Acute Mitral Regurgitation is a medical and surgical emergency characterized by the sudden, often catastrophic, leakage of blood backward through the mitral valve from the left ventricle into the left atrium during systole. Unlike chronic mitral regurgitation, which develops over years and allows the heart time to adapt, in acute MR, the heart has no time to compensate. This sudden volume and pressure overload on the previously normal-sized, non-compliant left atrium rapidly leads to acute pulmonary edema and often cardiogenic shock due to a severe drop in forward cardiac output.
1. Hemodynamics
In acute MR, the primary issue is a sudden volume overload in a non-compliant system.
- Left Atrial Pressure: The LA is small and non-compliant. The sudden regurgitant volume causes a massive spike in LA pressure, characterized by a prominent ‘v’ wave on pulmonary capillary wedge pressure (PCWP) tracings.
- Pulmonary Congestion: This high pressure is transmitted backward instantly into the pulmonary vasculature, leading to acute pulmonary edema.
- Forward Cardiac Output: A large portion of the LV stroke volume is ejected into the low-pressure LA rather than the aorta. This leads to a drop in systemic cardiac output and, in severe cases, cardiogenic shock.
- LV Function: Initially, the LV ejection fraction (LVEF) may appear “hyperdynamic” (high) because the ventricle is emptying into a low-pressure sink (the LA), but this masks the actual decrease in forward flow.
2. Common Causes
Acute MR usually results from a catastrophic structural failure of the mitral valve apparatus:
| Component | Common Etiologies |
| Chordae Tendineae | Myxomatous degeneration (MVP), Infective Endocarditis, or blunt chest trauma. |
| Papillary Muscle | Acute Myocardial Infarction (typically 2–7 days post-MI). The posteromedial papillary muscle is most vulnerable as it usually has a single blood supply (RCA). |
| Valve Leaflets | Infective Endocarditis (perforation or large vegetations preventing closure). |
| Prosthetic Valve | Dehiscence, thrombus, or structural failure of a bioprosthetic valve. |
3. Management
The goal of management is to reduce afterload (to encourage forward flow) and stabilize the patient for definitive repair.
Medical Stabilization
- Afterload Reduction: * Vasodilators: IV Sodium Nitroprusside is the gold standard if the patient is normotensive. It lowers systemic vascular resistance, making it “easier” for the LV to pump blood into the aorta than the LA.
- Diuretics: IV Furosemide to reduce pulmonary venous congestion.
- Inotropes: If the patient is hypotensive (cardiogenic shock), dobutamine may be used, though it must be balanced carefully as it can increase myocardial oxygen demand.
Mechanical Support
- Intra-aortic Balloon Pump (IABP): Highly effective for acute MR. It decreases afterload during systole (facilitating forward flow) and increases coronary perfusion during diastole. It serves as a vital bridge to surgery.
Definitive Treatment
- Surgery: Almost all cases of severe acute MR require urgent surgical intervention.
- Mitral Valve Repair: Preferred if the anatomy allows (e.g., chordal rupture).
- Mitral Valve Replacement: Often necessary in cases of papillary muscle rupture or extensive endocarditis.
- Transcatheter Options: In patients deemed prohibitively high risk for surgery, edge-to-edge repair is occasionally considered, though less common in the hyper-acute phase.
Comparison Summary
| Feature | Acute MR | Chronic MR |
| LA Size | Normal | Enlarged (dilated) |
| LA Compliance | Low (stiff) | High (compliant) |
| Symptoms | Sudden, severe (Flash Edema) | Gradual (DOE, fatigue) |
| V-wave | Large/Tall | Variable |