PRINCIPLES OF HUMAN PHYSIOLOGY THIRD EDITION Cindy L. Stanfield | William J. Germann PowerPoint ® Lecture Slides prepared by W.H. Preston, College of the Sequoias Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. 13 Part B The Cardiovascular System: Cardiac Function
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Cardiac Cycle Figure Ventricular filling Ventricular filling Mid-to-late diastole Atrial contraction Isovolumetric contraction Ventricular ejection Isovolumetric relaxation Left atrium Right atrium Right ventricle Left ventricle Systole Early diastole OpenAtrioventricular valves Aortic and pulmonary (semilunar) valves Phase Open Closed 12341
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Ventricular Systole Isovolumetric ventricular contraction AV and aortic valves closed Ventricular pressure increases until it exceeds atrial pressure Ventricular ejection Aortic valve opens Blood moves from ventricle to aorta
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Ventricular Diastole Isovolumetric ventricular relaxation Ventricle muscle relaxes so that pressure is less than aorta Aortic valve closes Pressure in ventricle continues dropping until it is less than atrial pressure Ventricular filling AV valve opens Blood moves from atria to ventricle Passive until atrium contracts
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Ventricular Pressure Figure 13.19
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Aortic Pressure Figure 13.20
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Figure Ventricular Volume EDV = end-diastolic volume, volume of blood in ventricle at the end of diastole ESV = end systolic volume, volume of blood in ventricle at the end of systole SV = stroke volume, volume of blood ejected from ventricle each cycle. SV = EDV -ESV
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Stroke Volume Volume of blood ejected by the ventricle each beat Stroke volume = end diastolic volume – end systolic volume = 130 mL – 60 mL = 70 mL
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Ejection Fraction Fraction of end-diastolic volume ejected during a heartbeat Ejection fraction = stroke volume / end diastolic volume = 70 mL / 130 mL = 0.54
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Heart Sounds Due to turbulent flow when valves close First heart sound Soft lubb AV valves close simultaneously Second heart sound Louder dubb Semilunar valves close simultaneously
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Heart Sounds Figure 13.22
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Cardiac Output Volume of blood pumped by each ventricle per minute Cardiac output = CO = SV x HR Average CO = 5 liters/min at rest Average blood volume = 5.5 liters
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Regulation of Cardiac Output Regulate heart rate and stroke volume Extrinsic and intrinsic regulation Extrinsic—neural and hormonal Intrinsic—autoregulation
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Autonomic Inputs to Heart Figure 13.23
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Heart Rate - Determined by SA Node Firing Rate SA node intrinsic firing rate = 100/min No extrinsic control on heart, HR = 100 SA node under control of ANS and hormones Rest: parasympathetic dominates, HR = 75 Excitement: sympathetic takes over, HR increases
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Effects of Sympathetic Activity on Heart Rate Increased sympathetic activity (nerves or epinephrine) Beta 1 receptors in SA node Increase open state of If and calcium channels Increase rate of spontaneous depolarization Increase heart rate
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Effects of Parasympathetic Activity on Heart Rate Increased parasympathetic activity (vagus nerve) Muscarinic Cholinergic Receptors in SA Node Increase open state of K channels and closed state of calcium channels Decrease rate of spontaneous depolarization and hyperpolarize cell Decrease heart rate
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Sympathetic Effects: SA Potentials Figure 13.25
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Affecting Cardiac Output: Stroke Volume Primary factors affecting stroke volume Ventricular contractility End-diastolic volume Afterload
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Stroke Volume Ventricles never completely empty of blood More forceful contraction will expel more blood Extrinsic controls of SV Sympathetic drive to ventricular muscle fibers Hormonal control Intrinsic controls of SV Changes in EDV
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Extrinsic Control of Stroke Volume Sympathetic innervation of contractile cells Cardiac nerves NE binds to 1 adrenergic receptors Increases cardiac contractility Parasympathetic innervation of contractile cells Not significant Hormones Thyroid hormones, insulin and glucagon increase force of contraction
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Figure Sympathetic Effects on Contractility Increased sympathetic activity Increased epinephrine release Increases strength of contraction Increases rate of contraction Increases rate of relaxation
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Principle of Frank-Starling’s Law Increased EDV stretches muscle fibers Fibers closer to optimum length Optimum length = greater strength of contraction Result = Increased SV
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Intrinsic Control - Frank-Starling’s Law Increase venous return Increase strength of contraction Increase stroke volume
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Starling’s Law Figure 13.28
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Starling’s Law Figure 13.29
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Affecting End-Diastolic Volume End-diastolic pressure = preload Filling time Atrial pressure Central venous pressure Afterload = pressure in aorta during ejection
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Influencing Stroke Volume Figure Stroke volume End-diastolic volume Venous return ContractilityArterial pressure (afterload) Sympathetic activity or Epinephrine Ventricle
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Influencing Stroke Volume Figure 13.30, step 1 Stroke volume End-diastolic volume Venous return Ventricle
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Influencing Stroke Volume Figure 13.30, step 2 Stroke volume End-diastolic volume Venous return Contractility Sympathetic activity or Epinephrine Ventricle
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Factors Influencing Stroke Volume Figure 13.30, step 3 Stroke volume End-diastolic volume Venous return ContractilityArterial pressure (afterload) Sympathetic activity or Epinephrine Ventricle
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings. Regulation of Cardiac Output Figure 13.31