Heart sounds are produced by the closure of cardiac valves and the rapid deceleration of blood flow. S1 is generated by closure of the mitral (M1) and tricuspid (T1) valves at the onset of ventricular systole — it marks the beginning of systole and is best heard at the apex (mitral area). S1 intensity increases with shortened PR interval, mitral stenosis (valve leaflets are wide open at onset of systole and slam shut), high cardiac output states, and tachycardia. S1 is diminished with prolonged PR interval (first-degree AV block — valve partially closed before systole), severe mitral regurgitation (incomplete closure), and reduced contractility. S2 is generated by closure of the aortic (A2) and pulmonic (P2) valves at the end of ventricular systole — it marks the beginning of diastole and is best heard at the base. Physiologic splitting of S2 occurs during inspiration: increased venous return to the right heart delays pulmonic valve closure (P2), producing an audible A2-P2 split that disappears on expiration. Fixed splitting of S2 (split does not vary with respiration) is pathognomonic of atrial septal defect...