What do hypotension and an audible third heart sound (S3) have in common regarding cardiac function?

Hypotension and S3 Heart Sound: Shared Pathophysiology

Both hypotension and an audible third heart sound (S3) indicate reduced cardiac output and severe left ventricular dysfunction, representing markers of cardiac decompensation and heart failure. 1, 2

Common Pathophysiologic Mechanism

Reduced Forward Cardiac Output

• Both findings reflect inadequate forward stroke volume and cardiac output from left ventricular failure 1
• In acute severe heart failure, patients simultaneously develop reduced forward output (manifesting as hypotension) and pulmonary congestion (associated with S3), creating a clinical picture of cardiogenic shock 1
• The hypotension results from systolic blood pressure <90 mmHg with inadequate tissue perfusion, while S3 reflects elevated left ventricular filling pressures (>20 mmHg) and volume overload 1, 2

Hemodynamic Derangement

• S3 is associated with elevated pulmonary pressures (mean 55 ± 15 mmHg in patients with S3 versus 41 ± 11 mmHg without) 3
• Both findings indicate severe hemodynamic alterations requiring comprehensive assessment and vigorous medical or surgical treatment 3
• The combination represents a low cardiac output state with cardiac index <1.8 L/min/m² and central filling pressure >20 mmHg, defining cardiogenic shock 1

Clinical Significance and Risk Stratification

Prognostic Implications

• The presence of S3 substantially increases perioperative risk and is an independent predictor of complications during noncardiac surgery, especially when combined with history of heart failure 2
• S3 is a reliable and highly specific indicator of cardiac decompensation in adults with decreased ejection fraction 2
• Patients with S3 are more likely to have class III-IV symptoms (55% versus 18% without S3) 3

Killip Classification Integration

• The Killip classification for acute myocardial infarction demonstrates this relationship: Stage II includes S3 with pulmonary congestion, while Stage IV represents cardiogenic shock with hypotension (SBP <90 mmHg) 1
• Mortality increases progressively: 2.2% in Stage I (no S3, normal BP) to 55.5% in Stage IV (shock) 1

Diagnostic Approach When Both Present

Immediate Assessment

• Exclude other causes of hypotension including hypovolemia, vasovagal reactions, electrolyte disturbances, and arrhythmias before attributing findings to cardiogenic shock 1
• Assess for additional signs of heart failure: pulmonary rales, peripheral edema, elevated jugular venous pressure, and hepatomegaly 2
• Obtain chest radiograph for cardiomegaly and pulmonary congestion 1

Echocardiographic Evaluation

• Perform urgent echocardiography to assess left ventricular systolic function, ejection fraction, chamber dimensions, and valvular function 4, 2
• Evaluate E/E' ratio and left ventricular filling pressures 2
• S3 correlates with restrictive filling patterns, severe regurgitation (regurgitant fraction ≥40%), and marked ventricular dilatation 3

Hemodynamic Monitoring

• Consider pulmonary artery catheterization to measure pulmonary capillary wedge pressure (target <20 mmHg) and cardiac index (target >2 L/min/m²) 1
• Monitor for evidence of end-organ hypoperfusion: oliguria (<0.5 mL/kg/h), confusion, cold clammy skin, and peripheral cyanosis 1

Management Priorities

Acute Stabilization

• In normotensive patients with S3, nitroprusside increases forward output and reduces mitral regurgitation by decreasing left ventricular size 1
• In hypotensive patients, avoid nitroprusside alone; use combination therapy with inotropic agents (dobutamine 2.5-10 μg/kg/min) plus nitroprusside 1
• Intra-aortic balloon counterpulsation increases forward output and mean arterial pressure while reducing regurgitant volume in refractory cases 1

Definitive Treatment

• Standard heart failure therapy including diuretics, ACE inhibitors/ARBs, beta-blockers, and aldosterone antagonists 2
• Consider urgent surgical intervention for mechanical complications (acute mitral regurgitation, ventricular septal defect) causing acute decompensation 1
• Percutaneous or surgical revascularization can improve survival in patients with severe heart failure or shock from acute myocardial infarction 1

Critical Pitfalls

• Do not assume S3 is benign in adults with hypotension—this combination indicates severe cardiac decompensation requiring urgent intervention 2, 3
• Recognize that S3 may be the only abnormal physical finding in acute severe mitral regurgitation when the systolic murmur is absent 1
• In acute settings, transthoracic echocardiography may underestimate lesion severity; proceed to transesophageal echocardiography if clinical suspicion remains high despite reassuring initial imaging 1