Valve stenosis (narrowed orifice) increases afterload on the upstream chamber, causing concentric hypertrophy and eventual dysfunction. Aortic stenosis causes LV hypertrophy, diastolic dysfunction, and ischemia; mitral stenosis increases LA and pulmonary pressures. Valve regurgitation (insufficient closure) causes volume overload, eccentric hypertrophy, and chamber dilation of the upstream chamber. Acute versus chronic regurgitation have different compensatory mechanisms—chronic regurgitation is better tolerated due to gradual chamber remodeling. Combined lesions (e.g., mitral stenosis + regurgitation) have complex hemodynamic consequences.
Study the hemodynamic consequences of each lesion using pressure-volume diagrams. Understand why aortic stenosis progresses to heart failure (increased afterload, myocardial ischemia). Trace the progression from compensation through decompensation in each lesion.
Stenotic lesions are not 'narrowed by fat'; they are from leaflet pathology (calcification, fibrosis, endocarditis). Regurgitation is not always hemodynamically significant early—the heart compensates through eccentric hypertrophy. Mitral stenosis (narrowing) increases pulmonary pressure, predisposing to atrial fibrillation and thrombus.
Valve disease follows directly from the cardiac cycle you already know: the heart is a pressure pump that relies on one-way valves to direct flow efficiently. The left ventricle generates ~120 mmHg of systolic pressure to eject blood into the aorta; this only works if the aortic valve opens fully and the mitral valve seals completely. Any deviation — a valve that won't open enough (stenosis) or a valve that won't close completely (regurgitation) — forces the heart to work differently, and understanding how the heart compensates reveals both why patients can remain asymptomatic for years and why they eventually decompensate.
Stenosis creates a pressure overload problem. In aortic stenosis, the left ventricle faces a narrowed outflow valve — it must generate much higher pressure to force the same flow across a smaller orifice. The response is concentric hypertrophy: the ventricular wall thickens (more sarcomeres added in parallel) to normalize wall stress per the law of Laplace. This initially preserves ejection fraction, but thick walls are stiff walls. The ventricle loses compliance (diastolic dysfunction), requiring higher filling pressures to achieve adequate preload. Patients develop the classic triad — angina (hypertrophied muscle outstrips coronary supply), syncope (fixed cardiac output cannot respond to vasodilation on exertion), and heart failure (elevated filling pressures cause pulmonary congestion). In mitral stenosis, the problem is upstream: the left atrium cannot empty efficiently, pressure backs up into the pulmonary veins, and elevated pulmonary capillary pressure causes dyspnea, pulmonary hypertension, and eventually right heart failure. The chronically elevated left atrial pressure also causes atrial enlargement and atrial fibrillation — which simultaneously eliminates the atrial "kick" that accounts for 20–30% of ventricular filling, further compromising hemodynamics.
Regurgitation creates a volume overload problem — a fundamentally different stress. In aortic regurgitation, blood ejected into the aorta refluxes back into the left ventricle during diastole. The ventricle now receives both normal pulmonary return and the regurgitant volume. It compensates with eccentric hypertrophy: the chamber dilates (sarcomeres added in series) to accommodate the extra volume, and increased preload (Frank-Starling mechanism) maintains stroke volume. Chronic regurgitation can be remarkably well tolerated for years — the gradual remodeling prevents sudden pressure rises. This is why acute regurgitation (from endocarditis or aortic dissection) is dramatically more dangerous: the ventricle has no time to remodel, filling pressure spikes suddenly, and pulmonary edema develops within hours. The challenge in managing chronic regurgitation is that compensation masks symptoms until the ventricle is irreversibly dilated and systolic function begins to fall — surgical timing aims to intervene before this point of no return.
The difference in compensation also predicts the ausculatory findings. Stenosis creates turbulence as blood is forced through a narrowed orifice — aortic stenosis produces a crescendo-decrescendo systolic ejection murmur (blood accelerates then decelerates through the stenotic valve); mitral stenosis produces a low-pitched diastolic rumble (blood flows through the narrowed mitral valve during ventricular filling). Regurgitation produces murmurs of backward flow — aortic regurgitation creates a high-pitched early diastolic decrescendo murmur; mitral regurgitation creates a holosystolic murmur radiating to the axilla. Each murmur tells you the phase of the cardiac cycle when backward or turbulent flow occurs, which traces directly back to the valve anatomy and the pressure gradients driving flow in each phase.
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