Heart failure is impaired myocardial contractility (systolic dysfunction) or relaxation (diastolic dysfunction) causing inadequate cardiac output. Neurohormonal compensation—sympathetic activation, RAAS, natriuretic peptides—initially maintains perfusion but eventually worsens remodeling.
Use ejection fraction (EF) to classify: reduced EF (HFrEF, EF <40%), mildly reduced (HFmrEF, EF 40-49%), preserved (HFpEF, EF ≥50%). Understand diastolic dysfunction as impaired filling despite normal contractility.
Low ejection fraction does not always cause symptoms—many patients are asymptomatic. HFpEF is not simply 'diastolic heart failure'; it involves complex interplay of stiffness, chronotropic incompetence, and vascular dysfunction.
Heart failure is best understood by returning to the fundamentals of cardiac output you studied as a prerequisite. Cardiac output equals stroke volume times heart rate. Stroke volume itself depends on three variables: preload (ventricular filling), afterload (resistance the ventricle pumps against), and contractility (the intrinsic force of myocardial contraction). Heart failure occurs when these variables are so disrupted that the heart cannot maintain output sufficient for metabolic demands—or can only do so at the cost of abnormally elevated filling pressures.
Systolic dysfunction (HFrEF) is the classic picture: the ventricle contracts weakly, ejection fraction falls below 40%, and stroke volume drops. This follows directly from your study of myocardial infarction—dead myocardium cannot contract, so ischemic cardiomyopathy is a leading cause. The body's initial compensation is neurohormonal: the sympathetic nervous system increases heart rate and contractility, and the renin-angiotensin-aldosterone system (RAAS) promotes sodium and water retention to increase preload. In the short term, these Frank-Starling compensations maintain output. Over time, however, chronically elevated sympathetic tone causes maladaptive remodeling—the ventricle dilates and becomes more spherical, wall stress increases (by the law of LaPlace, tension = pressure × radius / 2 × wall thickness), and the dilated geometry further impairs ejection efficiency. Compensation becomes the disease.
Diastolic dysfunction (HFpEF) is mechanistically distinct: the ventricle contracts normally (EF ≥ 50%) but is abnormally stiff and cannot relax adequately during diastole. Think of the difference between squeezing a water balloon (systolic) and filling a stiff rubber ball (diastolic). In HFpEF, impaired relaxation means the ventricle requires elevated filling pressures to accept the same stroke volume—those elevated pressures back up into the pulmonary circulation, causing exertional dyspnea and pulmonary edema even with preserved contractility. Hypertension, diabetes, and obesity are major drivers because they all cause concentric left ventricular hypertrophy and increased myocardial stiffness.
The neurohormonal response is a unifying theme across both types. Natriuretic peptides (BNP, NT-proBNP) are secreted by stretched ventricular myocytes as a counter-regulatory signal—they promote vasodilation and natriuresis. Clinically, elevated BNP is the biochemical signature of heart failure regardless of type. The treatment logic for HFrEF follows directly from pathophysiology: ACE inhibitors/ARBs reduce afterload and blunt RAAS; beta-blockers counteract maladaptive sympathetic activation; aldosterone antagonists reduce fibrosis and fluid retention. The remarkable finding is that these agents reduce mortality not just by relieving symptoms but by partially reversing remodeling. For HFpEF, no therapy has yet demonstrated comparable mortality benefit—a reflection of our still-incomplete understanding of its heterogeneous pathophysiology.