pressure-volume loop

The PV loop plots LV volume (x-axis) against LV pressure (y-axis) throughout one cardiac cycle, forming a counterclockwise loop with four key points and phases: (1) Mitral valve closure (start of isovolumetric contraction) - occurs at end-diastolic volume (EDV), pressure rises rapidly with no volume change as both valves are closed; (2) Aortic valve opening - occurs when LV pressure exceeds aortic pressure, marking the start of ejection phase where volume decreases as pressure continues to rise then fall; (3) Aortic valve closure (start of isovolumetric relaxation) - occurs at end-systolic volume (ESV), pressure falls rapidly with no volume change; (4) Mitral valve opening - occurs when LV pressure falls below left atrial pressure, marking the start of filling phase where volume increases with minimal pressure change.

Key parameters derived from the PV loop: - Stroke volume (SV) = EDV - ESV = width of the loop - Stroke work = area enclosed by the loop (represents mechanical work performed by ventricle) - Ejection fraction (EF) = SV/EDV

Two boundary lines define the loop: - End-systolic pressure-volume relationship (ESPVR): the upper left line representing maximal pressure the ventricle can generate at any given volume during systole; its slope represents contractility (Ees). Increased contractility shifts ESPVR left/steeper. - End-diastolic pressure-volume relationship (EDPVR): the lower right curved line representing ventricular compliance during diastole; it becomes steeper as the ventricle fills, reflecting decreased compliance at higher volumes.

Clinical applications and changes in pathology: - Increased preload: shifts the loop rightward, increases EDV and SV (Frank-Starling mechanism), loop widens - Increased afterload: increases ESV, decreases SV, loop shifts upward and narrows, aortic valve opens later - Increased contractility (e.g., catecholamines): ESPVR shifts left/steeper, decreases ESV, increases SV and stroke work - Heart failure with reduced EF (systolic dysfunction): ESPVR shifts right/flattens (decreased contractility), loop shifts right with increased ESV and EDV, decreased SV - Heart failure with preserved EF (diastolic dysfunction): EDPVR shifts up/left (decreased compliance, increased stiffness), impaired filling - Aortic stenosis: increased afterload, concentric hypertrophy shifts EDPVR left - Aortic regurgitation: increased preload and volume overload, widens loop - Mitral regurgitation: loop shape changes as there's no isovolumetric contraction/relaxation phase (blood ejects into LA throughout systole)

Understanding PV loops is essential for grasping cardiac physiology, the effects of valvular disease, heart failure phenotypes, and pharmacologic interventions (e.g., diuretics reduce preload, ACE inhibitors reduce afterload, inotropes increase contractility).