How the circulation adapts to valve disease: aortic and mitral lesions at rest and in exercise
- Mechanism
- Exam priority: medium
A narrow or leaky valve makes the heart work harder. The heart grows and blood volume rises, which works until exercise or time uncovers the limit.
Also called: Hemodynamics of valve disease, Phonocardiogram
See it in 3D: Mitral anterior leaflet · Aortic right coronary cusp · Left atrium · Left ventricle
What it is
Valve lesions overload the chamber behind them with pressure (stenosis) or volume (regurgitation). The left ventricle compensates by hypertrophy and the kidneys by retaining fluid, which keeps output near normal at rest for years. Exercise, which needs a quick rise in output, unmasks the lesion first; the left atrium and lungs suffer in mitral disease, the coronary supply in aortic disease.
How it works, step by step
- A stenotic valve raises the pressure the chamber must generate; a regurgitant valve adds back-flow that must be pumped again.
- Pressure load adds sarcomeres in parallel (thick wall, concentric hypertrophy); volume load adds them in series (large chamber, eccentric hypertrophy).
- Low output reduces renal perfusion, so the kidneys retain salt and water; volume rises by ≈ 10–20% and red cell mass increases slightly.
- Higher volume and filling pressure keep output near normal at rest (Frank–Starling), but cardiac reserve shrinks.
- In aortic lesions, thick muscle and high wall stress need more O₂ while coronary inflow is limited (low diastolic pressure in AR, compression in AS): ischemia.
- In mitral stenosis flow is limited by the orifice; atrial pressure rises, and in exercise tachycardia shortens diastole, raising atrial pressure further.
- Exercise needs output to rise several-fold; a fixed obstruction or large leak cannot follow, so dyspnea, angina or syncope appear first on exertion.
Left-ventricular pressure–volume loop
EDV 115 mLESV 51 mLSV 64 mLEF 56%ESP 206 mmHgLV peak ≈ 222 mmHg
Aortic stenosis
Aortic stenosis: the LV must build a very high systolic pressure to push through the narrow valve (the aorta sees much less); the loop is tall, SV tends to fall and concentric hypertrophy stiffens filling.
Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.
- Current loop
- Normal loop
- ESPVR (contractility, Ees)
- EDPVR (passive filling)
- Ea (arterial afterload)
- Stroke volume (SV)
Left-ventricular pressure–volume loop
EDV 170 mLESV 56 mLSV 114 mLEF 67%ESP 116 mmHgRegurgitant ≈ 51 mLForward SV ≈ 63 mL
Mitral regurgitation
Mitral regurgitation: the LV also ejects into the atrium from the start of contraction until it relaxes, so there are no true isovolumetric phases. EDV and total SV are large, but almost half goes back to the atrium: EF overstates function.
Tap a corner of the loop (MC, AO, AC, MO) to see the valve event.
- Current loop
- Normal loop
- ESPVR (contractility, Ees)
- EDPVR (passive filling)
- Ea (arterial afterload)
- Stroke volume (SV)
Sound frequencies (illustrative)
| Parameter | Value | Note |
|---|---|---|
| S1 and S2 | ≈ 40–500 Hz | short, ≈ 0.10–0.14 s each |
| S3 and S4 | ≈ 20–40 Hz | low-pitched, best heard with the bell |
| Murmurs | up to ≈ 1000 Hz | longer, from turbulent flow |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Typical adaptations
| Lesion | Load | Main compensation | First limit |
|---|---|---|---|
| Aortic stenosis | Pressure on LV | Concentric LVH | Exertional angina, syncope, later failure |
| Aortic regurgitation | Volume on LV | Eccentric LVH, large stroke volume | Low diastolic pressure, coronary shortfall, LV dilation |
| Mitral stenosis | Pressure on LA and lungs | LA dilation, higher volume | Pulmonary edema, atrial fibrillation, pulmonary hypertension |
| Mitral regurgitation | Volume on LA and LV | LA and LV dilation | Pulmonary congestion, atrial fibrillation |
Clinical notes
- Rheumatic heart disease, still common in Colombia, mainly affects the mitral valve and causes mitral stenosis years after streptococcal infection.
- Atrial fibrillation in mitral stenosis removes the atrial kick and shortens filling, which can sharply worsen pulmonary congestion.
- Exertional angina, syncope and dyspnea mark severe aortic stenosis.
Test yourself
Think of the answer, then tap the question to see it.
Why does severe aortic stenosis cause angina even with normal coronary arteries?
The hypertrophied LV has high O₂ demand and high wall stress, while coronary inflow is limited by compression of subendocardial vessels and high diastolic LV pressure.
Why does aortic regurgitation lower coronary perfusion?
Blood falls back into the ventricle in diastole, so aortic diastolic pressure, the main driving pressure for LV coronary flow, is low.
A patient with mitral stenosis develops atrial fibrillation at 140/min and becomes very dyspneic. Why?
Fast rate shortens diastole and loss of the atrial kick lowers flow across the narrow valve; left atrial pressure rises and fluid enters the lungs.
Why does blood volume rise in chronic valve disease?
Reduced output lowers renal perfusion, so the kidneys retain salt and water (and red cell mass rises slightly), raising venous return and output.
Connections
See it in 3D4
The structures of Durgical's 3D anatomy where it happens.
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Aortic Stenosis (StatPearls (NCBI Bookshelf), 2025); Aortic Insufficiency (StatPearls (NCBI Bookshelf), 2024); Mitral stenosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Rheumatic Heart Disease (StatPearls (NCBI Bookshelf), 2023).
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Representative model, for educational purposes only.