1. The Heart
Chapter 20

2. Function of the Heart Anatomy of the Heart Pumping the red stuff
Location – mediastinum, slightly to the left of center
Size – about that of your fist
Mass – 250 – 300 g

3. Organization of the Cardiovascular System

4. Location

5. Tissues of the Heart

6. Coverings of the Heart: Anatomy
Pericardium – a double-walled sac around the heart composed of:
A superficial fibrous pericardium
A deep two-layer serous pericardium
The parietal layer lines the internal surface of the fibrous pericardium
The visceral layer or epicardium lines the surface of the heart
They are separated by the fluid-filled pericardial cavity

7. Coverings of the Heart: Physiology
The pericardium:
Protects and anchors the heart
Prevents overfilling of the heart with blood
Allows for the heart to work in a relatively friction-free environment

8. Serous pericardium

9. General Anatomy

10. Heart Wall Epicardium – visceral layer of the serous pericardium
Myocardium – cardiac muscle layer forming the bulk of the heart
Fibrous skeleton of the heart – crisscrossing, interlacing layer of connective tissue
Endocardium – endothelial layer of the inner myocardial surface
Heart Wall

11. External Heart: Major Vessels of the Heart (Anterior View)
Vessels returning blood to the heart include:
Superior and inferior venae cavae
Right and left pulmonary veins
Vessels conveying blood away from the heart include:
Pulmonary trunk, which splits into right and left pulmonary arteries
Ascending aorta (three branches) – brachiocephalic, left common carotid, and subclavian arteries
External Heart: Major Vessels of the Heart (Anterior View)

12. External Heart: Vessels that Supply/Drain the Heart (Anterior View)
Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular arteries
Veins – small cardiac, anterior cardiac, and great cardiac veins
External Heart: Vessels that Supply/Drain the Heart (Anterior View)

13. Surface features of the heart

15. Cardiac Muscle Cells
Figure 20–5

16. External Heart: Major Vessels of the Heart (Posterior View)
Vessels returning blood to the heart include:
Right and left pulmonary veins
Superior and inferior venae cavae
Vessels conveying blood away from the heart include:
Aorta
Right and left pulmonary arteries
External Heart: Major Vessels of the Heart (Posterior View)

17. Posterior view

18. Atria of the Heart Atria are the receiving chambers of the heart
Each atrium has a protruding auricle
Pectinate muscles mark atrial walls
Blood enters right atria from superior and inferior venae cavae and coronary sinus
Blood enters left atria from pulmonary veins

19. Deep in your heart of hearts…

20. Ventricles of the Heart
Ventricles are the discharging chambers of the heart
Papillary muscles and trabeculae carneae muscles mark ventricular walls
Right ventricle pumps blood into the pulmonary trunk
Left ventricle pumps blood into the aorta

22. Note the differences in wall thickness

23. Heart valves ensure unidirectional blood flow through the heart
Atrioventricular (AV) valves lie between the atria and the ventricles
AV valves prevent backflow into the atria when ventricles contract
Chordae tendineae anchor AV valves to papillary muscles
Heart Valves

24. Heart Valves
Aortic semilunar valve lies between the left ventricle and the aorta
Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk
Semilunar valves prevent backflow of blood into the ventricles

25. The heart valves

26. Function of the bicuspid valve

27. Valve functions

29. Heart Sounds

30. Where to go to listen to heart sounds

31. Some heart valve disorders
Stenosis (narrowing) – the inability of a valve to open fully
Insufficiency (incompetence) – failure of the valve to prevent back flow or close properly
Mitral valve prolapse – one or both of the flaps blows back into the atrium during systole (contraction) of the ventricle allowing backflow into the atrium.
The aortic semilunar valves can also suffer from stenosis or insufficiency, allowing backflow into the ventricle.

32. Pathway of Blood Through the Heart and Lungs
Right atrium  tricuspid valve  right ventricle
Right ventricle  pulmonary semilunar valve  pulmonary arteries  lungs
Lungs  pulmonary veins  left atrium
Left atrium  bicuspid valve  left ventricle
Left ventricle  aortic semilunar valve  aorta
Aorta  systemic circulation
Pathway of Blood Through the Heart and Lungs

33. Systemic & pulmonary circuits

34. Blood flow

35. Coronary Circulation
Coronary circulation is the functional blood supply to the heart muscle itself
Collateral routes ensure blood delivery to heart even if major vessels are occluded

36. Coronary Circulation (arterial)

37. Coronary Circulation (venous)

39. Cardiac histology & physiology
Cardiac muscle is made of short, branched fibers
Striated
Uninucleate
There is now some evidence that it has limited mitotic capability (it is likely that regeneration is from migration of stem cells from the blood)
99% are contractile
1% are “autorhythmic” or “pacemaker” cells

40. Cardiac Muscle Tissue

42. Cardiac Muscle Cells Intercalated discs:
interconnect cardiac muscle cells
secured by desmosomes
linked by gap junctions
convey force of contraction
propagate action potentials

43. Characteristics of Cardiac Muscle Cells
Small size
Single, central nucleus
Branching interconnections between cells
Intercalated discs

44. Cardiac Cells vs. Skeletal Fibers
Table 20-1

45. The intrinsic conduction system
Sinoatrial node: the primary pacemaker – has an intrinsic firing rate of about 100 bpm but kept at 60 – 80 by parasympathetic tone
Generates pacemaker potentials from leakage of Ca++
Depolarization spreads via gap junctions in intercalated disks
Rate can be adjusted by ANS

46. Intrinsic conduction system
Signals from SA node travel to the Atrioventricular Node via the internodal pathway
The AV node has its own intrinsic firing rate of 40 – 60 bpm. In absence of SA node function it can establish a “junctional rhythm” that keeps the ventricles working

47. The conducting pathways
The signal is delayed about 0.1 s and then transmitted down the …
Bundle of His or AV bundle and the left & right bundle branches to the apex
And from there the depolarization is distributed by the Purkinje fibers

48. Fig a

50. Contraction of cardiac muscle fibers and the cardiac cycle

51. The Electrocardiogram
Figure 20–14b

52. NSR: Normal Sinus Rhythm

53. Prolonged contraction of cardiac muscle

54. Features of an ECG P wave: atria depolarize QRS complex:
ventricles depolarize
T wave:
ventricles repolarize

55. Resting Potential Of a ventricular cell: about —90 mV
Of an atrial cell:
about —80 mV

56. 3 Steps of Cardiac Action Potential
Rapid depolarization:
voltage-regulated sodium channels (fast channels) open

57. 3 Steps of Cardiac Action Potential
As sodium channels close:
voltage-regulated calcium channels (slow channels) open
balance Na+ ions pumped out
hold membrane at 0 mV plateau

58. 3 Steps of Cardiac Action Potential
Repolarization:
plateau continues
slow calcium channels close
slow potassium channels open
rapid repolarization restores resting potential

59. The Refractory Periods
Absolute refractory period:
long
cardiac muscle cells cannot respond
Relative refractory period:
short
response depends on degree of stimulus

60. Timing of Refractory Periods
Length of cardiac action potential in ventricular cell:
250–300 msecs
30 times longer than skeletal muscle fiber
long refractory period prevents summation and tetany

61. Electrical Activity and the Cardiac Cycle

62. Calcium and Contraction
Contraction of a cardiac muscle cell is produced by an increase in calcium ion concentration around myofibrils

63. 2 Steps of Calcium Ion Concentration
20% of calcium ions required for a contraction:
calcium ions enter cell membrane during plateau phase

64. 2 Steps of Calcium Ion Concentration
Arrival of extracellular Ca2+:
triggers release of calcium ion reserves from sarcoplasmic reticulum

65. Intracellular and Extracellular Calcium
As slow calcium channels close:
intracellular Ca2+ is absorbed by the SR
or pumped out of cell
Cardiac muscle tissue:
very sensitive to extracellular Ca2+ concentrations

66. CO is the amount of blood pumped by each ventricle in one minute
CO is the product of heart rate (HR) and stroke volume (SV)
HR is the number of heart beats per minute
SV is the amount of blood pumped out by a ventricle with each beat
Cardiac reserve is the difference between resting and maximal CO
The Cardiac Cycle

67. Phases of the Cardiac Cycle
Figure 20–16

68. Cardiac output CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)

69. Cardiac output
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle after contraction

70. Pressure and Volume in the Cardiac Cycle
Figure 20–17

71. Factors Affecting Stroke Volume
Preload – amount ventricles are stretched by contained blood
Contractility – cardiac cell contractile force due to factors other than EDV
Afterload – back pressure exerted by blood in the large arteries leaving the heart

72. Factors Affecting Stroke Volume
Changes in EDV or ESV
Factors Affecting Stroke Volume
Figure 20–23 (Navigator)

73. Frank-Starling Law of the Heart
Preload, or degree of stretch, of cardiac muscle cells before they contract is the critical factor controlling stroke volume
Slow heartbeat and exercise increase venous return to the heart, increasing SV
Blood loss and extremely rapid heartbeat decrease SV

74. Extrinsic Factors Influencing Stroke Volume
Contractility is the increase in contractile strength, independent of stretch and EDV
Increase in contractility comes from:
Increased sympathetic stimuli
Certain hormones
Ca2+ and some drugs

75. Factors Affecting Heart Rate and Stroke Volume

76. Extrinsic Factors Influencing Stroke Volume
Agents/factors that decrease contractility include:
Acidosis
Increased extracellular K+
Calcium channel blockers

77. Contractility and Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Figure 18.22

78. Regulation of Heart Rate
Positive chronotropic factors increase heart rate
Negative chronotropic factors decrease heart rate

79. Regulation of Heart Rate: Autonomic Nervous System
Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise
Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS
PNS dominates the autonomic stimulation, slowing heart rate and causing vagal tone
Regulation of Heart Rate: Autonomic Nervous System

80. Autonomic Innervation

81. Autonomic Pacemaker Regulation

82. Autonomic Pacemaker Regulation (1 of 3)
Sympathetic and parasympathetic stimulation:
greatest at SA node (heart rate)
Membrane potential of pacemaker cells:
lower than other cardiac cells

83. Autonomic Pacemaker Regulation (2 of 3)
Rate of spontaneous depolarization depends on:
resting membrane potential
rate of depolarization

84. Autonomic Pacemaker Regulation (3 of 3)
ACh (parasympathetic stimulation):
slows the heart
NE (sympathetic stimulation):
speeds the heart

85. Atrial (Bainbridge) Reflex
Atrial (Bainbridge) reflex – a sympathetic reflex initiated by increased blood in the atria
Causes stimulation of the SA node
Stimulates baroreceptors in the atria, causing increased SNS stimulation

86. CNS and ANS controls of Cardiac output

87. Chemical Regulation of the Heart
The hormones epinephrine and thyroxine increase heart rate
Intra- and extracellular ion concentrations must be maintained for normal heart function
InterActive Physiology®: Cardiovascular System: Cardiac Output
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88. Factors Involved in Regulation of Cardiac Output

89. How the heart starts

90. Examples of Congenital Heart Defects

91. Congestive Heart Failure (CHF)
Congestive heart failure (CHF) is caused by:
Coronary atherosclerosis
Persistent high blood pressure
Multiple myocardial infarcts
Dilated cardiomyopathy (DCM)

92. Arteriosclerosis

93. Fig

94. Age-Related Changes Affecting the Heart
Sclerosis and thickening of valve flaps
Decline in cardiac reserve
Fibrosis of cardiac muscle
Atherosclerosis