1.5 Valvular Heart Disease
Key Takeaways
- Aortic stenosis presents with a harsh, mid-systolic crescendo-decrescendo murmur at the RUSB radiating to the carotid arteries, and is clinically characterized by the SAD triad (Syncope, Angina, Dyspnea).
- Mitral stenosis is almost exclusively caused by Rheumatic Heart Disease and presents with a low-pitched, rumbling mid-diastolic murmur at the apex, preceded by a loud opening snap and snapping S1.
- Mitral regurgitation features a blowing holosystolic murmur at the apex radiating to the left axilla, and can present acutely as flash pulmonary edema following papillary muscle rupture.
- Aortic regurgitation is associated with a wide pulse pressure and hyperdynamic circulation (e.g., Water-Hammer pulse, De Musset's sign), presenting with a blowing diastolic decrescendo murmur at the LUSB.
- Dynamic auscultation helps differentiate murmurs: standing and Valsalva decrease venous return, reducing the intensity of valvular murmurs while increasing the intensity of MVP and HCM.
Valvular Heart Disease
PANCE High-Yield Focus: Valvular heart disease is heavily tested. PANCE candidates must master physical exam findings, murmur characteristics (timing, location, radiation), classic clinical syndromes, and hemodynamic changes with dynamic maneuvers.
Aortic Valve Disorders
Aortic Stenosis (AS)
Aortic stenosis is the most common primary valvular disease.
- Pathophysiology: In older adults (>=65 years), it is caused by progressive senile calcification. In younger adults (<65 years), it is typically due to a congenital bicuspid aortic valve, which accelerates calcific wear and tear. Narrowing of the valve orifice impedes left ventricular (LV) outflow, leading to concentric LV hypertrophy, decreased myocardial compliance, and eventual left heart failure.
- Clinical Presentation: The clinical course is characterized by a long asymptomatic phase, followed by rapid clinical decline upon the onset of symptoms. Memorize the classic "SAD" triad:
- S - Syncope: Exertional syncope due to a fixed cardiac output unable to meet peripheral demand during exercise.
- A - Angina: Exertional chest pain caused by increased myocardial oxygen demand of the hypertrophied LV, combined with compressed subendocardial capillaries.
- D - Dyspnea: Dyspnea on exertion representing left ventricular diastolic failure from hypertrophy and congestion.
- Physical Exam Findings:
- Murmur: A harsh, mid-systolic crescendo-decrescendo murmur heard best at the Right Upper Sternal Border (RUSB) that radiates to the carotid arteries.
- Pulsus Parvus et Tardus: Carotid pulses are weak (parvus) and delayed/sluggish (tardus).
- Heart Sounds: Soft or absent S2 (due to immobility of calcified leaflets) and paradoxical splitting of S2 (delayed LV ejection causes the aortic valve to close after the pulmonic valve during expiration). An S4 gallop is frequently present due to LV hypertrophy.
Aortic Regurgitation (AR)
Aortic regurgitation involves diastolic backflow of blood from the aorta into the LV.
- Pathophysiology: Can result from primary leaflet disease (calcific, bicuspid valve, infective endocarditis) or aortic root dilation (syphilitic aortitis, Marfan syndrome, Ehlers-Danlos syndrome, aortic dissection). Chronic volume overload leads to eccentric LV hypertrophy and dilation.
- Clinical Presentation: Patients present with progressive exertional dyspnea, orthopnea, fatigue, and palpitations (often described as a "pounding heart" due to high stroke volume). The wide pulse pressure (highly elevated systolic pressure and very low diastolic pressure) produces hyperdynamic peripheral circulation signs.
- Physical Exam Findings:
- Murmur: A high-pitched, blowing diastolic decrescendo murmur heard best at the Left Upper Sternal Border (LUSB) or third intercostal space with the patient sitting up, leaning forward, and holding their breath at end-expiration.
- Hyperdynamic Signs:
- Corrigan's Pulse (Water-Hammer Pulse): Rapidly rising and falling arterial pulse.
- De Musset's Sign: Rhythmic head bobbing synchronous with the heartbeat.
- Quincke's Pulse: Visible capillary pulsations in the nail beds.
- Duroziez's Sign: Systolic murmur over the femoral artery with proximal compression, and a diastolic murmur with distal compression.
Mitral Valve Disorders
Mitral Stenosis (MS)
Mitral stenosis is characterized by narrowing of the mitral valve orifice, obstructing flow from the left atrium (LA) to the LV.
- Pathophysiology: Almost exclusively caused by chronic Rheumatic Heart Disease, resulting in chronic inflammation, leaflet thickening, and commissural fusion (often decades after initial Group A Strep infection). The obstruction leads to elevated LA pressure, causing LA dilation, pulmonary venous hypertension, and secondary right-sided heart failure.
- Clinical Presentation: Exertional dyspnea is the most common presenting symptom. Pulmonary venous congestion can cause hemoptysis (rupture of dilated bronchial veins). Left atrial stretch frequently triggers atrial fibrillation, which can lead to thromboembolic stroke. LA enlargement may compress the recurrent laryngeal nerve, causing hoarseness (Ortner's syndrome), or compress the esophagus, causing dysphagia.
- Physical Exam Findings:
- Murmur: A low-pitched, rumbling mid-diastolic murmur heard best at the apex in the left lateral decubitus position with the bell of the stethoscope.
- Opening Snap: A sharp, high-pitched diastolic sound that precedes the murmur. The closer the opening snap is to S2, the more severe the stenosis.
- Heart Sounds: A loud, snapping S1 (as the stiff valve leaflets are slammed shut by ventricular systole).
Mitral Regurgitation (MR)
Mitral regurgitation involves retrograde flow of blood from the LV into the LA during ventricular systole.
- Pathophysiology: Primary causes include mitral valve prolapse (MVP, myxomatous degeneration), infective endocarditis, and rheumatic disease. Secondary (functional) MR is caused by LV dilation (dilated cardiomyopathy, ischemic heart disease) displacing the papillary muscles. Acute MR can be caused by papillary muscle rupture in the setting of an acute myocardial infarction.
- Clinical Presentation: Chronic MR presents with progressive fatigue, dyspnea, and left heart failure. Acute MR is a medical emergency presenting with sudden-onset severe dyspnea, flash pulmonary edema, and cardiogenic shock.
- Physical Exam Findings:
- Murmur: A blowing, holosystolic (pansystolic) murmur heard best at the apex that radiates to the left axilla.
- Heart Sounds: An S3 gallop may be heard due to rapid volume filling of the LV.
Dynamic Auscultation and Management
Dynamic maneuvers alter loading conditions to help differentiate murmurs.
| Maneuver | Hemodynamic Effect | Effect on Valvular Murmurs (AS, MR, AR, MS) | Effect on MVP & HCM |
|---|---|---|---|
| Valsalva (strain) / Standing | Decreases preload (venous return) | Decreases intensity | Increases intensity |
| Squatting / Leg Raise | Increases preload (venous return) | Increases intensity | Decreases intensity |
| Handgrip (sustained) | Increases afterload (SVR) | Increases MR and AR (backward flow); Decreases AS (reduces gradient) | Decreases HCM (larger LV chamber size); Decreases MVP |
Clinical Management Guidelines
- Aortic Stenosis: Definitive treatment is surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI). Avoid vasodilators (e.g., nitroglycerin) in severe AS, as cardiac output is fixed; vasodilation can cause profound hypotension.
- Mitral Stenosis: Percutaneous balloon mitral valvuloplasty is the first-line treatment for symptomatic, severe MS in the absence of left atrial thrombus.
- Anticoagulation for Mechanical Valves: Lifelong anticoagulation with Warfarin is mandatory. DOACs are contraindicated. Target INR is 2.0–3.0 for aortic and 2.5–3.5 for mitral mechanical valves.
A 43-year-old female presents to the clinic complaining of progressive shortness of breath during exertion and occasional coughing up of blood-tinged sputum. On physical examination, her blood pressure is 120/75 mmHg and her pulse is 88 bpm and irregular. Auscultation reveals a low-pitched, rumbling diastolic murmur at the apex, preceded by a sharp, high-pitched sound shortly after S2. Which of the following is the most likely pathophysiological mechanism responsible for this patient's clinical presentation?
A 32-year-old male with a history of Marfan syndrome presents for a routine evaluation. On physical exam, he is noted to have a rhythmic nodding of his head that matches his heartbeat. Auscultation of the heart reveals a high-pitched, blowing diastolic decrescendo murmur heard best at the left sternal border with the patient sitting up and leaning forward. Which of the following physical exam findings is most likely to also be present in this patient?
A clinician is evaluating a 65-year-old male who has a systolic heart murmur. To differentiate between aortic stenosis and hypertrophic cardiomyopathy, the clinician asks the patient to stand up from a squatting position. Which of the following describes the expected response of the aortic stenosis murmur upon standing?