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INTRODUCTION

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  • Heart failure (HF) is a progressive clinical syndrome caused by inability of the heart to pump sufficient blood to meet the body’s metabolic needs. HF can result from any disorder that affects the ability of the heart to contract (systolic dysfunction) and/or relax (diastolic dysfunction). HF with reduced systolic function (ie, reduced left ventricular ejection fraction, LVEF) is referred to as HF with reduced ejection fraction (HFrEF). Preserved LV systolic function (ie, normal LVEF) with presumed diastolic dysfunction is termed HF with preserved ejection fraction (HFpEF).

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PATHOPHYSIOLOGY

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  • Causes of systolic dysfunction (decreased contractility) are reduced muscle mass (eg, myocardial infarction [MI]), dilated cardiomyopathies, and ventricular hypertrophy. Ventricular hypertrophy can be caused by pressure overload (eg, systemic or pulmonary hypertension and aortic or pulmonic valve stenosis) or volume overload (eg, valvular regurgitation, shunts, and high-output states).

  • Causes of diastolic dysfunction (restriction in ventricular filling) are increased ventricular stiffness, ventricular hypertrophy, infiltrative myocardial diseases, myocardial ischemia and MI, mitral or tricuspid valve stenosis, and pericardial disease (eg, pericarditis and pericardial tamponade).

  • The leading causes of HF are coronary artery disease and hypertension.

  • Regardless of the index event, decreased cardiac output results in activation of compensatory responses to maintain circulation: (1) tachycardia and increased contractility through sympathetic nervous system activation; (2) the Frank–Starling mechanism, whereby increased preload (through sodium and water retention) increases stroke volume; (3) vasoconstriction; and (4) ventricular hypertrophy and remodeling. Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the symptoms of HF and contribute to disease progression.

  • In the neurohormonal model of HF, an initiating event (eg, acute MI) leads to decreased cardiac output; the HF state then becomes a systemic disease whose progression is mediated largely by neurohormones and autocrine/paracrine factors that drive myocyte injury, oxidative stress, inflammation, and extracellular matrix remodeling. These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, and arginine vasopressin.

  • Common precipitating factors that may cause a previously compensated HF patient to decompensate include myocardial ischemia and MI, atrial fibrillation, pulmonary infections, nonadherence with diet or drug therapy, and inappropriate medication use. Drugs may precipitate or exacerbate HF through negative inotropic effects, direct cardiotoxicity, or increased sodium and water retention.

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CLINICAL PRESENTATION

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  • Patient presentation may range from asymptomatic to cardiogenic shock.

  • Primary symptoms are dyspnea (especially on exertion) and fatigue, which lead to exercise intolerance. Other pulmonary symptoms include orthopnea, paroxysmal nocturnal dyspnea, tachypnea, and cough.

  • Fluid overload can result in pulmonary congestion and peripheral edema.

  • Nonspecific symptoms may include fatigue, nocturia, hemoptysis, abdominal pain, anorexia, nausea, bloating, ascites, poor appetite or early satiety, mental status changes, and weight gain.

  • Physical examination findings may include pulmonary crackles, S3 gallop, cool extremities, Cheyne–Stokes respiration, tachycardia, narrow pulse pressure, cardiomegaly, symptoms of pulmonary edema (extreme breathlessness and anxiety, sometimes with coughing and pink, frothy sputum), peripheral edema, jugular venous distention, hepatojugular reflux, and hepatomegaly.

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DIAGNOSIS

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