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INTRODUCTION

  • Heart failure (HF) is a progressive syndrome that can result from any changes in cardiac structure or function that impair the ability of the ventricle to fill with or eject blood. HF may be caused by an abnormality in systolic function, diastolic function, or both. 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).

PATHOPHYSIOLOGY

  • Causes of systolic dysfunction (decreased contractility) include 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, high-output states).

  • Causes of diastolic dysfunction (restriction in ventricular filling) include 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 (CO) 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 CO; 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 (AVP).

  • Chronic activation of the neurohormonal systems results in a cascade of events that affect the myocardium at the molecular and cellular levels. These events lead to changes in ventricular size (left ventricular hypertrophy), shape, structure, and function known as ventricular remodeling. The alterations in ventricular function result in further deterioration in cardiac systolic and diastolic functions that further promotes the remodeling process.

  • Common precipitating factors that may cause a previously compensated HF patient to decompensate include myocardial ischemia and MI, 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.

CLINICAL PRESENTATION

  • 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 (PND), tachypnea, and cough.

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

  • Nonspecific symptoms may include fatigue, nocturia, hemoptysis, abdominal ...

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