Cardiovascular Ph��_i_QJ Q9Y Notice Medicine is an ever-changing science As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy are required The authors and the publisher of this work have checked with sources believed to be reliable in their ef forts to provide information that is complete and generally in accord with the standards accepted at the time of publication However, in view of the possibility of human error or changes in medical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication of this work warrants that the information contained herein is in every respect accurate or complete, and they disclaim all responsibility for any errors or omissions or for the results obtained from use of the information contained in this work Readers are encouraged to confirm the information contained herein with other sources For example and in particular, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this work is accurate and that changes have not been made in the recommended dose or in the contraindications for administration This recommendation is of particular impor tance in connection with new or infrequently used drugs a LANGE medical book Cardiovascular Phy�i9JQgy 8th edition David E Mohrman, PhD Associate Professor Emeritus Department of Biomedical Sciences University of Minnesota Medical School Duluth, Minnesota Lois Jane Heller, PhD Professor Emeritus Department of Biomedical Sciences University of Minnesota Medical School Duluth, Minnesota llJIIMedical New York Milan Chicago New Delhi San Francisco Singapore Athens Sydney London Toronto Madrid Mexico City Copyright © 2014 by McGraw-Hill Education All rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-179312-4 MHID: 0-07-179312-7 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-179311-7, MHID: 0-07-179311-9 E-book conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the benefit of the trademark owner, with no intention of infringement of the trademark Where such designations appear in this book, they have been printed with initial caps McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs To contact a representative, please visit the Contact Us page at www.mhprofessional.com Previous editions copyright © 2010, 2006, 2003, 1997, 1991, 1986, 1981 by The McGraw-Hill Companies TERMS OF USE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work Use of this work is subject to these terms Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education's prior consent You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited Your right to use the work may be terminated if you fail to comply with these terms THE WORK IS PROV IDED "AS IS." McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HY PERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE McGraw-Hill Education and its licensors not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill Education has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise Contents Preface Chapter ix Overview of the Cardiovascular System Objectives I Homeostatic Role of the Cardiovascular System I The Basic Physics of Blood Flow I Material Transport by Blood Flow I The Heart I The Vasculature I 15 Blood I 17 Perspectives I 19 Key Concepts I 19 Study Questions I 20 Chapter Characteristics of Cardiac Muscle Cells 22 Objectives I 22 Electrical Activity of Cardiac Muscle Cells I 23 Mechanical Activity of the Heart I 38 Relating Cardiac Muscle Cell Mechanics to Ventricular Function I 48 Perspectives I 49 Key Concepts I 49 Study Questions I 50 Chapter The Heart Pump Objectives I 52 52 Cardiac Cycle I 53 Determinants of Cardiac Output I 60 Influences on Stroke Volume I 60 Summary of Determinants of Cardiac Output I 64 Cardiac Energetics I 68 Perspectives I 70 Key Concepts I 70 Study Questions I 71 Chapter Measurements of Cardiac Function Objectives I 73 Measurement of Mechanical Function I 73 Measurement of Cardiac Excitation-The Electrocardiogram I 7 v 73 vi I CONTENTS Perspectives I 87 Key Concepts I 87 Study Questions I 88 Chapter Cardiac Abnormalities 90 Objectives I 90 Electrical Abnormalities and Arrhythmias I 90 Cardiac Valve Abnormalities I 95 Perspectives I 98 Key Concepts I 99 Study Questions I 100 Chapter The Peripheral Vascular System 102 Objectives I 102 Transcapillary Transport I 104 Resistance and Flow in Networks ofVessels I 109 Normal Conditions in the Peripheral Vasculature I 112 Measurement ofArterial Pressure I 118 Determinants ofArterial Pressure I 119 Perspectives I 122 Key Concepts I 122 Study Questions I 124 Chapter Vascular Control 126 Objectives I 126 Vascular Smooth Muscle I 127 Control ofArteriolar Tone I 132 Control ofVenous Tone I 141 Summary of Primary Vascular Control Mechanisms I 142 Vascular Control in Specific Organs I 143 Perspectives I 154 Key Concepts I 154 Study Questions I 155 Chapter Hemodynamic Interactions 157 Objectives I 157 Key System Components I 158 Central Venous Pressure: An Indicator of Circulatory Status I 160 Perspectives I 170 Key Concepts I 170 Study Questions I 171 Chapter Regulation of Arterial Pressure Objectives I 172 Short-Term Regulation ofArterial Pressure I 173 172 CONTENTS I vii Long-Term Regulation of Arterial Pressure I 183 Perspectives I 189 Key Concepts I 190 Study Questions I 191 Chapter 10 Cardiovascular Responses to Physiological Stresses 193 Objectives I 193 Primary Disturbances and Compensatory Responses I 195 Effect of Respiratory Activity I 195 Effect of Gravity I 198 Effect of Exercise I 203 Normal Cardiovascular Adaptations I 208 Perspectives I 212 Key Concepts I 213 Study Questions I 214 Chapter 11 Cardiovascular Function in Pathological Situations 216 Objectives I 216 Circulatory Shock I 217 Cardiac Disturbances I 222 Hypertension I 231 Perspectives I 235 Key Concepts I 235 Study Questions I 236 Answers to Study Questions 238 Appendix A 256 AppendixB 257 AppendixC 258 AppendixD 259 AppendixE 262 Index 267 This page intentionally left blank Preface This text is intended to give beginning medical and serious physiology students a strong understanding of the basic operating principles of the intact cardiovascular system In the course of their careers, these students will undoubtedly encounter a blizzard of new research findings, drug company claims, etc Our basic rationale is that to be able to evaluate such new information, one must understand where it fits in the overall picture In many curricula, the study of cardiovascular physiology is a student's first exposure to a complete organ system Many students who have become masters at memorizing isolated facts understandably have some difficulty in adjusting their mindset to think and reason about a system as a whole We have attempted to fos ter this transition with our text and challenging study questions In short, our goal is to have students "understand" rather than "know" cardiovascular physiology We strongly believe that in order to evaluate the clinical significance of any new research finding, one must understand precisely where it fits in the basic interac tive framework of cardiovascular operation Only then can one appreciate all the consequences implied With the current explosion in reported new findings, the need for a solid foundation is more important than ever We are also conscious of the fact that cardiovascular physiology is allotted less and less time in most curricula We have attempted to keep our monograph as short and succinct as possible Our goal from the first edition in 1981 onward has been to help students understand how the "bottom-line" principles of cardio vascular operations apply to the various physiological and pathological challenges that occur in everyday life Thus, our monograph is presented throughout with its last two chapters in mind These chapters bring together the individual compo nents to show how the overall system operates under normal and abnormal situ ations We judged what facts to include in the beginning chapters on the basis of whether they needed to be referred to in these last two chapters In this eighth edition, we have attempted to improve conveying our overall mes sage through more precise language, more logical organization of some of the mate rial, smoother and more leading transitions between topics, incorporation of new facts that help clarifY our understanding of basic concepts, addition of"Perspectives" section in each chapter that identifies important issues that are currently unresolved, and inclusion of additional thought-provoking study questions and answers As always, we express sincere thanks to our mentors, colleagues, and students for all the things they have taught us over the years This may be our last edition, so, in closing, the authors would like to thank each other for the uncountable hours we have spent in discussion (and argument) in what has been a long, mutually beneficial, and enjoyable collaboration David E Mohrman, PhD Lois jane Heller, PhD ix Appendix E Analysis of the Arterial Baroreflex For most purposes, the simple "thermostat analogy" provides a sufficient understanding of how the arterial baroreflex operates However, in certain situations-especially when there are multiple disturbances on the cardiovascular system-a more detailed understanding is helpful Consequently, the operation of the arterial baroreflex is presented in this appendix with a more formal control system approach The complete arterial baroreceptor reflex pathway is a control system made up of two distinct portions, as shown in Figure E-1: (1) an effector portion, includ ing the heart and peripheral blood vessels; and (2) a neural portion, including the arterial baroreceptors, their afferent nerve fibers, the medullary cardiovascular centers, and the efferent sympathetic and parasympathetic fibers Mean arterial pressure is the output of the effector portion and simultaneously the input to the neural portion Similarly, the activity of the sympathetic (and parasympathetic) cardiovascular nerves is the output of the neural portion of the arterial barorecep tor control system and, at the same time, the input to the effector portion For convenience, we omit continual reference to parasympathetic nerve activity in the following discussion Throughout, however, an indicated change in sympathetic nerve activity should usually be taken to imply a reciprocal change in the activity of the cardiac parasympathetic nerves A host of reasons why mean arterial pressure increases when the heart and peripheral vessels receive increased sympathetic nerve activity are discussed in Chapters through All this information is summarized by the curve shown in the lower graph in Figure E-1, which describes the operation of the effector por tion of the arterial baroreceptor system alone In Chapter 9, how increased mean arterial pressure acts through the arterial baroreceptors and medullary cardiovas cular centers to decrease the sympathetic activity has also been discussed This information is summarized by the curve shown in the upper graph in Figure E-1, which describes the operation of the neural portion of the arterial baroreceptor system alone When the arterial baroreceptor system is intact and operating as a closed loop, the effector portion and neural portion retain their individual rules of opera tion, as described by their individual function curves in Figure E-1 Yet in the closed loop, the two portions of the system must interact until they come into balance with each other at some operating point with a mutually compatible 262 APPENDIX E I 263 Neural portion Sympathetic and parasympathetic nerve activity Mean arterial pressure Low Mean arterial pressure (input) High Low High Sympathetic nerve activity (input) Figure E-1 Neural and effector portions of the arterial baroreceptor control system combination of mean arterial pressure and sympathetic activity The analysis of the complete system begins by plotting the operating curves for the neural and effector portions of the systems together on the same graph as in Figure E-2A To accomplish this superimposition, the graph for the neural portion (the upper graph in Figure E-1) was flipped to interchange its vertical and horiwntal axes Consequently, the neural curve {but not the effector curve) in Figure E-2A must be read in the unusual sense that its independent variable, arterial pressure, is on the vertical axis and its dependent variable, sympathetic nerve activity, is on the horizontal axis Whenever there is any outside disturbance on the cardiovascular system, the operating point of the arterial baroreceptor system shifts This happens because all cardiovascular disturbances cause a shift in one or the other of the two curves in Figure E-2A For example, Figure E-2B shows how the operating point for the arterial baroreceptor system is shifted by a cardiovascular disturbance that 264 I APPENDIX E A Cl 200 I E Influence of mean s � ::::J Ill Ill Influence of sympathetic activity on mean 150 arterial pressure � a (ij ·;:: � 100 as c: as Gl ::!: 50 Low High Sympathetic nerve activity, impulses per second B 200 I I Cl I E s / / "Pressure-lowering" disturbance on the 150 � effector organs ::::J Ill Ill � a (ij 100 ·;:: � as c: as Gl 50 ::!: Low High Sympathetic nerve activity, impulses per second Figure E-2 Operation of the arterial baroreceptor control system: (A) normal balance and (B) operating point shift with disturbance on the effector portion lowers the operating curve of the effector portion The disturbance in this case could be anything that reduces the arterial pressure produced by the heart and vessels at each given level ofsympathetic activity Blood loss, for example, is such a disturbance because it lowers central venous pressure and, through Starling's law, lowers cardiac output and thus mean arterial pressure at any given level of car diac sympathetic nerve activity Metabolic vasodilation of arterioles in exercising APPENDIX E I 265 skeletal muscle is another example of a pressure-lowering disturbance on the effec tor portion of the system because it lowers the total peripheral resistance and thus the arterial pressure that the heart and vessels produce at any given level of sympathetic nerve activity As shown by point in Figure E-2B, any pressure-lowering disturbance on the heart or vessels causes a new balance to be reached within the baroreceptor system at a slightly lower than normal mean arterial pressure and a higher than normal sympathetic activity level Note that the point 1' in Figure E-2B indicates how far the mean arterial pressure would have fallen as a consequence of the disturbance, had not the sympathetic activity been automatically increased above normal by the arterial baroreceptor system As indicated previously in this chapter, many disturbances act on the neural portion of the arterial baroreceptor system rather than directly on the heart or vessels These disturbances shift the operating point of the cardiovascular system because they alter the operating curve of the neural portion of the system For example, the influences listed in Figure 9-4 that raise the set point for arterial pressure so by shifting the operating curve for the neural portion of the arterial baroreceptor system to the right, as shown in Figure E-3A, because they increase the level of sympathetic output from the medullary cardiovascular centers at each and every level of arterial pressure (ie, at each and every level of input from the arterial baroreceptors) For example, a sense of danger will cause the components of the arterial baroreceptor system to come into balance at a higher than normal arterial pressure and a higher than normal sympathetic activity, as shown by point in Figure E-3A Conversely, but not shown in Figure E-3, any of the set-point lowering influences listed in Figure 9-4 acting on the medullary cardiovascular centers will shift the operating curve for the neural portion of the arterial barore ceptor system to the left, and a new balance will be reached at lower than normal arterial pressure and sympathetic activity Many physiological and pathological situations involve simultaneous distur bances on both the neural and effector portions of the arterial baroreceptor system Figure E-3A illustrates this type of situation The set-point-increasing disturbance on the neural portion of the system alone causes the equilibrium to shift from point to point Superimposing a pressure-lowering disturbance on the heart or vessels further shifts the equilibrium from point to point Note that, although the response to the pressure-lowering disturbance in Figure E-3B (point to point 3) starts from a higher than normal arterial pressure, it is essen tially identical to that which occurs in the absence of a set-point-increasing influence on the cardiovascular center (see Figure E-2B) Thus, the response is an attempt to prevent the arterial pressure from falling below that at point The overall implication is that any of the set-point-increasing influences on the med ullary cardiovascular centers listed in Figure 9-4 cause the arterial baroreceptor system to regulate arterial pressure to a higher than normal value Conversely, the set-point-lowering influences on the medullary cardiovascular centers listed in Figure 9-4 would cause the arterial baroreceptor system to regulate arterial pres sure to a lower than normal value 266 I APPENDIX E A "Set-point-raising" influence on medullary centers \/ ' Low High Sympathetic nerve activity, impulses per second 13 , � "Pressure-lowering" I influence on effector organs / Low High Sympathetic nerve activity, impulses per second Figure E-3 The effect of neural influences on the arterial baroreceptor control system: (A) operating point shift with disturbance on the neural portion and (B) operating point shift with disturbances on both neural and effector portions Several situations that involve a higher than normal sympathetic activity at a time when arterial pressure is itself higher than normal are discussed in Chapters 10 and 11 It should be noted that higher than normal sympathetic activity and higher than normal arterial pressure can exist together only when there is a set-point-raising influence on the neural portion of the arterial baro receptor system Index Page numbers followed by fand t indicate figures and tables, respectively A Aquaporin, 106 Acetylcholine, 13 , 37, 134 , 140, 152 Arterial baroreceptor reflex analysis of, 262-266 Acetyl CoA, 68 Action potential, 12 , 23 associated with emotion, 180-181 central command and, 181 of cardiac cells, 27-33 cardiac ion channels, 30t conduction of, 33-36 central integration of, 175-176 chemoreceptor reflexes, 179 " fast-response" and "slow-response", components of, 174f control system 27f,28, 32/ Activation gate, 31 effect of neural influences on, 266f Active hyperemia, 136-137, 207 neural and effector portions of, 263/ Active tensions, 42 operation of, 264f development of, 43/ Acute coronary occlusion, 224-225 dive reflex, 180 Acute exercise, 203-207 Adenosine, 133 mechanisms of, 185/ factors influencing set point of, 182/ nonarterial baroreceptor influences and, 183 Adenosine triphosphate (ATP), 68, 128 Adenylate cyclase, 67 operation of, 176-178 pain, responses to, 181 Adrenergic sympathetic fibers, 13 pathways of Aerobic metabolism, 69 afferent, 174-175 efferent, 173-174 Afterload, 45 , 48, 62 from receptors in Albumins, 18 exercising skeletal muscle, 179-180 Aldosterone, 187 Alerting reaction, 180 heart and lungs, 178-179 temperature regulation, 181-182 a-Adrenergic receptors, 17, 139 �-Adrenergic receptor blockers, 229, 231, 240 Arterial chemoreceptors, 179 Alveolar hypoxia, 153 Anaphylactic shock, 219 Arterial pressure age-related changes in, 121/ Angina, 224 cardiovascular adjustments caused by, 177/ Angina pectoris, 223 determinants of, 119-122 mean pressure, 119-120 Angiotensin-converting enzyme (ACE) inhibitors, 187, 229 pulse pressure, 120-122 effect on baroreceptor nerve activity, 175/ Angiotensin I, 187 Angiotensin II, 141, 187, 220 long-term regulation of, 183 Angiotensin II receptor blockers (ARBs), 229 fluid balance, 184-186 urinary output rate, 186-189, Angiotensinogen, 187 Anterior hypothalamus, 181 Anticoagulants, 260 188f, 189/ measurement of, 118-119 Antidiuretic hormone (ADH), 141, 187 short-term regulation of arterial baroreceptor reflex, 173-178 other cardiovascular reflexes and Antigen- antibody reactions, 135 Aortic baroreceptors, 174 responses, 178-182 Aortic insufficiency, 98 Aortic stenosis, 96 , 245 Arteries and veins, elastic properties of, Aortic valve, 10 117-118 267 268 I INDEX Arteriolar smooth muscle, 17 Arteriolar tone, control of basal tone, 132 hormonal influences on arterioles Blood flow autoregulation of, 248 basic flow equation, Fick principle, angiotensin II, 141 fluid flow through a tube, 6, 7/ circulating catecholamines, material transport by, 8-9 140-141 vasopressin, 141 local influences on arterioles moment-to-moment control of, physics of, 6-8 Poiseuille equation, from chemical substances, 135-136 pressure difference, from endothelial cells, 134-135 rate of the substance's loss and, flow responses by local mechanisms, responses caused by local 136-139 metabolic influences, 132-134 transmural pressure, 136 neural influences on arterioles parasympathetic vasodilator nerves and, 140 sympathetic vasoconstrictor nerves and, 139-140 mechanisms, 137/ through the heart, 10/ tissue pressure hypothesis of, 139 vascular control of cerebral blood flow, 147-149 coronary blood flow, 144-146 of cutaneous blood flow, 151-152 pulmonary blood flow, 152-154 Arterioles, 16, 17, 132 of renal blood flow, 150-151 Aspirin, 260 skeletal muscle blood flow, Atherosclerosis, 211, 223 Atherosclerotic plaque, 114 146-147 splanchnic blood flow, 149-150 Atrial fibrillation, 93 vascular resistance of, Atrial flutter, 93 velocities, 112-114 Atrial gallop rhythm, 58 viscosity of, Atrial tachyarrhythmias, 180 Blood oxygen tension, 210 Atrioventricular node (AV node), 12, 7 Blood pressure, 114-115 Atrioventricular (AV) valves, 53 Auscultation technique, principles of, 118 Autoregulation of organ blood flow, 138-139, 138/ Autotransfusion, 220 auscultation technique for measurement of, 118, 119/ "fluid balance" model, 183 Blood vessels capacitance, 17 characteristics of, 15-17 B classification of, 15 Basal metabolism, of heart conduit, 16 tissue, 69, 70 Basal tone, 132 Basic flow equation, Blood, 17-18 cells in, 18 control of, 17 reflex, 17 types of, 15-16 arteries, 15 arterioles, 15 gas, capillaries, 15, 16-17 normal values of veins, 15 erythrocytes, 256 leukocytes, 256 platelets, 256 venules, 15 venous, 16-17 Blushing response, 180 plasma, 2, 18 Bone marrow, 18 volume, 114 Bradycardia, 92, 179, 180 Blood-brain barrier, 148, 149 Bradykinin, 134, 136, 152 Blood clotting, 259 Bundle branches, 12 Blood-conditioning organs, Bundle of His, 12 INDEX I 269 c conventions for use of Calcium channel blockers,224 Calmodulin,128 electrocardiograms,78-80 electrocardiogram,7 7-78 Calsequestrin,39 mean electrical axis and axis Capacitance vessels, 17 deviations,83-85 standard 12-lead electrocardiogram, Capillaries,16 filtration and reabsorption, 107 Cardiac abnormalities, 90 electrical abnormalities and arrhythmias, 90-92 supraventricular abnormalities,91f, 92-94 ventricular abnormalities, 91f,94-95 valvular abnormalities,95-98 aortic insufficiency,98 aortic stenosis,96 characteristics of, 97f 85-87 ventricular depolarization and the QRS complex,82-83,82/ ventricular repolarization and the Twave,83 mechanical function for cardiac index, 76-77 cardiac output,75-76 end-systolic pressure-volume relationship,74-75 imaging techniques,73-74 sympathetic neural influences on,67-68 mitral regurgitation,98 Cardiac glycosides,229 mitral stenosis,96-98 Cardiac angiography,74 Cardiac hypertrophy,49,230 Cardiac index,76-77 Cardiac arrhythmias,223 Cardiac ion channels Cardiac conduction system action potentials,27-33,27/ conduction velocity,34 consequences of, 34 characteristics of, 30t conceptual model of, 32/ gates of, 31 Cardiac muscle cells membrane potentials,24-26,25f,27/ Cardiac conversion,95 contractility of, 46-48 diastolic depolarization,28 Cardiac cycle electrical activity of, 23-38 arterial pressure waveform and, 120 diastole, 11,118 ventricular, 53-54 electrocardiogram of, 77/ action potentials,27-33,27/ conduction of action potentials, 33-36,34/ control of heart beating rate, 36-38 left pump,53-56,54f electrocardiograms and, 36 phases of, 54/ pressure development phase of, 70 membrane potentials,24-26,25f,27/ pressure-volume and length-tension relationships in,58-59 right pump,56-57,56/ systole, 11, 118 Cardiac dilation,49 Cardiac dipoles,80-82 during atrial depolarization,80/ magnitude and strength of, 80 single-cell voltage recordings,35/ time records of, 35/ fractional shortening of, 46 hypertrophy,96 length-tension cycle,59/ length-tension diagram,45 norepinephrine, effect of, 46,47/ pacemaker cells,28 pacemaker potential,28 Cardiac filling, 17 percent shortening of, 46 Cardiac function curves,65-67 phase depolarization,28 influence of cardiac sympathetic nerve activity on,66/ Cardiac functions,measurement of cardiac excitation,77-87 cardiac dipoles and electrocardiographic records,80-82 potassium equilibrium potential, 25 sodium equilibrium potential,26 transmembrane potentials,24 transmembrane protein structures, types of, 24 ventricular function of, 48-49 270 I INDEX Cardiac output (CO), 5, 11, 198 arterial pressure related to, 120 control of autonomic neural influences, 12-13 diastolic filling, 13-14 determinants of, 60, 64-65 measurement of, 75-76 echocardiography method for, 76 Fick principle for, 75-76 indicator dilution techniques for, 76 cardiac output and venous return, determination of, 164-168 as circulatory status indicator, 160-170 cardiac output and venous return, distinction between, 161/ and venous return, relationship between, 161-163, 162/ influence of peripheral venous pressure on, 163-164 Cardiac pacemaker potentials, 37/ Cerebral arterioles, 148 Cardiac parasympathetic fibers, 37 Cerebral blood flow, vascular control Cardiac parasympathetic nerves, 64 of, 147-149 Cardiac reserve, 207 Cerebral ischemic response, 179 Cardiac sympathetic nerves, 168 Cerebrospinal fluid (CSF), 149 Cardiac tamponade, 217 Chemoreceptor reflexes, 179 Cardiogenic shock, 217, 254 Cholinergic parasympathetic nerve Cardiopulmonary receptors, 178 Cardiovascular system arterial baroreceptor reflex (See arterial baroreceptor reflex) fibers, 13 tonic activity of, 38 Cholinergic sympathetic fibers, 152 Choroid plexes, 149 blood circulating in, Chronic bleeding disorders, 254 compensatory responses and, 195 Chronic exercise, 207-208 components of, 158-159, 158/ Chronic heart failure blood volume and pressure, distribution of, 160 mean circulatory filling pressure, 159-160 properties of, 159t diastolic dysfunction, 230-231 systolic dysfunction, 225-229 Chronic moderate depolarization, 33 Chronotropic effect, 38 Circulatory shock convective transport, process of, cardiovascular alterations in, 218/ emotion, responses associated with, compensatory mechanisms in, 180-181 functional arrangement of, 4f and hemorrhage, 167/ 220-221 decompensatory processes in, 221, 222/ primary disturbances and, 217-219 homeostatic role of, 2-6 Cold-induced vasodilation, 152 primary disturbances and, 195 Collagen, 259 transport system, 3/ Carotid massage, 180 Carotid sinus baroreceptors, 174 fibers, 16 Colloid osmotic pressure, 107 Compensatory reflex, 253 Compliance massage, 249 systemic circuit, 159 nerves, 175 vascular, 117 Catecholamines, 140-141 Cell membrane, hyperpolarization of, 131 Computed tomography angiography (CTA), 74 Central chemoreceptors, 179 Conduction blocks, 93 Central command, 181 Conduction velocity, 34 Central venous pool, 114 Congestive heart failure, 227 Central venous pressure Connexin, 33 abnormal, clinical implications of, 169-170 Contractile Proteins, 39 cardiac function and venous function Contractility curves, 166/ definition, 46 INDEX I 271 Convection, process of, E Convective transport, process of, Echocardiography, 74, 76 Conventions, for use of electrocardiograms, Edema, 108, 149 78-80 Einthoven's electrocardiographic conventions, 79/ Einthoven's electrocardiographic conventions, 79/ Einthoven's triangle, 79, 81 Cor Pulmonale, 231 Coronary angioplasty, 224 Ejection fraction, 63 Elastin fibers, 16 Coronary artery disease Electrical arrhythmia, 241 Electrical conduction system, of the heart, 13/ definition and physiological consequences of, 222-223 diagnosis, 223 treatments, 223-224 Electrical connections, low-resistance, 33 Electrical dipoles, 80 Electrocardiograms, 35f, 36, 55 Coronary blood flow, vascular control of, 144-146 cardiac dipoles and, 80-82 conventions for use of, 78-80 Coronary sinus, 144 Coughing, 197 Einthoven's conventions, 79/ of single cardiac cycle, 77/ standard 12-lead electrocardiogram, 85-87 Coumadin, 260 Cross-bridge cycling, 128 Cuff pressure, 119 Electrolytes, 18 Electromechanical coupling, 130-131 Cushing reflex, 179, 250 Embarrassment, states of, 180 Cutaneous blood flow, vascular control of, 151-152 Emotions, cardiovascular responses for, 180-181 Cyclic adenosine monophosphate End-diastolic volume (EDV), 12, 63 (cAMP), 131 Cyclic guanosine monophosphate Endothelial cells, 106, 112, 134-135 metabolism, 149 (cGMP), 132 Cyclic nucleotide-gated (HCN) Endothelin, 134 Endotoxin, 219 channels, 31-32 End-systolic pressure-volume relationship, 74-75 Cyclooxygenase inhibitors, 260 effect of increased contractility on, 75/ D End-systolic volume (ESV), 12, 55 Delayed outward current, 29 Energy sources, 69-70 Desmosomes, 33 Epinephrine, 131, 140 Developed tension, 42 Diastolic depolarization, 29, 31, 34 murmur, 58, 98 Excitement See Alerting reaction Exercise and cardiovascular mechanisms, 205/ cardiovascular responses to pressure, 56 Dicoumarol, 260 acute exercise, 203-207 chronic exercise, 207-208 cardiovascular variables, changes in, 204/ Dicrotic notch, 55 Diffusion, process of, Digitalis, 229 Distributive shock, 219 pressor response, 207 static, 206, 207 Extracellular fluids, 2, 131 osmolarity, 141 Dive reflex, 180 Doppler echocardiography, 74 F shifts, 76 Dromotropic effect, 38 Fainting, 250 Ductus arteriosis, 209 Fatty acids, 68 Dynamic exercise, 204-206 Fast inward current, 29 long-chain, 108 272 I INDEX Fetal alveoli,209 Fibrinogen,18 Fick principle,9,241 for calculation of cardiac output, 75-76 Filtration,106 Flow equations, 106, 109, 111, 120, 161,240 Fluid intake rate, 185-186, 190 Foramen ovale,209 Frank-Starling's Law of the heart,60-62, 114,249,255 Furosemide,229 G Gallop rhythms, 57 Gap junctions,33 between cardiac cells,38 electrical characteristics of, 34 Gender,cardiovascular responses and,212 Globulins, 18 Glomerular capillaries, 186 Glomerular filtrate, 186 Glomerular filtration rate, 186 Glossopharyngeal nerves, 175 Glycogen,68 Gravity,cardiovascular responses to body position changes and, 198-202 long-term bed rest and,202-203 Guanosine triphosphate-binding proteins (GTP-binding proteins),131, 139 H HCN channels, 30,32 Heart aortic valve, 10 blood flow through, 10/ cardiac cycle, 11 cardiac excitation of, 12 cardiac output,control of autonomic neural influences, 12-13 diastolic filling, 13-14 effective operation of, requirements for, 14 electrical conduction system of, 13/ Frank-Starling's Law,60-62 mean electrical axis of, 83 mechanical activity of cardiac muscle cell contraction,38-39 cardiac muscle contractility, 46-48 cardiac muscle mechanics,41-42 excitation-contraction coupling,39-41 isometric contractions,42-44 isotonic and afterloaded contractions, 44-46 length-tension relationships,42-44,46 mitral valve,10 pulmonic valve, 10 pumping action of, 9-12 ventricular, 11/ Starling's Law of, 13-14,14f, 17 tricuspid valve, 10 volume-pressure curves, 117/ Heart beating rate and compensatory pause,94 control of, 36-38 prolonged QT intervals,94-95 Heart blocks bundle branch blocks,94 first-degree, 93 hemiblocks, 94 second-degree, 93 third-degree, 93 Heart failure,225,228f, 230j See also Chronic heart failure with preserved systolic function, 230 Heart pumps, 9-10, 12, 164 cardiac cycle and heart sounds, 57-58 left pump and,53-56, 54f pressure-volume and length-tension relationships in, 58-59 right pump and, 56-57, 56f cardiac energetics and,68-70 energy sources,68 myocardial oxygen consumption, determinants of, 69-70 cardiac output determinants and,60 cardiac function curves,65-67 stroke volume,influences on cardiac muscle contractility,63-64 ventricular afterload,62-63,62f ventricular preload, 60-62,61f Heart rate (HR), 11, 70 Heart sounds, 57-58, 95 Korotkoff sounds,119 murmurs,58, 95,96,113,210 Hematocrits,17 Hemoglobin, 18 Hemorrhage, 108, 141 cardiovascular adjustments to, 167/ Hemostasis,259-261 Heparin,261 Hering's nerves, 175 INDEX I 273 Histamine, 108, 135, 136 Homeostasis,2 Hydrostatic pressure, 106, 153, 154 Hyperemia active, 136-137 exercise,136 postocclusion,137 reactive,137-138 Hypertension, 183, 189,211,230, 231-232 cause of, 234 facts about,232-234 renal function curves in,233/ treatment of diuretic therapy for,234 strategies for,234-235 Hypothalamic communications, 180 Hypothalamus, 176, 178 Hypovolemic shock, 217, 254 Hypoxic vasoconstriction, 153 I /-funny (if) current,29 Imaging techniques,73-74 Impedance cardiography,76 Inactivation gate,31 Incisura, 55 Inositol triphosphate (IP), 131 Inotropic effects, 46 Intercalated disks,33 Interstitial fluids, 18 composition of, Interstitial homeostasis,239 lntrarenal renin-angiotensin system, 151 Ion channels,24 Ion exchangers,24 Ion pumps,24 Ischemia,222, 223 Ischemic heart disease,212 Isometric contraction, 42-44, 43/ Isotonic (fixed load) contraction, 44-46 Isotonic saline, 18 lsovolumetric contraction phase, 55 Isovolumetric relaxation phase, 55 J Jugular venous pulse, 57 K Kallikrein, 136 Korotkoff sounds, 119 Krebs cycle,68 L Laminar flow, 112, 114{ Latent pacemakers,35 Law of Laplace,49,69,250,254 Leukocytes See White blood cells Leukotrienes,135 Ligand-gated channels,30 Lipopolysaccharide,219 Lusitropic effect,48 Lymph,109 Lymphatic system, 108-109 M Magnetic resonance imaging (MRI), 74, 76 Mean arterial pressure, 115 Mean circulatory filling pressure, 159-160 Mean electrical axis and axis deviations, 83-85,84/ Medulla oblongata, 175 Medullary cardiovascular centers, 175 Metabolic vasodilation, 147,207 Metabolic vasodilator hypothesis, 133/ Mitral regurgitation, 98 Mitral stenosis, 96-98,245 Mitral valve, 10 Multigated acquisition scan (MUGA scan) See Radionuclide ventriculography Murmurs, 58, 95, 96, 113,210 Muscle contraction,69 Muscle length, effect on resting and active tension,43/ Muscle relaxation,47 Myocardial contractility, 70 Myocardial hypertrophy,208 Myocardial infarction,145,224-225 Myocardial ischemia,223 Myocardial oxygen consumption,144 determinants of, 69-70 Myocardium (heart muscle),5, 93 Myogenic response, 136 Myosin filaments, 128 Myosin light-chain kinase (MLC kinase),128 Myosin phosphatase, 128 N Neurogenic shock,219 Neurogenic tone, 140 Neurogenic vasoconstriction, 141 Nitric oxide, 134, 219 Nitroglycerin,224 Norepinephrine, 140,239 274 I INDEX Norepinephrine (noradrenaline), 13,38,46 effect on cardiac muscle,47/ Physiological stresses,cardiovascular Normal sinus arrhythmia, 196 responses to age-dependent changes,211 Nucleus ambiguus, 176 exercise and,203-208 Nucleus tractus solitarius, 176 fetal circulation and changes at birth, 209-210,209/ gender and,212 Oncotic pressure, 107 gravity and, 198-202 Orthostatic hypotension,203 Osmolarity,2, 187,220 pediatric cardiovascular characteristics and,210 Osmotic pressures, 106,107 pregnancy and,208-209 Oxidative phosphorylation,68 Oxygen-binding protein myoglobin,68 respiratory activity and,195-198 Placenta, 209 Plaques,222 calcification of, 223 p Pacemaker cells,28,31 diastolic depolarization of, 60 Pain,reflex responses to, 181 Parasympathetic neural activity, 150 Parasympathetic vasodilator nerves,140 Paroxysmal atrial tachycardia,92 Peak systolic pressure, 55 Pericardium,9 Peripheral vascular resistances,115-116 Peripheral vascular system arterial pressure Plasma,18 normal constituents of, 257 proteins,107 proteins in, 18 volume, Platelets, 18 Poiseuille equation,7,238 Positive-pressure ventilators,198 Positron emission tomography (PET),74 Posterior hypothalamus,180 Postextrasystolic potentiation,94 determinants of, 119-122 Postganglionic fibers, 173 measurement of, 118-119 Postural hypotension,203 conditions in arteries and veins, 117-118 blood flow velocities, 112-114, 113/ blood pressures,113f, 114-115 blood volumes, 113f, 114 peripheral resistance, 116 vascular resistances, 113f, 115-116 resistance and flow in networks of vessels and, 109-112 Potassium equilibrium potential,25 Preganglionic fibers, 173 Pregnancy,cardiovascular changes of, 208-209 Preload,48,60 Premature ventricular contractions (PVCs),94 Pressure-volume relationship of arteries,121/ Primary cardiomyopathy,225 vessels in parallel, 111-112, 111/ Prostacyclin,134 vessels in series,109-111, 110/ Prostaglandins,135, 151 Pulmonary arterioles, 153 transcapillary transport lymphatic system,108-109 Pulmonary blood flow,vascular control transcapillary fluid movement, of, 152-154 Pulmonary circulation,4 106-108 transcapillary solute diffusion, 104-106 Pulmonary embolus,217 Pulmonary hypoxic vasoconstriction,153 Peripheral veins,142 Pulmonary veins, 10 Peripheral venous pool, 114 Pulmonary wedge pressure,170 Permeability, 104 Pulmonic valve, 10 of ions,24 Pharmacomechanical coupling, 130-131 Phospholamban,47 stenosis,244 Pulse pressure, 56 evaluations of, 76 Purkinje fibers, 12,35,81 INDEX I 275 Q Staircase phenomenon,48 QT syndrome, 95 Standard 12-lead electrocardiogram, R Starling hypothesis, 107 Radioactive isotopes,74 Starling's Law of heart, 13-14, 1-if, 17,60, 85-87,86/ Radionuclide ventriculography,74 64,165,239 Raphe nucleus, 176 Static exercise,206 Rapid ejection period, 55 Steady-state rate of consumption,9 Reabsorption, 106 "Stenotic" valve,241 Reactive hyperemia, 137-138,207 Stent,224 Receptor-operated channels, 131 See also Ligand-gated channels Streptokinase,225 Stroke volume (SV), 11-12,55,63,198,241 age-related changes in, 121/ Red blood cells, 18,74 Red flare, 152 Renal blood flow,vascular control of, 150-151 Renal function curves,in healthy and hypertensive people,233/ Renin, 187 Stroke work,69 Supraventricular arrhythmias,91/ Supraventricular tachycardia,92 Sweat glands, 152 Sympathectomy,248 Sympathetic vasoconstrictor nerves, 139-140,148 Renin-angiotensin-aldosterone system, 187,227 Syncope,217 Respiration,artificial support of, 198 Systemic circulation,4 Respiratory activity,cardiovascular Systolic responses to, 195-198 compression, 144 Respiratory cycle, 57 dysfunction,225-229 Respiratory inspiration,cardiovascular murmurs, 58,244 effects of, 196/ Respiratory pumps, 195, 197,251 T Resting length-tension curve, 42 Tachycardia,92, 179 Resting tension,42 Thiazides,229 development of, 43/ Threshold potential,29 Rhythmic contractions,147 Thrombin,259,260 Rostral ventrolateral medulla, 176 Thrombolytic agents,261 s Tissue plasminogen activator (tPA),261 Sarcomeres,38 Tissue pressure hypothesis,of blood flow, 139 Thromboxane, 135 Sarcoplasmic reticulum (SR),39 Titin,39 Sense of danger See Alerting reaction Tonic firing activity, 139 Septic shock,219,254 Torsades de pointes, 95 Serum, 18 Total body water,2 Shear stress, 112, 113 Total peripheral resistance (TPR), 116, Sinoatrial (SA) node,60 Sinoatrial node (SA node), 12,35 Skeletal muscles,68 blood flow,vascular control of,146-147 pumps, 142,200,251 reflexes from receptors in, 179 247,253 arterial pressure related to, 120 Total tension, 42 Transcapillaty diffusion,2, 16 pathways for,105/ of solutes,104-106 Skin blood flow,206,253 Transcapillaty fluid filtration, 108 Smooth muscle cells, 17 Transcapillaty fluid movement, 106-108 Sodium equilibrium potential,26 Splanchnic blood flow,vascular control of, 149-150 factors influencing, 108/ Transmembrane potentials,24 Transmembrane protein,types of, 24 276 I INDEX Transmembrane voltage,24 Vascular tone, 132 Tricuspid valve, 10 Vasoactive intestinal peptide, 134 Vasoconstriction, 133 regurgitation, 244 Triple response, 152 Vasodilation, 132 Turbulent flow, 113, 11'if Vasopressin, 141, 187-188 \'asovagal syncope,181,219 u Uremia,221 \'ectorcardiography,84, 85/ \'enous blood, 10 v \'enous function curve, 161, 163 effect of changes in blood volume and Vagus nerves,37 Valsalva maneuver, 197-198 Vascular control, 127 arteriolar tone, control of basal tone, 132 hormonal influences,140-141 venous tone on, 16'if families of, 166/ \'enous plexus, 151 \'enous return, 160 \'enous tone, control of, 141-142 \'entricular local influences,132-139 afterload, 58 arrhythmias, 91/ neural influences, 139-140 of cerebral blood flow, 147-149 depolarization, 85 of coronary blood flow, 144-146 fibrillation, 95 of cutaneous blood flow, 151-152 mechanisms for, 142-143 gallop rhythm, 58 preload, 58 tachycardia, 94 of pulmonary blood flow, 152-154 reflex control, 139 \'erapamil,224 of renal blood flow, 150-151 of skeletal muscle blood flow, 146-147 \'iscosity, blood, \'itamin K, 260 in specific organs, 143-144 \'oltage-gated channels,30 of splanchnic blood flow, 149-150 \'oltage-operated channel (\'OC), vascular smooth muscle (See vascular smooth muscle) venous tone, control of, 141-142 129, 130 \'olume-pressure curves, of arterial and venous compartments, 117/ Vascular resistance, 6, Vascular smooth muscle contractile processes, 127-129 w Wall tension, 69 W hite blood cells, 18 electromechanical versus pharmacomechanical coupling, 130-131 y functional characteristics of, 127 Yawning, 197 mechanisms for activation of, 130/ membrane potentials, 129 z relaxation mechanisms,131-132 Zero gravity,cardiovascular responses Vascular system, characteristics of, 15-17, 15/ to,202-203 ... Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit,... sary for life within the organism Thus, the temperature, oxygen concentration, pH, ionic composition, osmolarity, and many other important variables of our internal environment are closely controlled... many curricula, the study of cardiovascular physiology is a student's first exposure to a complete organ system Many students who have become masters at memorizing isolated facts understandably