Heart Sound Management Guideline

Characteristics and Clinical Significance

S3 is a mid-diastolic heart sound that occurs during the rapid filling phase of ventricular diastole, associated with elevated left ventricular filling pressures and volume overload, as stated by the European Society of Cardiology 1, 2, 3, 4
S4 is a late-diastolic heart sound that occurs during atrial contraction, and is most frequently found in patients with coronary heart disease, as noted by the American Heart Association 1, 2

Management Approach for S3

Primary Management Focus

The European Society of Cardiology recommends treating the underlying heart failure with standard heart failure therapy including diuretics, ACE inhibitors/ARBs, beta-blockers, and aldosterone antagonists, as S3 is a reliable indicator of cardiac decompensation 3

Monitoring and Assessment

Monitoring jugular venous pressure, which is often elevated in patients with S3, is recommended by the European Society of Cardiology, as well as assessing for other signs of heart failure such as pulmonary rales, peripheral edema, and hepatomegaly 3, 4

Diagnostic Workup

The American College of Cardiology recommends performing echocardiography to assess ventricular function, as S3 correlates with systolic and diastolic dysfunction 5, 4

Management Approach for S4

Monitoring and Assessment

The American Heart Association suggests monitoring blood pressure control, as improved blood pressure management may lead to resolution of S4, and assessing for left ventricular hypertrophy, which is commonly associated with S4 3, 6

Diagnostic Workup

The European Society of Cardiology recommends performing echocardiography to assess for left ventricular hypertrophy and diastolic function, as S4 may signal increased risk for developing heart failure if the underlying condition is not addressed 5, 6

Clinical Significance and Management of S3 and S4 Heart Sounds

Risk Stratification and Perioperative Considerations

The presence of S3 is a reliable indicator of cardiac decompensation and substantially increases perioperative risk, according to the American College of Cardiology, while S4 does not independently predict heart failure 7, 8, 9
Both S3 and signs of heart failure are associated with substantially increased risk during noncardiac surgery, as stated by the American Heart Association 7, 8, 9
S3 gallop is an independent predictor of perioperative risk when combined with history of congestive heart failure, pulmonary edema, paroxysmal nocturnal dyspnea, bilateral rales, or pulmonary vascular redistribution on chest X-ray, as recommended by the American College of Cardiology 7, 8, 9
In perimyocarditis, auscultation of a new S3 is indicative of myocardial involvement, according to the European Society of Cardiology 10
Patients with S3 require careful perioperative fluid management and hemodynamic monitoring, as suggested by the American Heart Association 7, 8, 9

Diagnostic Assessment

Consider cardiac MRI in selected cases to evaluate for infiltrative processes or myocardial fibrosis, as recommended by the American College of Cardiology 11

S3 Heart Sound Causes and Clinical Significance

Pathophysiologic Mechanism and Clinical Conditions

Young healthy individuals with hyperdynamic circulation can have S3 due to rapid early filling velocity without underlying cardiac disease, as noted by the European Heart Journal 12
The American College of Cardiology indicates that S3 is a reliable indicator of cardiac decompensation and substantially increases perioperative risk 13

Clinical Significance and Hemodynamic Determinants

The presence of S3 combined with history of heart failure, pulmonary edema, bilateral rales, or pulmonary vascular redistribution is an independent predictor of perioperative complications, according to the Journal of the American College of Cardiology 13

S3 and S4 Heart Sounds in Specific Patient Populations

Normal S3 Populations

In pregnant women, S3 is a normal physiologic finding due to increased circulating blood volume and cardiac output, as stated by the American Heart Association, and does not indicate pathology 14

S4 Heart Sound in Abnormal Populations

In patients with aortic stenosis, S4 is rather common in obstructive hypertrophic cardiomyopathy and valvular aortic stenosis, according to the American College of Cardiology 15

Clinical Significance of the S3 Heart Sound

Pathologic S3

The American Heart Association suggests that 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, pulmonary edema, bilateral rales, or pulmonary vascular redistribution, in patients with cardiac decompensation and heart failure 16
The presence of S3 is a reliable and highly specific indicator of cardiac decompensation and heart failure, associated with elevated left ventricular filling pressures and volume overload, in adults with decreased ejection fraction 16

Physiologic S3 (Normal Variants)

In pregnant women, S3 is present in most cases as a normal physiologic finding due to increased circulating blood volume and cardiac output, and does not indicate pathology, according to the American College of Cardiology 16

Diagnostic Workup When S3 is Detected

Echocardiography is recommended to assess ventricular function, as S3 correlates with systolic and diastolic dysfunction, and should include assessment of left ventricular systolic function and ejection fraction, by the American Society of Echocardiography 17
The echocardiographic evaluation should include measurement of E/E' ratio, evaluation of LV filling pressures, and assessment for left ventricular hypertrophy, as recommended by the European Society of Cardiology 17

Hemodynamic Implications of Combined Hypotension and an S3 Heart Sound

Pathophysiology

Combined hypotension (systolic blood pressure < 90 mmHg) and an audible S3 indicate a low‑output state with cardiac index < 1.8 L·min⁻¹·m⁻² and central filling pressure > 20 mmHg, defining cardiogenic shock. 18
In acute severe left‑ventricular failure, reduced forward stroke volume produces hypotension, while elevated left‑ventricular filling pressures (> 20 mmHg) generate the S3 sound. 18

Prognostic Significance

The Killip classification for acute myocardial infarction incorporates this relationship:

Killip Stage	Key Findings	In‑hospital Mortality
I (no S3, normal BP)	No S3, normal blood pressure	2.2 %
II (S3 with pulmonary congestion)	Presence of S3	—
IV (cardiogenic shock)	Hypotension (SBP < 90 mmHg)	55.5 %

Mortality rises progressively with worsening stage. 19

Diagnostic Assessment

Before attributing hypotension to cardiogenic shock, other causes (e.g., hypovolemia, vasovagal response, electrolyte imbalance, arrhythmia) must be excluded. 18
Chest radiography should be obtained to evaluate for cardiomegaly and pulmonary congestion. 18
Pulmonary‑artery catheterization is recommended to measure pulmonary capillary wedge pressure (target < 20 mmHg) and cardiac index (target > 2 L·min⁻¹·m⁻²). 18
End‑organ hypoperfusion should be monitored using surrogate markers such as oliguria (< 0.5 mL·kg⁻¹·h⁻¹), altered mental status, cool clammy skin, and peripheral cyanosis. [18][19]

Management Priorities

Normotensive patients with an S3: intravenous nitroprusside improves forward output and reduces mitral regurgitation by decreasing left‑ventricular size. 20
Hypotensive patients: nitroprusside should not be used alone; combine with an inotropic agent (e.g., dobutamine 2.5–10 µg·kg⁻¹·min⁻¹) to augment cardiac output while still providing vasodilation. [20][18]
In refractory shock, intra‑aortic balloon counter‑pulsation can raise mean arterial pressure, increase forward output, and lower regurgitant volume. 20
Urgent surgical correction is indicated for mechanical complications such as acute mitral regurgitation or ventricular septal defect causing decompensation. [20][18]
Revascularization (percutaneous or surgical) improves survival in patients with severe heart failure or shock secondary to acute myocardial infarction. [18][21]