Clinical meaning
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 (SVR, normal 800-1200 dynes·sec/cm⁵) for the left ventricle and pulmonary vascular resistance (PVR) for the right ventricle. Increased afterload (vasoconstriction, aortic stenosis, hypertension) increases myocardial oxygen demand and decreases stroke volume because the ventricle must generate higher pressure to open the aortic valve — chronically elevated afterload causes concentric left ventricular hypertrophy (LVH). Contractility (inotropy) is the intrinsic force of myocardial contraction independent of preload and afterload, determined by intracellular calcium availability and sarcomere sensitivity. Positive inotropes (dobutamine, milrinone, digoxin) increase contractility by increasing intracellular calcium; negative inotropes (beta-blockers, calcium channel blockers, severe acidosis, hypoxia) decrease contractility. Cardiac index (CI = CO/body surface area, normal 2.5-4.0 L/min/m²) provides a size-adjusted measure of cardiac function. In cardiogenic shock, the hemodynamic profile shows low CI (pump failure), high PCWP (blood backing up behind the failing ventricle), and high SVR (compensatory vasoconstriction) — treatment targets improving contractility (dobutamine), reducing preload (diuretics), and reducing afterload (vasodilators), NOT administering fluids. In septic shock, the profile shows low SVR (pathological vasodilation), initially high CI (hyperdynamic response), and low-normal PCWP — treatment targets restoring afterload (vasopressors like norepinephrine) and volume resuscitation.