1. Chapter 20 the heart

2. Anatomy review Electrical activity of the whole heart (EKG) Electrical activity of the heart cells The Cardiac Cycle Cardiac Input and Output (dynamics)

3. Heart review 4 chambers 2 atria 2 ventricles 4 valves 2 AV valves 2 semilunar valves 2 circuits systemic pulmonary receive send

4. fig. 20-9 external heart anatomy

5. fig. 20-6 internal heart anatomy

6. 100 keys (pg. 678) “The heart has four chambers, two associated with the pulmonary circuit (right atrium and right ventricle) and two with the systemic circuit (left atria and left ventricle). The left ventricle has a greater workload and is much more massive than the right ventricle, but the two chambers pump equal amounts of blood. AV valves prevent backflow from the ventricles into the atria, and semilunar valves prevent backflow from the aortic and pulmonary trunks into the ventricles.”

7. cardiac conduction system modified cardiac muscle cells SA node (sinoatrial node) wall of RA AV node (atrioventricular node) between atrium and ventricle conducting cells AV bundle (of His) conducting fibers Purkinje fibers

8. fig. 20-12a conducting system of heart

9. prepotential cannot maintain steady resting potential gradually drift toward threshold SA node80-100 bpm AV node40-60 bpm

10. fig. 20-12b

11. …it controls the heart rate (pacemaker) but heart rate is normally slower than 80-100 bpm (parasympathetics) if SA node is damaged, heart can still continue to beat, but at a slower rate because SA node is faster…

12. if heartbeat is slower than normal… … bradycardia if heartbeat is faster than normal… … tachycardia

13. impulse conduction fig. 20-13

14. impulse conduction SA node atria get signal - contract signal to AV Node AV node sends signal to ventricles (time delay) ventricles contract after atria are done damage to any part of conducting system may result in abnormalities (EKG)

15. ECG’s EKG’s electrocardiagram recording of the electrical activity of the heart (from the surface of the body) fig 20-14

16. ECG’s different components: P wave QRS complex T wave depolarization of the atria depolarization of the ventricles bigger stronger signal repolarization of the ventricles

17. ECG’s fig 20-14 EKG

18. ECG’s to analyze: size of voltage changes duration of changes timing of changes intervals

19. ECG’s fig 20-14 EKG

20. intervals: ECG’s P-R interval from start of atrial depolarization to start of QRS complex if longer than 200 msec can mean damage to conducting system time for signal to get from atrium to ventricles

21. intervals: ECG’s Q-T interval time for ventricular depolarization and repolarization (ventricular systole) if lengthened, may indicate, [ion] disturbances, medications, conducting problems, ischemia, or myocardial damage.

22. intervals: ECG’s T-P interval from end of ventricular repolarization to start of next atrial depolarization the time the “heart” is in diastole the “isoelectric line”

23. T-P interval fig 20-14 EKG

24. intervals: ECG’s abnormalities cardiac electrical activity = cardiac arrhythmias some are not dangerous others indicate damage to heart

25. 100 keys (pg. 688) “The heart rate is normally established by cells of the SA node, but that rate can be modified by autonomic activity, hormones, and other factors. From the SA node the stimulus is conducted to the AV node, the AV bundle, the bundle branches, and Purkinjie fibers before reaching the ventricular muscle cells. The electrical events associated with the heartbeat can be monitored in an electrocardiagram (ECG).”

26. 99 % of heart is contractile cells similar to skeletal muscle AP leads to Ca 2+ around myofibrils Ca 2+ bind to troponin on thin filaments initiates contraction (cross-bridges) Electrical activity of the heart cells but there are differences… nature of AP location of Ca 2+ storage duration of contraction

27. The action potential Electrical activity of the heart cells resting potential of heart cells ~ -90mV threshold is reached near intercalated discs signal is AP in an adjacent cell (gap junctions)

28. The action potential Electrical activity of the heart cells review skeletal muscle fig. 20-15

29. The action potential Electrical activity of the heart cells once threshold is reached the action potential proceeds in three steps.

30. The action potential - step 1 Electrical activity of the heart cells rapid depolarization (like skeletal muscle) Na + into cell through voltage-gated channels (fast channels)

31. The action potential - step 2 Electrical activity of the heart cells the plateau Na + channels close Ca 2+ channels open for a “long” time (slow calcium channels) Ca 2+ in balances Na + pumped out

32. The action potential - step 3 Electrical activity of the heart cells repolarization Ca 2+ channels begin closing slow K + channels begin opening K + rushes out restoring resting pot.

33. The action potential - step 3 Electrical activity of the heart cells Na + channels are still inactive cell will not respond to stimulus = refractory period repolarization

34. fig. 20-15a

35. The role of calcium Electrical activity of the heart cells extracellular Ca 2+ enters cells during the plateau phase (20%) Ca 2+ entering triggers release of Ca 2+ from sarcoplasmic reticulum... heart is highly sensitive to changes in [Ca 2+ ] of the ECF

36. The role of calcium Electrical activity of the heart cells in skeletal muscle, refractory period ended before peak tension developed… …summation was possible …tetanus. in cardiac muscle refractory period lasts until relaxation has begun… …no summation …no tetanus.

37. Clinical note:Heart attacks blockage of coronary vessels myocardium without blood supply… …cells die (infarction) myocardial infarction (MI) = heart attack

38. Clinical note:Heart attacks blockage of coronary vessels due to: CAD (coronary artery disease) (plaque in vessel wall) blocked by clot (thrombosis)

39. Clinical note:Heart attacks blockage of coronary vessels as O 2 levels fall, cardiac cells will: accumulate anaerobic enzymes die and release enzymes LDH SGOT CPK CK-MB lactose dehydrogenase serum glutamic oxaloacetic transaminase creatine phosphokinase cardiac muscle creatine phosphokinase

40. to here 3/26 lec # 31

41. Clinical note:Heart attacks anticoagulants(aspirin) clot-dissolving enzymes quick treatment will help reduce damage due to blockage

42. Clinical note:Heart attacks risk factors: smoking high blood pressure high blood cholesterol high [LDL] diabetes male severe emotional stress obesity genetic predisposition sedentary lifestyle any 2 more than doubles your risk of MI

43. The cardiac cycle contraction (systole) relax (diastole) fluid (blood) moves always moves from higher pressure… …toward lower pressure

44. fig. 20-16

45. The cardiac cycle atrial systole atrial diastole ventricular systole ventricular diastole generic heart rate 75 bpm together

46. fig. 20-17

47. The cardiac cycle atrial systole (100 msec) blood in atria is pushed through AV valves into ventricles “tops off” the ventricles blood in ventricles is called EDV (end diastolic volume) (follows path of least resistance) 1+2 3… end of atrial systole ventricular diastole begins

48. The cardiac cycle ventricular systole (270 msec) pressure start to rise in ventricle when it is greater than pressure in atria, the AV valves will close (chordae tendineae and papillary m.) pressure continues to build until it can force open the semilunar valves “lubb” …3 4

49. The cardiac cycle ventricular systole (270 msec) up until now, ventricles have been contracting but no blood has flowed: isovolumetric contraction ventricular volume has not changed but the pressure has increased 4

50. The cardiac cycle ventricular systole (270 msec) when pressure in ventricle is greater than pressure in the arteries, the semilunar valves will open ventricular ejection stroke volume some blood left behind end systolic volume (ESV) 5

51. The cardiac cycle ventricular systole (270 msec) as pressure drops below that of arteries, the semilunar valves will close again “Dupp” 6

52. The cardiac cycle ventricular diasatole (430 msec) semilunar valves are shut AV valves are shut too (temporarily) isovolumetric relaxation 7 when pressure gets below atrial pressure, AV valves will open and ventricle will begin to fill passively 8

53. fig. 20-17

54. Heart sounds lubb DUPP lubb DUPP auscultation stethoscope

55. Heart sounds lubb closing of the AV valves as ventricular contraction begins

56. Heart sounds DUPP closing of the semilunar valves as ventricular relaxation begins

57. Heart dynamics cardiac output heart rate stroke volume variation & adjustments

58. Heart dynamicsdefinitions EDVend diastolic volume ESVend systolic volume Stroke volume ventricle is full beginning to contract ventricle is done contracting (a little blood left inside) SV = EDV - ESV

59. Heart dynamicsdefinitions cardiac output (CO) CO = HR (heart rate) x SV how much blood the heart pumps in a minute both the SV and the HR can vary

60. Heart dynamics both the SV and the HR can vary fig. 20-20

61. Heart dynamics variation in HR autonomics dual innervation to SA node

62. Heart dynamicsHR parasympathetics releases ACh opens K+ channels lowers the resting potential (hyperpolarize cell) slows heart rate controlled by cardioinhibitory centers in the medulla oblongatat

63. Heart dynamicsHR parasympathetics controlled by cardioinhibitory centers in the medulla oblongata reflexeshypothalamus

64. Normal: Parasympathetics: fig 20-22

65. Heart dynamicsHR sympathetics releases NE binds to beta-1 receptors opens Na + /Ca 2+ channels depolarize cell speeds up heart rate

66. Heart dynamicsHR sympathetics controlled by cardioacceleratory centers in the medulla oblongata reflexeshypothalamus

67. Normal: Sympathetics: fig 20-22

68. Heart dynamicsHR atrial (Bainbridge) reflex increased venous return stretches atria stimulates stretch receptors stimulates sympathetics increase HR (and CO)

69. Heart dynamicsHR hormones E, NE, thyoid hormone affect SA node speed up HR

70. to here 3/30/07 lec# 33

71. Heart dynamics stroke volume (SV) remember SV = EDV - ESV

72. Heart dynamicsSV EDV the amount of blood in the ventricle at the end of its diastolic phase, just before contraction begins.

73. Heart dynamicsSV EDV affected by the filling time & venous return preload

74. Heart dynamicsSV EDV preload the degree of stretching of the ventricle during diastole preload is proportional to EDV preload affects heart muscles ability to generate tension

75. Heart dynamicsSV EDV preload

76. Heart dynamicsSV EDV preload “more in = more out” Frank-Starling principle

77. fig. 20-23

78. Heart dynamicsSV ESV preload contractility afterload

79. Heart dynamicsSV ESV contractility amount of force generated with a contraction increase decrease + inotropic action - inotropic action

80. Heart dynamicsSV ESV contractility factors that influence: ANS hormones

81. Heart dynamicsSV ESV contractility ANS sympathetic NS NE, E + inotropic effect parasympathetic NS ACh - inotropic effect

82. fig. 20-23

83. Heart dynamicsSV ESV contractility hormones (and drugs) NE, E, glucagon, thyroid hormones + inotropic effect dopamine, dobutamine isoproterenol digitalis

84. Heart dynamicsSV ESV contractility hormones (and drugs) propanolol timolol etc., (beta-blockers) - inotropic effect verapamil nifedipine (Ca 2+ blocker) (hypertension)

85. fig. 20-23

86. Heart dynamicsSV ESV preload contractility afterload the amount of tension needed to open semilunar valves and eject blood

87. Heart dynamicsSV ESV afterload the amount of tension needed to open semilunar valves and eject blood greater afterload longer isovolumetric contraction less ejected, larger ESV

88. Heart dynamicsSV ESV afterload restrict blood flow constrict peripheral vessels circulatory blockage inc. afterload

89. fig. 20-23

90. Summary Heart rate EDV ESV SV = EDV-ESV hormones venous return filling time venous return preload contractility afterload

91. 100 keys (pg. 703) “Cardiac output is the amount of blood pumped by the left ventricle each minute. It is adjusted on a moment-to-moment basis by the ANS, and in response to circulating hormones, changes in blood volume, and alternation in venous return. Most healthy people can increase cardiac output by 300-500 percent.”