adherence to antihypertensive medications as ordered.

1. Closely assess the patient’s blood pressure. Heart attack and stroke can result from high systolic and diastolic blood pressure. Advise treating hypertension in heart failure with decreased ejection fraction. The target blood pressure is 130/80 mmHg.

2. Obtain blood samples for lab tests. The following blood tests determine the risk for unstable blood pressure in patients with heart failure:

• Blood urea nitrogen and serum creatinine
• Electrolyte levels
• Thyroid function
• Cholesterol (lipid) levels
• Blood glucose levels
• Liver function

3. Review the patient’s current treatment. Medications and herbal remedies aggravate or induce heart failure because they affect the blood pressure and heart muscles’ ability to pump blood and interact with other treatments and medications for heart failure. Examples of medications include:

• Spironolactone, angiotensin-converting enzyme (ACE) inhibitor, and furosemide can lead to electrolyte imbalances and renal failure
• Opioids and stimulants disturb the natural balance of certain neurotransmitters in the body and brain (catecholamines)
• Ashwagandha, blue cohosh, and Yohimbe are herbs sold in the United States that can cause cardiac toxicity

4. Identify underlying conditions. Systemic diseases, cardiac disorders, and some genetic defects can result in heart failure. The most prevalent underlying causes of heart failure are coronary artery disease, hypertension, and a previous heart attack.

1. Treat the underlying condition. Treatment of heart failure starts with prevention by reducing the risk factors. Patients should work to manage their blood pressure through exercise, weight loss, diet, medications, and smoking cessation.

2. Alert the patient when to seek emergency care. Symptoms of hypertension or hypotension include:

• A rapid heartbeat 
• Dizziness or fainting
• Profuse sweating
• Blurred vision

3. Instruct on how to take an accurate blood pressure reading. If the patient is monitoring their blood pressure at home, ensure they adhere to the following:

• Try to take the blood pressure at the same times each day
• Rest for 5-10 minutes to allow the blood pressure to return to baseline
• Do not cross your legs or ankles while taking a blood pressure
• Do not talk while taking a blood pressure

Ensure the patient and/or family member are using the correct size cuff and placing it correctly on the arm.

4. Advise the patient to keep BP logs. Heart failure (HF) patients’ usual clinical practice includes checking their blood pressure regularly. It is generally recognized that increased BP predicts cardiovascular risk. Advise the patient to keep accurate records to allow the healthcare team to monitor the effectiveness of treatment.

• Ackley, B.J., Ladwig, G.B., Flynn Makic M.B., Martinez-Kratz, M., & Zanotti, M. (2019). Nursing diagnosis handbook: An evidence-based guide to planning care (12th edition). Mosby.
• American Heart Association. (2018, January 11). What is heart failure? www.heart.org. Retrieved February 2023, from https://www.heart.org/en/health-topics/heart-failure/what-is-heart-failure
• Blumenthal, R. & Jones, S. (2021). Congestive heart failure: Prevention, treatment, and research. https://www.hopkinsmedicine.org/health/conditions-and-diseases/congestive-heart-failure-prevention-treatment-and-research
• Brown AC. Heart Toxicity Related to Herbs and Dietary Supplements: Online Table of Case Reports. Part 4 of 5. J Diet Suppl. 2018 Jul 4;15(4):516-555. doi: 10.1080/19390211.2017.1356418. Epub 2017 Oct 5. PMID: 28981338.
• Cardiac Rehab for Heart Failure. (2017, May 31). American Heart Association. Retrieved January 26, 2022, from https://www.heart.org/en/health-topics/heart-failure/treatment-options-for-heart-failure/cardiac-rehab-for-heart-failure
• Centers for Disease Control and Prevention. (2022, October 14). Heart failure. Retrieved February 2023, from https://www.cdc.gov/heartdisease/heart_failure.htm
• Cleveland Clinic. (2022, January 21). Heart failure: Common symptoms, causes and treatment. Retrieved March 2023, from https://my.clevelandclinic.org/health/diseases/17069-heart-failure-understanding-heart-failure
• Doenges, M. E., Moorhouse, M. F., & Murr, A. C. (2008). Nurse’s Pocket Guide Diagnoses, Prioritized Interventions, and Rationales (11th ed.). F. A. Davis Company.
• Doenges, M.E., Moorhouse, M.F., & Murr, A.C. (2019). Nursing care plans: Guidelines for individualizing client care across the life span (10th edition). F.A. Davis Company.
• Dumitru, I., & Sharma, G. K. (2021, October 27). Heart Failure Treatment & Management: Approach Considerations, Nonpharmacologic Therapy, Pharmacologic Therapy. Medscape Reference. Retrieved January 26, 2022, from https://emedicine.medscape.com/article/163062-treatment
• Heart failure – Symptoms and causes. (2021, December 10). Mayo Clinic. Retrieved January 26, 2022, from https://www.mayoclinic.org/diseases-conditions/heart-failure/symptoms-causes/syc-20373142
• Heart Failure: Types, Symptoms, Causes & Treatments. (n.d.). Cleveland Clinic. Retrieved January 26, 2022, from https://my.clevelandclinic.org/health/diseases/17069-heart-failure-understanding-heart-failure
• Heckman, G. A., Patterson, C. J., Demers, C., St Onge, J., Turpie, I. D., & McKelvie, R. S. (2007). Heart failure and cognitive impairment: challenges and opportunities. Clinical interventions in aging, 2(2), 209–218.
• Mayo Clinic. (2021, December 10). Heart failure – Diagnosis and treatment – Mayo Clinic. Retrieved March 2023, from https://www.mayoclinic.org/diseases-conditions/heart-failure/diagnosis-treatment/drc-20373148
• Micaela, I. (2020, June 25). Heart failure – fluids and diuretics. MedlinePlus. Retrieved January 26, 2022, from https://medlineplus.gov/ency/patientinstructions/000112.htm
• National Center for Biotechnology Information. (2022, April 30). Heart failure and ejection fraction – StatPearls – NCBI bookshelf. Retrieved March 2023, from https://www.ncbi.nlm.nih.gov/books/NBK553115/
• Pellicori, P., Kaur, K., & Clark, A. L. (2015). Fluid Management in Patients with Chronic Heart Failure. Cardiac failure review, 1(2), 90–95. https://doi.org/10.15420/cfr.2015.1.2.90
• The Trustees of the University of Pennsylvania. (2020, August 27). Avoid these foods if you have heart failure – Penn medicine. Penn Medicine. Retrieved March 2023, from https://www.pennmedicine.org/updates/blogs/heart-and-vascular-blog/2020/august/avoid-these-foods-if-you-have-heart-failure
• Types of Heart Failure. (2017, May 31). American Heart Association. Retrieved January 26, 2022, from https://www.heart.org/en/health-topics/heart-failure/what-is-heart-failure/types-of-heart-failure
• WebMD. (2002, September 19). How do I get a diagnosis of heart failure? Retrieved March 2023, from https://www.webmd.com/heart-disease/heart-failure/heart-failure-diagnosis

13 Heart Failure Nursing Care Plans

Utilize this comprehensive nursing care plan and management guide to provide optimal care for patients with heart failure . Gain valuable insights on nursing assessment , interventions, goals, and nursing diagnosis specifically tailored for heart failure in this guide.

Table of Contents

What is heart failure, nursing problem priorities, nursing assessment, nursing diagnosis, nursing goals, 1. initiating interventions for decrease in cardiac output, 2. monitoring diagnostic procedures and laboratory studies, 3. administering medication and providing pharmacological interventions, 4. maintaining or improving respiratory function, 5. managing fluid volume and electrolyte imbalance, 6. providing perioperative nursing care, 7. managing acute pain and discomfort, 8. promoting adequate tissue perfusion and managing decreased cardiac tissue perfusion, 9. promoting optimal nutritional balance and adherence to low-sodium diet, 10. maintaining skin integrity & preventing pressure ulcers, 11. managing decreased tolerance to activity and fatigue, 12. reducing anxiety, fear and improving coping, 13. initiating health teaching and patient education, discharge and home care guidelines, discharge goals, documentation guidelines, recommended resources, references and sources.

Heart failure (HF) or Congestive Heart Failure (CHF) is a physiologic state in which the heart cannot pump enough blood to meet the body’s metabolic needs following any structural or functional impairment of ventricular filling or ejection of blood.

Heart failure results from changes in the systolic or diastolic function of the left ventricle . The heart fails when, because of intrinsic disease or structural, it cannot handle a normal blood volume or, in the absence of disease, cannot tolerate a sudden expansion in blood volume. Heart failure is a progressive and chronic condition managed by significant lifestyle changes and adjunct medical therapy to improve quality of life. Heart failure is caused by various cardiovascular conditions such as chronic hypertension , coronary artery disease, and valvular disease.

Heart failure is not a disease itself. Instead, the term refers to a clinical syndrome characterized by manifestations of volume overload, inadequate tissue perfusion , and poor exercise tolerance. Whatever the cause, pump failure results in hypoperfusion of tissues, followed by pulmonary and systemic venous congestion.

Clinical Manifestations

Heart failure can affect the heart’s left side, right side, or both sides. Though, it usually affects the left side first. The signs and symptoms of heart failure are defined based on which ventricle is affected—left-sided heart failure causes a different set of manifestations than right-sided heart failure.

Left-Sided Heart Failure

• Dyspnea on exertion
• Pulmonary congestion, pulmonary crackles
• Cough that is initially dry and nonproductive
• Frothy sputum that is sometimes blood-tinged
• Inadequate tissue perfusion
• Weak, thready pulse
• Tachycardia
• Oliguria, nocturia

Right-Sided Heart Failure

• Congestion of the viscera and peripheral tissues
• Edema of the lower extremities
• Enlargement of the liver (hepatomegaly)
• Anorexia , nausea
• Weight gain (fluid retention)

Because heart failure causes vascular congestion, it is often called congestive heart failure, although most cardiac specialists no longer use it. Other terms used to denote heart failure include chronic heart failure, cardiac decompensation, cardiac insufficiency, and ventricular failure.

Nursing Care Plans & Management

Nurses greatly influence the outcomes of patients with heart failure through education and monitoring despite high morbidity and mortality rates. Education empowers patients, improving adherence and preventing complications. Vigilant monitoring enables early intervention, reducing risks. Nurses play a crucial role in reducing HF morbidity and mortality.

The following are the nursing priorities for patients with congestive heart failure:

• Improve myocardial contractility and perfusion. Enhance heart’s pumping function to ensure adequate blood flow to organs through medications, monitoring vital signs, and optimizing fluid balance .
• Manage fluid volume. Monitor fluid balance, assess for signs of retention, administer diuretics , monitor weight, and promote adherence to a low- sodium diet.
• Prevent complications. Monitor for and manage complications such as pulmonary edema, arrhythmias, and thromboembolism through close monitoring, medication administration , and patient education.
• Promote activity tolerance . Encourage 30 minutes of daily physical activity (as tolerated), collaborate on a schedule, and prioritize activities.
• Reduce anxiety . Provide comfort , psychological support, and teach anxiety management techniques.
• Minimize powerlessness. Encourage patient expression of concerns and involve them in decision-making .
• Provide disease information and prevention education. Educate patients about heart failure, its impact, prognosis, lifestyle modifications, medication adherence, and seeking timely care to prevent worsening of symptoms.

Nursing assessment for patients with heart failure emphasizes evaluating the efficacy of treatment and the patient’s adherence to self-management strategies. Monitoring and reporting worsening signs and symptoms of heart failure are essential for adjusting therapy. Additionally, the nurse addresses the patient’s emotional well-being, as heart failure is a chronic condition linked to depression and psychosocial concerns

Health History

• Assess the signs and symptoms such as dyspnea, shortness of breath, fatigue , and edema.
• Assess for sleep disturbances, especially sleep suddenly interrupted by shortness of breath.
• Explore the patient’s understanding of HF, self management strategies, and the ability and willingness to adhere to those strategies.

Physical Examination

• Auscultate the lungs for presence of crackles and wheezes.
• Auscultate the heart for the presence of an S3 heart sound.
• Assess JVD for presence of distention.
• Evaluate the sensorium and level of consciousness.
• Assess the dependent parts of the patient’s body for perfusion and edema.
• Assess the liver for hepatojugular reflux.
• Measure the urinary output carefully to establish a baseline against which to assess the effectiveness of diuretic therapy.
• Weigh the patient daily in the hospital or at home.

Assess for the following subjective and objective data:

• Increased heart rate (tachycardia)
• ECG changes
• Changes in BP (hypotension/ hypertension )
• Extra heart sounds (S3, S4)
• Decreased urine output (oliguria)
• Diminished peripheral pulses
• Jugular vein distention
• Changes in vital signs
• Presence of dysrhythmias
• Diaphoresis
• Weight gain
• Respiratory distress
• Abnormal breath sounds

Assess for factors related to the cause of congestive heart failure:

• Altered circulation
• Altered myocardial contractility/inotropic changes
• Alterations in rate, rhythm, electrical conduction
• Decreased cardiac output
• Structural changes (e.g., valvular defects, ventricular aneurysm)
• Poor cardiac reserve
• Side effects of medication
• Imbalance between oxygen supply/demand
• Prolonged bed rest
• Reduced glomerular filtration rate (decreased cardiac output)/increased antidiuretic hormone (ADH) production, and sodium/water retention.
• Changes in glomerular filtration rate
• Use of diuretics
• Lack of understanding
• Misconceptions about interrelatedness of cardiac function/disease/failure
• Invasive procedures
• Prolonged hospitalization
• Alveolar edema secondary to increased ventricular pressure
• Retained secretions
• Increased metabolic rate secondary to pneumonia

Following a thorough assessment, a nursing diagnosis is formulated to specifically address the challenges associated with heart failure based on the nurse’s clinical judgement and understanding of the patient’s unique health condition. While nursing diagnoses serve as a framework for organizing care, their usefulness may vary in different clinical situations. In real-life clinical settings, it is important to note that the use of specific nursing diagnostic labels may not be as prominent or commonly utilized as other components of the care plan. It is ultimately the nurse’s clinical expertise and judgment that shape the care plan to meet the unique needs of each patient, prioritizing their health concerns and priorities. However, if you still find value in utilizing nursing diagnosis labels, here are some examples to consider:

• Decreased Cardiac Output related to impaired myocardial function as evidenced by signs of fatigue , dyspnea, and abnormal heart rate or blood pressure .
• Risk for Ineffective Health Maintenance related to lack of knowledge regarding diagnostic and laboratory procedures necessary for monitoring heart failure status.
• Impaired Gas Exchange related to fluid overload and pulmonary congestion as evidenced by [e.g., orthopnea, paroxysmal nocturnal dyspnea, and hypoxemia ].
• Excess Fluid Volume related to compromised heart function and renal perfusion as evidenced by [e.g., peripheral edema, ascites, and weight gain].
• Acute Pain related to decreased myocardial oxygenation as evidenced by [e.g., reports of chest pain or discomfort exacerbated by physical exertion or stress].
• Ineffective Tissue Perfusion (cardiopulmonary) related to decreased cardiac output as evidenced by [e.g., altered mental status, cool and clammy skin, and decreased urine output].
• Imbalanced Nutrition : Less Than Body Requirements related to dietary restrictions and fluid management in heart failure as evidenced by [e.g., confusion about low-sodium diet recommendations and fluid intake limits].
• Activity Intolerance related to imbalance between oxygen supply and demand as evidenced by [e.g., repotrs of fatigue , dyspnea on exertion, and decreased endurance].
• Anxiety related to changes in health status and uncertainty about the future due to heart failure diagnosis as evidenced by [e.g., patient’s verbalization of worries about their condition, noticeable restlessness, frequent questions about their prognosis, and expressed concerns regarding the effects of their illness on family roles and responsibilities].

Major goals for patients with heart failure include promoting physical activity, reducing fatigue, alleviating symptoms of fluid overload , managing anxiety, fostering patient empowerment in decision-making, and providing comprehensive health education to the patient and their family. Goals and expected outcomes may also include:

• The patient will exhibit optimal cardiac output, indicated by vital signs within acceptable ranges, absence/control of dysrhythmias, and absence of heart failure symptoms.
• The patient will engage in activities that reduce cardiac workload.
• The patient will actively participate in desired activities and meet their own self-care needs.
• The patient will maintain stable fluid volume, with balanced intake and output, clear/clearing breath sounds, vital signs within acceptable range, stable weight, and absence of edema.
• The patient will verbalize understanding of individual dietary and fluid restrictions.
• The patient will prioritize maintaining skin integrity .
• The patient will effectively manage pain.
• The patient will identify strategies to reduce anxiety.
• The patient will exhibit improved concentration.
• The patient will actively participate in their treatment regimen based on their abilities and situation.

Nursing Interventions and Actions

Therapeutic interventions and nursing actions for patients with congestive heart failure may include:

A decrease in cardiac output in heart failure occurs because the heart muscle weakens or becomes stiff, impairing its ability to contract and relax properly. Initiating nursing interventions for a decrease in cardiac output in patients with congestive heart failure is important because it can help prevent the progression of the disease and decrease the risk of complications. Early recognition and management of decreased cardiac output can improve patient outcomes and quality of life.

1. Auscultate apical pulse, assess heart rate. Tachycardia is an early sign of heart failure. An increase in heart rate is the body’s first response to compensate for reduced cardiac output (CO). Initially, this compensatory response has a favorable effect on cardiac output, but over time, persistent tachycardia is harmful and may worsen heart failure. Appropriate heart rate control has been associated with better clinical outcomes, including decreased hospitalizations and mortality (Yancy et al., 2017).

2. Obtain a comprehensive health history focusing on HF symptoms and self-management strategies. Understanding the patient’s health history helps identify signs and symptoms of worsening HF and assess the patient’s understanding and adherence to self-management strategies.

3. Note heart sounds. An extra heart sound S 3 or ventricular gallop may be heard during auscultation ( S 3 mixtape here ). This is caused by a large volume of fluid entering the ventricle at the beginning of diastole (Drazner et al., 2003). S 1 and S 2 may be weak because of decreased pumping action. Murmurs may reflect valvular incompetence. Auscultate the heart for S3 heart sound and assess heart rate and rhythm. S3 heart sound is an early sign of increased blood volume in the ventricle, indicating worsening HF. Monitoring heart rate and rhythm helps identify abnormalities that may contribute to decreased cardiac output and guides treatment decisions.

4. Assess rhythm and document dysrhythmias if telemetry is available. Both atrial and ventricular dysrhythmias are common. Myocardial stretch, fibrosis, and chamber dilation all alter the electrical paths of the heart. Atrial fibrillation (AF) is common in patients with HF, and occurrence increases with HF severity (Maisel et al., 2003; Yancy et al., 2007). Atrial fibrillation promotes thrombus formation within the atria. Other common dysrhythmias associated with HF include premature atrial contractions, paroxysmal atrial tachycardia, PVCs, multifocal atrial tachycardia, ventricular tachycardia, and ventricular fibrillation.

5. Assess for palpitations or irregular heartbeat. Palpitations can occur due to dysrhythmias secondary to chronic heart failure. Atrial fibrillation is the most common dysrhythmia in HF. It can also be a compensatory mechanism as the failing heart tries to accommodate for the lack of flow with a faster HR (Kemp et al., 2012). Patients may report fast or irregular heartbeat.

6. Palpate peripheral pulses. Decreased cardiac output may be reflected in diminished radial, popliteal, dorsalis pedis, and post-tibial pulses. Marked diminution or absence of peripheral pulses can indicate severely depressed stroked volume or the presence of severe occlusive vascular disease (Leier, 2007). Pulses may be fleeting or irregular to palpation , and pulsus alternans (a strong beat alternating with a weak beat) may be present. Evaluating peripheral pulses and skin perfusion helps determine the adequacy of peripheral perfusion. Decreased pulse volume and cool, pale, or cyanotic skin may indicate decreased cardiac output and guide interventions.

7. Monitor blood pressure (BP). In acute heart failure, BP may be elevated because of increased systemic vascular resistance (SVR). BP is often used to determine interventions (e.g., vasodilators , vasopressors, etc.). In chronic heart failure, BP is used as a parameter to determine the adequacy or excess dosage of pharmacological therapy (e.g., administration of ACE inhibitors).

8. Inspect the skin for mottling. Low cardiac output can result in decreased perfusion to the skin of the extremities and may result in mottling – a blue or gray coloring of the skin (Albert et al., 2010). Because of increased tissue capillary oxygen extraction in chronic HF, the skin may appear dusky.

9. Inspects the skin for pallor or cyanosis. Cool or clammy feeling to touch can occur with diminished perfusion; hypoperfusion in the limb will render pallor (Leier, 2007; Bolger, 2003). This finding, along with other signs of systemic hypoperfusion, will assist the primary care provider to choose proper pharmacotherapy and interventions needed to manage the patient’s condition.

10. Monitor urine output, noting decreasing output and concentrated urine . Urine output may be decreased due to decreased renal perfusion – kidneys react to reduced cardiac output by retaining water and sodium. The patient may also develop resistance to diuretics, resulting in decreased urinary output (De Bruyne et al., 2003). Urine output is usually low during the day because fluid shifts into tissues and increases at night (nocturia) due to increased renal perfusion during supine position (Redeker et al., 2012).

11. Note changes in sensorium: lethargy , confusion , disorientation, anxiety, and depression. Cerebral hypoperfusion occurs because of hypoxia to the brain from the decreased cardiac output. The patient may report this as confusion , forgetfulness, or restlessness. Through assessment is necessary to evaluate for possible related conditions, including psychological disorders. Depression is common among patients with heart failure and can lead to poor adherence to treatment plans. Studies have shown depression is 4 to 5 times more common in patients with heart failure and confers a twofold risk of mortality and higher readmission rates (Joynt et al., 2004; Rutledge et al., 2006).

12. Evaluate the patient’s level of consciousness for changes that may indicate decreased cerebral perfusion. Low cardiac output in HF can result in decreased oxygen delivery to the brain, potentially causing alterations in consciousness. Assessing the patient’s level of consciousness helps detect any changes and guides appropriate interventions.

13. Examine lower extremities for edema and rate its severity. Edema is a common manifestation of HF. Assessing its presence and severity helps evaluate fluid status and guide diuretic therapy and fluid management.

14. Assess the abdomen for tenderness, hepatomegaly, and signs of ascites. Abdominal assessment provides information on potential complications of HF, such as hepatic congestion and ascites. Identifying these findings guides interventions and treatment decisions.

15. Assess jugular vein distention (JVD). JVD is assessed to estimate central venous pressure and identify right ventricular failure. Abnormal JVD, defined as distention greater than 4 cm above the sternal angle, suggests increased venous pressure and guides treatment decisions.

16. Monitor results of laboratory and diagnostic tests. Signs and symptoms of heart failure are not highly specific and may mimic many other medical conditions (Yancy et al., 2017). The goal in diagnosis is to find the underlying cause of HF and the patient’s response to treatment.

17. Monitor oxygen saturation and ABGs. Baseline oxygen saturation is useful in establishing the diagnosis and severity of heart failure in acute settings (Masip et al., 2012; Milo-Cotter et al., 2009). Additionally, this provides information regarding the heart’s ability to perfuse distal tissues with oxygenated blood.

18. Give oxygen as indicated by the patient’s symptoms, oxygen saturation , and ABGs. Supplemental oxygen increases oxygen availability to the myocardium and can help relieve symptoms of hypoxemia, ischemia, and subsequent activity intolerance (Giordano, 2005; Haque et al., 1996). The need is based on the degree of pulmonary congestion and resulting hypoxia. Ongoing pulse oximetry monitors the need for and effectiveness of oxygen supplementation.

19. Provide a restful environment and encourage periods of rest and sleep; assist with activities. Minimizing controllable stressors and unnecessary disturbances reduces cardiac workload and oxygen demand (Rogers et al., 2015). Physical and emotional rest allows the patient to conserve energy. The degree of rest depends on the severity of HF. Patients with severe HF may need to rest in bed, while those with mild to moderate HF can be ambulatory with limited activity.

20. Encourage rest, semirecumbent in bed or chair. Assist with physical care as indicated. During acute or refractory HF, physical rest should be maintained to improve cardiac contraction efficiency and decrease myocardial oxygen demand/ consumption and workload. Enforce complete bed rest when necessary to decrease the cardiac workload on acute symptomatic attacks of HF.

21. Provide a quiet environment: explain therapeutic management, help the patient avoid stressful situations, listen, and respond to expressions of feelings. Psychological rest helps reduce emotional stress, which can produce vasoconstriction, elevating BP and increasing heart rate.

22. Assist the patient in assuming a high Fowler’s position . Allows for better chest expansion, thereby improving pulmonary capacity. In this position, the venous return to the heart is reduced, pulmonary congestion is alleviated, and pressure on the diaphragm is minimized. Additionally, heart failure with pulmonary congestion can cause a chronic nonproductive cough worsening in the recumbent position (Platz et al., 2017; Picano et al., 2010).

23. Check for calf tenderness, diminished pedal pulses, swelling, local redness, or pallor of extremity. The risk for thrombophlebitis increases with enforced bed rest, reduced cardiac output, and venous pooling.

24. Elevate legs, avoiding pressure under the knee or in a position comfortable to the patient. Decreases venous return and preload and may reduce the incidence of thrombus or embolus formation.

25. Reposition patient every two (2) hours . For patients under bed rest, prolonged immobility should be avoided because of its deconditioning effects and risk, such as pressure ulcers , especially in patients with edema. Decreased circulation in edematous areas also increases the risk of pressure ulcers.

26. Provide bedside commode, provide stool softeners as ordered. Have patient avoid activities eliciting a vasovagal response (straining during defecation, holding breath during position changes). Using a bedside commode decreases work of getting to the bathroom or struggling to use a bedpan. Patients with HF have autonomic dysfunction. Valsalva maneuver or similar behaviors reduces mean arterial blood pressure and cerebral blood flow, leaving patients vulnerable to hypoperfusion, ischemia, and stroke (Serber et al., 2014).

27. Encourage active and passive exercises. Increase activity as tolerated. For acute HF, bed rest may be temporarily indicated. Otherwise, a total of 30 minutes of physical activity every day should be encouraged (Yancy et al., 2017).

28. Administer medications as indicated. See Pharmacologic Management

29. Withhold digitalis preparation as indicated, and notify the physician if marked changes occur in cardiac rate or rhythm or signs of digitalis toxicity occur. The incidence of toxicity is high (20%) because of the narrow margin between therapeutic and toxic ranges. Digoxin may have to be discontinued in the presence of toxic drug levels, a slow heart rate, or low potassium level.

30. Administer IV solutions , restricting total amount as indicated. Avoid saline solutions. Because of existing elevated left ventricular pressure, the patient may not tolerate increased fluid volume ( preload ). The amount of fluid administered should be monitored closely (Bikdeli et al., 2015; Albert, 2012). Patients with HF also excrete less sodium, which causes fluid retention and increases cardiac workload.

31. Monitor for signs and symptoms of fluid and electrolyte imbalances . Fluid shifts and the use of diuretics can lead to excessive diuresis and may lead to electrolyte imbalances, such as hypokalemia (Oh et al., 2015). Signs of hypokalemia include ventricular dysrhythmias, hypotension, and generalized weakness . Hyperkalemia can occur with the use of ACE inhibitors, ARBs, or spironolactone .

32. Monitor serial electrocardiogram (ECG) and chest x-ray changes. Can indicate the underlying cause of HF. ST-segment depression and T-wave flattening can develop because of increased myocardial oxygen demand, even if no coronary artery disease is present. A chest X-ray may show an enlarged heart and pulmonary congestion.

33. Measure cardiac output and other functional parameters as indicated. Cardiac index, preload , afterload, contractility, and cardiac work can be measured noninvasively using the thoracic electrical bioimpedance (TEB) technique. Useful in determining the effectiveness of therapeutic interventions and response to activity.

34. Prepare for insertion and maintenance of pacemaker, if indicated. It may be necessary to correct bradydysrhythmias unresponsive to drug intervention. This can aggravate congestive failure and/or produce pulmonary edema.

35. Assist with mechanical circulatory support systems, such as the placement of a ventricular assist device (VAD). A battery-powered ventricular assist device (VAD) is positioned between the cardiac apex and the descending thoracic or abdominal aorta. This device receives blood from the left ventricle (LV) and ejects it into the systemic circulation, often allowing the patient to resume a nearly normal lifestyle while awaiting recovery, transplantation, or waiting for a decision (Yancy et al., 2017).

36. Recognize that some patients may need an intra-aortic balloon pump (IABP), and provide assistance. An intra-aortic balloon pump (IABP) may be inserted as temporary support to the failing heart in a critically ill patient with potentially reversible HF (Reid et al., 2005). When caring for a patient managed with IABP, the nurse must continually assess and measure the often subtle changes in patient’s condition. This requires expert knowledge of the cardiovascular system , therapeutic effects of IABP, and potential adverse events (Lewis et al., 2009). With end-stage HF, cardiac transplantation may be indicated.

37. Withhold digitalis preparation as indicated, and notify the physician if marked changes occur in cardiac rate or rhythm or signs of digitalis toxicity occur. The incidence of toxicity is high (20%) because of the narrow margin between therapeutic and toxic ranges. Digoxin may have to be discontinued in the presence of toxic drug levels, a slow heart rate, or low potassium level.

38. Administer IV solutions , restricting total amount as indicated. Avoid saline solutions. Because of existing elevated left ventricular pressure, the patient may not tolerate increased fluid volume (preload). The amount of fluid administered should be monitored closely (Bikdeli et al., 2015; Albert, 2012). Patients with HF also excrete less sodium, which causes fluid retention and increases cardiac workload.

39. Monitor for signs and symptoms of fluid and electrolyte imbalances . Fluid shifts and the use of diuretics can lead to excessive diuresis and may lead to electrolyte imbalances, such as hypokalemia (Oh et al., 2015). Signs of hypokalemia include ventricular dysrhythmias, hypotension, and generalized weakness. Hyperkalemia can occur with the use of ACE inhibitors, ARBs, or spironolactone.

40. Measure cardiac output and other functional parameters as indicated. Cardiac index, preload, afterload, contractility, and cardiac work can be measured noninvasively using the thoracic electrical bioimpedance (TEB) technique. Useful in determining the effectiveness of therapeutic interventions and response to activity.

Monitoring diagnostic procedures and laboratory studies is an essential aspect of caring for patients with heart failure. These assessments help healthcare professionals evaluate the severity of the condition, track progress, and guide treatment decisions. This helps healthcare providers make informed decisions about the patient’s care and adjust treatment plans as necessary.

1. Blood urea nitrogen (BUN) and creatinine. Elevation of BUN or creatinine reflects decreased renal perfusion, which may be caused by HF or medications (e.g., diuretics, ACE inhibitors).

2. Liver function studies (AST, LDH). May detect alterations in liver function which can demonstrate possible cause or effect. May also be elevated because of liver congestion and indicate a need for smaller dosages of medications.

3. Prothrombin time (PT) and activated partial thromboplastin time (aPTT) coagulation studies. Helps in identifying patients at risk for excessive clot formation and measures changes in coagulation processes or the effectiveness of anticoagulant therapy.

4. Atrial natriuretic peptide (ANP). ANP is a hormone secreted from the right atrial cells when pressure increases. It is increased in congestive HF.

5. Beta-type natriuretic peptide (BNP). BNP is secreted from the cardiac ventricles as a response to ventricular volume and fluid overload (Cowie & Mendez, 2002). BNP levels in the blood increases when symptoms of HF worsen.

6. Electrocardiogram (ECG). Can indicate the underlying cause of HF. ST-segment depression and T-wave flattening can develop because of increased myocardial oxygen demand, even if no coronary artery disease is present.

7. Echocardiogram . This ultrasound test provides detailed images of the heart’s structure and function, including the size and thickness of the heart chambers, the strength of the heart’s contractions, and the ejection fraction (the percentage of blood pumped out with each heartbeat). Echocardiograms are regularly performed to assess cardiac function and monitor changes over time.

8. Cardiac stress test. This test evaluates the heart’s response to physical exertion or pharmacological stress. It is used to assess exercise capacity, identify exercise-induced arrhythmias, and determine if there are any underlying coronary artery blockages contributing to heart failure symptoms.

9. Complete blood count (CBC). A CBC measures various components of the blood, including red and white blood cells and platelets. It helps identify anemia , infection , or other abnormalities that may impact heart failure management.

10. Kidney function tests. Blood tests such as serum creatinine and blood urea nitrogen (BUN) are used to assess kidney function. Impaired kidney function is common in heart failure and may affect treatment options and medication dosages.

11. Electrolyte levels. Blood tests measure electrolyte levels, such as sodium, potassium, and magnesium . Imbalances in these electrolytes can affect heart rhythm and overall cardiac function.

12. Chest X-ray A chest X-ray may show an enlarged heart and pulmonary congestion.

Administering medication and providing pharmacological interventions are critical components of caring for patients with heart failure. Medications are prescribed to manage symptoms, improve heart function, prevent complications, and enhance the patient’s quality of life. These interventions can also help slow the progression of the disease and improve overall outcomes for the patient.

1. Diuretics Diuretics are first-line drugs for all patients with signs of volume overload. Diuretics work by reducing blood volume, therefore, decreasing venous pressure, arterial pressure, pulmonary edema, peripheral edema, and cardiac dilation (Ellison et al., 2017; Brater, 2000). Diuretics are essential in managing fluid overload in patients with heart failure. Loop diuretics, thiazide diuretics, and aldosterone antagonists have different mechanisms of action in the kidney, promoting increased urine production and removal of excess extracellular fluid . Administering the prescribed diuretic helps alleviate symptoms of fluid overload and improve the patient’s overall condition. Data from several small controlled trials show that conventional diuretics appear to reduce the risk of death and worsening heart failure compared to a placebo in patients with CHF. About 80 deaths may be avoided for every 1000 people treated. Diuretics also increase the ability to exercise by about 28% to 33% more than other active drugs (Faris et al., 2012).

Commonly used diuretics for patients with heart failure include:

• Thiazide diuretics [hydrochlorothiazide (Microside)] are oral agents that produce moderate diuresis and are used for long-term therapy of heart failure when edema is moderate (Sica et al, 2011; De Bruyne et al, 2003). Thiazides are ineffective when the GFR is low and if the cardiac output is severely reduced. Adverse effects of thiazides include hypokalemia (thereby increasing risk of digoxin-induced dysrhythmias).
• Loop diuretics [ furosemide (Lasix), ethacrynic acid (Edecrin)] promote fluid loss even when GFR is low, in contrast with thiazides. Loop diuretics are the drug of choice for patients with severe heart failure (Felker, 2012). Other than hypokalemia, loop diuretics can also cause severe hypotension due to excessive fluid volume loss. Furosemide also reduces alveolar congestion, enhancing gas exchange .
• Potassium-sparing diuretics [spironolactone (Aldactone)] are used to counteract potassium loss caused by thiazide and loop diuretics, thereby reducing the risk of digoxin-induced dysrhythmias (Gao et al, 2007). Hyperkalemia is the principal adverse effect of these drugs (Brater, 2000).

Nursing interventions and actions for patients taking diuretics may include:

• Monitor and document the patient’s fluid intake and output, including daily weight measurements. Monitoring and documenting fluid intake and output, along with daily weight measurements, are crucial in evaluating the effectiveness of diuretic therapy. These parameters help assess the response to diuretics, determine the need for dosage adjustments, and identify any excessive fluid retention or depletion. Changes in weight can be an early indicator of fluid shifts. Tracking fluid intake and output provides valuable information on fluid balance. Comparing intake and output with weight changes helps evaluate the effectiveness of diuretic therapy and guides fluid management decisions.
• Monitor serum potassium levels regularly and report any abnormalities. Certain diuretics, such as loop diuretics and thiazide diuretics, increase potassium excretion, potentially leading to hypokalemia. Regular monitoring of serum potassium levels allows for early detection of imbalances and enables prompt intervention, such as adjusting the diuretic dosage or prescribing potassium supplements, to maintain optimal electrolyte balance.
• Educate the patient about the importance of adhering to a low-sodium diet and restricting fluid intake. A low-sodium diet, along with fluid restriction, helps reduce fluid overload and decrease the reliance on diuretics. Educating the patient about dietary modifications and fluid management strategies promotes self-care and empowers the patient to actively participate in their treatment plan, ultimately improving outcomes and reducing the burden of heart failure symptoms.
• Assess for signs and symptoms of orthostatic hypotension and kidney injury . Diuretic therapy can lead to orthostatic hypotension, especially in patients prone to volume depletion. Regular assessment for symptoms such as dizziness, lightheadedness, or syncope when changing positions helps identify orthostatic hypotension and guide appropriate interventions. Additionally, close monitoring for kidney injury, indicated by changes in urine output or renal function, is important to ensure early detection and management.
• Monitor serum creatinine and potassium levels frequently, especially during the initiation of aldosterone antagonists (e.g., spironolactone). Aldosterone antagonists, such as spironolactone, are potassium-sparing diuretics that require careful monitoring of serum creatinine and potassium levels. Close monitoring, particularly during the initial phase of treatment, helps detect any changes or abnormalities that may indicate renal impairment or potassium imbalance. Prompt intervention or dosage adjustments can then be made to ensure patient safety .
• Evaluate the patient’s response to diuretic therapy and assess for the development or worsening of cardiorenal syndrome. Monitoring the patient’s response to diuretic therapy is essential to evaluate its effectiveness in relieving

2. Vasodilators, arterial dilators, and combination drugs. Vasodilators treat heart failure by increasing cardiac output, reducing circulating volume, and decreasing systemic vascular resistance – ultimately reducing ventricular workload. Commonly used vasodilators include:

• Isosorbide dinitrate (ISDN) [Nitro Dur, Isordil] causes selective dilation of veins. For patients with severe refractory HF, ISDN can reduce congestive symptoms and improve exercise capacity (Ziaeian et al, 2017; Nyolczas et al, 2017; Cohn et al, 1991). Watch out for adverse effects such as orthostatic hypotension and reflex tachycardia.
• Hydralazine [Apresoline] causes selective dilation of arterioles, therefore, can help improve cardiac output and renal blood flow (Herman, 2017; Jacobs, 1984). Hydralazine is always used in combination with ISDN (e.g., BiDil – a fixed-dose combination of hydralazine and ISDN).
• Nitroglycerin when given intravenously, is a powerful vasodilator that produces a dramatic reduction in venous pressure. It is also used to relieve acute severe pulmonary edema (Levy et al, 2007). Hypotension and reflex tachycardia are its main adverse effects.
• Sodium nitroprusside [Nitropress] rapidly dilates arterioles and veins. Arteriolar dilation reduces afterload and thereby increasing cardiac output. Venodilation reduces venous pressure, thereby reducing pulmonary and peripheral congestion. Note: Blood pressure must be monitored continuously when taking this drug.
• Nesiritide administration leads to a rapid and balanced vasodilatory effect, which results in a significant decrease in right and left ventricular filling pressures and systemic vascular resistance and at the same time in an increase in stroke volume and cardiac output without a change in heart rate. (Elkayam et al, 2002). Nesiritide treatment significantly increased left ventricular ejection fraction, cardiac index, and 24- and 72-hour urine volumes. The drug safely improves global cardiac and systemic function for patients with heart failure (Zhao et al, 2020).

3. Angiotensin-converting Enzyme Inhibitors (ACE Inhibitors) [benazepril (Lotensin), captopril (Capoten), lisinopril (Prinivil), enalapril (Vasotec), quinapril (Accupril), ramipril (Altace), moexipril (Univasc)] blocks the renin-angiotensin-aldosterone-system (RAAS) by inhibiting the conversion of angiotensin I to angiotensin II. They decrease mortality, morbidity, hospitalizations, and symptoms in patients with heart failure (Yancy et al., 2017). These drugs also decrease the release of aldosterone and suppress the degradation of kinins. As a result, they improve hemodynamics and favorably alter cardiac remodeling. Additionally, observe for symptomatic hypotension, hyperkalemia, cough, and worsening renal function. Additional nursing interventions for patients taking ACE inhibitors may include:

• Monitor vital signs, including blood pressure, before and after administering ACE inhibitors. Monitoring vital signs, especially blood pressure, is essential when initiating ACE inhibitor therapy. These medications promote vasodilation, which can potentially cause hypotension. Regular monitoring allows for early detection and intervention in case of significant changes in blood pressure.
• Monitor serum potassium levels regularly. ACE inhibitors can cause hyperkalemia (increased potassium levels) due to their effect on inhibiting aldosterone secretion. Monitoring serum potassium levels allows for early detection of hyperkalemia, especially in patients concurrently receiving diuretics that may also affect potassium balance. Appropriate interventions can then be implemented to prevent complications.
• Educate the patient about the importance of compliance with medication regimen and regular follow-up appointments. Ensuring patient understanding and adherence to the prescribed ACE inhibitor regimen is crucial for optimal treatment outcomes. Education should include information about the benefits of ACE inhibitors, potential side effects, and the importance of attending regular follow-up appointments to monitor medication effectiveness, adjust dosages, and address any concerns or adverse reactions.
• Assess for the presence of a dry, persistent cough and report it to the primary care provider. A dry, persistent cough is a common side effect of ACE inhibitors. It is important to assess and monitor the patient for this adverse effect, as it may persist and affect the patient’s quality of life. Additionally, a persistent cough may also indicate a worsening of ventricular function and heart failure, necessitating further evaluation and intervention.
• Monitor for signs and symptoms of angioedema, such as swelling of the face, lips, or throat, and report immediately. Although rare, angioedema can occur as an allergic reaction to ACE inhibitors. It is a potentially life-threatening condition, particularly if it affects the oropharyngeal area and impairs breathing. Immediate discontinuation of the ACE inhibitor and provision of emergency care are essential to ensure patient safety and prevent further complications.
• Collaborate with the healthcare provider to adjust ACE inhibitor dosage based on the patient’s blood pressure, fluid status, renal function, and severity of heart failure. The optimal dosage of ACE inhibitors depends on various factors, including the patient’s blood pressure, fluid status, renal function, and severity of heart failure. Collaborating with the healthcare provider helps determine the appropriate dosage for each patient, ensuring that the medication is effective while minimizing the risk of adverse effects.

4. Angiotensin II receptor blockers (ARBs) [eprosartan (Teveten), irbesartan (Avapro), valsartan (Diovan)] are for patients who are unable to tolerate ACE inhibitors (usually owing to intractable cough). They prevent the vasoconstrictor and aldosterone-secreting effects of angiotensin II by binding to the angiotensin II receptor sites. ARBs promote afterload reduction and vasodilation, improve LV ejection fraction, reduce heart failure symptoms, increase exercise tolerance, decrease hospitalization, enhance the quality of life, and reduce mortality (Yancy et al., 2017). Monitoring is the same as ACE inhibitors.

5. Cardiac glycosides [Digitalis (Lanoxin)] Digoxin is a cardiac glycoside that increases the myocardial contractile force (positive inotropic action). By increasing contractile force, digoxin can increase cardiac output. It also slows the conduction of the heart through the AV node. Unfortunately, digitalis does not result in decreased mortality rates in patients with HF though effective in preventing hospital readmission and decreasing symptoms of systolic HF (Alkhawam et al., 2019; Qamer et al., 2019). Digitalis is considered a second-line agent for heart failure and was widely used in the past. Monitor the renal function and serum potassium levels of patients taking digitalis. Regular monitoring of renal function and serum potassium levels is essential to adjust digoxin dosage and prevent toxicity. Clinical manifestations of digoxin toxicity, such as anorexia, nausea, visual disturbances, confusion , and bradycardia, should be assessed and documented. Serum digoxin levels are obtained if renal function changes or toxicity symptoms occur. Patient education about digoxin toxicity signs, adherence to medication and monitoring, and prompt reporting of concerning symptoms is crucial.

6. Inotropic agents [amrinone (Inocor), milrinone (Primacor), vesnarinone (Arkin-Z), dobutamine [Dobutrex]] . These medications are useful for short-term or acute treatment of HF unresponsive to cardiac glycosides, vasodilators, and diuretics to increase myocardial contractility and produce vasodilation. They are given intravenously. Positive inotropic properties have reduced mortality rates by 50% and improved quality of life.

Additional nursing interventions for patients taking inotropic agents:

• Administer IV inotropes, such as milrinone (Primacor) or dobutamine (Dobutrex), to hospitalized patients with acute decompensated heart failure (HF) who do not respond to routine pharmacologic therapy. IV inotropes are used in patients with severe ventricular dysfunction and acute decompensated HF who do not respond to standard pharmacologic treatments. Milrinone and dobutamine increase myocardial contractility and can be effective in improving cardiac function. Administering these medications helps support cardiac output and perfusion in critically ill patients.
• Monitor blood pressure closely before and during the administration of milrinone, as it can cause hypotension. Milrinone promotes vasodilation, leading to decreased preload and afterload. Monitoring blood pressure before and during administration is crucial, especially in hypovolemic patients, as rapid drops in blood pressure can occur. Close monitoring allows for timely intervention and adjustment of medication dosage to maintain hemodynamic stability.
• Monitor blood pressure, ECG, and cardiac rhythm closely during and following infusions of milrinone. Close monitoring of blood pressure, electrocardiogram (ECG), and cardiac rhythm during and after milrinone infusions is necessary. Hypotension and increased ventricular dysrhythmias are major side effects of milrinone. Regular assessment of these parameters allows for early detection of adverse reactions and prompt interventions, ensuring patient safety.
• Administer dobutamine to patients with significant left ventricular dysfunction and hypoperfusion. Dobutamine is an IV medication used in patients with significant left ventricular dysfunction and inadequate tissue perfusion . It stimulates beta-1 adrenergic receptors, increasing cardiac contractility and renal perfusion, which enhances urine output. Administering dobutamine improves cardiac function and promotes adequate organ perfusion in critically ill patients.
• Monitor heart rate and rhythm closely during dobutamine administration, as it can increase heart rate and precipitate ectopic beats and tachydysrhythmias. Dobutamine action in stimulating beta-1 adrenergic receptors increases heart rate and can lead to the development of ectopic beats and tachydysrhythmias. Regular monitoring of heart rate and rhythm allows for early detection of any abnormalities or adverse effects. Prompt intervention can be implemented to manage dysrhythmias and ensure patient stability.
• Monitor and document hemodynamic data, including cardiac function and volume status, when utilizing IV inotropes, vasodilators, and diuretics. Monitoring and documenting hemodynamic data, including cardiac function and volume status, is crucial in managing patients receiving IV inotropes, vasodilators, and diuretics. Hemodynamic data provide valuable information about cardiac performance, fluid status, and response to therapy. These parameters guide treatment decisions, dose adjustments, and overall patient management in the intensive care unit (ICU) setting.
• Assess the patient’s need for continuous IV inotropic therapy at home if they cannot be weaned from IV inotropes and have end-stage heart failure. In some cases, patients with end-stage heart failure may require continuous IV inotropic therapy at home if they cannot be weaned off IV inotropes. Assessing the patient’s response to treatment, stability, and overall prognosis helps determine the need for home-based therapy. Continuous therapy requires careful monitoring and coordination with healthcare providers to ensure safety and optimal management of heart failure.

7. Beta-Blockers: Beta-adrenergic receptor antagonists [carvedilol (Coreg), bisoprolol (Zebeta), metoprolol (Lopressor)]. Beta-blockers are considered first-line therapy in the management of heart failure. They block the adverse effects of the sympathetic nervous system , leading to vasodilation, reduced blood pressure, decreased afterload, and decreased cardiac workload. Administering beta-blockers helps improve functional status, reduce mortality and morbidity, and prevent the onset of heart failure symptoms in patients with asymptomatic systolic dysfunction. Careful control of the dosage of beta-blockers can improve patient status by improving LV ejection fraction, increasing exercise tolerance, slowing HF progression, reducing the need for hospitalization, and prolong survival (Butler et al., 2006; Barrese et al., 2013). Side effects to look out for include worsening HF symptoms, hypotension, fatigue, and bradycardia. Additional nursing interventions for patients with heart failure taking beta blockers may include:

• Monitor vital signs, including blood pressure and heart rate, before and after administering beta-blockers. Monitoring vital signs, especially blood pressure and heart rate, is essential when initiating beta-blocker therapy. These medications lower blood pressure and can cause bradycardia. Regular monitoring allows for early detection and intervention in case of significant changes in blood pressure or heart rate.
• Educate the patient about the gradual titration of beta-blocker dosage and the expected delay in therapeutic effects. Beta-blockers are started at a low dose and gradually titrated up over several weeks to minimize potential side effects. It is important to educate the patient about this dosing regimen and explain that therapeutic effects may not be seen immediately. Providing this information helps manage patient expectations and promotes adherence to the treatment plan.
• Assess and document the patient’s response to beta-blocker therapy, including the presence of side effects. Monitoring the patient’s response to beta-blocker therapy is crucial to ensure effectiveness and detect any adverse effects. Close assessment and documentation of side effects, such as dizziness, hypotension, bradycardia, fatigue, and depression, are important to inform healthcare providers and guide appropriate interventions or dosage adjustments.
• Provide support and reassurance to patients experiencing side effects during the initial phase of beta-blocker treatment. Side effects of beta-blockers are most common in the early weeks of treatment. Patients may experience symptoms such as dizziness, hypotension, bradycardia, fatigue, and depression. Offering support, reassurance, and education about the temporary nature of these side effects can help alleviate patient concerns and enhance adherence to the treatment plan.
• Assess the patient’s respiratory status, especially in those with a history of bronchospastic diseases such as uncontrolled asthma . Beta-blockers can cause bronchoconstriction, which can be problematic for patients with a history of bronchospastic diseases like uncontrolled asthma . Regular assessment of respiratory status helps identify any worsening of symptoms or potential complications related to bronchoconstriction, allowing for prompt intervention and adjustment of the treatment plan if necessary.
• Document and report any significant changes or concerns related to the patient’s cardiovascular or respiratory status to the primary care provider. Timely documentation and reporting of significant changes or concerns related to the patient’s cardiovascular or respiratory status are crucial for ongoing monitoring and appropriate interventions. This information helps healthcare providers make informed decisions regarding dosage adjustments, additional therapies, or potential medication changes to optimize patient outcomes .

8. Morphine sulfate Decreases vascular resistance and venous return, reducing myocardial workload, especially when pulmonary congestion is present. The use of morphine should be reserved for patients with myocardial ischemia who are refractory to drugs that favorably alter myocardial oxygen supply and demand. Morphine should not be used in patients whose chest pain syndrome has not been treated with nitrates and beta-blockers (Conti, 2011). Additionally, morphine can help allay anxiety and break anxiety’s feedback cycle to catecholamine release to anxiety.

9. Antianxiety agents and sedatives. Promote rest, reducing oxygen demand and myocardial workload. Patients with HF are likely to be restless and anxious and may feel overwhelmed by breathlessness due to their difficulty maintaining adequate oxygenation (Hinkle et al., 2017). Emotional stress can stimulate the SNS, ultimately increasing cardiac workload. By decreasing anxiety, the patient’s cardiac workload also decreases (De Jong et al., 2011). Additionally, patients with HF have a high incidence of depression and is linked with increased morbidity and mortality (Joynt et al., 2014). (see: Anxiety nursing diagnosis)

10. Anticoagulants: low-dose heparin , warfarin ( Coumadin ). Prescribed to patients with a history of atrial fibrillation or thromboembolic event. Anticoagulants are used prophylactically to prevent thrombus and embolus formation in the presence of risk factors such as venous stasis, enforced bed rest, cardiac dysrhythmias, and history of previous thrombotic episodes (Kim et al., 2018; Amin et al., 2019). Regular monitoring of the patient’s INR and PT is essential to evaluate the effectiveness and safety of anticoagulant therapy. These laboratory values provide information about the patient’s coagulation status and the therapeutic range of the anticoagulant being administered. Monitoring allows for dosage adjustments and ensures that the patient is within the target therapeutic range, minimizing the risk of bleeding or clotting complications.

11. Bronchodilators: aminophylline Increases oxygen delivery by dilating small airways and exerts mild diuretic effect to aid in reducing pulmonary congestion.

Maintaining or improving respiratory function is necessary for the care of patients with heart failure. As heart failure progresses, it can lead to fluid accumulation in the lungs, causing respiratory symptoms and compromising breathing. Nurses play a vital role in maintaining and improving respiratory function in patients with heart failure. Their proactive monitoring, patient education, and collaboration with the healthcare team help optimize respiratory care, reduce respiratory symptoms, and enhance the overall well-being of individuals with heart failure.

1. Assess respiratory rate, use of accessory muscles, signs of air hunger, lung excursion, cyanosis, and significant changes in vital signs. Monitoring respiratory parameters provides information on the patient’s respiratory status, the severity of pulmonary congestion, and the effort required for breathing. It helps identify potential respiratory complications and guides appropriate interventions. These are warning signs of increasing respiratory distress that requires immediate attention.

2. Auscultate breath sounds, noting crackles and wheezes. Reveals presence of pulmonary congestion and collection of secretions, indicating the need for further intervention. Decreased breath sounds can be a sign of fluid overload or altered ventilation. Crackles indicate the sudden opening of edematous airways and alveoli, while wheezes may suggest bronchospasm associated with pulmonary congestion. Identifying abnormal lung sounds aids in the assessment of HF severity and guides treatment decisions.

3. Monitor oxygen saturation and ABG findings. A 92% or less pulse oximetry value, decreased PaO 2 , and increased PaCO 2 are signs of decreasing oxygenation.

4. Observe the color of skin, mucous membranes, and nail beds, noting the presence of peripheral cyanosis. Cyanosis of nail beds may represent vasoconstriction or the body’s response to fever / chills.

5. Monitor potassium levels. A possibility of hypokalemia is evident in patients taking diuretics.

6. Instruct patient in effective coughing and deep breathing. Clears airways and facilitates oxygen delivery.

7. Encourage frequent position changes. Helps prevent atelectasis and pneumonia .

8. Position the patient in a High Fowler’s position with the head of the bed elevated up to 90°. Promote maximal inspiration and enhance expectoration of secretions to improve ventilation.

9. Suction secretions PRN To clear the airway when secretions are blocking the airway.

10. Graph graph serial ABGs, pulse oximetry. Hypoxemia can be severe during pulmonary edema. Compensatory changes are usually present in chronic HF. Note: Research suggests pulse oximeter measurements may exceed actual oxygen saturation by up to 7% in patients with abnormal cardiac index.

11 Administer supplemental oxygen as indicated. For patients with ADHF, high-flow oxygen is given via a non-rebreathing mask, positive airway pressure devices, or endotracheal intubation and mechanical intubation. If it improves, oxygen is titrated to maintain pulse oximetry readings greater than 92%.

12. Administer medications as indicated . See Pharmacologic Management

13. Assist patient to use relaxation techniques Reduces muscle tension , decreases work of breathing

The patient’s fluid status is closely monitored through methods like auscultating the lungs, tracking daily body weight, and supporting the patient in following a low-sodium diet. Severe heart failure patients may undergo IV diuretic therapy, while those with milder symptoms usually receive oral diuretics. It’s important to note that a single dose of a diuretic can lead to a significant volume of fluid being excreted shortly after administration. Nursing interventions focus on monitoring fluid balance, promoting fluid restriction, administering diuretic medications, and providing patient education to optimize fluid balance and alleviate symptoms.

1. Monitor urine output, noting amount and color, as well as the time of day when diuresis occurs. Urine output may be scanty and concentrated (especially during the day) because of reduced renal perfusion. Recumbency favors diuresis; therefore, urine output may be increased at night and/or during bed rest. Monitoring urinary output helps evaluate renal function and the effectiveness of diuretic therapy. Oliguria or anuria may indicate renal dysfunction, requiring further assessment and intervention.

2. Monitor and calculate 24-hour intake and output (I&O) balance. In patients receiving IV fluids and medications, close monitoring of fluid intake is crucial. Consultation with the primary provider or pharmacist can help determine if it is possible to maximize medication dosage within the same volume of IV fluid, such as double concentrating to reduce fluid volume. It’s important to note that diuretic therapy may lead to a sudden loss of fluid, resulting in circulating hypovolemia , even if edema or ascites persists.

3. Maintain chair or bed rest in semi-Fowler’s position during an acute phase. Positioning plays a crucial role in facilitating breathing for patients with respiratory difficulties. This can be achieved by increasing the number of pillows, elevating the head of the bed, or having the patient sit in a recliner. These positions help reduce venous return to the heart, alleviate pulmonary congestion, and minimize pressure on the diaphragm. Supporting the lower arms with pillows can also relieve fatigue and strain on the shoulder muscles caused by the patient’s weight.

4. Establish a fluid intake schedule if fluids are medically restricted, incorporating beverage preferences when possible. Give frequent mouth care. Ice chips can be part of the fluid allotment. Involving patients in the therapeutic regimen may enhance a sense of control and cooperation with restrictions.

5. Weigh daily. Frequently monitor blood urea nitrogen, creatinine, and serum potassium, sodium, chloride, and magnesium levels. Monitoring and documenting changes in edema is important to assess the effectiveness of therapy in managing fluid retention. In heart failure patients, a weight gain of 5 pounds is roughly equivalent to 2 liters of fluid accumulation. Conversely, the use of diuretics can lead to excessive fluid shifts and subsequent weight loss . By collaborating with the patient, the nurse can assist in developing a fluid intake plan that adheres to prescribed restrictions while accommodating the patient’s dietary preferences. This comprehensive approach promotes balanced fluid management and supports the patient in maintaining a healthy diet.

6. Assess for distended neck and peripheral vessels. Inspect dependent body areas for edema (check for pitting); note the presence of generalized body edema (anasarca). Excessive fluid retention may be manifested by venous engorgement and edema formation. Peripheral edema begins in feet and ankles (or dependent areas) and ascends as failure worsens. Pitting edema is generally obvious only after retention of at least 10 lb of fluid. Increased vascular congestion (associated with RHF) eventually results in systemic tissue edema.

7. Auscultate breath sounds, noting decreased and/or adventitious sounds (crackles, wheezes). Note presence of increased dyspnea, tachypnea, orthopnea, paroxysmal nocturnal dyspnea, persistent cough. Excess fluid volume can cause pulmonary congestion, leading to symptoms such as dyspnea, cough, and orthopnea. To effectively manage fluid levels, the patient’s fluid status is carefully monitored through lung auscultation, daily body weight measurements, and adherence to a low-sodium diet. It is important to note that symptoms of pulmonary edema associated with left-sided heart failure may have a more acute onset, while respiratory symptoms related to right-sided heart failure may develop more gradually and be harder to alleviate.

8. Investigate reports of sudden extreme dyspnea and air hunger, need to sit straight up, a sensation of suffocation, feelings of panic, or impending doom. May indicate the development of complications (pulmonary edema and/or embolus) and differs from orthopnea paroxysmal nocturnal dyspnea in that it develops much more rapidly and requires immediate intervention.

9. Administer oral diuretics in the morning. Oral diuretics are commonly prescribed for patients with heart failure with less severe symptoms. Administering them in the morning helps prevent interference with the patient’s nighttime rest and reduces the likelihood of nocturia, urinary urgency, or incontinence , especially in older patients.

10. Monitor fluid status closely. Regular monitoring of the patient’s fluid status is essential. Auscultating the lungs helps assess for signs of pulmonary congestion, while daily body weight measurements provide information on fluid retention. Weight gain in patients with heart failure typically indicates fluid accumulation.

11. Promote adherence to a low-sodium diet. Assist the patient in adhering to a low-sodium diet by educating them on reading food labels and avoiding high-sodium foods, such as canned, processed, and convenience foods. Sodium restriction helps prevent fluid retention and reduces the workload on the heart.

12. Plan fluid intake throughout the day. If the patient requires fluid restriction, collaborate with them to plan fluid intake throughout the day while considering their dietary preferences. This approach promotes adherence to the prescribed fluid restriction while maintaining hydration.

13. Monitor IV fluids and consult with the primary provider or pharmacist. If the patient receives IV fluids and medications, closely monitor the fluid volume and consult with the primary provider or pharmacist regarding the possibility of maximizing medication concentration in the same volume of IV fluid. This approach helps minimize the overall fluid intake while ensuring effective medication administration.

14. Position the patient for optimal breathing. Assist the patient in assuming positions that facilitate easier breathing, such as elevating the head of the bed, using extra pillows, or sitting in a recliner. These positions reduce venous return to the heart (preload), alleviate pulmonary congestion, and minimize pressure on the diaphragm, thus improving respiratory comfort .

15. Assess for and prevent pressure ulcers. Edematous areas are at an increased risk of pressure ulcers due to decreased circulation. Regularly assess the patient’s skin for signs of breakdown and implement preventive measures. Positioning techniques that relieve pressure and frequent changes in position help prevent pressure ulcers and maintain skin integrity .

16. Monitor BP and central venous pressure (CVP) Hypertension and elevated CVP suggest fluid volume excess and may reflect developing pulmonary congestion, heart failure.

17. Assess bowel sounds. Note complaints of anorexia, nausea, abdominal distension, constipation . Visceral congestion (occurring in progressive heart failure) can alter intestinal function.

18. Obtain patient history to ascertain the probable cause of the fluid disturbance. May include increased fluids or sodium intake or compromised regulatory mechanisms.

19. Monitorfor distended neck veins and ascites Indicates fluid overload.

20. Evaluate urine output in response to diuretic therapy. In HF management, severe cases often require IV diuretic therapy, while less severe symptoms are treated with oral diuretics. Administering oral diuretics in the morning helps prevent disruption of the patient’s nighttime rest. It is important to consider timing of medication administration, particularly for older patients who may experience urinary urgency or incontinence . A single dose of diuretic can lead to significant fluid excretion shortly after taking the medication. The focus is on monitoring the response to the diuretics rather than the actual amount voided.

21. Assess the need for an indwelling urinary catheter. Treatment focuses on diuresis of excess fluid.

22. Auscultate breath sounds q 2hr and pm for the presence of crackles and monitors for frothy sputum production When increased pulmonary capillary hydrostatic pressure exceeds oncotic pressure, fluid moves within the alveolar septum and is evidenced by the auscultation of crackles. Frothy, pink-tinged sputum is an indicator that the client is developing pulmonary edema.

23. Assess for the presence of peripheral edema. Do not elevate legs if the client is dyspneic. Decreased systemic blood pressure to stimulation of aldosterone, which causes increased renal tubular reabsorption of sodium Low-sodium diet helps prevent increased sodium retention, which decreases water retention. Fluid restriction may be used to decrease fluid intake, hence decreasing fluid volume excess.

24. Measure abdominal girth, as indicated. In progressive right-sided heart failure, fluid may shift into the peritoneal space, causing increasing abdominal girth (ascites).

25. Palpate abdomen. Note reports of right upper quadrant pain and tenderness. Advancing HF leads to venous congestion, resulting in abdominal distension, liver engorgement (hepatomegaly), and pain. This can alter liver function and prolong drug metabolism.

26. Encourage verbalization of feelings regarding limitation s. Expression of feelings may decrease anxiety, which is an energy drain that can contribute to feelings of fatigue.

27. Weigh the patient daily and compare to the previous measurement. Bodyweight is a sensitive indicator of fluid balance, and an increase indicates fluid volume excess. Daily weight monitoring is essential for assessing fluid balance in patients with heart failure. Significant weight gain may indicate fluid retention, prompting adjustments in medication, such as diuretic dosing.

28. Follow a low-sodium diet and/or fluid restriction The client senses thirst because the body senses dehydration . Oral care can alleviate the sensation without an increase in fluid intake.

29. Encourage or provide oral care q2 Heart failure causes venous congestion, resulting in increased capillary pressure. When hydrostatic pressure exceeds interstitial pressure, fluids leak out of the capillaries and present as edema in the legs and sacrum. Elevation of legs increases venous return to the heart.

30. Change position frequently. Elevate feet when sitting. Inspect skin surface, keep dry, and provide padding as indicated. To prevent pressure ulcers, the nurse assesses the patient for skin breakdown and implements preventive measures, considering the increased risk in areas affected by edema. This includes proper positioning to alleviate pressure and regular repositioning. The nurse recognizes that edema, impaired circulation, inadequate nutrition, and prolonged immobility, such as bed rest, are factors that can collectively compromise skin integrity . Close monitoring and proactive interventions are essential in maintaining skin health.

31. Provide small, frequent, easily digestible meals. Reduced gastric motility can adversely affect digestion and absorption. Small, frequent meals may enhance digestion/ prevent abdominal discomfort.

32. Institute/instruct patient regarding fluid restrictions as appropriate. This helps reduce extracellular volume.

33. Administer medications as indicated . See Pharmacologic Management

34. Maintain fluid and sodium restrictions as indicated. Reduces total body water and prevents fluid reaccumulation.

35. Consult with a dietitian. It may be necessary to provide a diet that meets caloric needs within sodium restriction to the patient.

36. Monitor chest x-ray. Reveals changes indicative of resolution of pulmonary congestion.

37. Assist with rotating tourniquets and/or phlebotomy, dialysis, or ultrafiltration as indicated. Although not frequently used, mechanical fluid removal rapidly reduces circulating volume, especially in pulmonary edema refractory to other therapies.

Providing perioperative nursing care for patients with heart failure requires special attention and consideration to ensure their safety and optimize outcomes. By implementing these perioperative nursing interventions, nurses contribute to the safe and effective management of patients with heart failure throughout the surgical journey. Their expertise, close monitoring, and collaborative approach help ensure patient safety, minimize complications and promote positive surgical outcomes.

There are several surgeries that may be performed for the treatment of heart failure, including:

1. Coronary artery bypass graft (CABG) surgery. Coronary artery bypass graft (CABG) surgery involves creating a new pathway for blood to flow to the heart by bypassing blocked or narrowed coronary arteries. Nursing interventions for CABG surgery may include:

• Monitor the patient’s vital signs, including blood pressure, heart rate, and oxygen saturation levels.
• Assess the patient’s pain and administer pain medication as needed.
• Monitor for signs of bleeding or infection.
• Assist the patient with deep breathing and coughing exercises to prevent respiratory complications.
• Provide patient education on wound care and activity restrictions postoperatively.

2. Heart valve replacement surgery. Heart valve replacement surgery involves replacing a damaged or diseased heart valve with a prosthetic valve. Nursing interventions for heart valve replacement surgery may include:

• Monitor the patient’s vital signs and cardiac function.
• Administer medications to manage pain, prevent infection, and prevent blood clots.
• Provide patient education on medications, activity restrictions, and follow-up care.

3. Angioplasty. Angioplasty is a minimally invasive procedure used to open blocked or narrowed blood vessels, typically arteries supplying the heart. During angioplasty, a thin tube with a balloon at the tip is inserted into the blocked vessel and inflated to widen the artery and improve blood flow. Nursing interventions for angioplasty include:

• Obtain informed consent from the patient.
• Prepare the patient physically and emotionally for the procedure, and address any concerns or questions.
• Assist the healthcare team in positioning the patient for the procedure.
• Monitor the patient’s vital signs, including blood pressure, heart rate, and oxygen saturation levels, throughout the procedure.
• Assist with documentation.
• Provide instructions to the patient on post-procedure care, including wound care , activity restrictions, and medications.

4. Cardiomyoplasty. Cardiomyoplasty is an experimental procedure in which the latissimus dorsi muscle is wrapped around the heart and electrically stimulated to contract with each heartbeat. It may be done to augment ventricular function while the patient is awaiting cardiac transplantation or when transplantation is not an option. The benefit of cardiomyoplasty in the treatment of HF remains unclear (Bocchi, 2001). The challenge for the clinical application of cardiomyoplasty is that it is a major surgical procedure, and the benefits obtained are limited. Cardiomyoplasty is usually not recommended due to unfavorable results.

5. Transmyocardial revascularization. Other new surgical techniques include transmyocardial revascularization (percutaneous [PTMR]) using CO2 laser technology, in which a laser is used to create multiple 1-mm diameter channels in viable but underperfused cardiac muscle.

6. Prepare for insertion and maintenance of pacemaker, if indicated. It may be necessary to correct bradydysrhythmias unresponsive to drug intervention. This can aggravate congestive failure and/or produce pulmonary edema.

7. Assist with mechanical circulatory support systems, such as the placement of a ventricular assist device (VAD). A battery-powered ventricular assist device (VAD) is positioned between the cardiac apex and the descending thoracic or abdominal aorta. This device receives blood from the left ventricle (LV) and ejects it into the systemic circulation, often allowing the patient to resume a nearly normal lifestyle while awaiting recovery, transplantation, or waiting for a decision (Yancy et al., 2017).

8. Recognize that some patients may need an intra-aortic balloon pump (IABP), provide assistance. An intra-aortic balloon pump (IABP) may be inserted as temporary support to the failing heart in a critically ill patient with potentially reversible HF (Reid et al., 2005). When caring for a patient managed with IABP, the nurse must continually assess and measure the often subtle changes in patient’s condition. This requires expert knowledge of the cardiovascular system, therapeutic effects of IABP, and potential adverse events (Lewis et al., 2009). With end-stage HF, cardiac transplantation may be indicated.

Heart failure can cause a variety of symptoms that can lead to distress and discomfort for patients. Acute pain may arise from factors such as angina (chest pain) due to reduced blood flow to the heart, musculoskeletal strain, or complications of heart failure, such as pleural effusion or edema. The effective management of acute pain and discomfort in heart failure patients is essential for improving their overall well-being, promoting rest and recovery, and enhancing their quality of life. By implementing appropriate interventions, healthcare professionals, including nurses, can help alleviate pain and provide comfort to patients experiencing acute episodes or ongoing discomfort.

1. Assess patient pain for intensity using a pain rating scale, location, and precipitating factors. To identify intensity, precipitating factors, and location to assist in accurate diagnosis.

2. Monitor vital signs, especially pulse and blood pressure, every 5 minutes until pain subsides. Tachycardia and elevated blood pressure usually occur with angina and reflect compensatory mechanisms secondary to sympathetic nervous system stimulation.

3. Assess the response to medications every 5 minutes Assessing response determines the effectiveness of medication and whether further interventions are required.

4. Administer or assist with self-administration of vasodilators, as ordered. The vasodilator nitroglycerin enhances blood flow to the myocardium. It reduces the amount of blood returning to the heart, decreasing preload, decreasing its workload.

5. Provide comfort measures. To provide non-pharmacological pain management.

6. Establish a quiet environment. A quiet environment reduces the energy demands on the patient.

7. Elevate the head of the bed. Elevation improves chest expansion and oxygenation.

8. Teach patient relaxation techniques and how to use them to reduce stress. Anginal pain is often precipitated by emotional stress that can be relieved by non-pharmacological measures such as relaxation .

9. Teach the patient how to distinguish between angina pain and signs and symptoms of myocardial infarction . In some cases, chest pain may be more serious than stable angina. The patient needs to understand the differences to seek emergency care in a timely fashion.

Please visit Acute Pain Nursing Care Plan and Management for a more detailed interventions on the management of pain .

Promoting adequate tissue perfusion and effectively managing decreased cardiac tissue perfusion are crucial aspects of caring for patients with heart failure. Optimal tissue perfusion is vital for delivering oxygen and nutrients to the body’s organs and tissues, ensuring their proper function and health. Inadequate tissue perfusion in heart failure patients can result in various complications and symptoms, including fatigue, dizziness, reduced exercise tolerance, organ dysfunction, and impaired healing. Nurses play a pivotal role in promoting adequate tissue perfusion and managing decreased cardiac tissue perfusion in patients with heart failure. They collaborate closely with the healthcare team to develop individualized care plans tailored to each patient’s specific needs.

2. Monitor vital signs, especially pulse and blood pressure every 15 minutes or more frequently if unstable. Watch out for any reduction greater than 20 mm Hg over the patient’s baseline or related changes such as dizziness and changes in mental status. A major side effect of the medical management of heart failure is hypotension which can also result from the disease.

3. Assess the extremities for color, temperature, capillary refill, pulse presence, and amplitude. Signs of peripheral vasoconstriction due to sympathetic nervous system compensation include pallor, coolness, delayed capillary refill time (more than 2 seconds), and decreased pulse amplitude. The presence of edema in the extremities may be observed due to fluid overload.

4. Assess cardiac and circulatory status. This assessment establishes a baseline and detects changes that may indicate a change in cardiac output or perfusion.

5. Assess changes in mental status such as anxiety, memory loss, confusion, depression, restlessness, lethargy, stupor, and coma. This may signal reduced cerebral perfusion and decreased oxygen level.

6. Assess the response to medications every 5 minutes. Assessing response determines the effectiveness of medication and whether further interventions are required.

7. Assess results of cardiac markers—creatinine phosphokinase, CK- MB, total LDH, LDH-1, LDH-2, troponin, and myoglobin ordered by the physician. These enzymes elevate in the presence of myocardial infarction at differing times and assist in ruling out a myocardial infarction as the cause of chest pain.

8. Monitor cardiac rhythms on patient monitor and results of 12 lead ECG. Notes abnormal tracings that would indicate ischemia.

9. Administer or assist with self-administration of vasodilators, as ordered. The vasodilator nitroglycerin enhances blood flow to the myocardium. It reduces the amount of blood returning to the heart, decreasing preload, decreasing its workload.

10. Give beta-blockers as ordered. Beta-blockers decrease oxygen consumption by the myocardium and are given to prevent subsequent angina episodes.

11. Establish a quiet environment. A quiet environment reduces the energy demands on the patient.

12. Elevate the head of the bed. Elevation improves chest expansion and oxygenation.

13. Provide oxygen and monitor oxygen saturation via pulse oximetry, as ordered. Oxygenation increases the amount of oxygen circulating in the blood and, therefore, increases the amount of available oxygen to the myocardium, decreasing myocardial ischemia and pain.

14. Teach the patient relaxation techniques and how to use them to reduce stress. Anginal pain is often precipitated by emotional stress that can be relieved by non-pharmacological measures such as relaxation.

15. Teach the patient how to distinguish between angina pain and signs and symptoms of myocardial infarction. In some cases, chest pain may be more serious than stable angina. The patient needs to understand the differences to seek emergency care in a timely fashion.

16. Reposition the patient every 2 hours To prevent bedsores

17. Instruct patient on eating small frequent feedings To prevent heartburn and acid indigestion

Nursing interventions for heart failure nutrition include educating patients about a low-sodium diet, monitoring adherence, involving family support, collaborating with a dietitian, and evaluating the patient’s response.

1. Assess the patient’s ability to comply with the recommended dietary sodium restriction and consider individual preferences, cultural food patterns, and nutritional needs when designing the diet plan. Each patient has unique dietary preferences, cultural food patterns, and nutritional needs. Assessing the patient’s ability to comply with the recommended sodium restriction allows for the development of a personalized diet plan. Collaborating with the patient helps strike a balance between sodium restriction and the patient’s ability to adhere to the prescribed diet, ensuring nutritional adequacy and promoting dietary compliance .

2. Educate the patient about the importance of following a low-sodium diet, typically no more than 2 g/day, to reduce fluid retention and symptoms of peripheral and pulmonary congestion. Educating the patient about the benefits of a low-sodium diet is crucial in managing heart failure. A low-sodium diet helps reduce fluid retention and alleviate symptoms associated with congestion. Providing information about sodium restriction empowers the patient to make dietary choices that support fluid balance and decrease myocardial workload.

3. Monitor the patient’s adherence to the low-sodium diet and assess for dietary indiscretions that may exacerbate heart failure symptoms. Regular monitoring of the patient’s adherence to the low-sodium diet is essential for optimizing heart failure management. Assessing for dietary indiscretions helps identify any deviations from the prescribed diet that may lead to severe exacerbations of heart failure symptoms. Early identification of nonadherence allows for interventions to reinforce the importance of the diet and prevent complications requiring hospitalization.

4. Involve family members in supporting the patient’s adherence to the low-sodium diet and encourage their participation in following the diet as well. Family support plays a significant role in helping patients adhere to a low-sodium diet. Involving family members and encouraging their participation in following the diet fosters a supportive environment for the patient. Studies have shown that patients whose family members also adhere to the low-sodium diet have better adherence themselves. Engaging family members in the patient’s dietary management improves outcomes and enhances the patient’s ability to adhere to the prescribed dietary restrictions.

5. Collaborate with a dietitian or nutritionist to provide comprehensive nutritional guidance and support for the patient. Collaboration with a dietitian or nutritionist can provide specialized expertise in developing and implementing a low-sodium diet plan for patients with heart failure. Collaboration allows for comprehensive nutritional guidance and support tailored to the patient’s specific needs. It ensures that the diet plan is nutritionally balanced, promotes dietary compliance, and supports overall heart failure management.

6. Evaluate the patient’s response to the low-sodium diet, including the resolution of symptoms, weight management, and overall improvement in heart failure status. Regular evaluation of the patient’s response to the low-sodium diet helps assess the effectiveness of dietary interventions in managing heart failure. Monitoring symptom resolution, weight changes, and overall improvement in heart failure status provides valuable feedback on the impact of the diet plan.

Maintaining skin integrity is a critical aspect of care for patients with heart failure. Heart failure can lead to various physiological changes and complications that can impact the health and integrity of the skin. Maintaining skin integrity in heart failure patients is essential to prevent complications such as pressure ulcers, skin breakdown, and infections. Healthy skin serves as a protective barrier against pathogens, and its integrity plays a vital role in the overall well-being of patients. Nursing interventions focus on promoting skin hygiene, implementing pressure relief strategies, providing wound care as needed, and educating patients and caregivers on skin care practices.

1. Inspect skin, noting skeletal prominences, presence of edema, areas of altered circulation, or obesity and/or emaciation. Skin is at risk because of impaired peripheral circulation, physical immobility, and alterations in nutritional status.

2. Check the fit of shoes and slippers and change as needed. Dependent edema may cause shoes to fit poorly, increasing the risk of pressure and skin breakdown on the feet.

3. Provide gentle massage around reddened or blanched areas. Improves blood flow, minimizing tissue hypoxia. Note: Direct massage of the compromised area may cause tissue injury.

4. Encourage frequent position changes and assist with active and passive range of motion (ROM) exercises. Reduces pressure on tissues, improves circulation, and reduces time in any area is deprived of full blood flow.

5. Provide frequent skincare: minimize contact with moisture and excretions. Excessive dryness or moisture damages skin and hastens breakdown.

6. Avoid intramuscular route for medication. Interstitial edema and impaired circulation impede drug absorption and predispose to tissue breakdown and development of infection.

7. Provide alternating pressure, egg-crate mattress, sheepskin elbow, and heel protectors. Reduces pressure on the skin, and may improve circulation.

Managing decreased tolerance to activity and fatigue in congestive heart failure is important to improve the patient’s quality of life and overall well-being. For patients with other conditions (such as arthritis ) and a longer duration of heart failure, it can be challenging to adhere to exercise training, which is vital for them to derive benefits from it. Temporary bed rest may be necessary if there is an acute illness that worsens heart failure symptoms or requires hospitalization. However, in all other cases, it is important to encourage some form of daily physical activity. Exercise training offers numerous benefits to heart failure patients, such as enhanced functional capacity, reduced dyspnea, and improved quality of life (Georgantas, Dimopoulos, Tasoulis, et al., 2014).

1. Check vital signs before and immediately after activity, especially if the patient receives vasodilators, diuretics, or beta-blockers. Orthostatic hypotension can occur with activity because of medication effect (vasodilation), fluid shifts (diuresis), or compromised cardiac pumping function.

2. Document cardiopulmonary response to activity. Note tachycardia, dysrhythmias, dyspnea, diaphoresis, and pallor. Compromised myocardium and inability to increase stroke volume during activity may cause an immediate increase in heart rate and oxygen demands, thereby aggravating weakness and fatigue.

3. Assess for other causes of fatigue (treatments, pain, medications). Medications such as beta-blockers, tranquilizers, and sedatives can cause fatigue as a side effect. Pain and stressful procedures can also diminish the patient’s energy can cause fatigue.

4. Identify factors that could affect the desired level of activity and motivation . Age, pain, breathing problems, impaired visual acuity, hearing problems, functional decline, etc., are all factors that could hinder interventions from improving activity tolerance . Other factors unrelated to heart failure could affect the client’s participation in interventions to improve activity tolerance (Chew et al., 2019). Fatigue affects both the client’s actual and perceived ability to participate in activities.

5. Monitor and evaluate the patient’s response to activities. Regular monitoring of vital signs and oxygen saturation levels is crucial before, during, and after physical activity to ensure they remain within the desired range. The heart rate should return to baseline within 3 minutes after activity. Moderate continuous training, recommended by the Heart Failure Association Guidelines, is safe, effective, and well-tolerated by patients with heart failure. Adjusting the intensity, duration, and frequency of exercise based on the patient’s response is essential, both in the hospital and at home. Adherence to exercise training may be challenging for some patients, and referral to a cardiac rehabilitation program can provide additional support, especially for newly diagnosed patients with heart failure or those requiring extra guidance. If the patient is hospitalized, monitor vital signs and oxygen saturation levels before, during, and after physical activity to ensure they remain within the desired range. If the patient is at home, assess the degree of fatigue experienced after activity. Monitoring the patient’s response helps evaluate tolerance and adjust the intensity, duration, and frequency of activity accordingly.

6. Consider the use of the 6-minute walk test (6MWT) to determine the patient’s physical ability. 6MWT is an exercise test that entails measuring the distance walked over a span of 6 minutes (Enright, 2003). It helps gauge the patient’s cardiopulmonary response . More information about the 6MWT can be found here .

7. Assist in identifying and overcoming barriers to physical activity. Identify barriers that may hinder the patient’s ability to engage in physical activity and discuss strategies to overcome them. For example, suggesting sitting while performing tasks like chopping or peeling vegetables can help conserve energy. By addressing barriers, patients are more likely to incorporate physical activity into their daily routine.

8. Encourage daily physical activity. Patients with heart failure often experience reduced physical activity, leading to physical deconditioning and worsening symptoms. Encouraging daily physical activity helps improve exercise tolerance, functional capacity, and quality of life in patients with heart failure.

9. Collaborate with the primary provider and patient to develop a personalized exercise schedule. A collaborative approach involving the primary provider, nurse, and patient is essential in developing an exercise schedule that promotes pacing and prioritization of activities. This helps ensure that activities are balanced with periods of rest and prevents excessive energy consumption.

10. Provide guidelines for safe physical activity. Start slow and low. Before engaging in physical activity, the patient should be given guidelines to follow, such as starting with low-impact activities like walking , incorporating warm-up and cool-down periods, avoiding extreme weather conditions, waiting 2 hours after meals before exercising, and ensuring the ability to talk during activity. These guidelines promote safety and prevent complications during exercise.

11. Evaluate accelerating activity intolerance. May denote increasing cardiac decompensation rather than overactivity. Three factors that affect the risk of exercise include age, heart disease presence, and exercise intensity (Piña et al., 2003). Sudden cardiac death during exercise is rare in apparently healthy individuals. Individuals with cardiac disease seem to be at a greater risk for sudden cardiac arrest during vigorous exercise (such as jogging) than are healthy individuals (Fletcher et al., 2001). Reduced physical activity in heart failure (HF) patients leads to physical deconditioning and worsens symptoms. It is important to encourage daily physical activity while considering the patient’s limitations and risks. Exercise training has numerous benefits, including increased functional capacity, decreased dyspnea, and improved quality of life.

12. Promote adherence to exercise training. Adherence to exercise training is crucial for patients to benefit from it. Patients may face challenges due to comorbidities or the duration of HF. Referral to a cardiac rehabilitation program can provide supervised exercise sessions, structured environments, educational support, regular encouragement, and interpersonal contact.

13. Assist with self-care activities as necessary. Encourage independence within prescribed limits. Assisting with ADLs ensure that the patient’s need is met while reducing cardiac workload. As much as possible and as tolerated by the patient, involve them in promoting a sense of control and reducing helplessness.

14. Slow the pace of care and provide adequate rest before and after periods of exertion (e.g., bathing, eating, exercise). Allow the patient extra time to carry out physical tasks, especially on geriatric clients. Older patients are more vulnerable to falls and injuries due to decreased muscle strength, reduced balance, etc.

15. Organize nursing care activities to allow rest periods. Intersperse activity periods with rest periods by developing a schedule that promotes pacing and prioritizes activities to meet the patient’s personal care needs without undue myocardial stress and excessive oxygen demand (Cattadori et al., 2018; Piña et al., 2003). Grouping nursing care allows adequate time for the patient to recharge.

16. Implement a graded cardiac rehabilitation program. Strengthens and improves cardiac function under stress if cardiac dysfunction is not irreversible. Gradual increase in activity avoids excessive myocardial workload and oxygen consumption. Cardiac rehabilitation offers an effective model of care for older patients with heart failure (Austin et al., 2005). The potential benefit of increasing exercise performance by increasing training load from moderate to higher doses of exercise should be weighed against the lack of an improvement in cardiac vagal modulation and the possible increase in the risk of adverse events (Volterrani & Iellamo, 2016).

17. Adjust the client’s daily activities and reduce the intensity of the level. Discontinue activities that cause undesired physiological and psychological changes . It prevents straining and overexertion, which may aggravate symptoms. Stop all activity if severe shortness of breath, pain, or dizziness develops. Additionally, instruct the patient or significant other to recognize the signs of overexertion. One way to ensure the patient is not overexerting during physical ability is if they can talk during the routine; if they cannot do so, decrease the intensity of activity.

18. Encourage patient to have adequate bed rest and sleep; provide a calm and quiet environment. It relaxes the body and promotes comfort. Temporary bed rest should also be implemented during an acute exacerbation of heart failure symptoms.

19. Initiate interventions and safeguards to promote safety and prevent risk for injury during activity. Interventions include:

• Assist the patient during ambulation, if necessary.
• Ascertain the patient’s ability to stand and move about and degree of assistance needed or use of movement aids or equipment.
• Instruct or demonstrate physical activities that may be unfamiliar with the patient.
• Start with warm-up activity and end with cool-down activities.
• Avoid performing physical activities outside extreme temperatures or during humid weather.
• Wait 2 hours after eating a meal before performing a physical activity.

20. Encourage the client to maintain a positive attitude; provide evidence of daily or weekly progress. It helps enhance the patient’s sense of well-being and raises the patient’s motivation and morale. Motivation is necessary for patients with HF who are attempting to become more physically active but may not be sufficient to initiate physical activity. In addition to a high level of motivation to be physically active, patients with HF must have a high degree of self-efficacy (Klompstra et al., 2018). Provide a positive atmosphere during the exercise regimen to help minimize patient frustration.

Patients with heart failure may display signs and symptoms of anxiety. Alongside psychosocial factors contributing to anxiety, there are also physiological compensatory mechanisms involved, such as the activation of neurohormones, including catecholamines (Chapa et al., 2014). Anxiety stems from factors like the fear of shocks, role adjustments, and concerns about the patient’s ability to perform daily activities. When the patient shows symptoms of anxiety, the nurse takes measures to facilitate physical comfort and provide psychological support.

1. Assess for restlessness and anxiety as potential indicators of hypoxia from pulmonary congestion. Restlessness and anxiety may suggest inadequate oxygenation, which can occur in HF due to pulmonary congestion. Prompt recognition of these signs allows for appropriate interventions to improve oxygenation.

2. Promote physical comfort and provide psychological support. When the patient exhibits anxiety, it is essential for the nurse to prioritize the patient’s physical comfort and provide psychological support. Creating a calming environment and ensuring the patient feels safe and secure can help reduce anxiety levels. Physical comfort measures, such as allowing the patient to sit in a recliner, can enhance relaxation and decrease anxiety.

3. Assess physical reactions to anxiety. Anxiety also plays a role in somatoform disorders, characterized by physical symptoms such as pain, nausea, weakness, or dizziness that have no apparent physical cause.

4. Administer oxygen during acute events. During acute episodes of anxiety, administering oxygen can help diminish the work of breathing and increase the patient’s comfort. Adequate oxygenation contributes to a sense of ease and relaxation.

5. Validate observations by asking the patient, “Are you feeling anxious now?” Anxiety is a highly individualized, physical, and psychological response to internal or external life events.

6. Recognize awareness of the patient’s anxiety. Acknowledgment of the patient’s feelings validates the feelings and communicates acceptance of those feelings.

7. Interact with patients in a calm, peaceful manner. This approach may help decrease anxiety so that patient’s cardiac work is also decreased.

8. Encourage the patient to express fears, feelings regarding the condition. Recognizing one’s feelings allows communication, thus decreasing fear.

9. Identify present and past measures that the patient uses to cope with fear. This information helps determine the effectiveness of coping strategies practiced by the patient.

10. Assess for factors contributing to a sense of powerlessness. Identifying the related factors with powerlessness can benefit in recognizing potential causes and building a collaborative plan of care.

11. Assess for feelings of apathy, hopelessness, and depression. These moods may be an element of powerlessness.

12. Evaluate the patient’s decision-making competence. Powerlessness is the feeling that one has lost the implicit power to control their own interests.

13. Know situations/interactions that may add to the patient’s sense of powerlessness. Healthcare providers must recognize the patient’s right to refuse certain procedures. Some routines are done on patients without their consent fostering a sense of powerlessness.

14. Appraise the impact of powerlessness on the patient’s physical condition (e.g., appearance, oral intake, hygiene, sleep habits). Individuals may seem as though they are powerless to establish basic aspects of life and self-care activities.

15. Assess the role of illness plays in the patient’s sense of powerlessness. The dilemma about events, duration, course of illness, prognosis, and dependence on others for guidance and treatments can contribute to powerlessness.

16. Evaluate the results of the information given on the patient’s feelings and behavior. Patients facing powerlessness may overlook information. Too much information may overwhelm the patient and add to feelings of powerlessness. A patient simply experiencing a knowledge deficit may be mobilized to act in their own best interest after the information is presented and options are explored. The act of providing information about heart failure may strengthen a patient’s sense of independence.

17. Encourage a calm and quiet environment. This intervention avoids or decreases the sensory overload that may cause fear.

18. Familiarize patients with the environment and new experiences or people as needed. Awareness of the environment promotes comfort and may decrease anxiety experienced by the patient. Anxiety may intensify to a panic level if the patient feels threatened and unable to control environmental stimuli. A decrease in anxiety will also mean that patient’s cardiac work is also decreased.

19. Administer oxygen during the acute stage. Oxygen therapy diminishes the work of breathing and increases comfort.

20. When the patient displays anxiety, promote physical comfort and psychological support. A family member’s presence may provide reassurance; pet visitation or animal-assisted therapy can also be helpful.

21. Converse using simple language and brief statements. When experiencing moderate to severe anxiety , patients may not understand anything more than simple, clear, and brief instructions.

22. When the patient is comfortable, teach ways to control anxiety and avoid anxiety-provoking situations. Anxiety may intensify to a panic state with excessive conversation, noise, and equipment around the patient. Increasing anxiety may become frightening to the patient and others.

23. Assist in identifying factors that contribute to anxiety. Talking about anxiety-producing situations and anxious feelings can help the patient perceive the situation realistically and recognize anxiety-related factors.

24. Help patient determine precipitants of anxiety that may indicate interventions. Obtaining insight allows the patient to reevaluate the threat or identify new ways to deal with it.

25. Screen for depression, which often accompanies or results from anxiety. Symptoms of depression and anxiety are present in about one-third of patients with heart failure. Studies found evidence confirming “markedly higher” rates of depression and anxiety disorders among patients with heart failure compared to the general population.

26. Allow the patient to talk about anxious feelings and examine anxiety-provoking situations if they are identifiable. Talking about anxiety-producing situations and anxious feelings can help the patient perceive the situation realistically and recognize anxiety-related factors.

27. Assist the patient in developing new anxiety-reducing skills (e.g., relaxation, deep breathing, positive visualization, and reassuring self-statements). Discovering new coping methods provides the patient with a variety of ways to manage anxiety.

28. Avoid unnecessary reassurance; this may increase undue worry. Reassurance is not helpful for the anxious individual.

29. Intervene when possible to eliminate sources of anxiety. Anxiety is a normal response to actual or perceived danger; the response will stop if the threat is eliminated.

30. Explain all activities, procedures, and issues that involve the patient; use non-medical terms and calm, slow speech. Do this in advance of procedures when possible, and validate the patient’s understanding. With preadmission patient education, patients experience less anxiety and emotional distress and have increased coping skills because they know what to expect. Uncertainty and lack of predictability contribute to anxiety.

31. Educate patient and family about the symptoms of anxiety. If the patient and family can identify anxious responses, they can intervene earlier than otherwise.

32. Teach patients to visualize or fantasize about the absence of anxiety or pain, successful experience of the situation, resolution of conflict, or outcome of the procedure. The use of guided imagery has been useful for reducing anxiety.

33. Maintain a relaxed and accepting demeanor while communicating with the patient. The patient’s feeling of stability increases in a peaceful and non-threatening environment.

34. Use simple language and easy-to-understand statements regarding diagnostic procedures and treatment regimens. Simple, clear, and brief instructions are important for the patient to understand any explanations during excessive fear.

35. Provide patients and significant others with emotional support. The support system from the family and other significant others is important for the patient in decreasing their level of fear.

36. Allow the patient to have rest periods. Relaxation improves the ability to cope. The nurse needs to pace activities, especially for older adults, to conserve the patient’s energy.

37. Listen actively to patients often. This approach creates a supportive environment and sends a message of caring.

38. Encourage the patient to identify strengths. This will aid the patient in recognizing inner strengths.

39. Provide the patient with decision-making opportunities with increasing frequency and significance. This approach enhances the patient’s independence.

40. Help the patient in reexamining negative perceptions of the situation. The patient may have their own perceptions that are unrealistic for the situation.

41. Provide encouragement and praise while identifying the patient’s progress. This approach creates a supportive environment and sends a message of caring.

42. Assist the patient in differentiating between factors that can be controlled and those that cannot. The patient may have their own perceptions that are unrealistic for the situation.

43. Avoid using coercive power when approaching the patient. This approach may increase the patient’s feelings of powerlessness and result in decreased self-esteem .

44. Eliminate the unpredictability of events by allowing adequate preparation for tests or procedures. Information in advance of a procedure can provide the patient with a sense of control.

45. Support in planning and creating a timetable to manage increased responsibility in the future. Use of realistic short-term goals for resuming aspects of self-care foster confidence in one’s abilities.

46. Provide safety measures within the home when indicated (e.g., alarm system, safety devices in showers, bathtubs). The patient’s fear will not be reduced or resolved if the home environment is unsafe.

Treating heart failure involves intricate therapeutic regimens that necessitate substantial lifestyle adjustments for both the patient and their family. Hospital readmissions are frequently caused by noncompliance with prescribed diet, fluid restrictions, and medications. Furthermore, inadequate coordination of care and insufficient clinical follow-up contribute to unfavorable outcomes (Albert et al., 2015). Nurses play a crucial role in managing episodes of acute decompensated HF and creating a comprehensive teaching and discharge plan. This plan aims to prevent hospital readmissions and enhance the patient’s quality of life.

1. Discuss normal heart function. Include information regarding the patient’s variance from normal function. Explain the difference between heart attack and HF. Knowledge of disease processes and expectations can facilitate adherence to the prescribed treatment regimens.

2. Reinforce treatment rationale. Include SOs in teaching as appropriate, especially for complicated regimens such as dobutamine infusion home therapy when the patient does not respond to customary combination therapy or cannot be weaned from dobutamine or those awaiting a heart transplant. Patients may believe it is acceptable to alter the postdischarge regimen when feeling well and symptom-free or when feeling below par, which can increase the risk of exacerbating symptoms. Understanding of regimen, medications, and restrictions may augment cooperation with control of symptoms. Home IV therapy requires a significant commitment by caregivers to troubleshoot infusion pumps, change the dressing for peripherally inserted central catheter (PICC) line, monitor I&O and signs and symptoms of HF.

3. Encourage developing a regular home exercise program, and provide guidelines for sexual activity. Promotes maintenance of muscle tone and organ function for the overall sense of well-being. Changing sexual habits may be difficult (sex in the morning when well-rested, patient on top, inclusion of other physical expressions of affection) but provides an opportunity for continuing a satisfying sexual relationship.

4. Discuss the importance of being as active as possible without becoming exhausted and rest between activities. Excessive physical activity or overexertion can further weaken the heart, exacerbating failure, and necessitates adjustment of exercise program.

5. Discuss the importance of sodium limitation. Provide a list of the sodium content of common foods that are to be avoided and limited. Encourage reading of labels on food and drug packages. Dietary intake of sodium of more than 3 grams per day can offset the effect of diuretics. The most common source of sodium is table salt and obviously salty foods, although canned soups, luncheon meats, and dairy products also may contain high sodium levels.

6. Refer to a dietitian for counseling specific to individual dietary customs. Identifies dietary needs, especially in the presence of nausea, vomiting , and resulting wasting syndrome (cardiac cachexia). Eating six small meals and using liquid dietary supplements and vitamin supplements can limit inappropriate weight loss.

7. Review medications, purpose, and side effects. Provide both oral and written instructions. Understanding therapeutic needs and the importance of prompt reporting of side effects can prevent the occurrence of drug-related complications. Anxiety may block comprehension of input or details, and patient/ SO may refer to written material later to refresh memory.

8. Recommend taking diuretic early in the morning. Provides adequate time for drug effects before bedtime to prevent interruption of sleep.

9. Instruct and receive return demonstration of ability to take and record daily pulse and blood pressure and when to notify health care provider: parameters above or below preset rate, changes in rhythm, and regularity. Promotes self-monitoring of drug effects. Early detection of changes allows for timely intervention and may prevent complications, such as digitalis toxicity .

10. Explain and discuss the patient’s role in controlling risk factors (smoking, unhealthy diet) and precipitating or aggravating factors (high-salt diet, inactivity, overexertion, exposure to extremes in temperature). It adds to the body of knowledge and permits the patient to make informed decisions regarding condition control and prevention of complications. Smoking potentiates vasoconstriction; sodium intake promotes water retention or edema formation; improper balance between activity and rest and exposure to temperature extremes may result in exhaustion and/or increased myocardial workload and increased risk of respiratory infections. Alcohol can depress cardiac contractility. Limitation of alcohol use to social occasions or a maximum of 1 drink per day may be tolerated unless cardiomyopathy is alcohol-induced (requiring complete abstinence).

11. Review signs and symptoms that require immediate medical attention: rapid and significant weight gain, edema, shortness of breath, increased fatigue, cough, hemoptysis, fever. Self-monitoring increases patient responsibility in health maintenance and aids in the prevention of complications, e.g., pulmonary edema, pneumonia. Weight gain of more than 3 lb in a week requires medical adjustment of diuretic therapy. Note: Patient should weigh self daily in morning without clothing, after voiding, and before eating.

12. Provide opportunities for patients and SO to ask questions, discuss concerns, and make necessary lifestyle changes. HF’s chronicity and debilitating nature often exhaust both the patient’s and significant other’s coping abilities and supportive capacity, leading to depression.

13. Discuss general health risks (such as infection), recommending avoidance of crowds and individuals with respiratory infections, obtaining yearly influenza immunization and one-time pneumonia immunization. This population is at increased risk for infection because of circulatory compromise.

14. Stress importance of reporting signs and symptoms of digitalis toxicity: development of gastrointestinal (GI) and visual disturbances, changes in pulse rate and rhythm, worsening of heart failure. Early recognition of developing complications and involvement of healthcare providers may prevent toxicity.

15. Identify community resources and support groups and visiting home health nurses as indicated. Encourage participation in an outpatient cardiac rehabilitation program. May need additional assistance with self-monitoring, home management, especially when HF is progressive.

16. Discuss the importance of advance directives and communicating plans and wishes to family and primary care providers. Up to 50% of all deaths from heart failure are sudden, with many occurring at home, possibly without significant worsening of symptoms. If the patient chooses to refuse life-support measures, an alternative contact person (rather than 911) should be designated, should cardiac arrest occur.

17. Assess the patient with underlying coronary artery disease for consideration of coronary artery revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass surgery. Patients with heart failure and underlying coronary artery disease may benefit from coronary artery revascularization procedures. Assessing the patient’s eligibility and suitability for PCI or coronary artery bypass surgery helps determine the appropriate surgical approach to improve coronary blood flow and potentially enhance ventricular function.

18. Identify patients with severe left ventricular dysfunction at high risk for life-threatening dysrhythmias and consider the placement of an implantable cardioverter defibrillator (ICD). Patients with severe left ventricular dysfunction and a high risk of life-threatening dysrhythmias may benefit from an ICD. Identifying eligible candidates, typically those with an ejection fraction (EF) less than 35% and NYHA functional class II or III, helps prevent sudden cardiac death and extends survival. Collaboration with the healthcare team ensures appropriate selection and placement of the ICD device.

19. Evaluate patients who do not respond to standard therapy for cardiac resynchronization therapy (CRT) and consider the use of a biventricular pacemaker to treat electrical conduction defects. Patients with heart failure who do not improve with standard therapy may benefit from CRT. Identifying patients with a prolonged QRS duration on the electrocardiogram (ECG) indicating left bundle branch block helps identify those who may benefit from CRT. Placement of a pacing device with leads in the right atrium , right ventricle, and left ventricular cardiac vein synchronizes ventricular contractions, optimizing cardiac output, reducing mitral regurgitation, and improving overall ventricular function.

20. Monitor patients receiving ultrafiltration for severe fluid overload, especially those resistant to diuretic therapy. Ultrafiltration is an alternative intervention for patients with severe fluid overload who do not respond to diuretic therapy. Monitoring the patient’s output of filtration fluid, blood pressure, and hemoglobin levels helps assess volume status and response to ultrafiltration. Regular monitoring ensures patient safety and allows for adjustments in the filtration process as needed.

21. Consider referral for cardiac transplantation in patients with end-stage heart failure who are eligible for long-term survival. For patients with end-stage heart failure who have exhausted other treatment options, cardiac transplantation may be the best option for long-term survival. Referring eligible patients for consideration of transplantation ensures access to a potentially life-saving intervention. Collaboration with the healthcare team and transplant centers facilitates appropriate evaluation and selection of candidates.

22. Provide nursing surveillance for older male patients receiving diuretics to monitor for bladder distention caused by urethral obstruction from an enlarged prostate gland. Older male patients receiving diuretics may be at risk of bladder distention due to urethral obstruction from an enlarged prostate gland. Regular monitoring of urinary symptoms, such as urinary frequency, urgency, and signs of bladder fullness, helps detect potential complications. Nursing interventions, such as ultrasound scanning or palpation of the suprapubic area, aid in assessing bladder fullness and managing urinary issues in older patients with limited mobility .

23. Address the unique symptoms and challenges faced by older adults with heart failure, including atypical symptoms, decreased renal function, and mobility limitations. Older adults with heart failure may present with atypical symptoms, such as weakness and somnolence, instead of typical symptoms like shortness of breath. Assessing and addressing these symptoms helps ensure appropriate management. Additionally, older adults may have decreased renal function, affecting diuretic response, and limited mobility , which can exacerbate challenges related to urinary symptoms. Taking these factors into account during nursing care optimizing outcomes for older patients with heart failure.

For the expected patient outcomes , the following are evaluated:

• Demonstration of tolerance for increased activity.
• Maintenance of  fluid balance .
• Less anxiety.
• Decides soundly regarding care and treatment.
• Adherence to self-care regimen.

The nurse should provide education and involve the patient in the therapeutic regimen .

• Patient education . Teach the patient and their families about medication management, low-sodium diets, activity and exercise recommendations, smoking cessation, and learning to recognize the signs and symptoms of worsening HF.
• Encourage the patient and their families to ask questions so that information can be clarified and understanding enhanced.
• Cardiac output adequate for individual needs.
• Complications prevented/resolved.
• Optimum level of activity/functioning attained.
• Disease process/prognosis and therapeutic regimen understood.
• Plan in place to meet needs after discharge.

The following data should be documented appropriately:

• Assessment findings
• I&O fluid balance
• Degree o f fluid retention
• Results of laboratory tests and diagnostic studies.
• Response to interventions, teachings, and actions performed.
• Attainment or progress toward desired outcomes .

Other recommended site resources for this nursing care plan:

• Nursing Care Plans (NCP): Ultimate Guide and Database MUST READ! Over 150+ nursing care plans for different diseases and conditions. Includes our easy-to-follow guide on how to create nursing care plans from scratch.
• Nursing Diagnosis Guide and List: All You Need to Know to Master Diagnosing Our comprehensive guide on how to create and write diagnostic labels. Includes detailed nursing care plan guides for common nursing diagnostic labels.

Other nursing care plans for cardiovascular system disorders:

• Angina Pectoris (Coronary Artery Disease)
• Cardiac Arrhythmia (Digitalis Toxicity)
• Cardiac Catheterization
• Cardiogenic Shock
• Congenital Heart Disease
• Decreased Cardiac Output & Cardiac Support
• Heart Failure
• Hypertension
• Hypovolemic Shock
• Impaired Tissue Perfusion & Ischemia
• Myocardial Infarction
• Pacemaker Therapy

Recommended nursing diagnosis and nursing care plan books and resources.

Disclosure: Included below are affiliate links from Amazon at no additional cost from you. We may earn a small commission from your purchase. For more information, check out our privacy policy .

Ackley and Ladwig’s Nursing Diagnosis Handbook: An Evidence-Based Guide to Planning Care We love this book because of its evidence-based approach to nursing interventions. This care plan handbook uses an easy, three-step system to guide you through client assessment, nursing diagnosis, and care planning. Includes step-by-step instructions showing how to implement care and evaluate outcomes, and help you build skills in diagnostic reasoning and critical thinking.

Nursing Care Plans – Nursing Diagnosis & Intervention (10th Edition) Includes over two hundred care plans that reflect the most recent evidence-based guidelines. New to this edition are ICNP diagnoses, care plans on LGBTQ health issues, and on electrolytes and acid-base balance.

Nurse’s Pocket Guide: Diagnoses, Prioritized Interventions, and Rationales Quick-reference tool includes all you need to identify the correct diagnoses for efficient patient care planning. The sixteenth edition includes the most recent nursing diagnoses and interventions and an alphabetized listing of nursing diagnoses covering more than 400 disorders.

Nursing Diagnosis Manual: Planning, Individualizing, and Documenting Client Care  Identify interventions to plan, individualize, and document care for more than 800 diseases and disorders. Only in the Nursing Diagnosis Manual will you find for each diagnosis subjectively and objectively – sample clinical applications, prioritized action/interventions with rationales – a documentation section, and much more!

All-in-One Nursing Care Planning Resource – E-Book: Medical-Surgical, Pediatric, Maternity, and Psychiatric-Mental Health   Includes over 100 care plans for medical-surgical, maternity/OB, pediatrics, and psychiatric and mental health. Interprofessional “patient problems” focus familiarizes you with how to speak to patients.

Recommended journals, books, and other interesting materials to help you learn more about heart failure nursing care plans and nursing diagnosis:

• Albert, N. M. (2012). Fluid management strategies in heart failure . Critical care nurse , 32 (2), 20-32.
• Albert, N., Trochelman, K., Li, J., & Lin, S. (2010). Signs and symptoms of heart failure: are you asking the right questions? . American Journal of Critical Care , 19 (5), 443-452.
• Alkhawam, H., Abo-Salem, E., Zaiem, F., Ampadu, J., Rahman, A., Sulaiman, S., … & Vittorio, T. J. (2019). Effect of digitalis level on readmission and mortality rate among heart failure reduced ejection fraction patients . Heart & Lung , 48 (1), 22-27.
• Allen, J. K., & Dennison, C. R. (2010). Randomized trials of nursing interventions for secondary prevention in patients with coronary artery disease and heart failure: systematic review . Journal of Cardiovascular Nursing , 25 (3), 207-220.
• Amin, A., Garcia Reeves, A. B., Li, X., Dhamane, A., Luo, X., Di Fusco, M., … & Keshishian, A. (2019). Effectiveness and safety of oral anticoagulants in older adults with non-valvular atrial fibrillation and heart failure . PloS one , 14 (3), e0213614.
• Austin, J., Williams, R., Ross, L., Moseley, L., & Hutchison, S. (2005). Randomised controlled trial of cardiac rehabilitation in elderly patients with heart failure . European Journal of Heart Failure , 7 (3), 411-417.
• Barrese, V., & Taglialatela, M. (2013). New advances in beta-blocker therapy in heart failure . Frontiers in physiology , 4 , 323.
• Bikdeli, B., Strait, K. M., Dharmarajan, K., Li, S. X., Mody, P., Partovian, C., … & Krumholz, H. M. (2015). Intravenous fluids in acute decompensated heart failure . JACC: Heart Failure , 3 (2), 127-133.
• Bocchi, E. A. (2001). Cardiomyoplasty for treatment of heart failure . European journal of heart failure , 3 (4), 403-406.
• Bolger, A. P., Coats, A. J., & Gatzoulis, M. A. (2003). Congenital heart disease: the original heart failure syndrome . European Heart Journal , 24 (10), 970-976.
• Brater, D. C. (2000). Pharmacology of diuretics . The American journal of the medical sciences , 319 (1), 38-50.
• Brennan, E. J. (2018). Chronic heart failure nursing: integrated multidisciplinary care . British Journal of Nursing , 27 (12), 681-688.
• Brunner, L. S. (2010). Brunner & Suddarth’s textbook of medical-surgical nursing (Vol. 1). Lippincott Williams & Wilkins.
• Butler, J., Young, J. B., Abraham, W. T., Bourge, R. C., Adams, K. F., Clare, R., … & ESCAPE Investigators. (2006). Beta -blocker use and outcomes among hospitalized heart failure patients . Journal of the American College of Cardiology , 47 (12), 2462-2469.
• Cattadori, G., Segurini, C., Picozzi, A., Padeletti, L., & Anzà, C. (2018). Exercise and heart failure: an update . ESC heart failure , 5 (2), 222-232.
• Chew, H. S. J., Sim, K. L. D., & Cao, X. (2019). Motivation, challenges and self-regulation in heart failure self-care: a theory-driven qualitative study . International journal of behavioral medicine , 26 (5), 474-485.
• Conti, C. R. (2011). Intravenous morphine and chest pain . Clinical cardiology , 34 (8), 464.
• Cowie, M. R., & Mendez, G. F. (2002). BNP and congestive heart failure . Progress in cardiovascular diseases , 44 (4), 293-321.
• De Bruyne, L. K. M. (2003). Mechanisms and management of diuretic resistance in congestive heart failure . Postgraduate medical journal , 79 (931), 268-271.
• De Jong, M. J., Chung, M. L., Wu, J. R., Riegel, B., Rayens, M. K., & Moser, D. K. (2011). Linkages between anxiety and outcomes in heart failure . Heart & Lung , 40 (5), 393-404.
• Drazner, M. H., Rame, J. E., & Dries, D. L. (2003). Third heart sound and elevated jugular venous pressure as markers of the subsequent development of heart failure in patients with asymptomatic left ventricular dysfunction . The American journal of medicine , 114 (6), 431-437.
• Elkayam, U., Akhter, M. W., Tummala, P., Khan, S., & Singh, H. (2002). Nesiritide: a new drug for the treatment of decompensated heart failure . Journal of cardiovascular pharmacology and therapeutics , 7 (3), 181-194.
• Ellison, D. H., & Felker, G. M. (2017). Diuretic treatment in heart failure . New England Journal of Medicine , 377 (20), 1964-1975.
• Enright, P. L. (2003). The six-minute walk test . Respiratory care , 48 (8), 783-785.
• Faris, R. F., Flather, M., Purcell, H., Poole‐Wilson, P. A., & Coats, A. J. (2012). Diuretics for heart failure . Cochrane Database of Systematic Reviews , (2).
• Felker, G. M., Ellison, D. H., Mullens, W., Cox, Z. L., & Testani, J. M. (2020). Diuretic therapy for patients with heart failure: JACC state-of-the-art review . Journal of the American College of Cardiology , 75 (10), 1178-1195.
• Fletcher, G. F., Balady, G. J., Amsterdam, E. A., Chaitman, B., Eckel, R., Fleg, J., … & Bazzarre, T. (2001). Exercise standards for testing and training: a statement for healthcare professionals from the American Heart Association. Circulation , 104 (14), 1694-1740.
• Friederich, J. A., & Butterworth, J. F. (1995). Sodium nitroprusside: twenty years and counting . Anesthesia & Analgesia , 81 (1), 152-162.
• Gao, X., Peng, L., Adhikari, C. M., Lin, J., & Zuo, Z. (2007). Spironolactone reduced arrhythmia and maintained magnesium homeostasis in patients with congestive heart failure . Journal of cardiac failure , 13 (3), 170-177.
• Giordano, F. J. (2005). Oxygen, oxidative stress, hypoxia, and heart failure . The Journal of clinical investigation, 115(3), 500-508.
• Grady, K. L., Dracup, K., Kennedy, G., Moser, D. K., Piano, M., Stevenson, L. W., & Young, J. B. (2000). Team management of patients with heart failure: a statement for healthcare professionals from the Cardiovascular Nursing Council of the American Heart Association . Circulation , 102 (19), 2443-2456.
• Haque, W. A., Boehmer, J., Clemson, B. S., Leuenberger, U. A., Silber, D. H., & Sinoway, L. I. (1996). Hemodynamic effects of supplemental oxygen administration in congestive heart failure . Journal of the American College of Cardiology , 27 (2), 353-357.
• Herman, L. L., & Tivakaran, V. S. (2017). Hydralazine .
• Hinkle, J. L., & KH, C. (2017). Brunner & Suddarth’s textbook of medical‑surgical nursing. Vol. 1.
• Holme, M. R., & Sharman, T. (2020). Sodium nitroprusside .
• Jaarsma, T., Strömberg, A., De Geest, S., Fridlund, B., Heikkila, J., Mårtensson, J., … & Thompson, D. R. (2006). Heart failure management programmes in Europe . European Journal of Cardiovascular Nursing , 5 (3), 197-205.
• Jacobs, M. (1984). Mechanism of action of hydralazine on vascular smooth muscle . Biochemical pharmacology , 33 (18), 2915-2919.
• Joynt, K. E., Whellan, D. J., & O’connor, C. M. (2004). Why is depression bad for the failing heart? A review of the mechanistic relationship between depression and heart failure . Journal of cardiac failure , 10 (3), 258-271.
• Jurgens, C. Y., Goodlin, S., Dolansky, M., Ahmed, A., Fonarow, G. C., Boxer, R., … & Rich, M. W. (2015). Heart failure management in skilled nursing facilities: a scientific statement from the American Heart Association and the Heart Failure Society of America . Circulation: Heart Failure , 8 (3), 655-687.
• Kemp, C. D., & Conte, J. V. (2012). The pathophysiology of heart failure . Cardiovascular Pathology , 21 (5), 365-371.
• Kim, W., & Kim, E. J. (2018). Heart failure as a risk factor for stroke . Journal of stroke , 20 (1), 33.
• Klompstra, L., Jaarsma, T., & Strömberg, A. (2018). Self-efficacy mediates the relationship between motivation and physical activity in patients with heart failure . The Journal of cardiovascular nursing , 33 (3), 211.
• Krämer, B. K., Schweda, F., & Riegger, G. A. (1999). Diuretic treatment and diuretic resistance in heart failure . The American journal of medicine , 106 (1), 90-96.
• Leier, C. V., & Chatterjee, K. (2007). The physical examination in heart failure—Part I . Congestive Heart Failure , 13 (1), 41-47.
• Levy, P., Compton, S., Welch, R., Delgado, G., Jennett, A., Penugonda, N., … & Zalenski, R. (2007). Treatment of severe decompensated heart failure with high-dose intravenous nitroglycerin: a feasibility and outcome analysis . Annals of emergency medicine , 50 (2), 144-152.
• Lewis, P. A., Ward, D. A., & Courtney, M. D. (2009). The intra-aortic balloon pump in heart failure management: implications for nursing practice . Australian critical care , 22 (3), 125-131.
• Maisel, W. H., & Stevenson, L. W. (2003). Atrial fibrillation in heart failure: epidemiology, pathophysiology, and rationale for therapy . The American journal of cardiology , 91 (6), 2-8.
• Masip, J., Gayà, M., Páez, J., Betbesé, A., Vecilla, F., Manresa, R., & Ruíz, P. (2012). Pulse oximetry in the diagnosis of acute heart failure . Revista Española de Cardiología (English Edition) , 65 (10), 879-884.
• Milo-Cotter, O., Cotter, G., Kaluski, E., Rund, M. M., Felker, G. M., Adams, K. F., … & Weatherley, B. D. (2009). Rapid Clinical Assessment of Patients with Acute Heart Failure: First Blood Pressure and Oxygen Saturation–Is That All We Need ? . Cardiology , 114 (1), 75-82.
• Mullens, W., Abrahams, Z., Francis, G. S., Skouri, H. N., Starling, R. C., Young, J. B., … & Tang, W. W. (2008). Sodium nitroprusside for advanced low-output heart failure . Journal of the American College of Cardiology , 52 (3), 200-207.
• Nicholson, C. (2007). Heart failure: A clinical nursing handbook (Vol. 31). John Wiley & Sons.
• Nyolczas, N., Dekany, M., Muk, B., & Szabo, B. (2017). Combination of hydralazine and isosorbide-dinitrate in the treatment of patients with heart failure with reduced ejection fraction . Heart Failure: From Research to Clinical Practice , 31-45.
• Oh, S. W., & Han, S. Y. (2015). Loop diuretics in clinical practice . Electrolytes & Blood Pressure , 13 (1), 17-21.
• Pereira, J. D. M. V., Cavalcanti, A. C. D., Lopes, M. V. D. O., Silva, V. G. D., Souza, R. O. D., & Gonçalves, L. C. (2015). Accuracy in inference of nursing diagnoses in heart failure patients . Revista brasileira de enfermagem , 68 , 690-696.
• Picano, E., Gargani, L., & Gheorghiade, M. (2010). Why, when, and how to assess pulmonary congestion in heart failure: pathophysiological, clinical, and methodological implications . Heart failure reviews , 15 (1), 63-72.
• Piña, I. L., Apstein, C. S., Balady, G. J., Belardinelli, R., Chaitman, B. R., Duscha, B. D., … & Sullivan, M. J. (2003). Exercise and heart failure: a statement from the American Heart Association Committee on exercise, rehabilitation, and prevention . Circulation , 107 (8), 1210-1225.
• Platz, E., Merz, A. A., Jhund, P. S., Vazir, A., Campbell, R., & McMurray, J. J. (2017). Dynamic changes and prognostic value of pulmonary congestion by lung ultrasound in acute and chronic heart failure: a systematic review . European journal of heart failure , 19 (9), 1154-1163.
• Qamer, S. Z., Malik, A., Bayoumi, E., Lam, P. H., Singh, S., Packer, M., … & Ahmed, A. (2019). Digoxin use and outcomes in patients with heart failure with reduced ejection fraction . The American journal of medicine , 132 (11), 1311-1319.
• Redeker, N. S., Adams, L., Berkowitz, R., Blank, L., Freudenberger, R., Gilbert, M., … & Rapoport, D. (2012). Nocturia, sleep and daytime function in stable heart failure. Journal of Cardiac Failure , 18 (7), 569-575 .
• Reid, M. B., & Cottrell, D. (2005). Nursing care of patients receiving: Intra-aortic balloon counterpulsation. Critical care nurse , 25 (5), 40-49.
• Rogers, C., & Bush, N. (2015). Heart failure: Pathophysiology, diagnosis, medical treatment guidelines, and nursing management . The Nursing Clinics of North America , 50 (4), 787-799.
• Rutledge, T., Reis, V. A., Linke, S. E., Greenberg, B. H., & Mills, P. J. (2006). Depression in heart failure: a meta-analytic review of prevalence, intervention effects, and associations with clinical outcomes . Journal of the American college of Cardiology , 48 (8), 1527-1537.
• Scott, L. D., Setter-Kline, K., & Britton, A. S. (2004). The effects of nursing interventions to enhance mental health and quality of life among individuals with heart failure . Applied Nursing Research , 17 (4), 248-256.
• Serber, S. L., Rinsky, B., Kumar, R., Macey, P. M., Fonarow, G. C., & Harper, R. M. (2014). Cerebral blood flow velocity and vasomotor reactivity during autonomic challenges in heart failure . Nursing research , 63 (3), 194.
• Sica, D. A., Carter, B., Cushman, W., & Hamm, L. (2011). Thiazide and loop diuretics . The journal of clinical hypertension , 13 (9), 639-643.
• Volterrani, M., & Iellamo, F. (2016). Cardiac Rehabilitation in patients with heart failure: New perspectives in exercise training . Cardiac failure review , 2 (1), 63.
• Yancy, C. W., Jessup, M., Bozkurt, B., Butler, J., Casey Jr, D. E., Colvin, M. M., … & Westlake, C. (2017). 2017 ACC/AHA/HFSA focused update of the 2013 ACCF/AHA guideline for the management of heart failure: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Failure Society of America . Journal of the American College of Cardiology , 70 (6), 776-803.
• Zhao, X., Zhang, D. Q., Song, R., & Zhang, G. (2020). Nesiritide in patients with acute myocardial infarction and heart failure: a meta-analysis . Journal of International Medical Research , 48 (1), 0300060519897194.
• Ziaeian, B., Fonarow, G. C., & Heidenreich, P. A. (2017). Clinical effectiveness of hydralazine–isosorbide dinitrate in African-American patients with heart failure . JACC: Heart Failure , 5 (9), 632-639.

First published on July 14, 2013. 

23 thoughts on “13 Heart Failure Nursing Care Plans”

good explanation

GOOD NDx keep it up`yeah jah bless

Very good work. You’ve always made my work easier

Thank you! :)

Thank you are really helping me

Am a student nurse and this is really helping me a lot

Thanks alot,had a problem with this but now I feel I can do better

A really benefit websites

This notes are lit and helping alot thanks and keep updating especially pharmacology am astudent nurse

A very nice explanation keep it up!

Thanks much. This is a great jobe well done. Be blessed

Thank you Caleb, check out our other nursing care plans and nursing diagnoses !

I wish you would add some patient education information, sometimes it seems like it may be common knowledge, but I’d like to see specifically focused education topics! Please and thank you!

You can check the deficient knowledge nursing diagnosis for this care plan.

This is great!! I am a student nurse, currently working on my unit for Chronic health conditions. This has really helped me a lot.

Thank you! Gina

this site has been very helpful for me in my studies, very grateful.

Thanks so much, I’m a student nurse currently working on my care study and it has really been helpful.

Please,can I also have a detailed pathophysiology of peripartum cardiomyopathy as well as its nursing care plans. Thanks a lot once again.

This is such a comprehensive nursing care plan for heart failure. I appreciate the author. Kudos to you!

Wow!! These are great!! I wish this site had been around when I was in school!! Even now as an NP. These are a wonderful resource to review processes.. don’t know who came up with this site but kudos to you!!!

So much hands on information. Where can we get it as PDF info

This is good and commendable

Leave a Comment Cancel reply

87 Heart Failure Essay Topic Ideas & Examples

🏆 best heart failure topic ideas & essay examples, ✍️ heart failure essay topics for college, 🎓 simple & easy heart failure essay titles, 🔎 good research topics about heart failure.

• Congestive Heart Failure Etiology and Treatment Introduction Congestive heart failure (CHF) is a “progressive and debilitating disease” that is characterized by the congestion of body tissues (Nair & Peate, 2013, p. 237). Five percent of all medical admissions in hospitals are due to CHF. When an individual has this disease, his or her heart is not able to pump adequate blood […]
• Hypertension and Congestive Heart Failure In conclusion, the patient experiences a range of issues related to hypertension, which is likely to cause left-sided congestive heart failure since it is the most common in the population.
• Heart Failure and Chronic Obstructive Pulmonary Disease Respiratory: The patient is diagnosed with COPD and continues to smoke up to two packs a day. Psychosocial: The patient is conscious and able to communicate with the staff, informing them of his state of […]
• Congestive Heart Failure Treatment Innovations The relevance of the problem of this disease for health care is conditioned by the prevalence of pathology and the high economic costs of its treatment.
• Preventing Heart Failure: Case Study In addition to the signs of heart failure, Mrs. The use of oxygen through nasal cannulas reduces the load on the heart, and it is rational.
• Importance of Dashboard in Heart Failure Preventing Thorough testing of the heart failure dashboard is essential to ensure its successful work and contribute to the reduction of the risk of hospitalization for heart failure.
• Analysis of Heart Failure: Diagnosis and Treatment The current paper examines the two types of HF – systolic and diastolic – and explains the differences between the varieties based on the case study.
• Video Consultations Between Patients and Clinicians in Diabetes, Cancer, and Heart Failure Services For example, during one of my interactions with the patient, I was asked whether the hospital had the policy to avoid face-to-face interaction during the pandemic with the help of video examinations.
• Hypertension and Risk of Heart Failure Therefore, it is essential to reduce the circulating volume with the help of diuretics, a low-sodium diet, and ACE inhibitors that block the activation of the RAAS.
• Impact of Cognitive Dysfunctions on Patients With Heart Failure Based on the statement, which has been the initial assumption, impaired cognitive functions correlate with a lack of participation in the treatment of heart failure. The frame in which the structural concepts of the research […]
• Heart Failure: Prevent Readmissions and Noncompliance With Chronic Management The Heart failure (HF) is a rising healthcare burden which is common among many admitted patients. The project will introduce preventive interventions and measures for HF.
• Congestive Heart Failure: Diagnosis and Treatment Congestive Heart Failure is a condition characterized by decreasing pumping capacity of the heart muscles of a person resulting in the congestion of the body.
• Heart Failure: Diagnosis and Pharmacologic Treatment In addition, due attention should be paid to effective strategies for the prevention of symptoms and treatment of concomitant diseases to improve the quality of life of patients with heart failure.
• The Different Types of Heart Failure Right-sided heart failure occurs when the right chamber of the heart has not enough power to pump blood to the lungs. The role of a nurse is to assess and educate a patient with heart […]
• Pathophysiology of Congestive Heart Failure Cardiac output and stroke volume is lowered due to vasoconstriction. It causes pressure overload, which leads to congestion.
• Congestive Heart Failure (CHF): Causes, Treatment and Prevention Congestive Heart Failure is a condition that occurs when the heart is unable to pump enough blood to meet the needs of the entire body.
• Health Issues of Heart Failure and Pediatric Diabetes As for the population, which is intended to participate in the research, I am convinced that there is the need to specify the patients who should be examined and monitored.
• Systolic and Diastolic Heart Failure Second, the high sinus rhythm indicates the man’s irregular heartbeat, which is the result of the emergence of the specified event, and it is referred to as cardiac arrhythmias.
• Chronic Obstructive Pulmonary Disease, Hypertension, and Heart Failure: The Case Study The most likely cause of the symptom is fluid accumulation and congestion in the pulmonary system due to the failed heart that reduces the kidneys’ perfusion, thus causing an increase in the production of renin.
• Prevention of Heart Failure Hospital Readmissions This paper describes on improving patient’s health literacy and providing specialized nursing care will prevent heart failure hospital readmissions.
• Readmission in Hypertension and Heart Failure Patients In research, the independent variables are presented by CHF interventions, mortality rates, and population size, whereas the dependent variable is the possible results of their use for people with PH.
• The Role of Education in the Treatment of Congestive Heart Failure Home treatment plan is critical for the treatment and management of congestive heart failure, which is experienced by Mr.P. Hence, comprehensive education is central to the treatment and management of the congestive heart failure in […]
• Hospital Readmission and Health Related Quality of Life in Patients With Heart Failure The article analyzes the treatment of patients and the bettering of care. And the third is the discharge itself and the plans that organize its carrying out.
• Chronic Heart Failure: Symptoms and Self-Management Finally, the other cause of CHF includes endocarditis or myocarditis, a condition that affects the heart valves or the muscles of the heart.
• Left-Sided Heart Failure and Nursing Intervention Thus left-sided heart failure or left ventricular failure refers to a condition where the left part of the heart is unable to propel adequate oxygenated blood from the pulmonary transmission to the body through the […]
• Congestive Heart Failure – One of the Most Devastating Diseases Based on the guideline, the study will be focused on all aspects in the management of CHF. This is a very efficient theory in addressing nursing issues and more precisely the management of CHF.
• Home Health Care vs. Telemonitoring: Reducing Hospital Readmissions for Patients With Heart Failure In the United States, chronic heart failure is regarded as the number one cause of both the hospitalization and readmission of patients.
• Why the Elders Delay Responding to Heart Failure Symptoms The paper would discuss the reasons the elderly delay in responding to the symptoms of heart failure. It incorporates the history of the problem and seeks to use the current technology to solve the problem.
• Remote Care Costs for Congestive Heart Failure Various aspects of the article including the significance of the chosen problem, methods, and approaches, the reliability of results and the articles structure will be discussed and evaluated.
• Heart Failure: Prevention of the Disease Heart failure is now occurring in younger people and it is vital to make them cautious and have a healthy lifestyle to prevent the disease. The purpose of the leaflet is to draw people’s attention […]
• Congestive Heart Failure Case Management Program A multidisciplinary strategy can be observed and applied to the outpatient’s supervision of the CHF conditions with the attempt to facilitate the functionality and to bring down the statistics of readmission of the CHF patients […]
• Breathlessness as an Element of Congestive or Chronic Heart Failure It was done in order to preserve the focus of the analysis on the factor of breathlessness itself. The article allows nurses and other medical specialists to gain a more in-depth understanding of breathlessness among […]
• The Syndrome of Chronic Heart Failure Chronic heart failure is a syndrome of various diseases of the cardiovascular system, leading to a decrease in the pumping function of the heart, chronic hyperactivation of neurohormonal systems.
• Measures to Avoid Re-Hospitalization of Patients With Congestive Heart Failure The idea of this project is to print out a supplement for the hospital’s 28-page guide in English and Spanish, which will have the essential recommendations and references to page numbers.
• Patient Education: Congestive Heart Failure These statistics suggest that hospitals have a substantial number of patients with CHF, and adjusting their practice and guidelines to suit the requirements of these patients is a necessity.
• Congestive Heart Failure and Coronary Artery Disease The overall result of this is the development of a clump of fatty material covered by a smooth muscle and fibrous tissue on the inside of the artery; this is known as an atherosclerotic plaque.
• Chronic Diseases: Heart Failure and Cancer The first article examines the role of genetic testing of molecular markers that determine the occurrence and progression of cancer in individuals. The article recommends oncology nurses to keep abreast of advances in genomics for […]
• Chronic Heart Failure: Symptoms, Diagnosis, and Treatment The diagnosis of the condition is made when signs and symptoms of congestion along with reduced tissue perfusion are documented in the presence of abnormal systolic or diastolic cardiac function. When it comes to the […]
• Heart Failure: Health and Physical Assessment DJ has a bad sleeping pattern, and no remitting factors were found. DJ has no medication intolerances.
• Heart Failure: Risk Factors and Treatment A comprehension of the risk aspects for heart failure is crucial for the generation of effective interventions that seek to prevent the occurrence of the condition.
• Heart Failure: Cardiology and Treatment The patients suffering from the left-sided heart failure persistently wake up several times at night because of the shortness of breath and gain weight significantly.
• Heart Failure Among Older Adult Males The purpose of this paper is to evaluate the problem of heart failure in adult males of 65 years of age and older, identify risk factors, pathophysiology, typical lab, and diagnostic health data, and goals […]
• What Influences Physical Activity in People With Heart Failure When the literature on related research was reviewed, it was noted that all of the previous research that had been done on the issue of physical activities for people with heart failure conditions had centered […]
• Congestive Heart Failure in Older Adults The research will narrow down to the readmission and admission rates for the period between January 2010 and March 2011 as well as the relevant data that will facilitate the development of a case management […]
• Resource Identification, Evaluation and Selection: Congestive Heart Failure Below is modification of search terms that were most resourceful Heart failure OR congestive heart failure Congestive heart failure AND re-admission Heart failure+ causes and symptoms Congestive heart failure AND edema Congestive heart failure AND […]
• Angiogenic Endothelial Cell Signaling in Cardiac Hypertrophy and Heart Failure
• Acute Myocardial Infarction Cause Heart Failure: Cardiomyocyte Death and Scar Formation
• Heart Failure in Alcohol Addicted People: Risks and Outcomes
• Acute Kidney Disease After Acute Decompensated Heart Failure
• Caregiving for Patients With Heart Failure: Impact on Patients
• Specialist Palliative Care to People With Heart Failure
• High Health Expenditure on Heart Failure in Different Countries
• Hypokalemia-Induced Arrhythmias and Heart Failure
• Comparison of Heart Failure Patients and Tumor Patients
• The Connection Between Aging and Congestive Heart Failure
• Current and Future Directions of Exercise Therapy for Muscle Atrophy Induced by Heart Failure
• The Duke Heart Failure Program Is a World Leader
• Multi-Biomarker Profiling and Recurrent Hospitalizations in Heart Failure
• Heart Failure Risk: How Race and Ethnicity Play a Role
• Sleep-Disordered Breathing During Congestive Heart Failure
• Causes Sudden Death in Heart Failure: Heart Attack
• Biomarkers for Heart Failure Prognosis: Proteins, Genetic Scores, and Non-coding RNAs
• Chronic Heart Failure in Heart Transplant Recipients: Presenting Features and Outcome
• Right-Sided Heart Failure: Severe Peripheral Pitting Edema
• Congestive Heart Failure in Older Adults
• Heart Failure Alert System Using Rfid Technology
• Heart Failure in Type 2 Diabetes: Current Perspectives on Screening, Diagnosis, and Management
• Influence of Socioeconomic Deprivation on Care and Treatment of Patients With Heart Failure
• Types of Drugs That Can Bring on Heart Failure
• The Difference Between Acute and Congestive Heart Failure
• Markers for Early Signs of Heart Failure Decompensation
• Alcoholic Cardiomyopathy: A Distinct Form of Congestive Heart Failure
• The Difference Between Left and Right Heart Failure
• A Process of Decision-Making by Caregivers of Family Members With Heart Failure
• Pediatric Congestive Heart Failure: Background, Etiology
• Immunity, Inflammation and Heart Failure: Their Role on Cardiac Function and Iron Status
• Supplemental Oxygen Helps Heart Failure: Reducing the Heart’s Workload
• How to Enjoy the Highest Quality of Life Possible With Congestive Heart Failure
• Cardiac and Vascular Remodeling in Heart Failure
• Cardioprotection and Thyroid Hormones in the Clinical Setting of Heart Failure
• First Gene Therapy for Heart Failure in Clinical Trials
• Cardiac Regeneration: New Insights Into the Frontier of Ischemic Heart Failure Therapy
• The Transition From Hypertension to Heart Failure
• Classification of Heart Failure in the Atherosclerosis Risk
• Approaches to Modeling the Mechanics of Human Heart Failure for Drug Discovery
• Blood Pressure Ideas
• Myocardial Infarction Research Ideas
• Anatomy Ideas
• Diabetes Questions
• Smoking Research Topics
• Stress Titles
• Obesity Ideas
• Anorexia Essay Ideas
• Chicago (A-D)
• Chicago (N-B)

IvyPanda. (2024, February 28). 87 Heart Failure Essay Topic Ideas & Examples. https://ivypanda.com/essays/topic/heart-failure-essay-topics/

"87 Heart Failure Essay Topic Ideas & Examples." IvyPanda , 28 Feb. 2024, ivypanda.com/essays/topic/heart-failure-essay-topics/.

IvyPanda . (2024) '87 Heart Failure Essay Topic Ideas & Examples'. 28 February.

IvyPanda . 2024. "87 Heart Failure Essay Topic Ideas & Examples." February 28, 2024. https://ivypanda.com/essays/topic/heart-failure-essay-topics/.

1. IvyPanda . "87 Heart Failure Essay Topic Ideas & Examples." February 28, 2024. https://ivypanda.com/essays/topic/heart-failure-essay-topics/.

Bibliography

IvyPanda . "87 Heart Failure Essay Topic Ideas & Examples." February 28, 2024. https://ivypanda.com/essays/topic/heart-failure-essay-topics/.

• DOI: 10.1002/ejhf.3390
• Corpus ID: 271456956

Efficacy and safety of hypertonic saline therapy in ambulatory patients with heart failure: The SALT-HF trial.

• M. Cobo Marcos , R. de la Espriella , +16 authors J. Núñez
• Published in European Journal of Heart… 26 July 2024

19 References

Dietary sodium and fluid intake in heart failure. a clinical consensus statement of the heart failure association of the esc, design and baseline characteristics of salt‐hf trial: hypertonic saline therapy in ambulatory heart failure, sodium loading in ambulatory patients with heart failure with reduced ejection fraction: mechanistic insights into sodium handling, the added value of hypertonic saline solution to furosemide monotherapy in patients with acute decompensated heart failure: a meta‐analysis and trial sequential analysis, practical outpatient management of worsening chronic heart failure, 2021 esc guidelines for the diagnosis and treatment of acute and chronic heart failure, ultrasound imaging of congestion in heart failure: examinations beyond the heart, real world use of hypertonic saline in refractory acute decompensated heart failure: a u.s. center's experience., heart ambulatory treatment of worsening heart failure with intravenous loop diuretics: a four-year experience., effects of hypertonic saline solution on body weight and serum creatinine in patients with acute decompensated heart failure, related papers.

Showing 1 through 3 of 0 Related Papers

Continuous Identification of Sepsis-Associated Acute Heart Failure Patients: An Integrated LSTM-Based Algorithm

New citation alert added.

This alert has been successfully added and will be sent to:

You will be notified whenever a record that you have chosen has been cited.

To manage your alert preferences, click on the button below.

New Citation Alert!

Please log in to your account

Information & Contributors

Bibliometrics & citations, view options, recommendations, comorbidity trajectory network in heart failure patients based on prefixspan algorithm.

Due to the evolution and improvement of the medicare quality in the world and the improvement of healthcare system in Taiwan over the past few decades, the ageing population is increasing and the global population is getting older. In addition, the ...

Regularity of Heart Rate Fluctuations Analysis in Congestive Heart Failure Patients Using Information-Based Similarity

Congestive Heart Failure (CHF) is a chronic progressive condition that affects the pumping power of your heart muscle. There are a number of works investigating Obstructive Sleep Apnea (OSA) detection based on heart rate variability and obtain ...

Telemedical support in patients with chronic heart failure: experience from different projects in Germany

The great epidemiological significance and costs associated with chronic heart failure pose a challenge to health systems inWestern industrial countries. In the past few years, controlled randomised studies have shown that patients with chronic heart ...

Information

Published in.

Kunming University of Science and Technology, Kunming, China

https://ror.org/03qt6ba18Georgia State University, Atlanta, GA, USA

https://ror.org/02der9h97University of Connecticut, Storrs, CT, USA

Springer-Verlag

Berlin, Heidelberg

Publication History

Author tags.

• deep learning
• continuous prediction
• hierarchical diagnosis
• sepsis-associated acute heart failure

Contributors

Other metrics, bibliometrics, article metrics.

• 0 Total Citations
• 0 Total Downloads
• Downloads (Last 12 months) 0
• Downloads (Last 6 weeks) 0

View options

Login options.

Check if you have access through your login credentials or your institution to get full access on this article.

Full Access

Share this publication link.

Copying failed.

Share on social media

Affiliations, export citations.

• Please download or close your previous search result export first before starting a new bulk export. Preview is not available. By clicking download, a status dialog will open to start the export process. The process may take a few minutes but once it finishes a file will be downloadable from your browser. You may continue to browse the DL while the export process is in progress. Download
• Download citation
• Copy citation

We are preparing your search results for download ...

We will inform you here when the file is ready.

Your file of search results citations is now ready.

Your search export query has expired. Please try again.

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

• View all journals
• Explore content
• About the journal
• Publish with us
• Sign up for alerts
• Open access
• Published: 30 July 2024

Early risk predictors of acute kidney injury and short-term survival during Impella support in cardiogenic shock

• Nikolaos Patsalis 1 ,
• Julian Kreutz 1 ,
• Giorgos Chatzis 1 ,
• Styliani Syntila 1 ,
• Maryana Choukeir 1 ,
• Bernhard Schieffer 1 &
• Birgit Markus 1  

Scientific Reports volume  14 , Article number:  17484 ( 2024 ) Cite this article

Metrics details

• Cardiac device therapy
• Cardiovascular diseases
• Predictive markers
• Risk factors

Acute kidney injury (AKI) is one of the most frequent and prognostic-relevant complications of cardiogenic shock (CS) complicating myocardial infarction (MI). Mechanical circulatory assist devices (MCS) like left ventricular Impella microaxial pump have increasingly been used in the last decade for stabilization of hemodynamics in those patients. Moreover, a protective effect of Impella on renal organ perfusion could recently be demonstrated. However, data identifying early risk predictors for developing AKI during Impella support in CS are rare. Data of hemodynamics and renal function from 50 Impella patients (January 2020 and February 2022) with MI-related CS (SCAI stage C), were retrospectively analyzed using e.g. multivariate logistic regression analysis as well as Kaplan–Meier curves and Cox regression analysis. 30 patients (60%) developed AKI. Central venous pressure as an indicator for venous congestion (OR 1.216, p = 0.02), GFR at admission indicating existing renal damage (OR 0.928, p = 0.002), and reduced central venous oxygen saturation (SvO 2 ) as a marker for decreased tissue perfusion (OR 0.930, p = 0.029) were independently associated with developing an AKI. The 30-day mortality rate was significantly higher in patients with AKI stage 3 (Stage 1: 0%, Stage 2: 0%, Stage 3; 41.6%, p = 0.014) while AKI stage 3 (HR 0.095, p = 0.026) and norepinephrine dosage (HR 1.027, p = 0.008) were independent predictors for 30-day mortality. AKI as a complication of MI-related CS occurs frequently with a major impact on prognosis. Venous congestion, reduced tissue perfusion, and an already impaired renal function are independent predictors of AKI. Thus, timely diagnostics and a focused treatment of the identified factors could improve prognosis and outcome.

Introduction

Cardiogenic shock (CS) is a feared complication in approximately 10% of acute myocardial infarction (MI) with a 30-day mortality of up to 40% 1 . The impairment of myocardial contractility in CS is the most relevant pathophysiological problem. A reduced cardiac output (CO) results in reduced blood pressure, which in turn further impairs organ and coronary perfusion and, consequently, myocardial contractility. As part of the development of this so-called downward shock spiral, tissue and end-organ perfusion thus deteriorates considerably with corresponding consequences in terms of organ failure 2 .

Acute kidney injury (AKI) is one of the most frequent complications of a reduced CO in CS with a cumulative risk of 20–35% and a significant impact on prognosis 3 . Patients with AKI are accompanied by a 12 times greater 90-day mortality and the additional necessity of renal replacement therapy (RRT) further increases intrahospital mortality (62% vs. 46%) 3 , 4 , 5 , 6 . To stabilize hemodynamics, high dosages of vasopressors are very often being substituted. However, vasoconstrictors only achieve a pseudo normalization of blood pressure while the systemic vascular resistance and hence the cardiac afterload rise, which in turn further burdens myocardial contractility and organ perfusion. During the past years, percutaneous left ventricular assist devices (pLVAD) such as the Impella micro axial pump have increasingly been used to improve CO, reduce vasopressor dosages, and thus optimize tissue and end-organ perfusion and at least function 7 , 8 , 9 . While some studies have investigated the prevalence of AKI in CS, data analyzing patients with CS being supported with Impella are rare. The goal of this study was to evaluate early risk factors and define subsequent predictor characteristics for developing AKI during Impella support in CS as well as to identify potential therapeutic options during Impella support concerning the predisposing factors of AKI.

Study design

This was a retrospective data analysis of patients with CS and Impella support, admitted to the University Hospital of Marburg from January 2020 to February 2022. To be included in this analysis, patients had to present with CS due to myocardial infarction, corresponding to stage C of the SCAI classification. Data of patients with single kidney and underlying autoimmune or polycystic kidney disease were not included in this analysis.

Risk predictors for developing AKI and the influence of AKI on survival were retrospectively evaluated.

The definition of CS predisposed the presence of the following three factors: (1) impaired systolic blood pressure < 90 mmHg, longer than 30 min or necessary catecholamine support to maintain systolic blood pressure ≥ 90 mmHg, (2) onset of pulmonary congestion (3) clinical evidence of burdened end-organ perfusion (one or more of the following: serum lactate above 2.0 mmol/L, cold and wet cutis, urine output below 30 ml/h, pathological mental function), corresponding to SCAI stage C 10 .

AKI was defined as an elevation of serum creatinine ≥ 0.3 mg/dl during the initial 48 h after admission to the hospital according to the Kidney Disease Improving Global Outcomes (KDIGO) criteria 11 . Urine output criteria were not considered since the initial administration of diuretics could represent a relevant confounder 12 . For patients without any recent data regarding creatinine levels (n = 3), we assessed baseline creatinine by implementing an estimated glomerular filtration rate (eGFR) of 75 ml/min/1.73 m 2 (eGFR approach) 13 , 14 , 15 . Stages of chronic kidney disease (CKD) were determined by assessment of baseline (admission to the hospital) creatinine levels according to current KDIGO guidelines 16 .

In all patients, the implantation of Impella and the pulmonary artery catheter (PAC) for invasive hemodynamic measurements were performed within the first 120 min after admission according to standard operating procedures in the catheterization laboratory before the PCI procedure of the culprit lesion took place (suppl. Table 1 ). Before implantation of the Impella, the LVEF was measured using echocardiography.

Invasive hemodynamic measurement

PAC was implemented to obtain hemodynamic parameters like cardiac output (CO), systolic arterial pulmonary pressure (sPAP), diastolic arterial pulmonary pressure (dPAP) and mean arterial pulmonary pressure (meanPAP), pulmonary capillary wedge pressure (PCWP), central venous pressure (CVP), central venous oxygen saturation (SvO 2 ), systemic vascular resistance (SVR) and pulmonary artery pulsatility index (PAPi). Parameters were taken within the first 24 h after admission to the hospital, after the patient´s arrival on the ICU with ongoing Impella support.

Comorbidities, clinical parameters, and ICU scores

Comorbidities and clinical and treatment-related parameters, like systolic, diastolic, and mean arterial pressure, heart rate, catecholamine dosages and fluids, laboratory parameters including serum creatinine and GFR and lactate were registered and evaluated during the in-hospital stay. The common ICU scores (SAPS II, SOFA) and the Horowitz Index were documented within the first 24 h after admission.

Clinical outcomes

Primary endpoint was the development of AKI. Risk factors for the development of AKI, all-cause mortality and risk factors for mortality were defined as secondary endpoints.

Statistical analysis

This was a retrospective data analysis. Data are presented as absolute variables and percentages (%) for categorical variables and either median with interquartile range (IQR: 25th–75th percentile) or mean with standard deviation according to the distribution of the variables. Normality was assessed by using Kolmogorov–Smirnov as well as the Shapiro–Wilk test. After testing for normal distribution, the Student’s t-test or Mann–Whitney test was implemented to test for differences between various characteristics. For categorical variables, Fisher’s exact test or chi-square test was used, as appropriate. We implemented binary logistic regression analysis to identify variables associated with AKI. Considering significant associations of univariate analysis (p < 0.1 accepted for retention), multivariate logistic regression with backward elimination and probability of occurrence of 0.05 and removal of 0.10 was performed to identify independent predictors. Pearson's correlation was implemented to analyze for correlations with a p < 0.05 considered statistically significant. Kaplan–Meier curves with log-rank (Mantel-Cox) test was used to analyze 30-day survival. Cox regression analysis was performed to identify independent predictors considering variables with significant association at univariate analysis (retention p < 0.1). All analyses were made using SPSS 28 (IBM Corp., USA) and GraphPad Prism 8.0. A two-sided p-value < 0.05 was considered statistically significant.

Ethics approval and consent to participate

The data analysis was performed according to the Declaration of Helsinki and was approved by the Ethics Committee of the University Hospital of Marburg (protocol code: study 136/17, date of approval: 11 October 2019). Informed consent was acquired from all patients involved.

Overall cohort

Data from 50 patients were analyzed. The demographics, baseline characteristics, and relevant comorbidities of the overall cohort are displayed in Table 1 . All patients presented with shock stadium C according to the SCAI classification. Only Impella MCS was used in this study cohort. None of the patients' hemodynamic situation deteriorated during Impella support and none suffered cardiac arrest. The study population had a mean age of 67 ± 13 years with 74% male individuals. 18 (36%) of the patients were accompanied by a 3-vessel coronary heart disease (CHD), 19 (38%) had a 2-vessel CHD and in 13 (26%) a 1-vessel CHD was diagnosed. Culprit lesions were in 4 patients (8%) in the left main coronary artery (LMCA), in 19 patients (38%) in the left anterior descending (LAD), in 6 patients (12%) in the LAD and first diagonal branch, in 4 patients (8%) in the LAD and in the second diagonal branch, in 6 patients (12%) in the intermediary branch, in 8 patients (16%) in the LCX, and in 3 patients (6%) in the right posterolateral branch. None of the patients presented a right ventricular infarction (Suppl. Table 1 ). Every patient underwent coronary angiography with appropriate percutaneous coronary intervention and implantation of left ventricular Impella (CP) under fluoroscopic control in the catheter laboratory. In all patients, arterial access was established via the femoral artery. 43 (86%) patients had a medical history of arterial hypertension (aHT), 35 (70%) were accompanied by known dyslipidemia, and in 19 (38%) patients diabetes mellitus was diagnosed. In the overall cohort, the mean LVEF was 37 ± 12% and the mean duration of Impella support was 9 ± 6 days, without any significant differences in the subgroups (AKI, Non-AKI). No relevant hemolysis (significant hemoglobine decrease, macrohematuria, bilirubin increase, free hemoglobine) could be detected. Data on renal function and hemodynamic data of the overall cohort are shown in Tables 2 and 3 respectively.

Prevalence of AKI and risk factors

40 (80%) patients had a known medical history of chronic kidney disease (CKD). In 10 (20%) patients CKD stadium G1 had been diagnosed and 20 (40%) patients had a known CKD stadium G2 whereas 15 (30%) and 5 (10%) individuals were accompanied by CKD stadium G3a and G3b respectively. At admission, the whole cohort had a mean creatinine of 1.39 ± 0.69 mg/dl and in 13 (26%) patients AKI was diagnosed according to 2012 KDIGO criteria whereas, after the first 48 h, a total of 30 (60%) patients developed AKI. 4 (8%) of these patients were classified at AKI stage1, 2 (4%) at AKI stage 2 and 24 (48%) at AKI stage 3. In 24 (48%) patients renal replacement therapy with continuous hemodiafiltration (CVVHDF) had to be conducted (Table 2 ).

Comparing the no AKI and AKI subgroups patients with AKI had a significantly higher SOFA and SAPS II score (6 (6) vs. 11 (5), p = 0.001 and 36.3 ± 11.9 vs. 50.17 ± 14.51, p = 0.001 respectively) (Table 1 ). Furthermore, AKI patients were accompanied by a significantly lower GFR at admission (43.27 ± 17.89 ml/min vs. 70.5 ± 26.01 ml/min, p < 0.001) as well as by a significantly reduced lowest GFR level (37.23 ± 14.3 ml/min vs. 63.7 ± 20.51 ml/min, p < 0.001) (Table 2 ).

On the other hand, no significant differences of SAP, MAP, heart rate, and CO were documented. Interestingly CVP was significantly elevated in the AKI subgroup (12.33 ± 6.01 vs. 7.9 ± 5.1, p = 0.007) while the tissue perfusion-related values of lactate and SvO 2 were reduced in AKI individuals (1.9 ± 1.96 mmol/l vs. 1.3 ± 0.68 mmol/l, p = 0.07 and 59.12 ± 12.63% vs. 66.9 ± 17.19%, p = 0.07 respectively) but p values missed slightly statistical significance. Furthermore, regarding dosages of vasopressors and inotropics, no relevant differences between the two subgroups were documented (Table 3 ).

In the univariate analysis, a highly significant association of chronic kidney disease (CKD) history (OR 4.846, p = 0.04), CVP at admission (OR: 1.185, p = 0–014), SvO 2 at admission (OR 0.942, p < 0.001) and GFR at admission GFR at admission (OR 0.951, p = 0.002) with the development of AKI could be demonstrated. Moreover, multivariate analysis revealed CVP at admission (OR 1.216, p = 0.020), and SvO 2 at admission (OR 0.93, p = 0.029) as independent predictors for the onset of AKI. Due to the collinearity of the onset of AKI and GFR at admission, GFR was not included in the multivariate analysis (Table 4 ).

Analysis of survival

The 30-day mortality of the whole cohort was 22%. Patients with AKI were accompanied by a significantly higher 30-day mortality than patients without AKI (n = 10/30 (33%) vs. n = 1/20 (5%); p = 0.019). The overwhelming percentage of diseased patients was in AKI stadium 3 (n = 10/24; 41, 6%) and, consequently, this subgroup was accompanied by an even higher 30-day mortality rate (Figs. 1 , 2 and 3 ).

Study cohort.

30-Day cumulative survival. Red: patients with acute kidney injury (AKI), green: patients without AKI (Non-AKI) (Kaplan–Meyer analysis).

30-Day cumulative survival. Orange: no kidney injury, blue: AKI stages 1 and 2, purple: AKI stage 3 (Kaplan–Meyer analysis).

In the univariate analysis, lactate at admission (HR 1.489, p = 0.004), the dosage of norepinephrine (HR 1.027, p = 0.012), and AKI stage 3 (HR 0.074, p = 0.013) were significantly associated with survival. GFR at admission was also strongly associated with 30-day mortality but the p-value did not reach statistical significance (p = 0.054). In the Cox regression analysis, AKI stage 3 (HR = 0.095, p = 0.026) and norepinephrine dosage (HR 1.027, p = 0.008) were independently associated with 30-day mortality (Table 5 ).

We here defined early predictors for the occurrence of AKI during Impella support, which may be useful to optimize therapy control in CS. To our knowledge, this is the first study to analyze the occurrence of AKI according to the KDIGO criteria in CS patients during Impella support, including the evaluation of a wide range of patient characteristics, invasively obtained hemodynamics, laboratory parameters, and other indices that may influence renal function in shock.

In our Impella cohort, the prevalence of AKI was 60%, in accordance with other published data 3 , 17 , 18 . The development of AKI was significantly more common in patients with CKD, possibly reflecting a reduced compensatory ability caused by the development of chronic renal organ damage. Moreover, as expected, patients developing AKI had a significantly lower GFR at admission.

Ultimately, three independent and early predictors of AKI could be defined in our cohort, namely GFR, CVP, and SvO 2 . While pre-existing patient-associated parameters such as CKD and thus reduced GFR on admission cannot be directly influenced, the two other hemodynamic parameters CVP and SvO2 can be improved by therapeutic methods (fluid management, catecholamines) and possibly also by MCS such as the Impella.

According to our data, hemodynamic parameters that reflect myocardial function and organ and tissue perfusion in CS seem to play an outstanding role in the occurrence of AKI and renal organ failure. However, the quality and effectiveness of the interaction between the individual treatment options used and the parameters monitored and adjusted, could ultimately determine the outcome and be decisive for the preservation of organ function in CS.

In patients with AKI, in univariate analysis, SvO 2 was noteworthy lower and, correspondingly, although the p-value moderately missed statistical significance, lactate level was found to be considerably higher compared to non-AKI patients indicating an impaired tissue and end-organ perfusion as a consequence of low cardiac output. While AKI patients presented no significant differences of MAP and PCWP, CVP and sPAP on the other hand were notably elevated reflecting a substantial venous congestion and right ventricular burden. Whereas the elevated CVP and sPAP in AKI patients could pathophysiological be attributed to systemic overload in the situation of compromised hemodynamics as well as to oliguria or anuria in CS, the left ventricular unloading with the Impella seems to effectively support left ventricle function since PCWP values of patients with and without AKI presented comparable.

In addition, the vicious circle of impaired tissue and organ perfusion, which may also be caused by increased venous congestion, leads to the activation of a cascade of neuro-hormonal and inflammatory mechanisms that further deteriorate organ function 19 , 20 , 21 . Moreover, in combination with oxidative stress, the so-called glycosaminoglycan (CAG) networks could be damaged 22 . The CAGs, which are responsible for buffering sodium, influence endothelial function. An impaired function of the CAGs leads to an elevation of vascular resistance and imbalanced endothelial nitric oxide production. The resulting endothelial dysfunction requires an increased workload for both, the left and right myocardial ventricle, further impairing end-organ perfusion 23 . Thus, in case, right ventricular filling pressure increases for example in a situation of CS complicating right ventricular MI, a backward failure may lead to a further increase of CVP. Furthermore, also left ventricular failure with consecutive congestion could cause pulmonary edema with secondary deterioration of right ventricular function and consecutive abdominal organ congestion. Among all complications of AKI, volume overload aggravating venous congestion seems to be the one with the greatest impact on mortality 24 . At the same time, recent data emphasize that venous congestion and CVP are also one of the most important pathomechanisms for the development of CKD 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 . This seems in line with to pathophysiological understanding, as a backward failure can usually also be accompanied by a forward failure with consecutive organ minder perfusion. According to the findings of this study cohort, the elevated CVP could be attributed to left ventricular systolic function impairment with consecutive post capillary congestion leading to elevated sPAP burdening right ventricular function ultimately increasing venous congestion.

Therefore, in our opinion, the reduction of venous congestion through diuretics or early RRT while improving left ventricular function and organ perfusion, possibly by additional Impella support may be beneficial for a more favourable outcome.

As mentioned above, SvO 2 at admission could be identified as an independent and early predictor for the occurrence of AKI. This association underscores the relevance of adequate organ and tissue perfusion in the situation of CS to avoid end-organ failure. The use of catecholamines and vasopressors in CS often temporarily stabilizes blood pressure at the expense of severely increasing systemic peripheral vascular resistance and cardiac afterload 33 , 34 , 35 . Interestingly, as we were able to show, AKI stage 3 and norepinephrine dosages were independent predictors of 30-day mortality. Therefore, the reduction of vasopressor doses during CS should be aimed for. In this regard, the use of MCS such as the Impella is an option that may be considered in hemodynamically unstable patients, as during Impella support the CO and SvO 2 increase 9 .

As it is known from the current literature, in the situation of CS, the 30-day mortality remains higher than 50% without any noteworthy changes in the last two decades 3 . The 30-day mortality of our cohort, however, was lower at 22%. This may be attributed to the fact that the patients of this cohort received early hemodynamic support with left ventricular Impella implemented according to standard algorithms in CS. However, the high SOFA score of this cohort of 10 (IQR:5) with an expected mortality between 33 and 50%, which is in line with the known mortality rates in the current literature contradicts this explanation at first glance 36 . On the other side, one may postulate, that the interaction of myocardial function and hemodynamic support by MCS may improve the negative prognosis predicted by the scores.

In summary, early targeted monitoring of relevant parameters, as demonstrated here, should be recommended to enable timely adaptation of therapeutic approaches, in particular relieving venous congestion, increasing CO, and reducing peripheral vascular resistance to improve tissue and organ oxygenation, which in turn may reduce the prevalence of AKI 37 , 38 , 39 . The use of MCS may also be supportive in this respect 40 .

Limitations

The relatively small number of patients and the single center experience belong to the limitations of this study. Furthermore, the retrospective analysis also limits the interpretation of the data. However, to our knowledge, this is the first study to analyze early and subsequent predictors of AKI according to the KDIGO criteria in CS patients with Impella support using a broad spectrum of parameters and characteristics. To further evaluate the clinical relevance of these data, larger prospective randomized studies are needed that include a broader cohort of patients with different stages of CS as defined by the SCAI classification.

Conclusions

Renal function is one of the most relevant key factors regarding the prognosis of patients with CS and AKI deteriorates outcome dramatically. Increased venous congestion, reduced SvO 2, and GFR on admission are early independent predictors for AKI complicating CS in patients supported with Impella, while catecholamine dosages and the onset of AKI are independent predictors of mortality. The reduction of catecholamine dosages during ongoing support with pVLAD like the Impella and the decrease of venous congestion by additional volume restriction and if indicated the early use of RRT may improve prognosis.

Data availability

Data will be made available upon individual request (contact: corresponding author).

Samsky, M. D. et al. Cardiogenic shock after acute myocardial infarction: A review. JAMA 326 (18), 1840–1850 (2021).

Article   PubMed   PubMed Central   Google Scholar  

Thiele, H., Ohman, E. M., de Waha-Thiele, S., Zeymer, U. & Desch, S. Management of cardiogenic shock complicating myocardial infarction: An update 2019. Eur. Heart J. 40 (32), 2671–2683 (2019).

Article   CAS   PubMed   Google Scholar  

Tarvasmäki, T. et al. Acute kidney injury in cardiogenic shock: Definitions, incidence, haemodynamic alterations, and mortality. Eur. J. Heart Fail. 20 (3), 572–581 (2018).

Article   PubMed   Google Scholar  

Mezhonov, E. M., Vialkina, I. A., Vakulchik, K. A. & Shalaev, S. V. Acute kidney injury in patients with ST-segment elevation acute myocardial infarction: Predictors and outcomes. Saudi J. Kidney Dis. Transpl. 32 (2), 318–327 (2021).

Cosentino, N. et al. Acute kidney injury and in-hospital mortality in patients with ST-elevation myocardial infarction of different age groups. Int. J. Cardiol. 344 , 8–12 (2021).

Vallabhajosyula, S. et al. Temporal trends, predictors, and outcomes of acute kidney injury and hemodialysis use in acute myocardial infarction-related cardiogenic shock. PLoS ONE 14 (9), e0222894 (2019).

Article   CAS   PubMed   PubMed Central   Google Scholar  

Karatolios, K. et al. Impella support compared to medical treatment for post-cardiac arrest shock after out of hospital cardiac arrest. Resuscitation 126 , 104–110 (2018).

Lüsebrink, E. et al. Percutaneous transvalvular microaxial flow pump support in cardiology. Circulation 145 (16), 1254–1284 (2022).

Patsalis, N. et al. Renal protection and hemodynamic improvement by impella microaxial pump in patients with cardiogenic shock. J. Clin. Med. 11 (22), 6817 (2022).

Naidu, S. S. et al. SCAI SHOCK stage classification expert consensus update: A review and incorporation of validation studies: This statement was endorsed by the American College of Cardiology (ACC), American College of Emergency Physicians (ACEP), American Heart Association (AHA), European Society of Cardiology (ESC) Association for Acute Cardiovascular Care (ACVC), International Society for Heart and Lung Transplantation (ISHLT), Society of Critical Care Medicine (SCCM), and Society of Thoracic Surgeons (STS) in December 2021. J. Am. Coll. Cardiol. 79 (9), 933–946 (2022).

Kidney Disease, Improving Global Outcomes (KDIGO). Kidney Int. Suppl. 2 , 19–36 (2012).

Sims, A. J., Hussein, H. K., Prabhu, M. & Kanagasundaram, N. S. Are surrogate assumptions and use of diuretics associated with diagnosis and staging of acute kidney injury after cardiac surgery?. Clin. J. Am. SocNephrol. 7 (1), 15–23 (2012).

Article   Google Scholar  

Siew, E. D. & Matheny, M. E. Choice of reference serum creatinine in defining acute kidney injury. Nephron 131 (2), 107–112 (2015).

Bellomo, R., Ronco, C., Kellum, J. A., Mehta, R. L. & Palevsky, P. Acute Dialysis Quality Initiative Workgroup: Acute renal failure – definition, outcome measures, animal models, fluid therapy and information technology needs: the second international consensus conference of the acute dialysis quality initiative (ADQI) group. Crit. Care 8 , R204–R212 (2004).

National Kidney Foundation K/DOQI Clinical Practice Guidelines for Chronic Kidney Disease. Evaluation, classification and stratification. Am. J. Kidney Dis. 39 (2 Suppl 1), S76–S92 (2002).

Google Scholar  

Kidney International Supplements (2013) 3, 4.

Fuernau, G. et al. Prognostic impact of established and novel renal function biomarkers in myocardial infarction with cardiogenic shock: A biomarker substudy of the IABP-SHOCK II-trial. Int. J. Cardiol. 191 , 159–166 (2015).

Werdan, K., Ruß, M., Buerke, M., Delle-Karth, G., Geppert, A., Schöndube, F. A., German Cardiac Society, German Society of Intensive Care and Emergency Medicine, German Society for Thoracic and Cardiovascular Surgery (Austrian Society of Internal and General Intensive Care Medicine; German Interdisciplinary Association of Intensive Care and Emergency Medicine; Austrian Society of Cardiology; German Society of Anaesthesiology and Intensive Care Medicine; German Society of Preventive Medicine and Rehabilitation. Cardiogenic shock due to myocardial infarction: diagnosis, monitoring and treatment: a German-Austrian S3 Guideline. DtschArztebl Int. 109 (19), 343–351 (2012).

Harjola, V. P. et al. Organ dysfunction, injury and failure in acute heart failure: from pathophysiology to diagnosis and management. A review on behalf of the Acute Heart Failure Committee of the Heart Failure Association (HFA) of the European Society of Cardiology (ESC). Eur. J. Heart Fail. 19 (7), 821–836 (2017).

Calfee, C. S. & Matthay, M. A. Clinical immunology: Culprits with evolutionary ties. Nature 464 (7285), 41–42 (2010).

Article   ADS   CAS   PubMed   PubMed Central   Google Scholar  

Rudiger, A. Understanding cardiogenic shock. Eur. J. Heart Fail. 17 (5), 466–467 (2015). https://doi.org/10.1002/ejhf.265 . Erratum in: Eur. J. Heart Fail. 17 (6), 639 (2015).

Nijst, P. et al. The pathophysiological role of interstitial sodium in heart failure. J. Am. Coll. Cardiol. 65 (4), 378–388 (2015).

Marti, C. N. et al. Endothelial dysfunction, arterial stiffness, and heart failure. J. Am. Coll. Cardiol. 60 (16), 1455–1469 (2012).

Payen, D. et al. A positive fluid balance is associated with a worse outcome in patients with acute renal failure. Crit. Care 12 (3), 74 (2008).

Sheikh, O., Nguyen, T., Bansal, S. & Prasad, A. Acute kidney injury in cardiogenic shock: A comprehensive review. Catheter Cardiovasc. Interv. 98 , E91–E105 (2021).

McCallum, W. & Sarnak, M. J. Cardiorenal syndrome in the hospital. Clin. J. Am. Soc. Nephrol. 18 (7), 933–945 (2023).

Andrei, S., Bahr, P. A., Nguyen, M., Bouhemad, B. & Guinot, P. G. Prevalence of systemic venous congestion assessed by Venous Excess Ultrasound Grading System (VExUS) and association with acute kidney injury in a general ICU cohort: a prospective multicentric study. Crit. Care 27 (1), 224 (2023).

D’Marco, L. Congestive nephropathy. Int. J. Environ. Res. Public Health 19 (5), 2499 (2022).

Palazzuoli, A. et al. Chronic kidney disease and worsening renal function in acute heart failure: Different phenotypes with similar prognostic impact?. Eur. Heart J. Acute Cardiovasc. Care 5 (8), 534–548 (2016).

van den Akker, J. P. C., Bakker, J., Groeneveld, A. B. J. & den Uil, C. A. Risk indicators for acute kidney injury in cardiogenic shock. J. Crit. Care 50 , 11–16 (2019).

Legrand, M., Mebazaa, A., Ronco, C. & Januzzi, J. L. Jr. When cardiac failure, kidney dysfunction, and kidney injury intersect in acute conditions: The case of cardiorenal syndrome. Crit. Care Med. 42 (9), 2109–2117 (2014).

Mullens, W. et al. Importance of venous congestion for worsening of renal function in advanced decompensated heart failure. J. Am. Coll. Cardiol. 53 (7), 589–596 (2009).

Upadhyaya, V. D. et al. Outcomes of renal function in cardiogenic shock patients with or without mechanical circulatory support. J. Clin. Med. Res. 13 (5), 283–292 (2021).

Flaherty, M. P. et al. Hemodynamic support with a microaxial percutaneous left ventricular assist device (Impella) protects against acute kidney injury in patients undergoing high-risk percutaneous coronary intervention. Circ. Res. 120 (4), 692–700 (2017).

Singer, M. et al. The Third International Consensus Definitions for Sepsis and Septic Shock (Sepsis-3). JAMA 315 (8), 801–810 (2016).

Nohria, A. et al. Clinical assessment identifies hemodynamic profiles that predict outcomes in patients admitted with heart failure. J. Am. Coll. Cardiol. 41 (10), 1797–1804 (2003).

Mullens, W. & Nijst, P. Cardiac output and renal dysfunction: Definitely more than impaired flow. J. Am. Coll. Cardiol. 67 , 2209–2212 (2016).

Hanberg, J. S. et al. Reduced cardiac index is not the dominant driver of renal dysfunction in heart failure. J. Am. Coll. Cardiol. 67 , 2199–2208 (2016).

Chatzis, G. et al. Early Impella support in postcardiac arrest cardiogenic shock complicating acute myocardial infarction improves short- and long-term survival. Crit. Care Med. 49 (6), 943–955 (2021).

Download references

Open Access funding enabled and organized by Projekt DEAL. This study acquired no external funding.

Author information

Authors and affiliations.

Department of Cardiology, Angiology, and Intensive Care Medicine, University Hospital, Philipps University of Marburg, Baldinger Str., 35043, Marburg, Germany

Nikolaos Patsalis, Julian Kreutz, Giorgos Chatzis, Styliani Syntila, Maryana Choukeir, Bernhard Schieffer & Birgit Markus

You can also search for this author in PubMed   Google Scholar

Contributions

Conceptualization, NP, BS, and BM; Data curation, NP, GC, MC, JK; Data analysis, NP, GC, MC, JK; Methodology, NP, BS, and BM; Project administration, SS; Resources, BS and BM; Software, NP, JK, and GC; Supervision, BS; Validation, NP, GC, BS, and BM; Visualization, NP, JK, GC, and SS; Writing – original draft, NP and BM; Writing – review & editing, GC, SS, MC, BS, and BM.

Corresponding author

Correspondence to Birgit Markus .

Ethics declarations

Competing interests.

B.M. received research funding from Abiomed; J.K., G.C., B.S., and B.M. receive speaker’s honoraria from Abiomed; no other of the remaining authors declared any disclosures.

Additional information

Publisher's note.

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary Information

Supplementary information., rights and permissions.

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ .

Reprints and permissions

About this article

Cite this article.

Patsalis, N., Kreutz, J., Chatzis, G. et al. Early risk predictors of acute kidney injury and short-term survival during Impella support in cardiogenic shock. Sci Rep 14 , 17484 (2024). https://doi.org/10.1038/s41598-024-68376-w

Download citation

Received : 31 March 2024

Accepted : 23 July 2024

Published : 30 July 2024

DOI : https://doi.org/10.1038/s41598-024-68376-w

Share this article

Anyone you share the following link with will be able to read this content:

Sorry, a shareable link is not currently available for this article.

Provided by the Springer Nature SharedIt content-sharing initiative

• Cardiogenic shock
• Acute kidney injury (AKI)
• Left ventricular Impella
• Predictors of AKI

By submitting a comment you agree to abide by our Terms and Community Guidelines . If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.

Quick links

• Explore articles by subject
• Guide to authors
• Editorial policies

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings
• My Bibliography
• Collections
• Citation manager

Save citation to file

Email citation, add to collections.

• Create a new collection
• Add to an existing collection

Add to My Bibliography

Your saved search, create a file for external citation management software, your rss feed.

• Search in PubMed
• Search in NLM Catalog
• Add to Search

Increase of serum pancreatic enzymes during hospitalization for acute heart failure

Affiliations.

• 1 University of Groningen, Department of Cardiology, University Medical Centre Groningen, Groningen, The Netherlands.
• 2 Department of Gastroenterology and Hepatology, St. Antonius Hospital, Nieuwegein, The Netherlands.
• PMID: 39056408
• DOI: 10.1002/ehf2.14985

Aims: Acute heart failure (AHF) is associated with end-organ dysfunction. The effect of AHF on the pancreas has not been studied. We aim to evaluate serum markers of pancreatic damage during hospitalization for AHF.

Methods and results: In data from the Pragmatic Urinary Sodium-based treatment algoritHm in Acute Heart Failure (PUSH-AHF) study, amylase and lipase values were extracted from available serum samples at baseline, and at 24 and 72 h after hospitalization. The differences between pancreatic enzymes between timepoints were evaluated using the Friedman test. Associations with N-terminal pro-B-type natriuretic peptide (NT-proBNP) were tested using linear regression analysis. The study population consisted of 274 patients. Mean age was 73 ± 11 years, and 117 (43%) were women. Mean left ventricular ejection fraction (LVEF) was 38 ± 14%; 53 (19%) patients had HF with a preserved LVEF (≥50%). At baseline, median amylase and lipase were within normal range (47 [33-63] U/L and 30 [21-44] U/L, respectively). Both enzymes significantly increased in the first 72 h (P-value for trend <0.001); mean change was 9 ± 22 U/L for amylase, and 10 ± 22 U/L for lipase. Moreover, NT-proBNP at baseline showed a positive correlation with mean change in pancreatic enzymes in 72 h (P = 0.02 for amylase and P = 0.006 for lipase).

Conclusion: Patients admitted for AHF exhibited a significant increase in serum values of pancreatic enzymes in the first 72 h, suggesting that an episode of AHF affects the pancreatic tissue. This rise in pancreatic enzymes was associated with HF severity, as reflected by NT-proBNP.

Keywords: Acute heart failure; Amylase; Lipase; Pancreas.

© 2024 The Author(s). ESC Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

PubMed Disclaimer

• McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Bohm M, et al. 2021 ESC guidelines for the diagnosis and treatment of acute and chronic heart failure. Eur Heart J 2021;42:3599‐3726. doi:10.1093/eurheartj/ehab368
• Metra M, Cotter G, Davison BA, Felker GM, Filippatos G, Greenberg BH, et al. Effect of serelaxin on cardiac, renal, and hepatic biomarkers in the Relaxin in Acute Heart Failure (RELAX‐AHF) development program: Correlation with outcomes. J Am Coll Cardiol 2013;61:196‐206. doi:10.1016/j.jacc.2012.11.005
• Biegus J, Hillege HL, Postmus D, Valente MAE, Bloomfield DM, Cleland JGF, et al. Abnormal liver function tests in acute heart failure: relationship with clinical characteristics and outcome in the PROTECT study. Eur J Heart Fail 2016;18:830‐839. doi:10.1002/ejhf.532
• Dams OC, Vijver MAT, van Veldhuisen CL, Verdonk RC, Besselink MG, van Veldhuisen DJ. Heart failure and pancreas exocrine insufficiency: Pathophysiological mechanisms and clinical point of view. J Clin Med 2022;11:4128. doi:10.3390/jcm11144128
• Vijver MAT, Dams OC, Verdonk RC, van Veldhuisen DJ. Pancreatic exocrine insufficiency in heart failure, preliminary results from a pilot study. Eur J Heart Fail 2023;254.

LinkOut - more resources

Full text sources, research materials.

• NCI CPTC Antibody Characterization Program

Miscellaneous

• NCI CPTAC Assay Portal

• Citation Manager

NCBI Literature Resources

MeSH PMC Bookshelf Disclaimer

The PubMed wordmark and PubMed logo are registered trademarks of the U.S. Department of Health and Human Services (HHS). Unauthorized use of these marks is strictly prohibited.

An official website of the United States government

The .gov means it’s official. Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

The site is secure. The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

• Publications
• Account settings

Preview improvements coming to the PMC website in October 2024. Learn More or Try it out now .

• Advanced Search
• Journal List
• Card Fail Rev
• v.1(2); 2015 Oct

The Key Roles for the Nurse in Acute Heart Failure Management

The key roles for the nurse in the management of heart failure have largely focused on the follow up and monitoring of patients at high risk of hospital (re)admission. Studies reported an improvement in outcome for patients followed up by a multidisciplinary care team in which a nurse was a key player. Such level of care is now recognised in international guidelines. More recent emphasis on the management of acute heart failure has led to a focus on the contribution by nurses to the entire heart failure journey and their roles in improving patient outcome and the delivery of quality care. This paper focuses on the in-patient admission for acute or decompensated heart failure and discusses the involvement of nurses in achieving an effective heart failure service.

The specialised role of the heart failure nurse rose to prominence during the 1990s. Studies of heart failure disease management reported a reduction in the risk of hospital readmission in services with structured follow up that focused on the optimisation of therapy, out-patient follow up, education for self-care and the coordination of care.[ 1 ] Nurses had already established their role in the long-term management of patients with chronic disease and quickly confirmed their role within heart failure disease management services. Such level of care became recognised in international guidelines and as a marker of a quality service.[ 2 ] More recently there has been a developing interest in optimising patient outcome through a greater focus on the in-patient admission, faster diagnosis of acute or decompensated heart failure, in-patient management in an appropriate care environment and planned discharge which includes referral to a heart failure disease management programme. Recent recommendations for the early in-patient period acknowledge the clear roles for the nurse in the heart failure team and discussed in this article ( Table 1 ).[ 3 ]

Source: adapted from Mebazza et al, 2015.[ 3 ]

Immediate Assessment and Triage

From a patient perspective, the acute heart failure journey generally starts with increasing shortness of breath, sometimes accompanied by non-specific signs and symptoms of oedema, fatigue, loss of appetite and changes in weight. Patients seek professional help when their own self-care resources fail or through the encouragement of family or friends. For some, the onset of symptoms is rapid.[ 4 ] Either way, patients generally have worsening shortness of breath when they present to a hospital emergency department. The UK National Heart Failure Audit provides a detailed picture of the patient admitted to hospital. It reports that almost 80 % of those admitted to hospital with acute or decompensated heart failure present with shortness of breath on at least moderate exercise during their first hospital admission: New York Heart Association (NYHA) III 44 %, NYHA IV 35 %. At subsequent hospitalisations, the proportion of patients presenting with severe shortness of breath increases modestly: NYHA III 44 %, NYHA IV,40 %.[ 5 ] On arrival in the emergency department, prompt recognition, management and transfer to an appropriate environment for care are necessary to alleviate both the physical and emotional symptoms of breathlessness and optimise outcome. Unlike the focus on triage of the patient presenting with acute-onset chest pain, emergency departments do not generally have an acute heart failure triage nurse. Therefore the initial patient triage is frequently undertaken by a nurse practitioner who elicits the patient history, assesses the severity of the clinical status and refers to the relevant team. In this way, such nurses play a key role within the multi-professional team by helping to distinguish the cause of breathlessness and initiating prompt symptom relieving therapy.

Key issues in the nurse’s initial clinical assessment of suspected acute heart failure are summarised in Table 2 and adapted from the most recent recommendations on management.[ 3 ] Nurse practitioners generally have an ‘expanded’ skill set that enables them to also perform clinical examination to identify signs of congestion and refer for chest X-ray. Identifying clinical stability is an important first step in triage and enables the prompt transfer of the patient to the appropriate level of care for safe and effective therapy. This is largely influenced by the local organisation of services and skill sets of ward nurses. However, a patient at high risk of clinical deterioration or one requiring invasive cardiopulmonary support should ideally be transferred to the emergency resuscitation area, or an intensive or coronary care unit offering a lower patient-to-nurse ratio, closer patient monitoring and medical staff more available to support decision making.

Ongoing Monitoring and Management

The management of acute breathlessness or cardiopulmonary instability is generally carried out simultaneously with diagnosis. Once the diagnosis of acute heart failure is made, diuretics are administered to relieve dyspnoea. Ideally the dose should be the lowest needed to reduce fluid congestion and so balance the positive action with any potential negative effect on renal function. Close monitoring of renal function, fluid balance and urine output are therefore needed. There is often a tendency to assume urinary catheterisation for the close monitoring of urine output. However, urinary tract infection attributed to urinary catheterisation is the most frequent cause of hospital-acquired infection and in acute hospitals may account for as many as 20 % of all hospital-acquired infections. Risk increases the longer a catheter is in situ , with a daily risk estimated as between 3–7 %.[ 6 ] This risk is likely to be increased further in the older adult with more health problems. The consequences of such an infection are likely to vary, increasing the risk of a prolonged hospital stay and the development of in-hospital confusion, particularly in older adults. Alongside nursing actions to prevent infection, good practice also includes limiting the use of urinary catheters and, when they are necessary, removal as soon as possible. National and international guidelines suggest best practice in their use.[ 7 , 8 ] In the context of acute heart failure this guidance can be interpreted to suggest urinary catheterisation should be restricted to those patients with cardiopulmonary instability and low cardiac output, when hourly urine output monitoring is needed.

The ongoing monitoring of response to treatment and cardiopulmonary status also necessitates close monitoring of key haemodynamic parameters. In the immediate period of stabilisation, overly aggressive management with diuretics and vasodilators may lead to hypotension. Equally, patients may be undertreated or their underlying condition may deteriorate. Early warning scores allocate and weight points to vital signs outside pre-agreed ranges. These points are then summed to provide a single composite score. An increase in score will identify those patients who will benefit from escalation of monitoring or treatment. For example, they may benefit from an increased frequency of observationor ugent medical review. Escalation of treatment and alterations in management are then made in line with the ‘score’. To provide standardisation and limit misunderstanding the UK has adopted the National Early Warning Score (NEWS)[ 9 ] (see Figure 1 ) for use in routine recording of clinical data, replacing traditional observation charts. Such tools have been reported to improve the ability of ward staff (both nursing and medical) to identify and respond to indicators of clinical change.[ 10 ]

Reproduced with permission from the Royal College of Physicians. National Early Warning Score (NEWS): Standardising the assessment of acute illness severity in the NHS. Report of a working party. London: RCP, 2012. Copyright © 2012 Royal College of Physicians.

Close monitoring requires a care environment where nurses have the time and expertise to identify and respond appropriately to changes in physiological data. The association between the competence of nurses and quality of care has long been recognised and more recently the association between nurse staffing, nurse expertise and patient outcome has been confirmed. A study of more than 400,000 patients in 300 acute hospitals in nine European countries reported an association between an increase in the number of nurses and the risk of death. An increase in a nurse’s workload by one patient increased the likelihood of a patient dying by 7 % (OR 1.068, 95 % CI [1.031–1.106]). Conversely, the risk of death was reduced where patients were cared for by academically prepared nurses; every 10 % increase in the number of bachelor-degree nurses on the ward decreased the likelihood of death by 7 % (OR 0.929, 95% CI [0.886–0.973]).[ 11 ] The authors concluded that patients in hospitals in which 60 % of nurses held bachelor degrees and in which the nurse-to-patient ratio was 1:6 would have an almost 30 % reduced risk of death than patients in hospitals in which only 30 % of nurses had bachelor degrees and each cared for eight patients.[ 11 ] Within the context of heart failure the UK National Heart Failure audit revealed that in-hospital mortality is lower when patient care is managed in specialist cardiology wards rather than general medical wards (7.8 % vs 13.2 %).[ 5 ] Taken together these papers suggest that outcome is improved when in-patient care is provided by a specialised team and by ward nurses familiar with the management of heart failure. Countries will need to decide locally how to interpret and implement these findings but they point to an association between the quality of nursing care and patient outcome.

It is not always possible for every patient to receive in-patient care on a specialist cardiology ward and some will be best cared for on general medical or care-of-the-elderly wards where nursing staff have specific expertise in managing the care needs of the frail, older adult. The heart failure management of the older adult is complicated by concomitant comorbid conditions, altered pharmacokinetics, frailty and cognitive impairment. Consequently their hospital length of stay is likely to be longer and also influenced by the availability of post-discharge social support. The UK National Audit data reports an increased length of stay (LOS) in heart failure patients not cared for on cardiology wards and this relates to the majority of those patients aged above 74 years (mean LOS 12.7 days (cardiology ward) vs 13.1 days (general medical) and 14.7 days (other ward areas)).[ 5 ] The in-patient hospital stay allows review of all medication, as well as combinations that may increase the risk of side effects. The in-patient admission also provides time for the safe introduction of new heart failure medication and this is likely to be slower in the older patient. When accompanied by close monitoring of physiological variables and assessment of the patient’s ability to manage potential effects, such as lower systolic blood pressure or increased diuresis, the in-patient stay can increase the safe prescription of medication, as well as positively influence patient compliance. For example, nurses can remind patients to stand up slowly to reduce their risk of dizziness and falls, teach them to modify the timing of diuretics to enable activities outside the home and facilitate the supply of continence aids when necessary. Where in-patient care is not provided on a cardiology ward this can be facilitated by regular outreach by the heart failure team and the heart failure specialist nurse has a central role in this, providing advice, education and liaison between the health-care teams directly involved in providing care and the heart failure specialist team.

Regardless of the place care is delivered, ideally patients with heart failure should be identified and followed up during their hospital stay by a specialist heart failure team. Using medical admission records the heart failure specialist nurse can identify patients with suspected heart failure, act as a point of contact for advice and ensure appropriate discharge planning and follow up. Once stabilised patients should be started or restarted on evidence medicines. Various models for such outreach exist but the exact model will depend on the local organisation of care.[ 12 ]

Discharge Planning

In-patient management extends beyond haemodynamic monitoring and initiation of medication to planning for discharge and the smooth transition to a community heart failure disease management programme. It is now well recognised that patients are at high risk of hospital re-admission during the first few months following discharge. This has led to recommendations for follow up early in the post-discharge period and ideally within the first one to two weeks.[ 3 ] Disease management programmes are now established in many European countries. A recent survey of countries of the ESC reported that heart failure clinics are present in 75 % of those countries that completed the survey and that a heart failure nurse specialist was employed in the majority of those clinics.[ 13 ]

Discharge planning commences once the patient is stabilised and discussions include the heart failure specialist team, the patient and, where necessary, the patient’s family. Preparing for discharge requires assessment of social environment into which the patient will be discharged as well as their capacity to self-care. Patients admitted to hospital with heart failure are frequently elderly with multiple comorbidities. They have reduced physiological reserve to adapt to change and stress and may require a period of rehabilitation and supportive community resources in the initial post-discharge phase. In such situations the heart failure nurse co-ordinates discussions to develop a collaborative discharge plan. In a quasi-experimental study in Sweden of 248 elderly patients hospitalised with heart failure Ulin and colleagues report an earlier hospital discharge in patients whose discharge plan was a collaborative process between the heart failure team and social/community team. They report a mean of 6.7 in-hospital bed days compared with 9.2 days in patients who did not receive a co-ordinated discharge plan.[ 14 ] Such an approach may have particular advantage when hospital discharge is delayed due to social circumstances.

Regardless of age, discharge from hospital is frequently cited as a period of high anxiety for both patients and their families. A coordinated care plan that estimates time to euvolamia and commencement of heart failure medication can be communicated and discussed at an early stage and so help prepare both the patient and their family for discharge.

Patient Education

The in-hospital period is also an ideal time to provide education about heart failure, its monitoring and management. It is possible that some hospital admissions are preventable if worsening heart failure is recognised early; some patients and family wish to be involved in self-care e.g. by monitoring their condition, recognising significant change and taking appropriate action. They should be introduced to these concepts during the in-patient stay. There is often a mismatch between a patent’s understanding of their heart failure management and the information provided by the health professional. For example, the Euroheart failure survey reported that patients recalled only 46 % of the self-care advice given[ 15 ] whilst Ekman and colleagues, in a sub-study of the COMET study, reported that adherence to medication was associated with patient beliefs about their medication.[ 16 ] Results such as these point to the complexity of providing the patient with education for self-care and are recognised in the current focus on individualising patient education. A patient’s capacity to learn and retain new information may be reduced whilst hospitalised, in part due to higher levels of anxiety and cognitive dysfunction. It is therefore good practice to use the hospital admission to provide the patient with verbal information that is supported by written material. Some nurses use the ‘teach-back technique’ whereby they ask the patient to repeat, using their own words, the information they have given them.[ 17 ] This enables the patient to confirm their understanding and the nurse to rephrase any information that is misunderstood. Such a technique involves the nurse and patient in the repetition of information and increases the time the nurse spends with the patient discussing heart failure and its management. It is possible that this increased time spent in patient education provides benefit in terms of knowledge retention and may be particularly valuable when interacting with the person with low educational or health literacy. Both the education provided and the patient’s understanding should be communicated to the heart failure disease management team and should form a basis for ongoing education and support.

End-of-life Care

Mortality is high in patents discharged from hospital following an acute heart failure admission. Despite advances in care about 14 % of patients still die within six months of hospital discharge.[ 18 ] Various factors are likely to increase this risk such as age, frailty, number of hospital admissions in the preceding 12 months and presence of cachexia.[ 2 ] The hospital admission provides time to identify patients with a worse prognosis and introduce palliative and supportive measures. Such care actions include providing pain relief, discussions around future care planning and preferred place of death. There is a growing recognition of the need for such discussions and hospitals increasingly provide a palliative care service jointly between the heart failure and palliative care nurse. Where such services exist studies report a reduction in symptom burden and depression and improvements in quality of life.[ 19 ] Such services also report an increase in advance care planning.[ 20 ] This may help address the currently reported mismatch between patients’ preferred and actual place of death.

Conclusions

Patients with acute heart failure benefit from early diagnosis, close monitoring and management provided by skilled heart failure teams that include a heart failure nurse specialist and by cardiology ward nurses with sufficient education to support safe practice. As part of the team, the heart failure nurse specialist is well placed to also provide an outreach service to patients throughout the acute heart failure pathway and this requires close collaboration with nurses in non-cardiology specialist areas such as the emergency department and general medical/care-of-the-elderly wards. In contrast to the evidence base to support the heart failure nurse in long-term disease management, the nurse’s role in the acute heart failure pathway is less clearly defined. We now need to turn our attention to this in-patient period and strengthen the evidence that supports the role, number and skill set required of nurses to underpin effective heart failure treatment throughout the entire patient journey.