Preload, Afterload, Contractility

Cardiac output (CO) — the volume of blood ejected by the heart per minute — is the product of heart rate (HR) and stroke volume (SV), where stroke volume is determined by three interdependent hemodynamic variables: preload, afterload, and contractility. Preload is the volume of blood in the ventricles at the end of diastole (end-diastolic volume, EDV), which stretches the myocardial sarcomeres before contraction. According to the Frank-Starling mechanism, increased preload stretches sarcomeres toward their optimal length (~2.2 micrometers), maximizing actin-myosin cross-bridge formation and increasing the force of contraction and stroke volume — up to a point. Beyond optimal stretch, the sarcomeres become over-distended, cross-bridge overlap decreases, and further preload increases produce no additional stroke volume (the flat portion of the Starling curve), with excess preload causing pulmonary congestion (left-sided) or peripheral edema (right-sided). Preload is estimated clinically by pulmonary capillary wedge pressure (PCWP, normal 6-12 mmHg) for the left ventricle and central venous pressure (CVP, normal 2-6 mmHg) for the right ventricle. Afterload is the resistance the ventricle must overcome to eject blood, determined primarily by systemic vascular resistance...