Cardiac Output Cardiac Output (CO) = Stroke Volume (SV) x Heart Rate (HR) Oxygen delivery = CO x arterial oxygen content (CaO2) Cardiac output must be the same in both sides of the heart except patients with regurgitant murmurs patients with structural heart abnormalities Fick principle VO2 = (Ca-Cv) x CO volume of oxygen consumed = tissue extraction of oxygen times CO applies "conservation of mass" concept to oxygen consumption in body CO = O2 consumption / [ (O2 in pulmonary vein) - (O2 in pulmonary artery) ] Key the equation above refers to difference of oxygen content between the pulmonary vein (oxygenated blood) and pulmonary artery (deoxygenated blood) when dealing with systemic circulation, one has to substract O2 in systemic veins (deoxygenated blood) from O2 in systemic arteries (oxygenated blood) to avoid negative values Changes in CO ↓ SV in ventricular tachycardia if HR is too high, diastolic filling is incomplete and CO decreases exercise CO maintained by SV in early stages of exercise CO maintained by HR in late stages of exercise Stroke Volume Stroke Volume (SV) SV = CO/HR = End-Diastolic Volume (EDV) - End-Systolic Volume (ESV) volume of blood ejected per heart beat SV ~ 70 mL Variables (assessed by echocardiogram) EDV volume of blood in ventricle before ejection ESV volume of blood in ventricle after ejection Changes in SV ↑ SV in anxiety, exercise, pregnancy ↓ SV in failing heart "SV CAP" Stroke Volume affected by Contractility, Afterload, Preload ↑ SV via (1) ↑ contractility, (2) ↓ afterload, (3) ↑ preload ↑ Contractility, ↑ SV via catecholamines ↑ activity of Ca2+ pump in SR ↑ intracellular Ca2+ ↓ extracellular Na+ ↓ activity of Na+/Ca2+ exchanger digitalis ↑ intracellular Na+ → ↑ intracellular Ca2+ ↓ Contractility, ↓ SVvia β1 blockade ↓ cAMP heart failure systolic dysfunction acidosis hypoxia/hypercapnea ↓ PO2/↑ PCO2 non-dihydropyridine Ca2+ channel blockers ↑ Myocardial O2 demand via ↑ afterload (∝ arterial pressure) ↑ contractility ↑ HR ↑ heart size aka ↑ wall tension Ejection Fraction Ejection Fraction (EF) = SV/EDV fraction of EDV ejected per SV an index of ventricular effectiveness ↓ EF via systolic heart failure an index of cardiac contractility ↑ EF, ↑ contractility EF ~ 0.55 or 55% Pulse Pressure Pulse Pressure (PP) = Systolic Pressure - Diastolic Pressure PP reflects volume of blood ejected from left ventricle on a single beat PP ∝ SV Mean Arterial Pressure Mean Arterial Pressure (MAP) average pressure in a complete cardiac cycle Equations MAP = CO x Total Peripheral Resistance (TPR) MAP = 2/3 Diastolic Pressure + 1/3 Systolic Pressure MAP = 1/3 PP + Diastolic Pressure as HR increases, diastole decreases and systole increases in the percentage of time spent, thus influencing the MAP Preload and Afterload Preload aka ventricular EDV preload "pumps up the heart" ↑ preload by exercise (slightly) ↑ blood volume e.g., over-transfusion excitement sympathetics Pathology right wall myocardial infarction (inferior wall) ST elevation seen in leads II, III, and avF preload dependent for cardiac function, thus do not diurese Afterload aka MAP ∝ TPR Pharmacology venodilators (e.g., nitroglycerin) ↓ preload vasodilators (e.g., hydrAlAzine) ↓ Afterload (Arterial)