Cardiovascular

Early systole, after mitral valve closure but before aortic valve opening. Both valves are closed, so ventricular pressure rises rapidly while ventricular volume (the end-diastolic volume) is unchanged.

S1 is produced by closure of the mitral and tricuspid (atrioventricular) valves at the onset of systole. S2 is produced by closure of the aortic and pulmonic (semilunar) valves at the end of systole.

S3 occurs in early diastole during rapid passive ventricular filling. It reflects a dilated, volume-overloaded ventricle with decreased compliance — normal in children/young adults and athletes, but pathologic in dilated cardiomyopathy, systolic heart failure, and high-output states.

S4 occurs in late diastole when the atrium contracts against a stiff, non-compliant ventricle. It signals decreased ventricular compliance — seen in ventricular hypertrophy (e.g., from hypertension or aortic stenosis) and diastolic dysfunction. It is always abnormal in this setting.

Going clockwise: (1) mitral valve closure → isovolumetric contraction (rising pressure, constant volume); (2) aortic valve opening → systolic ejection (volume falls); (3) aortic valve closure → isovolumetric relaxation (falling pressure, constant volume); (4) mitral valve opening → diastolic filling (volume rises). Width = stroke volume.

Stroke volume (SV) = end-diastolic volume (EDV) − end-systolic volume (ESV). Ejection fraction (EF) = SV / EDV. Normal EF is ~55–70%. EF is reduced in systolic (HFrEF) failure and typically preserved in diastolic (HFpEF) failure.