PSL301H Lecture 4: Regulation of Cardiac Output PDF

PSL301H – Lecture 4: Regulation of cardiac output How is cardiac output regulated? Silverthorn 7th ed: 468-472 Silverthorn 8th ed: 466-472 ESPVR and EDPVR Cardiac Performance in Ventricles ESV = end systolic volume (~65 ml) EDV = end diastolic volume (~135 ml) Stroke volume...

PSL301H – Lecture 4: Regulation of cardiac output How is cardiac output regulated? Silverthorn 7th ed: 468-472 Silverthorn 8th ed: 466-472 ESPVR and EDPVR Cardiac Performance in Ventricles ESV = end systolic volume (~65 ml) EDV = end diastolic volume (~135 ml) Stroke volume SV = EDV-ESV Amount of blood pumped by 1 ventricle in 1 contraction Cardiac output CO = HR x SV Amount of blood pumped per ventricle per unit time ~5L/min (~70 beats/min * 70 ml/beat=4.9L/min) Normal blood volume is ~ 5L Cardiac reserve difference between resting and maximal CO  The CV System as a series of “bags” with different compliances Copyright © 2009 Pearson Education, Inc. Stroke Volume Frank-Starling law states stroke volume increases as EDV increases (“Starling curve” shown below) Length-force relationships in intact heart Starling curve Figure 14-28 How does an increased EDV lead to increased SV? Stretch increases # of crossbridges and approaches optimal sarcomere length Stroke Volume EDV is affected by venous return Venous return is affected by Skeletal muscle pump Respiratory pump Sympathetic innervation  Check all that apply. What would happen to cardiac function if you Increased the pressure in the venous “bag”? A. increased SV B. increased EDV C. increased ESV D. increased CO E. increased HR Copyright © 2009 Pearson Education, Inc. “Extrinsic” Factors Influencing Stroke Volume Contractility is the increase in contractile strength independent of stretch independent of EDV Increase in contractility comes from: Increased sympathetic stimuli Certain hormones Ca2+ and some drugs Catecholamines Modulate Cardiac Contraction Epinephrine and norepinephrine bind to b1-receptors that activate cAMP second messenger system resulting in phosphorylation of Voltage-gated Ca2+ channels Phospholamban Open time increases Ca2+-ATPase on SR Ca2+ entry from ECF Ca2+ stores in SR Ca2+ removed from cytosol faster Shortens Ca-troponin Ca2+ released KEY binding time SR = Sarcoplasmic reticulum Shorter ECF = Extracelllular More forceful duration fluid contraction of contraction Inotropic Effect The effect of norepinepherine on contractility of the heart Altering the Inotropic State of the Heart Changes the Slope of the ESPVR Autonomic Nervous System: Extrinsic Regulation Heart Rate KEY Integrating center Cardiovascular control Efferent path center in medulla Effector oblongata Tissue response Sympathetic neurons Parasympathetic (NE) neurons (Ach) b1-receptors of Muscarinic receptors autorhythmic cells of autorhythmic cells Na+ and Ca2+ influx K+ efflux; Ca2+ influx Hyperpolarizes cell and Rate of depolarization rate of depolarization Heart rate Heart rate Summary Slide: Stroke Volume and Heart Rate Determine Cardiac Output CARDIAC OUTPUT CO = HR x SV is a function of Heart rate Stroke volume determined by determined by Rate of depolarization Force of contraction in in autorhythmic cells ventricular myocardium b1R, Gas, NE/epinephrine, Increased cAMP/PKA is influenced by more I(f) Decreases Increases increases Contractility End-diastolic volume Sympathetic b1R, Gas, Due to innervation and NE/epinephrine which varies with parasympathetic innervation epinephrine Increased cAMP/PKA VGCC, SERCA = SR Ca2+ increases Venous constriction Venous return M2R , Gai, ACh, lowered cAMP/PKA, less I(f) aided by Skeletal muscle Respiratory pump pump