Intro to the Cardiovascular System – Heart II (Jahn) .pdf

Intro to the Cardiovascular System – Heart II Stephan C. Jahn, Ph.D. Cardiac Output Cardiac output (CO)—amount ejected by each ventricle in 1 minute Cardiac output = heart rate x stroke volume  About 4 to 6 L/min at rest  Vigorous exercise increases CO to...

Intro to the Cardiovascular System – Heart II Stephan C. Jahn, Ph.D. Cardiac Output Cardiac output (CO)—amount ejected by each ventricle in 1 minute Cardiac output = heart rate x stroke volume  About 4 to 6 L/min at rest  Vigorous exercise increases CO to 21 L/min for a fit person and up to 35 L/min for a world-class athlete 19-2 Heart Rate Pulse—surge of pressure produced by heart beat that can be felt by palpating a superficial artery  Infants have HR of 120 bpm or more  Young adult females = 72 - 80 bpm  Young adult males = 64 - 72 bpm  Adult male = 70-72 bpm  Adult female = 80-82 bpm  Heart rate rises again in the elderly 19-3 Heart Rate Tachycardia—resting adult heart rate above 100 bpm  Stress, anxiety, drugs, heart disease, or fever Bradycardia—resting adult heart rate of less than 60 bpm  Insleep, low body temperature, and endurance-trained athletes Positive chronotropic agents—factors that raise the heart rate Negative chronotropic agents—factors that lower the heart rate 19-4 Chronotropic Effects of the Autonomic Nervous System Autonomic nervous system does not initiate the heartbeat  Modulates rhythm and force Cardiac centers in the medulla oblongata initiate autonomic output to the heart Cardiostimulatory effect  Sympathetic pathway Cardioinhibitory effect  Parasympathetic 19-5 pathway Chronotropic Effects of the Autonomic Nervous System Sympathetic postganglionic fibers are adrenergic  They release norepinephrine  Bind to β-adrenergic fibers in the heart  Activate cAMP second-messenger system  Lead to opening of Ca2+ channels in plasma membrane 19-6  Chronotropic Effects of the Autonomic Nervous System Sympathetic postganglionic fibers are adrenergic (continued)  Norepinephrine increases heart rate as high as 230 bpm Accelerates both contraction and relaxation,  At excessively high heart rates (>160 bpm) diastole becomes too brief for adequate filling Both stroke volume and cardiac output are reduced 19-7  Chronotropic Effects of the Autonomic Nervous System Parasympathetic vagus nerves have cholinergic, inhibitory effects on SA and AV nodes  Acetylcholine (ACh) binds to muscarinic receptors  Opens K+ gates in the nodal cells  As K+ leaves the cells, they become hyperpolarized and fire less frequently  Heart slows down 19-8  Chronotropic Effects of the Autonomic Nervous System Inputs to cardiac centers in medulla are diverse  Sources include higher brain centers such as cerebral cortex, limbic system, hypothalamus Sensory or emotional stimuli  Medulla also receives input from muscles, joints, arteries, and brainstem Proprioceptors in muscles and joints inform cardiac centers about changes in activity HR increases before metabolic demands on muscle arise 19-9 Chronotropic Effects of Chemicals Electrolytes  K+ has greatest chronotropic effect Hyperkalemia—excess K+ diffuses into cardiocytes  Myocardium less excitable, heart rate slows and becomes irregular Hypokalemia—deficiency in K+  Cells hyperpolarized, require increased stimulation  Calcium Hypercalcemia—excess of Ca2+  Increases heart rate and contraction strength  Sodium Hypernatremia—excess of Na+  Increases heart rate 19-10 Stroke Volume The other factor in cardiac output, besides heart rate, is stroke volume (SV) Three variables govern stroke volume  Preload  Contractility  Afterload 19-11 Preload Preload—the amount of tension in ventricular myocardium immediately before it begins to contract  Increased preload causes increased force of contraction  Exercise increases venous return and stretches myocardium  Cardiocytes generate more tension during contraction  Increased cardiac output matches increased venous return 19-12 Contractility Contractility refers to how hard the myocardium contracts for a given preload Positive inotropic agents increase contractility  Hypercalcemia can cause strong, prolonged contractions and even cardiac arrest in systole  Catecholamines increase calcium levels  Digitalis raises intracellular calcium levels and contraction strength Negative inotropic agents reduce contractility  Hypocalcemia can cause weak, irregular heartbeat  Hyperkalemia reduces strength of myocardial action potentials 19-13  Afterload Afterload—sum of all forces opposing ejection of blood from ventricle Largest part of afterload is blood pressure in aorta and pulmonary trunk  Opposes the opening of semilunar valves  Limits stroke volume Hypertension increases afterload and opposes ventricular ejection 19-14