Heart Failure

Heart failure (HF) or congestive heart failure (CHF) is a clinical syndrome of abnormal ventricular filling and elevated cardiac filling pressures caused by a reduction in cardiac systolic fuction, diastolic function, or both. CHF is typically characterized by cardinal symptoms of dyspnea, fatigue, orthopnea, and paroxysmal nocturnal dyspnea, and by signs of pulmonary rales, elevated jugular venous pressure, presence of an S₃ heart sound, and lower-extremity edema. In this section, we will cover:

• Left-Heart Failure

• Right-Heart Failure

Left-Heart Failure

Left-heart failure is broadly categorized as follows:

• Heart failure with reduced ejection fraction (HFrEF): Patients with this class of heart failure have a left ventricular ejection fraction (LVEF) of ≤40%. These patients tend to have adverse neurohormonal changes because of reduced LVEF, and certain medications and interventions have been proven to reduce morbidity and mortality in randomized, controlled trials.

  • Causes include myocardial infarction, tachycardia, drugs (e.g., alcohol), medications (e.g., chemotherapy), infections (e.g., myocarditis, Chagas disease), pregnancy, hyperthyroidism, infiltrative diseases (e.g., hemochromatosis, sarcoidosis), genetic factors, and idiopathic disease.

• Heart failure with preserved ejection fraction (HFpEF): Patients in this class generally have an LVEF ≥50%. The pathophysiology of CHF in this class is multifactorial.

  • Causes include impaired relaxation from ventricular stiffness and early-stage cardiomyopathies that will eventually lead to reduced LVEF (e.g., myocardial infarction and coronary disease, hypertrophic cardiomyopathy, amyloidosis, sarcoidosis).

  • Note: Valvular diseases and pericardial diseases may mimic HFpEF, but CHF symptoms should improve with management of these underlying causes. Aside from treating the underlying etiology, management of HFpEF involves lifestyle modifications and is symptom driven, but recent evidence suggests that sodium-glucose cotransporter-2 inhibitors may improve outcomes regardless of diabetes mellitus status.

• Heart failure with mildly reduced ejection fraction (HFmrEF): Patients in this more-recently defined group have an LVEF of 41% to 49%. Optimal management in this group is uncertain, but typically such patients are treated with the therapies used in patients with HFrEF.

• Heart failure with improved ejection fraction (HFimpEF): These individuals previously had HFrEF, and their LVEF improved to >40% with treatment. They should remain indefinitely on drugs indicated for HFrEF based on evidence of a decrease in LVEF if discontinued.

For evaluation of heart failure, patients should undergo comprehensive testing to determine an underlying etiology, which may include laboratory tests (N-terminal pro-brain natriuretic peptide [NT-proBNP] and B-type natriuretic peptide [BNP] have prognostic utility), chest x-ray, electrocardiogram (ECG), echocardiogram, coronary angiography, cardiac MRI, technetium pyrophosphate scintigraphy, positron emission tomography, and/or genetic testing.

Classification by stages: Sometimes reduced LVEF or cardiomyopathy is diagnosed for reasons other than CHF symptoms, and to incorporate the full spectrum of patients with heart failure, heart failure is also classified by stages:

• stage A: at risk for developing heart failure

• stage B: structural heart changes but no CHF signs or symptoms

• stage C: structural heart disease with prior or current symptoms, which are further classified based on the New York Heart Association (NYHA) classification system from I to IV

• stage D: refractory heart-failure symptoms despite medical therapy; these patients should be evaluated for transplant or more-advanced support

Treatment

Acute decompensated heart failure: When patients present with acute decompensation, treatment is based on whether they have low cardiac output (“cold” vs. “warm”) and whether they have elevated filling pressures (“wet” vs. “dry”). Most patients hospitalized with acute decompensated heart failure have volume overload and require preload reduction. However, it’s important to optimize cardiac output in “cold” patients, and many may require inotropes, vasodilators, or both to improve forward flow before diuretics can work effectively.

Most therapies target one of the following processes, with some overlap:

• preload reduction: diuretics, nitrates

• afterload reduction: angiotensin-converting-enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), angiotensin receptor-neprilysin inhibitors (ARNIs), hydralazine, nitrates, nitroprusside, dobutamine, milrinone

• contractility enhancement: dobutamine, milrinone, dopamine

Although pulmonary artery catheterization (see video) has not been shown to improve outcomes when routinely used for the management of heart failure, it can be very helpful for select patients with right-heart failure without left-heart failure, mixed etiologies for shock, or uncertain intravascular volume status by physical examination.

Some patients have such severe cardiac dysfunction that they need mechanical circulatory support, such as an intra-aortic balloon pump (IABP), a left ventricular assist device (LVAD), or extracorporeal membrane oxygenation (ECMO).

Chronic HFrEF and acute decompensated HFrEF that has been effectively controlled:

• Medical treatment includes a combination of the following, which are typically indicated in stage C heart failure, except for beta-blockers, ACE inhibitors, and ARBs, which are indicated in stage B.

  • loop diuretics: mainly for congestive symptoms; no known mortality benefit

  • thiazide diuretics: may be added cautiously to loop diuretics in patients with inadequate diuresis

  • ACE inhibitor, ARB, or ARNI (e.g., sacubitril-valsartan): ARNI is recommended over ACE inhibitors or ARBs in patients who can tolerate and afford it; sacubitril inhibits degradation of B-type natriuretic peptide (BNP) to enhance BNP’s beneficial action

  • beta-blockers: mortality benefit only shown for metoprolol succinate, carvedilol, and bisoprolol

  • aldosterone antagonists: indicated for symptomatic patients whose estimated glomerular filtration rate (eGFR) is >30 mL/min/1.73 m² and serum potassium is <5.0 mEq/L

  • Sodium-glucose cotransporter-2 inhibitors: shown to reduce heart-failure hospitalization and cardiovascular mortality regardless of diabetes mellitus status in clinical trials

  • hydralazine and nitrates: shown to reduce heart-failure hospitalization and mortality in self-identified African Americans; generally considered if symptomatic despite maximally tolerated doses of the above medications or intolerant of them

  • ivabradine: slows conduction in the sinoatrial (SA) node and indicated in patients with LVEF ≤35%, receiving a beta-blocker at maximum dose, in sinus rhythm, and with a resting heart rate <70 beats per minute; does not improve mortality

  • antiarrhythmic drug therapy, catheter ablation to maintain sinus rhythm; atrial fibrillation can be a cause and consequence of heart failure, and when feasible, rhythm control should be pursued with a combination of medications (most often amiodarone) and catheter ablation

• Device-based treatment:

  • Implantable cardioverter-defibrillator (ICD): Placement should be considered in patients whose LVEF is ≤35%. In a 2016 study of patients with heart failure not caused by coronary artery disease, ICD implantation was associated with a significant reduction in sudden cardiac death but not with a significantly lower long-term rate of all-cause mortality. However, guidelines continue to recommend ICD use in this setting.

  • Cardiac resynchronization therapy (CRT): Consider for patients whose LVEF is ≤35% and whose QRS duration on ECG is either ≥120 msec if left bundle branch block (LBBB) morphology is present or ≥150 msec if LBBB morphology is not present. Please see Arrhythmias in this rotation guide for more information on ICD and CRT.

  • Percutaneous edge-to-edge mitral valve repair: For patients with reduced LVEF and mitral regurgitation secondary to heart failure who have persistent symptoms despite guideline-directed medical therapy, this procedure can improve symptoms.

• Revascularization: In patients with heart failure due to obstructive multivessel coronary artery disease (CAD) and LVEF <35%, current guidelines recommend coronary artery bypass surgery to improve survival. However, those guidelines are based on older data. Results of a recent clinical trial suggest that routine revascularization may not have significant benefits, and further research is needed to identify which patients with HFrEF and CAD benefit the most from revascularization in the modern era of HF treatment.

(Source: 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation 2022. Reprinted with permission. ©2022, American Heart Association, Inc.)

Right-Heart Failure

The most common cause of right-heart failure is left-heart failure leading to elevated left atrial pressure transmitted to the pulmonary vasculature and increased right ventricular afterload. However, in patients who have signs of peripheral congestion, such as elevated jugular venous pressure (JVP) and leg edema, but no evidence of pulmonary congestion, isolated right-heart failure should be considered. Pulmonary artery catheterization can help distinguish whether there is isolated right-heart failure by assessing right- and left-heart filling pressures and cardiac outputs.

Acute causes of right-heart failure include the following:

• pulmonary embolism (see Cardiopulmonary Emergencies in the Emergency Medicine rotation guide)

• myocardial infarction involving the right ventricle (RV), which is rare to see without concurrent left-ventricle (LV) involvement

• acute respiratory distress syndrome (see ARDS in the Critical Care rotation guide)

• subacute RV dysfunction unmasked by improved venous return (e.g., after LVAD implantation)

Chronic causes of right-heart failure are:

• most commonly, pulmonary hypertension (see Pulmonary Hypertension in the Pulmonology rotation guide)

• less commonly, cardiomyopathies that affect both ventricles, and congenital heart diseases

Treatment

The treatment of right-heart failure depends on the underlying etiology and is similar to the management principles for left-heart failure, with attention toward optimizing preload, afterload, and contractility of the RV. Improving pulmonary hypertension, whether it is secondary to left-heart disease or other processes, is key in most cases.