Acute rise in LA pressure → pulmonary oedema & cardiogenic shock → end-diastolic pressure in LVrises sharply → compensation by increasing heart rate and contractility (Starling's law), but this fails to maintain normal stroke volume
Medical emergency with high mortality
Pathophys of chronic AR
LV volume & pressure overload -> increased wall tension -> compensated hypertrophy -> can sustain this for decades -> eventually LV systolic dysfunction supervenes LV end-diastolic pressure rises -> symptomatic CHF