1. 1 Chapter 19 Lecture Outline See PowerPoint Image Slides for all figures and tables pre-inserted into PowerPoint without notes. Copyright (c) The McGraw-Hill Companies, Inc. Permission required for reproduction or display.

2. 2 Circulatory System: The Heart  Gross anatomy of the heart  Overview of cardiovascular system  Cardiac conduction system and cardiac muscle  Electrical and contractile activity of heart  Blood flow, heart sounds, and cardiac cycle  Cardiac output

3. 3 Circulatory System: The Heart  Circulatory system heart, blood vessels and blood heart, blood vessels and blood  Cardiovascular system heart, arteries, veins and capillaries heart, arteries, veins and capillaries Two major divisions:  Pulmonary circuit - right side of heart carries blood to lungs for gas exchange carries blood to lungs for gas exchange  Systemic circuit - left side of heart supplies blood to all organs of the body supplies blood to all organs of the body

4. 4 Cardiovascular System Circuit

5. 5 Position, Size, and Shape  Located in mediastinum, between lungs  Base - broad superior portion of heart  Apex - inferior end, tilts to the left, tapers to point

6. 6 Heart Position

7. 7 Pericardium  Allows heart to beat without friction, room to expand and resists excessive expansion  Parietal pericardium outer, tough, fibrous layer of CT outer, tough, fibrous layer of CT  Pericardial cavity filled with pericardial fluid filled with pericardial fluid  Visceral pericardium (a.k.a. epicardium of heart wall) inner, thin, smooth, moist serous layer inner, thin, smooth, moist serous layer covers heart surface covers heart surface

8. 8 Pericardium and Heart Wall Pericardial cavity contains 5-30 ml of pericardial fluid

9. 9 Heart Wall  Epicardium (a.k.a. visceral pericardium) serous membrane covers heart serous membrane covers heart  Myocardium thick muscular layer thick muscular layer fibrous skeleton - network of collagenous and elastic fibers fibrous skeleton - network of collagenous and elastic fibers provides structural support and attachment for cardiac muscleprovides structural support and attachment for cardiac muscle electrical nonconductor, important in coordinating contractile activityelectrical nonconductor, important in coordinating contractile activity  Endocardium - smooth inner lining

10. 10 Heart Chambers  4 chambers right and left atria right and left atria two superior, posterior chamberstwo superior, posterior chambers receive blood returning to heartreceive blood returning to heart right and left ventricles right and left ventricles two inferior chamberstwo inferior chambers pump blood into arteriespump blood into arteries

11. 11 External Anatomy - Anterior

12. 12 External Anatomy - Posterior

13. 13 Heart Chambers - Internal  Interatrial septum wall that separates atria wall that separates atria  Pectinate muscles internal ridges of myocardium in right atrium and both auricles internal ridges of myocardium in right atrium and both auricles  Interventricular septum wall that separates ventricles wall that separates ventricles  Trabeculae carneae internal ridges in both ventricles internal ridges in both ventricles

14. 14 Internal Anatomy - Anterior

15. 15 Heart Valves  Atrioventricular (AV) valves right AV valve has 3 cusps (tricuspid valve) right AV valve has 3 cusps (tricuspid valve) left AV valve has 2 cusps (mitral, bicuspid valve) left AV valve has 2 cusps (mitral, bicuspid valve) chordae tendineae - cords connect AV valves to papillary muscles (on floor of ventricles) chordae tendineae - cords connect AV valves to papillary muscles (on floor of ventricles)  Semilunar valves - control flow into great arteries pulmonary: right ventricle into pulmonary trunk pulmonary: right ventricle into pulmonary trunk aortic: from left ventricle into aorta aortic: from left ventricle into aorta

16. 16 Heart Valves

17. 17 Heart Valves

18. 18 AV Valve Mechanics  Ventricles relax pressure drops pressure drops semilunar valves close semilunar valves close AV valves open AV valves open blood flows from atria to ventricles blood flows from atria to ventricles  Ventricles contract AV valves close AV valves close pressure rises pressure rises semilunar valves open semilunar valves open blood flows into great vessels blood flows into great vessels

19. 19 Operation of Atrioventricular Valves

20. 20 Operation of Semilunar Valves

21. 21 Blood Flow Through Heart

22. 22 Coronary Circulation  Left coronary artery (LCA) anterior interventricular branch anterior interventricular branch supplies blood to interventricular septum and anterior walls of ventriclessupplies blood to interventricular septum and anterior walls of ventricles circumflex branch circumflex branch passes around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventriclepasses around left side of heart in coronary sulcus, supplies left atrium and posterior wall of left ventricle  Right coronary artery (RCA) right marginal branch right marginal branch supplies lateral R atrium and ventriclesupplies lateral R atrium and ventricle posterior interventricular branch posterior interventricular branch supplies posterior walls of ventriclessupplies posterior walls of ventricles

23. 23 Coronary Vessels - Anterior

24. 24 Venous Drainage of Heart  20% drains directly into all 4 chambers via the thebesian veins  80% returns to right atrium via: great cardiac vein great cardiac vein blood from anterior interventricular sulcusblood from anterior interventricular sulcus middle cardiac vein middle cardiac vein from posterior sulcusfrom posterior sulcus left marginal vein left marginal vein coronary sinus coronary sinus collects blood and empties into right atriumcollects blood and empties into right atrium

25. 25 Coronary Vessels - Posterior

26. 26 Angina and Heart Attack  Angina pectoris partial obstruction of coronary blood flow can cause chest pain partial obstruction of coronary blood flow can cause chest pain pain caused by ischemia, often activity dependent pain caused by ischemia, often activity dependent  Myocardial infarction complete obstruction causes death of cardiac cells in affected area complete obstruction causes death of cardiac cells in affected area pain or pressure in chest that often radiates down left arm pain or pressure in chest that often radiates down left arm

27. 27 Nerve Supply to Heart  Sympathetic nerves from upper thoracic spinal cord, through sympathetic chain to cardiac nerves upper thoracic spinal cord, through sympathetic chain to cardiac nerves directly to ventricular myocardium directly to ventricular myocardium can raise heart rate to 230 bpm can raise heart rate to 230 bpm  Parasympathetic nerves right vagal nerve to SA node right vagal nerve to SA node left vagal nerve to AV node left vagal nerve to AV node vagal tone – normally slows heart rate to 70 - 80 bpm vagal tone – normally slows heart rate to 70 - 80 bpm

28. 28 Cardiac Conduction System  Properties myogenic - heartbeat originates within heart myogenic - heartbeat originates within heart autorhythmic – regular, spontaneous depolarization autorhythmic – regular, spontaneous depolarization  Components next slide next slide

29. 29 Cardiac Conduction System  SA node: pacemaker, initiates heartbeat, sets heart rate  fibrous skeleton insulates atria from ventricles  AV node: electrical gateway to ventricles  AV bundle: pathway for signals from AV node  Right and left bundle branches: divisions of AV bundle that enter interventricular septum  Purkinje fibers: upward from apex spread throughout ventricular myocardium

30. 30 Cardiac Conduction System

31. 31 Structure of Cardiac Muscle  Short, branched cells, one central nucleus   Sarcoplasmic reticulum, large T-tubules admit more Ca 2+ from ECF admit more Ca 2+ from ECF  Intercalated discs join myocytes end to end interdigitating folds -  surface area interdigitating folds -  surface area mechanical junctions tightly join myocytes mechanical junctions tightly join myocytes electrical junctions - gap junctions allow ions to flow electrical junctions - gap junctions allow ions to flow

32. 32 Structure of Cardiac Muscle Cell

33. 33 Metabolism of Cardiac Muscle  Aerobic respiration  Rich in myoglobin and glycogen  Large mitochondria  Organic fuels: fatty acids, glucose, ketones  Fatigue resistant

34. 34 Cardiac Rhythm  Systole – ventricular contraction  Diastole - ventricular relaxation  Sinus rhythm set by SA node at 60 – 100 bpm set by SA node at 60 – 100 bpm adult at rest is 70 to 80 bpm (vagal inhibition) adult at rest is 70 to 80 bpm (vagal inhibition)

35. 35 Depolarization of SA Node  SA node - no stable resting membrane potential  Pacemaker potential gradual depolarization from -60 mV, slow influx of Na + gradual depolarization from -60 mV, slow influx of Na +  Action potential occurs at threshold of -40 mV occurs at threshold of -40 mV depolarizing phase to 0 mV depolarizing phase to 0 mV fast Ca 2+ channels open, (Ca 2+ in)fast Ca 2+ channels open, (Ca 2+ in) repolarizing phase repolarizing phase K + channels open, (K + out)K + channels open, (K + out) at -60 mV K + channels close, pacemaker potential starts overat -60 mV K + channels close, pacemaker potential starts over  Each depolarization creates one heartbeat SA node at rest fires at 0.8 sec, about 75 bpm SA node at rest fires at 0.8 sec, about 75 bpm

36. 36 SA Node Potentials

37. 37 Impulse Conduction to Myocardium  SA node signal travels at 1 m/sec through atria  AV node slows signal to 0.05 m/sec thin myocytes with fewer gap junctions thin myocytes with fewer gap junctions delays signal 100 msec, allows ventricles to fill delays signal 100 msec, allows ventricles to fill  AV bundle and purkinje fibers speeds signal along at 4 m/sec to ventricles speeds signal along at 4 m/sec to ventricles  Ventricular systole begins at apex, progresses up spiral arrangement of myocytes twists ventricles slightly spiral arrangement of myocytes twists ventricles slightly

38. 38 Contraction of Myocardium  Myocytes have stable resting potential of -90 mV  Depolarization (very brief) stimulus opens voltage regulated Na + gates, (Na + rushes in) membrane depolarizes rapidly stimulus opens voltage regulated Na + gates, (Na + rushes in) membrane depolarizes rapidly action potential peaks at +30 mV action potential peaks at +30 mV Na + gates close quickly Na + gates close quickly  Plateau - 200 to 250 msec, sustains contraction slow Ca 2+ channels open, Ca 2+ binds to fast Ca 2+ channels on SR, releases  Ca 2+ into cytosol: contraction slow Ca 2+ channels open, Ca 2+ binds to fast Ca 2+ channels on SR, releases  Ca 2+ into cytosol: contraction  Repolarization - Ca 2+ channels close, K + channels open, rapid K + out returns to resting potential

39. 39 Action Potential of Myocyte 1) Na + gates open 2) Rapid depolarization 3) Na + gates close 4) Slow Ca 2+ channels open 5) Ca 2+ channels close, K + channels open

40. 40 Electrocardiogram (ECG)  Composite of all action potentials of nodal and myocardial cells detected, amplified and recorded by electrodes on arms, legs and chest

41. 41 ECG  P wave SA node fires, atrial depolarization SA node fires, atrial depolarization atrial systole atrial systole  QRS complex ventricular depolarization ventricular depolarization (atrial repolarization and diastole - signal obscured) (atrial repolarization and diastole - signal obscured)  ST segment - ventricular systole  T wave ventricular repolarization ventricular repolarization

42. 42 Normal Electrocardiogram (ECG)

43. 43 1) atrial depolarization begins 2) atrial depolarization complete (atria contracted) 3) ventricles begin to depolarize at apex; atria repolarize (atria relaxed) 4) ventricular depolarization complete (ventricles contracted) 5) ventricles begin to repolarize at apex 6) ventricular repolarization complete (ventricles relaxed) Electrical Activity of Myocardium

44. 44 Diagnostic Value of ECG  Invaluable for diagnosing abnormalities in conduction pathways, MI, heart enlargement and electrolyte and hormone imbalances

45. 45 ECGs, Normal and Abnormal

46. 46 Cardiac Cycle  One complete contraction and relaxation of all 4 chambers of the heart  Atrial systole, Ventricle diastole  Atrial diastole, Ventricle systole  Quiescent period

47. 47  Resistance opposes flow great vessels have positive blood pressure great vessels have positive blood pressure ventricular pressure must rise above this resistance for blood to flow into great vessels ventricular pressure must rise above this resistance for blood to flow into great vessels Principles of Pressure and Flow  Pressure causes a fluid to flow pressure gradient - pressure difference between two points pressure gradient - pressure difference between two points

48. 48 Heart Sounds  Auscultation - listening to sounds made by body  First heart sound (S 1 ), louder and longer “lubb”, occurs with closure of AV valves  Second heart sound (S 2 ), softer and sharper “dupp” occurs with closure of semilunar valves

49. 49 Phases of Cardiac Cycle  Quiescent period all chambers relaxed all chambers relaxed AV valves open and blood flowing into ventricles AV valves open and blood flowing into ventricles  Atrial systole SA node fires, atria depolarize SA node fires, atria depolarize P wave appears on ECG P wave appears on ECG atria contract, force additional blood into ventricles atria contract, force additional blood into ventricles ventricles now contain end-diastolic volume (EDV) of about 130 ml of blood ventricles now contain end-diastolic volume (EDV) of about 130 ml of blood

50. 50 Isovolumetric Contraction of Ventricles  Atria repolarize and relax  Ventricles depolarize  QRS complex appears in ECG  Ventricles contract  Rising pressure closes AV valves - heart sound S1 occurs  No ejection of blood yet (no change in volume)

51. 51 Ventricular Ejection  Rising pressure opens semilunar valves  Rapid ejection of blood  Reduced ejection of blood (less pressure)  Stroke volume: amount ejected, 70 ml at rest  End-systolic volume: amount left in heart

52. 52 Ventricles- Isovolumetric Relaxation  T wave appears in ECG  Ventricles repolarize and relax (begin to expand)  Semilunar valves close (dicrotic notch of aortic press. curve) - h eart sound S 2 occurs  AV valves remain closed  Ventricles expand but do not fill (no change in volume)

53. 53 Major Events of Cardiac Cycle  Quiescent period  Ventricular filling  Isovolumetric contraction  Ventricular ejection  Isovolumetric relaxation

54. 54 Events of the Cardiac Cycle

55. 55 Cardiac Output (CO)  Amount ejected by ventricle in 1 minute  Cardiac Output = Heart Rate x Stroke Volume about 4 to 6L/min at rest about 4 to 6L/min at rest vigorous exercise  CO to 21 L/min for fit person and up to 35 L/min for world class athlete vigorous exercise  CO to 21 L/min for fit person and up to 35 L/min for world class athlete  Cardiac reserve: difference between a persons maximum and resting CO  with fitness,  with disease  with fitness,  with disease

56. 56 Heart Rate  Pulse = surge of pressure in artery infants have HR of 120 bpm or more infants have HR of 120 bpm or more young adult females avg. 72 - 80 bpm young adult females avg. 72 - 80 bpm young adult males avg. 64 to 72 bpm young adult males avg. 64 to 72 bpm HR rises again in the elderly HR rises again in the elderly  Tachycardia: resting adult HR above 100 stress, anxiety, drugs, heart disease or  body temp. stress, anxiety, drugs, heart disease or  body temp.  Bradycardia: resting adult HR < 60 in sleep and endurance trained athletes in sleep and endurance trained athletes

57. 57 Inputs to Cardiac Center  Higher brain centers affect HR cerebral cortex, limbic system, hypothalamus cerebral cortex, limbic system, hypothalamus sensory or emotional stimuli (rollercoaster, IRS audit)sensory or emotional stimuli (rollercoaster, IRS audit)  Proprioceptors inform cardiac center about changes in activity, HR  before metabolic demands arise inform cardiac center about changes in activity, HR  before metabolic demands arise  Baroreceptors signal cardiac center aorta and internal carotid arteries aorta and internal carotid arteries pressure , signal rate drops, cardiac center  HRpressure , signal rate drops, cardiac center  HR if pressure , signal rate rises, cardiac center  HRif pressure , signal rate rises, cardiac center  HR

58. 58 Inputs to Cardiac Center  Chemoreceptors sensitive to blood pH, CO 2 and oxygen sensitive to blood pH, CO 2 and oxygen aortic arch, carotid arteries and medulla oblongata aortic arch, carotid arteries and medulla oblongata primarily respiratory control, may influence HR primarily respiratory control, may influence HR  CO 2 (hypercapnia) causes  H + levels, may create acidosis (pH < 7.35)  CO 2 (hypercapnia) causes  H + levels, may create acidosis (pH < 7.35) Hypercapnia and acidosis stimulates cardiac center to  HR Hypercapnia and acidosis stimulates cardiac center to  HR

59. 59 Stroke Volume (SV)  Governed by three factors: 1. preload 2. contractility 3. afterload  Example  preload or contractility causes  SV  preload or contractility causes  SV  afterload causes  SV  afterload causes  SV

60. 60 Preload  Amount of tension in ventricular myocardium before it contracts   preload causes  force of contraction exercise  venous return, stretches myocardium (  preload), myocytes generate more tension during contraction,  CO matches  venous return exercise  venous return, stretches myocardium (  preload), myocytes generate more tension during contraction,  CO matches  venous return  Frank-Starling law of heart - SV  EDV ventricles eject as much blood as they receive ventricles eject as much blood as they receive more they are stretched (  preload) the harder they contractmore they are stretched (  preload) the harder they contract

61. 61 Afterload  Pressure in arteries above semilunar valves opposes opening of valves   afterload  SV any impedance in arterial circulation  afterload any impedance in arterial circulation  afterload  Continuous  in afterload (lung disease, atherosclerosis, etc.) causes hypertrophy of myocardium, may lead it to weaken and fail

62. 62 Exercise and Cardiac Output  Proprioceptors HR  at beginning of exercise due to signals from joints, muscles HR  at beginning of exercise due to signals from joints, muscles  Venous return muscular activity  venous return causes  SV muscular activity  venous return causes  SV   HR and  SV cause  CO  Exercise produces ventricular hypertrophy  SV allows heart to beat more slowly at rest  SV allows heart to beat more slowly at rest  cardiac reserve  cardiac reserve