Cardiac Output - Gulf Medical University PDF
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Gulf Medical University
Dr. Ghada Elgarawany
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This document covers cardiac output, including definitions, measurement methods, physiological and pathological variations, factors affecting cardiac output, and the regulation of cardiac output. It also includes review questions.
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Cardiac Output Dr. Ghada Elgarawany Assistant professor of Medical Physiology www.gmu.ac.ae COLLEGE OF MEDICINE Define cardiac output and list the methods of measurement. Enumerate the Physiological and pathological variations of Cardiac Output List and describe Factors affecting Cardiac Output Desc...
Cardiac Output Dr. Ghada Elgarawany Assistant professor of Medical Physiology www.gmu.ac.ae COLLEGE OF MEDICINE Define cardiac output and list the methods of measurement. Enumerate the Physiological and pathological variations of Cardiac Output List and describe Factors affecting Cardiac Output Describe the regulation of Cardiac Output Remember End diastolic volume is the volume of blood in each ventricle at the end of diastole. (End diastolic volume= 120ml ) End systolic volume is the volume of blood that remains in each ventricle at the end of systole.(End systolic volume= 50ml) Stroke Volume is the amount of blood ejected by each ventricle per stroke (Stroke volume = EDV-ESV= 70 ml) Cardiac Output Definition: volume of blood pumped by ventricle per minute Cardiac output= stroke volume x Heart rate C.O.= SV x HR ( 70 X 70 = 4900 , about 5- 5.5 liter ). N.B: Cardiac output can increase up to 25L/min during exercise and to 35L/min in athletes. Minute volume = C.O. at rest Cardiac index is the volume of blood pumped by each ventricles per meter square body surface area per minute (3.2 L/m2/min), Venous return is the volume of blood returning to the right side of the heart in a minute. It is equal to C.O. Ejection Fraction Ejection fraction is the percentage ratio of stroke volume to the end diastolic volume. =70/120X100= 65% Normally, EF is >60%. It is most commonly measured using echocardiography. This non-invasive technique provides good estimates of end-diastolic (EDV) and end-systolic volumes (ESV), and stroke volume (SV). It is an indicator of myocardial contractility. It decreases in heart failure. Measurement of Cardiac Output 1- Echocardiography 2- Fick's principal C.O. = amount of O2 added (O2 Consumption) Arterial PO2 - Venous PO2 3- Dye dilution method Variations in cardiac output Physiological variations Pathological variations Pathological increase in C.O. Pathological decrease in C.O. Physiological variations of C.O. 1. Posture : C.O decreases in standing position. 2. Digestion: C.O decreases ?? 3. Temperature : increases in high temperature?? And very low temperature ?? 4. Excitement : increases 5. Exercise : increases 6. Pregnancy : increases Pathological variations Pathological increase in C.O. Pathological decrease in C.O. Aortic regurge (All heart disease decrease C.O except ?????) 1. Anemias 1. Paroxysmal tachycardia 2. Hyperthyroidism & fever 2. Complete heart block 3. Aortic regurge 3. Myocardial ischemia and infarction 4. Shock 5. Mitral stenosis or regurge & Aortic stenosis 6. Heart failure Factors affecting cardiac output Preload Venous return Afterload Arterial blood pressure Heart rate Ventricular contraction A- Venous return ( preload) Preload is the End diastolic volume which determine the initial length of the muscle (degree of stretch of the myocardium). Increased venous return (exercise) Increase SV (Starling law) Increase HR (Bainbridge reflex) This increases the stroke volume and cardiac output. Factors affecting venous return 1. Pumping action of the heart : increase V.R 2. Right atrial pressure (RAP) 3. Respiratory movement 4. Gravity 5. Diameter of arterioles and veins and opening of capillary 6. Skeletal muscle contraction 7. Blood volume B- Arterial blood pressure (Afterload) Afterload is the resistance in front of the blood after starting ventricular contraction and ejection Aortic pressure, arterial wall rigidity and blood viscosity (Arterial blood pressure, ABP ) Sudden rise in ABP→ decrease SV ( 1st systole or beat) then ????? In the second systole (beat), EDV is increased → increase contraction (Starling law) C- Heart Rate Increase (change) HR With constant VR Moderate physiological change from 50 to 200b/min (No C.O effect) Increase HR With increase VR as in muscle exercise (increased C.O) Marked pathological change (decreased C.O) 1- > 200 b/min as in Paroxysmal tachycardia: shortening of the diastole → decrease filling → marked decrease in S.V. 2-