Clinical meaning
The cardiac pressure-volume (PV) loop is a graphical representation of the mechanical work performed by the ventricle during a single cardiac cycle, plotting left ventricular pressure (y-axis) against left ventricular volume (x-axis). The loop traces four phases: (1) isovolumetric contraction (mitral valve closes, aortic valve still closed — pressure rises at constant volume), (2) ejection (aortic valve opens when LV pressure exceeds aortic diastolic pressure — volume decreases as blood is ejected), (3) isovolumetric relaxation (aortic valve closes, mitral valve still closed — pressure falls at constant volume), and (4) filling (mitral valve opens when LV pressure falls below left atrial pressure — volume increases). The width of the PV loop represents stroke volume (SV = end-diastolic volume minus end-systolic volume), while the area enclosed represents stroke work. The Frank-Starling mechanism describes how increasing preload (end-diastolic volume) stretches sarcomeres toward their optimal length (~2.2 micrometers), increasing the number of actin-myosin cross-bridge interactions and thus contractile force — this is represented on the PV loop as a rightward shift along the end-diastolic pressure-volume relationship (EDPVR). The EDPVR slope reflects ventricular compliance (diastolic stiffness): a steep slope indicates a stiff, non-compliant ventricle (restrictive cardiomyopathy, hypertrophic cardiomyopathy, cardiac tamponade) where small volume increases produce large pressure rises, causing pulmonary congestion at relatively low filling volumes. The end-systolic pressure-volume relationship (ESPVR) represents contractility independent of loading conditions — its slope (Ees, end-systolic elastance) increases with positive inotropes (dobutamine, milrinone) and decreases with systolic heart failure. Afterload, the pressure the ventricle must overcome to eject blood, is clinically approximated by systemic vascular resistance (SVR = [MAP - CVP]/CO × 80). Increased afterload (hypertension, aortic stenosis) shifts the ESPVR upward and narrows the PV loop (reduced stroke volume, increased end-systolic volume, increased myocardial oxygen demand). In heart failure with reduced ejection fraction (HFrEF), the PV loop shifts rightward (increased EDV from volume overload) and narrows (decreased SV from impaired contractility), with an elevated end-diastolic pressure that transmits retrograde to the pulmonary vasculature, causing pulmonary edema (PCWP >18 mmHg). HFpEF shows a steep EDPVR (impaired relaxation and increased stiffness) with preserved EF but elevated filling pressures — the ventricle generates adequate systolic function but cannot fill adequately at normal diastolic pressures. Understanding PV loops enables the NP to predict hemodynamic effects of interventions: vasodilators (nitroprusside) decrease afterload and widen the loop, diuretics decrease preload and shift the loop leftward, and inotropes increase the ESPVR slope and widen the loop.