S3 gallop

**Timing and sound:** S3 occurs in early diastole, after S2, during the rapid passive ventricular filling phase. It is low-pitched and best heard with the BELL of the stethoscope at the apex, with the patient in the left lateral decubitus position, at end-expiration. Right-sided S3 is louder at the left lower sternal border and increases with inspiration. Cadence: "Ken-TUCK-y" (S1 – S2 – S3), a ventricular gallop.

**Pathophysiology:** Blood rushes from the atrium into a ventricle that is dilated, has high end-diastolic volume or pressure, or is poorly compliant. This causes abrupt tensing of the chordae tendineae and ventricular wall, producing vibration. The cause is volume overload and/or reduced systolic function, not diastolic stiffness (which causes S4).

**Pathologic causes (adults >40):** - Systolic heart failure (dilated cardiomyopathy, post-MI) with elevated LV filling pressure and reduced EF. It is a sign of decompensation, and the S3 correlates with elevated BNP and a worse prognosis. - Volume-overload valvular lesions: mitral regurgitation, aortic regurgitation, and VSD or PDA with large left-to-right shunts. - High-output states: thyrotoxicosis, anemia, AV fistula. - Right-sided S3: cor pulmonale, severe pulmonary hypertension, tricuspid regurgitation. - Constrictive pericarditis: the "pericardial knock" occurs slightly earlier and is higher pitched.

**Physiologic S3:** Normal in children, adolescents, young adults, athletes, and pregnancy, because of rapid filling with a compliant ventricle. It is usually gone by about age 40. Persistence beyond that age should prompt a search for pathology.

**Maneuvers:** - Louder with: exercise, leg raise, or any increase in venous return (increased preload). Left-sided S3 is also louder with expiration. - Softer with: standing and Valsalva (decreased preload).

**S3 vs. S4 (high-yield comparison):** - S3: early diastole, ventricular filling, dilated/volume-overloaded ventricle, systolic HF. It is "Ken-tuck-y." - S4: late diastole, just before S1, atrial contraction against a stiff, noncompliant ventricle (LVH, HTN, aortic stenosis, hypertrophic cardiomyopathy, acute MI/ischemia). Absent in atrial fibrillation. It is "Ten-nes-see."

**Board pearls:** - A new S3 in a patient with dyspnea, orthopnea, JVD, rales, and edema indicates acute decompensated heart failure. - S3 has high specificity but low sensitivity for LV dysfunction. - S3 in mitral regurgitation reflects volume overload rather than necessarily reduced EF. - Management follows the underlying cause. In HF this means diuretics for congestion, plus GDMT (ACE-I/ARB/ARNI, beta-blocker, MRA, SGLT2 inhibitor).