1. Copyright 2009, John Wiley & Sons, Inc. Chapter 20: The Cardiovascular System: The Heart 2/7/20091

2. Disorders: Homeostatic Imbalances End of Chapter 19 Study pp. 711-712 Anemia Sickle-Cell Disease Hemophilia Leukemia Copyright 2009, John Wiley & Sons, Inc. 2/7/20092

3. Copyright 2009, John Wiley & Sons, Inc. Anatomy of the Heart Located in the mediastinum – anatomical region extending from the sternum to the vertebral column, the first rib and between the lungs Apex at tip of left ventricle Base is posterior surface Anterior surface deep to sternum and ribs Inferior surface between apex and right border Right border faces right lung Left border (pulmonary border) faces left lung 2/7/20093

4. Copyright 2009, John Wiley & Sons, Inc. 2/7/20094

5. Copyright 2009, John Wiley & Sons, Inc. Pericardium  Membrane surrounding and protecting the heart  Confines while still allowing free movement  2 main parts Fibrous pericardium – tough, inelastic, dense irregular connective tissue – prevents overstretching, protection, anchorage Serous pericardium – thinner, more delicate membrane – double layer (parietal layer fused to fibrous pericardium, visceral layer also called epicardium) Pericardial fluid reduces friction – secreted into pericardial cavity 2/7/20095

6. Copyright 2009, John Wiley & Sons, Inc. Pericardium and Heart Wall 2/7/20096

7. Copyright 2009, John Wiley & Sons, Inc. Layers of the Heart Wall 1.Epicardium (external layer)  Visceral layer of serous pericardium  Smooth, slippery texture to outermost surface 2. Myocardium  95% of heart is cardiac muscle 3. Endocardium (inner layer)  Smooth lining for chambers of heart, valves and continuous with lining of large blood vessels 2/7/20097

8. Copyright 2009, John Wiley & Sons, Inc. Chambers of the Heart  2 atria – receiving chambers Auricles increase capacity  2 ventricles – pumping chambers  Sulci – grooves Contain coronary blood vessels  Coronary sulcus – encircles most of heart; boundary between atria and ventricles; rt. coronary, circumflex coronary and coronary sinus  Anterior interventricular sulcus – boundary between rt. and lt. ventricles; LAD  Posterior interventricular sulcus – distinction between rt. and lt. ventricles; rt. coronary 2/7/20098

9. Copyright 2009, John Wiley & Sons, Inc. Structure of the Heart 2/7/20099

10. 20_03b

11. Copyright 2009, John Wiley & Sons, Inc. 20_03c 2/7/200911

12. Copyright 2009, John Wiley & Sons, Inc. Right Atrium  Receives blood from Superior vena cava Inferior vena cava Coronary sinus  Interatrial septum has fossa ovalis Remnant of foramen ovale  Blood passes through tricuspid valve (right atrioventricular valve) into right ventricle 2/7/200912

13. Copyright 2009, John Wiley & Sons, Inc. Right Ventricle  Forms anterior surface of heart  Trabeculae carneae – ridges formed by raised bundles of cardiac muscle fiber Part of conduction system of the heart  Tricuspid valve connected to chordae tendinae connected to papillary muscles  Interventricular septum  Blood leaves through pulmonary valve (pulmonary semilunar valve) into pulmonary trunk and then right and left pulmonary arteries 2/7/200913

14. Copyright 2009, John Wiley & Sons, Inc. Internal Anatomy of the Heart 2/7/200914

15. Copyright 2009, John Wiley & Sons, Inc. 20_04b 2/7/200915

16. 20_04c

17. Copyright 2009, John Wiley & Sons, Inc. Left Atrium  About the same thickness as right atrium  Receives blood from the lungs through pulmonary veins  Passes through bicuspid/ mitral/ left atrioventricular valve into left ventricle 2/7/200917

18. Copyright 2009, John Wiley & Sons, Inc. Left Ventricle  Thickest chamber of the heart  Forms apex  Chordae tendinae attached to papillary muscles  Blood passes through aortic valve (aortic semilunar valve) into ascending aorta  Some blood flows into coronary arteries, remainder to body  During fetal life ductus arteriosus shunts blood from pulmonary trunk to aorta (lung bypass) closes after birth with remnant called ligamentum arteriosum 2/7/200918

19. Copyright 2009, John Wiley & Sons, Inc. Myocardial thickness  Thin-walled atria deliver blood under less pressure to ventricles  Right ventricle pumps blood to lungs Shorter distance, lower pressure, less resistance  Left ventricle pumps blood to body Longer distance, higher pressure, more resistance  Left ventricle works harder to maintain same rate of blood flow as right ventricle 2/7/200919

20. Copyright 2009, John Wiley & Sons, Inc. Fibrous skeleton  Dense connective tissue that forms a (1) structural foundation, (2) point of insertion for muscle bundles, and (3) electrical insulator between atria and ventricles 2/7/200920

21. Copyright 2009, John Wiley & Sons, Inc. Heart Valves and Circulation of Blood Atrioventricular valves  Tricuspid and bicuspid valves  Atria contracts/ ventricle relaxed AV valve opens, cusps project into ventricle In ventricle, papillary muscles are relaxed and chordae tendinae slack  Atria relaxed/ ventricle contracts Pressure drives cusps upward until edges meet and close opening Papillary muscles contract tightening chordae tendinae  Prevents regurgitation 2/7/200921

22. Copyright 2009, John Wiley & Sons, Inc. 2/7/200922

23. Copyright 2009, John Wiley & Sons, Inc. Semilunar valves  Aortic and pulmonary valves  Valves open when pressure in ventricle exceeds pressure in arteries  As ventricles relax, some backflow permitted but blood fills valve cusps closing them tightly  How blood is passed to coronary arteries No valves guarding entrance to atria  As atria contracts, compresses and closes opening 2/7/200923

24. 20_06d

25. All valves with atria removed; Semilunars closed 2/7/2009 Copyright 2009, John Wiley & Sons, Inc. 25

26. Copyright 2009, John Wiley & Sons, Inc. Systemic and pulmonary circulation - 2 circuits in series  Systemic circuit Left side of heart Receives blood from lungs Ejects blood into aorta Systemic arteries, arterioles Gas and nutrient exchange in systemic capillaries Systemic venules and veins lead back to right atrium  Superior vena cava, inferior vena cava, and coronary sinus  Pulmonary circuit Right side of heart Receives blood from systemic circulation Ejects blood into pulmonary trunk then pulmonary arteries Gas exchange in pulmonary capillaries Pulmonary veins takes blood to left atrium 2/7/200926

27. Copyright 2009, John Wiley & Sons, Inc. 2/7/200927

28. Copyright 2009, John Wiley & Sons, Inc. Coronary circulation  Myocardium has its own network of blood vessels  Coronary arteries branch from ascending aorta Anastomoses provide alternate routes or collateral circuits Allows heart muscle to receive sufficient oxygen even if an artery is partially blocked  Coronary capillaries  Coronary veins Collects in coronary sinus Empties into right atrium 2/7/200928

29. Copyright 2009, John Wiley & Sons, Inc. Coronary Circulation 2/7/200929

30. Copyright 2009, John Wiley & Sons, Inc. Cardiac Muscle Tissue and the Cardiac Conduction System Histology  Shorter and less circular than skeletal muscle fibers  But striated like skeletal muscle  Branching gives “stair-step” appearance  Usually one centrally located nucleus  Ends of fibers connected by intercalated discs  Discs contain desmosomes (hold fibers together) and gap junctions (allow action potential conduction from one fiber to the next)  Mitochondria are larger and more numerous than skeletal muscle  Same arrangement of actin and myosin 2/7/200930

31. Copyright 2009, John Wiley & Sons, Inc. 2/7/200931

32. Copyright 2009, John Wiley & Sons, Inc. Autorhythmic Fibers  Specialized cardiac muscle fibers  Self-excitable  Repeatedly generate action potentials that trigger heart contractions  2 important functions 1.Act as pacemaker 2.Form conduction system 2/7/200932

33. Copyright 2009, John Wiley & Sons, Inc. Conduction system 1. Begins in sinoatrial (SA) node in right atrial wall; at junction with SVC Unstable resting potential; depolarize to threshold spontaneously Spontaneous depolarization = pacemaker potential Propagates action potential through atria via gap junctions Atria contact 2. Reaches atrioventricular (AV) node in interatrial septum; just anterior to coronary sinus 2/7/200933

34. Copyright 2009, John Wiley & Sons, Inc. Conduction system 3. Enters atrioventricular (AV) bundle (Bundle of His) Only site where action potentials can conduct from atria to ventricles; elsewhere, fibrous skeleton electrically insulates the atria from the ventricles 4. Enters right and left bundle branches which extends through interventricular septum toward apex 5. Finally, large diameter Purkinje fibers rapidly conduct action potential to remainder of ventricular myocardium Ventricles contract; pushing blood up and out 2/7/200934

35. Frontal plane Right atrium Right ventricle Left atrium Left ventricle Anterior view of frontal section Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE 1 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE 1 2 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) 1 2 3 Right atrium Right ventricle Frontal plane Left atrium Left ventricle Anterior view of frontal section SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES 1 2 3 4 Right atrium Right ventricle Frontal plane SINOATRIAL (SA) NODE ATRIOVENTRICULAR (AV) NODE Left atrium Left ventricle Anterior view of frontal section ATRIOVENTRICULAR (AV) BUNDLE (BUNDLE OF HIS) RIGHT AND LEFT BUNDLE BRANCHES PURKINJE FIBERS 1 2 3 4 5 Right atrium Right ventricle 2/7/200935

36. Copyright 2009, John Wiley & Sons, Inc. Conduction System SA node acts as natural pacemaker  Faster than other autorhythmic fibers  Initiates 100 times per second Nerve impulses from autonomic nervous system (ANS) and hormones modify timing and strength of each heartbeat  Do not establish fundamental rhythm 2/7/200936

37. Copyright 2009, John Wiley & Sons, Inc. Action Potentials and Contraction  Action potential initiated by SA node spreads out to excite “working” fibers called contractile fibers 1.Depolarization 2.Plateau 3.Repolarization 2/7/200937

38. Copyright 2009, John Wiley & Sons, Inc. Action Potentials and Contraction 1.Depolarization – contractile fibers have stable resting membrane potential Voltage-gated fast Na + channels open – Na + flows in Then deactivate and Na + inflow decreases 2.Plateau – period of maintained depolarization Due in part to opening of voltage-gated slow Ca 2+ channels – Ca 2+ moves from interstitial fluid into cytosol Ultimately triggers contraction Depolarization sustained due to voltage-gated K + channels balancing Ca 2+ inflow with K + outflow 2/7/200938

39. Copyright 2009, John Wiley & Sons, Inc. Action Potentials and Contraction 3.Repolarization – recovery of resting membrane potential  Resembles that in other excitable cells  Additional voltage-gated K + channels open  Outflow K + of restores negative resting membrane potential  Calcium channels closing 4.Refractory period – time interval during which second contraction cannot be triggered  Lasts longer than contraction itself  Tetanus (maintained contraction) cannot occur  Blood flow would cease 2/7/200939

40. DepolarizationRepolarization Refractory period Contraction Membrane potential (mV) Rapid depolarization due to Na + inflow when voltage-gated fast Na + channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 1 1 DepolarizationRepolarization Refractory period Contraction Membrane potential (mV) Rapid depolarization due to Na + inflow when voltage-gated fast Na + channels open Plateau (maintained depolarization) due to Ca 2+ inflow when voltage-gated slow Ca 2+ channels open and K + outflow when some K + channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 1 1 2 DepolarizationRepolarization Refractory period Contraction Membrane potential (mV) Repolarization due to closure of Ca 2+ channels and K + outflow when additional voltage-gated K + channels open Rapid depolarization due to Na + inflow when voltage-gated fast Na + channels open Plateau (maintained depolarization) due to Ca 2+ inflow when voltage-gated slow Ca 2+ channels open and K + outflow when some K + channels open 0.3 sec + 20 0 –20 –40 – 60 – 80 –100 2 1 3 1 2 3 Action Potential in a ventricular contractile fiber

41. Copyright 2009, John Wiley & Sons, Inc. Electrocardiogram  ECG or EKG  Composite record of action potentials produced by all the heart muscle fibers  Compare tracings from different leads with one another and with normal records  3 recognizable waves P, QRS, and T 2/7/200941

42. Copyright 2009, John Wiley & Sons, Inc. Correlation of ECG Waves and Systole Systole – contraction / diastole – relaxation 1.Cardiac action potential arises in SA node P wave appears 2.Atrial contraction/ atrial systole 3.Action potential enters AV bundle and out over ventricles QRS complex Masks atrial repolarization 4.Contraction of ventricles / ventricular systole Begins shortly after QRS complex appears and continues during S-T segment 5.Repolarization of ventricular fibers T wave 6.Ventricular relaxation / diastole 2/7/200942

43. 1 Depolarization of atrial contractile fibers produces P wave 0.20 Seconds Action potential in SA node P 1 Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.20 Seconds 0.20 Seconds Action potential in SA node P P 2 1 Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.20.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P 2 3 P 1 Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.20.40 Seconds 0.20.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P 2 3 4 P 1 5 Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.20.40 Seconds 0.20.40 Seconds 0.20.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T 2 3 4 5 P 1 6 Ventricular diastole (relaxation) 5 Repolarization of ventricular contractile fibers produces T wave Ventricular systole (contraction) Depolarization of ventricular contractile fibers produces QRS complex Atrial systole (contraction) Depolarization of atrial contractile fibers produces P wave 0.60.20.400.8 Seconds 0.60.20.40 Seconds 0.20.40 Seconds 0.20.40 Seconds 0.20 Seconds 0.20 Seconds Action potential in SA node R S Q P P P P T P 2 3 4 5 6 P 2/7/200943 Copyright 2009, John Wiley & Sons, Inc.

44. Cardiac Cycle All events associated with one heartbeat Systole and diastole of atria and ventricles In each cycle, atria and ventricles alternately contract and relax  During atrial systole, ventricles are relaxed  During ventricle systole, atria are relaxed Forces blood from higher pressure to lower pressure During relaxation period, both atria and ventricles are relaxed  The faster the heart beats, the shorter the relaxation period  Systole and diastole lengths shorten slightly 2/7/200944

45. 1 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 1 Atrial depolarization 1 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 2 1 2 Atrial depolarization Begin atrial systole 1 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle End (ventricular) diastolic volume 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 2 3 1 2 3 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 4 1 2 3 4 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization End (ventricular) diastolic volume 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 4 5 1 2 3 4 5 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction End (ventricular) diastolic volume 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 4 6 1 2 3 4 5 6 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction Begin ventricular ejection End (ventricular) diastolic volume 5 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle Stroke volume 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 4 7 1 2 3 4 5 6 7 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction Begin ventricular ejection End (ventricular) systolic volume End (ventricular) diastolic volume 6 5 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle Stroke volume 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 8 1 2 3 4 5 6 7 8 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction Begin ventricular ejection End (ventricular) systolic volume Begin ventricular repolarization End (ventricular) diastolic volume 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle Stroke volume 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 8 9 1 2 3 4 5 6 7 8 9 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction Begin ventricular ejection End (ventricular) systolic volume Begin ventricular repolarization Isovolumetric relaxation End (ventricular) diastolic volume 0 20 40 60 80 100 120 (d) Volume in ventricle (mL) (c) Heart sounds (b) Pressure (mmHg) (a) ECG P R Q S Dicrotic wave Left atrial pressure Aortic pressure Left ventricular pressure T 130 60 0 Atrial contraction Atrial contraction Isovolumetric contraction Isovolumetric relaxation Ventricular ejection Ventricular filling (e) Phases of the cardiac cycle Stroke volume 0.3 sec 0.1 sec 0.4 sec Ventricular systole Relaxation period Atrial systole S1S2S3S4 10 1 2 3 4 5 6 7 8 9 Atrial depolarization Begin atrial systole End (ventricular) diastolic volume Ventricular depolarization Isovolumetric contraction Begin ventricular ejection End (ventricular) systolic volume Begin ventricular repolarization Isovolumetric relaxation Ventricular filling End (ventricular) diastolic volume 8 9 2/7/200945

46. Copyright 2009, John Wiley & Sons, Inc. Heart Sounds Auscultation Sound of heartbeat comes primarily from blood turbulence caused by closing of heart valves 4 heart sounds in each cardiac cycle – only 2 loud enough to be heard  Lubb – AV valves close  Dupp – SL valves close S3 due to blood turbulence during rapid ventricular filling S4 from blood turbulence during atrial systole 2/7/200946

47. Copyright 2009, John Wiley & Sons, Inc. Cardiac Output CO = volume of blood ejected from left (or right) ventricle into aorta (or pulmonary trunk) each minute CO = stroke volume (SV) x heart rate (HR) In typical resting male  5.25L/min = 70mL/beat x 75 beats/min Entire blood volume flows through pulmonary and systemic circuits each minute Cardiac reserve – difference between maximum CO and CO at rest  Average cardiac reserve 4-5 times resting value 2/7/200947

48. Copyright 2009, John Wiley & Sons, Inc. Regulation of stroke volume  3 factors ensure left and right ventricles pump equal volumes of blood 1.Preload 2.Contractility 3.Afterload 2/7/200948

49. Copyright 2009, John Wiley & Sons, Inc. Preload  Degree of stretch on the heart before it contracts  Greater preload increases the force of contraction  Frank-Starling law of the heart – the more the heart fills with blood during diastole, the greater the force of contraction during systole Preload proportional to end-diastolic volume (EDV)  2 factors determine EDV 1. Duration of ventricular diastole 2. Venous return – volume of blood returning to right ventricle 2/7/200949

50. Copyright 2009, John Wiley & Sons, Inc. Contractility  Strength of contraction at any given preload  Positive inotropic agents increase contractility Often promote Ca 2+ inflow during cardiac action potential Increases stroke volume Epinephrine, norepinephrine, digitalis  Negative inotropic agents decrease contractility Anoxia, acidosis, some anesthetics, and increased K + in interstitial fluid 2/7/200950

51. Copyright 2009, John Wiley & Sons, Inc. Afterload  Pressure that must be overcome before a semilunar valve can open  Increase in afterload causes stroke volume to decrease Blood remains in ventricle at the end of systole  Hypertension and atherosclerosis increase afterload 2/7/200951

52. Copyright 2009, John Wiley & Sons, Inc. Regulation of Heart Beat  Cardiac output depends on heart rate and stroke volume  Adjustments in heart rate important in short-term control of cardiac output and blood pressure  Autonomic nervous system and epinephrine/ norepinephrine most important 2/7/200952

53. Copyright 2009, John Wiley & Sons, Inc. Autonomic regulation  Originates in cardiovascular center of medulla oblongata  Increases or decreases frequency of nerve impulses in both sympathetic and parasympathetic branches of ANS  Norepinephrine has 2 separate effects In SA and AV node speeds rate of spontaneous depolarization In contractile fibers enhances Ca 2+ entry increasing contractility  Parasympathetic nerves release acetylcholine which decreases heart rate by slowing rate of spontaneous depolarization 2/7/200953

54. Copyright 2009, John Wiley & Sons, Inc. Nervous System Control of the Heart 2/7/200954

55. Copyright 2009, John Wiley & Sons, Inc. Chemical regulation of heart rate  Hormones Epinephrine and norepinephrine increase heart rate and contractility Thyroid hormones also increase heart rate and contractility  Cations Ionic imbalance can compromise pumping effectiveness Relative concentration of K +, Ca 2+ and Na + important 2/7/200955

56. Copyright 2009, John Wiley & Sons, Inc. 2/7/200956

57. Clinical Connections Pericarditis p. 720 Myocarditis and endocarditis p. 720 Myocardial ischemia and infarction p. 730 Heart murmurs p. 740 Congestive heart failure p. 742 2/7/2009 Copyright 2009, John Wiley & Sons, Inc. 57

58. Disorders: Homeostatic imbalances Coronary artery disease pp. 750-752 Arrhythmias pp. 753-755 2/7/2009 Copyright 2009, John Wiley & Sons, Inc. 58

59. Copyright 2009, John Wiley & Sons, Inc. End of Chapter 20 Copyright 2009 John Wiley & Sons, Inc. All rights reserved. Reproduction or translation of this work beyond that permitted in section 117 of the 1976 United States Copyright Act without express permission of the copyright owner is unlawful. Request for further information should be addressed to the Permission Department, John Wiley & Sons, Inc. The purchaser may make back-up copies for his/her own use only and not for distribution or resale. The Publishers assumes no responsibility for errors, omissions, or damages caused by the use of theses programs or from the use of the information herein. 2/7/200959