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Chapter 20: Cardiac Output, Venous Return, And Their Regulation Guyton and Hall, Textbook of Medical Physiology, 12 edition Normal Values for CO at Rest and During Activity • Factors Directly Affecting Cardiac Output (CO) a. The basic level of body metabolism b. Whether the person in exercising c. Age d. Body size Normal Values for CO at Rest and During Activity • Effect of Age on CO—cardiac index is the CO per square meter of body surface area Fig. 20.1 Control of CO by Venous Return • Frank-Starling Law of the Heart a. When increased quantities of blood flow into the heart, the increased blood stretches the walls of the chambers. As a result the heart contracts with increased force, and this empties the extra blood into the systemic circulation. b. Stretching of the heart causes the heart to pump faster at an increased rate— Bainbridge Reflex Control of CO by Venous Return • CO Regulation-sum of blood flow regulation in all of the local tissues of the body Fig. 20.2 Control of CO by Venous Return • Effect of Total Peripheral Resistance on LongTerm CO Fig. 20.3 Control of CO (cont.) • Effect of Total Peripheral Resistance on LongTerm CO Control of CO • Limits for CO Fig. 20.4 CO curves for the normal heart and for hypoefffective and hypereffective hearts Control of CO • Factors That Cause a Hypereffective Heart a. Nervous excitation: sympathetic stimulation or parasympathetic inhibition b. Increased pumping effectiveness caused by hypertrophy of the cardiac muscle (but not to the point of damaging the heart Control of CO • Factors That Cause a Hypoeffective Heart a. Increased arterial pressure against which the heart must pump (i.e. hypertension) b. Inhibition of nervous excitation c. Pathological factors causing abnormal rhythm or rate of heart beat d. Coronary artery blockage e. Valvular heart disease f. Congenital heart disease g. Myocarditis h. Cardica hypoxia Control of CO • Role of the Nervous System Fig. 20.5 Experiment in a dog to demonstrate the importance of nervous maintenance of the arterial pressure as a prerequisite for cardiac output control. Control of CO • Low Cardiac Output Caused by Cardiac Factors a. Severe coronary vessel blockage and myocardial infarction b. Severe valvular heart disease c. Myocarditis d. Cardiac tamponade e. Cardiac metabolic derangements Fig. 20.6 CO in different pathological conditions. The number in parentheses indicate the number of patients studied in each condition. Control of CO (cont.) • Decrease Caused by Non-cardiac Peripheral Factors a. Decreased blood volume b. Acute venous dilation c. Obstruction of large veins d. Decreased tissue mass, especially skeletal muscle e. Decreased metabolic rate of the tissuesa Quantitative Analysis of CO Regulation • Fig. 20.7 Effect of External Pressure Outside the Heart on CO curves Quantitative Analysis of CO Regulation • Factors That Can Shift the CO Curve a. Cyclical changes in intrapleural pressure during respiration b. Breathing against a negative pressure c. Positive pressure breathing d. Opening the thoracic cage e. Cardiac tamponade (fluid accumulation in the pericardial cavity • Simultaneous Changes in External Cardiac Pressure and the Effectiveness of the Heart as a Pump Fig. 20.8 Venous Return Curves • Three Principal Factors Affecting Venous Return to the Heart a. Right atrial pressure b. Mean systemic filling pressure c. Resistance to blood flow Venous Return Curves • Normal Venous Return Curve Fig. 20.9 Normal venous return curve Venous Return Curves • Venous Return Curves a. Plateau at negative atrial pressure caused by collapse of large veins b. Effect of blood volume on mean circulatory filling pressure (psf ) c. Effect of sympathetic stimulation of circulation on mean circulatory filling pressure (psf) The greater the distance between the psf and right atrial pressure, the greater the venous return Fig. 20.11 Fig. 20.11 Resistance to Venous Return VR = Venous return Psf = Mean systemic filling pressure PRA = Right atrial pressure RVR = Resistance to venous return Resistance to Venous Return • Effect of Resistance to Venous Return on the Venous Return Curve Fig. 20.12 Resistance to Venous Return • Combinations of Venous Return Patterns Fig. 20.13 Resistance to Venous Return • Effect of Increased Blood Volume on Cardiac Output Fig. 20.14 The two solid curves demonstrate an analysis of cardiac output and right atrial pressure when the CO (red line) and venous return (blue line) lines are normal. Transfusion of blood equal to 20 per cent of the blood volume causes the venous return curve to become the dashed line; as a result, the cardiac output and right atrial pressure shift from point A to point B Resistance to Venous Return • Further Compensatory Effects a. Increased CO increases capillary pressure b. Reduces mean systemic pressure (stress-relaxation) c. Increases the resistance to venous return Resistance to Venous Return • Effects of Sympathetic Stimulation on CO Fig. 20.15 Resistance to Venous Return • Effects of Sympathetic Inhibition on CO Fig. 20.16