A papillary muscle rupture causes a murmur due to acute mitral regurgitation (MR) resulting from the failure of the mitral valve to close properly. Here’s a concise explanation of the mechanism, tied to the context of your previous questions about murmurs, EKGs, and cardiac pharmacology:
Mechanism of Murmur in Papillary Muscle Rupture
- Anatomy:
- The papillary muscles, located in the left ventricle, anchor the mitral valve leaflets via chordae tendineae.
- They contract during systole to prevent mitral valve prolapse or regurgitation by keeping the valve closed.
- Rupture Cause:
- Most commonly occurs 2–7 days post-myocardial infarction (MI), particularly with inferior or posterior MI (right coronary artery occlusion, which supplies the posteromedial papillary muscle).
- Other causes: trauma, endocarditis, or severe ischemia.
- Pathophysiology:
- Rupture (complete or partial) disrupts chordae tendineae, causing one or both mitral valve leaflets to flail or prolapse into the left atrium during systole.
- This leads to acute mitral regurgitation, where blood flows backward from the left ventricle to the left atrium during systole.
- The turbulent, high-velocity regurgitant jet creates a holosystolic murmur.
- Murmur Characteristics:
- Type: Harsh, holosystolic murmur
- Location: Best heard at the apex (5th intercostal space, midclavicular line), often radiating to the axilla.
- Associated Findings: May be accompanied by a thrill; murmur may be softer than expected due to rapid pressure equalization between ventricle and atrium in severe MR.
- Other Signs: Acute heart failure (pulmonary edema, hypotension, tachycardia) due to volume overload in the left atrium and lungs.
Why the Murmur Occurs
- The murmur is caused by the turbulent blood flow across the incompetent mitral valve during systole.
- The severity of the murmur depends on the degree of regurgitation and pressure gradient. In acute MR from papillary muscle rupture, the murmur may be less loud than chronic MR because:
- The left atrium is non-compliant (not dilated), leading to rapid pressure equalization.
- Cardiogenic shock or low cardiac output may reduce flow velocity.
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