1. The Cardiovascular System: The Heart
Chapter 19
The Cardiovascular System: The Heart
Part A

2. Heart Anatomy Approximately the size of your fist Location
Superior surface of diaphragm
Left of the midline
Anterior to the vertebral column, posterior to the sternum

3. Heart Anatomy
Figure 19.1

9. Heart Covering Pericardial physiology Protects and anchors heart
Prevents overfilling
Figure 19.2

10. Heart Covering Pericardial anatomy Fibrous pericardium
Serous pericardium (separated by pericardial cavity)
Epicardium (visceral layer)
Figure 19.2

11. 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

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

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

14. External Heart: Anterior View
Figure 19.4b

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

18. External Heart: Vessels that Supply/Drain the Heart (Posterior View)
Arteries – right coronary artery (in atrioventricular groove) and the posterior interventricular artery (in interventricular groove)
Veins – great cardiac vein, posterior vein to left ventricle, coronary sinus, and middle cardiac vein

19. External Heart: Posterior View
Figure 19.4d

20. Gross Anatomy of Heart: Frontal Section

21. Gross Anatomy of Heart: Frontal Section
Figure 19.4e

22. 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

23. 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

25. The Cardiovascular System: The Heart
Chapter 19
The Cardiovascular System: The Heart
Part B

26. Pathway of Blood through the Heart and Lungs
Figure 19.5

27. Coronary Circulation
Figure 19.7a

28. Coronary Circulation
Figure 19.7b

29. Heart Valves
Heart valves insure unidirectional blood flow through the heart
Atrioventricular (AV) valves lie between the atria and the ventricles
Also called the Tricuspid and Bicuspid (Mitral) valves
AV valves prevent backflow into the atria when ventricles contract
Chordae tendineae anchor AV valves to papillary muscles
Papillary muscles pre-tense the chordae prior to ventricular contraction

30. Heart Valves
Figure 19.9

35. 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

37. Heart Valves
Figure 19.10

38. The Cardiovascular System: The Heart
Chapter 19
The Cardiovascular System: The Heart
Histology & Microanatomy

39. Microscopic Heart Muscle Anatomy
Cardiac muscle is striated, short, fat, branched, and interconnected
Connective tissue endomysium acts as both tendon and insertion
Intercalated discs anchor cardiac cells together and allow free passage of ions
Heart muscle behaves as a functional syncytium

40. Cardiac Muscle Contraction
Heart muscle:
Is stimulated by nerves and self-excitable (automaticity or autorhythmicity)
Contracts as a unit (functional syncytium)
Has a long (250 ms) absolute refractory period compared to skeletal’s (~ 5ms)
Cardiac muscle contraction is similar to skeletal muscle contraction (sliding filament theory)

41. Figure 14-10: Cardiac muscle
Cardiac Muscle Cells:
Autorhythmic
Myocardial Characteristics:
Intercalated discs
Desmosomes
Gap Junctions
Fast signals
Cell to cell
Many mitochondria
Large T tubes
Figure 14-10: Cardiac muscle

42. Figure 14-10: Cardiac muscle
Cardiac Muscle Cells:
Figure 14-10: Cardiac muscle

43. Microscopic Heart Muscle Anatomy
Figure 19.11b

45. Cardiac Muscle

46. Ions

47. Heart Physiology: Intrinsic Conduction System
Autorhythmic cells:
Initiate action potentials
Have unstable resting potentials called pacemaker potentials
Use calcium influx (rather than sodium) for rising phase of the action potential

48. The Cardiovascular System: The Heart
Chapter 19
The Cardiovascular System: The Heart
Electrophysiology

49. Purkinje fibers 40X

50. * Purkinje fibers 100X

55. Heart Physiology: Intrinsic Conduction System
Figure 19.13

56. Heart Physiology: Sequence of Excitation
Sinoatrial (SA) node generates impulses about 75 times/minute
Atrioventricular (AV) node delays the impulse approximately 0.1 second
Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His)

57. Heart Physiology: Sequence of Excitation
AV bundle splits into two pathways in the interventricular septum (bundle branches)
Bundle branches carry the impulse toward the apex of the heart
Purkinje fibers carry the impulse to the heart apex and ventricular walls

58. Heart Physiology: Sequence of Excitation
Figure 19.14a

59. Electrocardiography
Electrical activity is recorded by electrocardiogram (ECG or EKG)
P wave corresponds to depolarization of SA node
QRS complex corresponds to ventricular depolarization
T wave corresponds to ventricular repolarization
Atrial repolarization record is masked by the larger QRS complex

60. Electrocardiography
Figure 19.16

62. Extrinsic Innervation of the Heart
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
Figure 19.15

63. Cardiac Cycle
Cardiac cycle refers to all events associated with blood flow through the heart
Systole – contraction of heart muscle
Diastole – relaxation of heart muscle

64. Phases of the Cardiac Cycle
Ventricular filling – mid-to-late diastole
Heart blood pressure is low as blood enters atria and flows into ventricles
AV valves are open then atrial systole occurs

65. Phases of the Cardiac Cycle
Ventricular systole
Atria relax
Rising ventricular pressure results in closing of AV valves
Isovolumetric contraction phase
Ventricular ejection phase opens semilunar valves

66. Phases of the Cardiac Cycle
Isovolumetric relaxation – early diastole
Ventricles relax
Backflow of blood in aorta and pulmonary trunk closes semilunar valves
Dicrotic notch – brief rise in aortic pressure caused by backflow of blood rebounding off semilunar valves

67. Phases of the Cardiac Cycle
Figure 19.19a

68. Phases of the Cardiac Cycle
Figure 19.19b

70. Heart Sounds
Heart sounds (lub-dup) are associated with closing of heart valves
Figure 19.20

74. Cardiac Output (CO) and Reserve
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

75. Cardiac Output: Example
CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
CO = 5250 ml/min (5.25 L/min)

76. Regulation of Stroke Volume
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
SV = EDV-ESV
EDV = amount of blood collected in a ventricle during diastole
ESV = amount of blood remaining in a ventricle after contraction

77. 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

78. 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

79. Preload and Afterload
Figure 19.21

80. The Cardiovascular System: The Heart
Chapter 19
The Cardiovascular System: The Heart
Part D

81. 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
Agents/factors that decrease contractility include:
Acidosis
Increased extracellular potassium
Calcium channel blockers

82. Contractility and Norepinephrine
Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system
Figure 19.22

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

84. Extrinsic Innervation of the Heart
Heart is stimulated by the sympathetic cardioacceleratory center
Heart is inhibited by the parasympathetic cardioinhibitory center
Figure 19.15

85. 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

86. Factors Involved in Regulation of Cardiac Output

87. Factors Involved in Regulation of Cardiac Output

88. Factors Involved in Regulation of Cardiac Output

89. Factors Involved in Regulation of Cardiac Output

90. Factors Involved in Regulation of Cardiac Output

91. Developmental Aspects of the Heart
Embryonic heart chambers
Sinus venous
Atrium
Ventricle
Bulbus cordis
Figure 19.24

92. Developmental Aspects of the Heart
Fetal heart structures that bypass pulmonary circulation
Foramen ovale connects the two atria
Ductus arteriosus connects pulmonary trunk and the aorta

96. Normal Heart Sound Mitral valve prolapse

97. Chapter 19
Pathologies
Part D

98. Endocarditis-symptoms
Paleness
Persistent cough
Swelling in your feet, legs or abdomen
Unexplained weight loss
Blood in your urine
A new heart murmur
Tenderness in your spleen
Fever
Chills
Weakness
Fatigue
Aching joints and muscles
Night sweats
Shortness of breath

99. Endocarditis
Endocarditis occurs when germs enter your bloodstream, travel to your heart and lodge on abnormal heart valves or damaged heart tissue. Bacteria are the cause of most cases, but fungi, viruses or other microorganisms also may be responsible.
Sometimes the culprit is one of many common bacteria that live in your mouth, upper respiratory tract or other parts of your body. In other cases, the offending organism may gain entry to your bloodstream through:
Certain dental or medical procedures.
An infection or other medical condition..
Catheters or needles..
Common activities..

100. Endocarditis
Typically, your immune system destroys bacteria that make it into your bloodstream. Even if bacteria reach your heart, they may pass through without causing an infection.
Most people who develop endocarditis have a diseased or damaged heart valve — an ideal spot for bacteria to settle. This damaged tissue in the endocardium provides bacteria with the roughened surface they need to attach and multiply.

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

103. Homeostatic Imbalances
Hypocalcemia – reduced ionic calcium depresses the heart
Hypercalcemia – dramatically increases heart irritability and leads to spastic contractions
Hypernatremia (Na ??!!)– blocks heart contraction by inhibiting ionic calcium transport
Hyperkalemia (K) – leads to heart block and cardiac arrest

104. Homeostatic Imbalances
Tachycardia – heart rate over 100 beats/min
Bradycardia – heart rate less than 60 beats/min
Pericarditis
inflammation of the pericardium
Reduces cardiac output
Antibiotics, anti-inflammatory

105. Congestive Heart Failure (CHF)
Congestive heart failure (CHF), caused by:
Coronary atherosclerosis
Increased blood pressure in aorta
Successive myocardial infarcts
Dilated cardiomyopathy (DCM)

106. Cardiopathologies Congestive Heart Failure
If RIGHT side fails, then peripheral congestion because the blood can’t return from the body to the right atrium causing edema in the extremities.
Ultimately, since the failure of one side now strains the effectiveness of the healthy side, the myocardium weakens over time and a heart transplant is inevitable.
Temporary treatment is to lower blood volume, reducing exertion, lowering BP

107. Cardiopathologies Atherosclerosis (CAD)
Blockage of coronary arteries from deposition of LDL due to tissue insult of tunica interna.
Stenosis relieved by balloon angioplasty, insertion of stent, coronary by-pass.

110. Illust.

111. Illust.

112. Illust.
Coronary Artery
Fatty Deposit
Stenosis

113. Illust.

114. Illust.

115. Illust.

116. Illust.

120. Cardiopathologies Myocardial Infarction
Ischemia (holding back blood) is due to a stenosis caused by atheroschlosis. The pain, angina pectoris is usually an indicator of a TIA (transient ischemic attack)
Necrosis (death) of myocardium due to ischemia associated w/ the stenosis.
Myocardia is amitotic and therefore will not repair itself. Scar tissue instead.
Seriousness depends on location/extent
Treatment would include dealing w/ stenosis, vasodilators, beta-blockers (reduce blood pressure), heart transplant, LVAD.

122. Cardiopathologies Valvular Stenosis
Stiffening of valves constrict opening to next vessel.
Increases cardiac workload
Valve replacement if needed.

123. Cardiopathologies Arrhythmia Ectopic Signals (extrasystole)
Damage to SA node, AV node, bundle branches (need pacemaker, drugs)
Ventricualar fibrillation is most extreme case of extrasystole.
Tachycardia – could lead to Vfib
Bradycardia caused by many factors (faulty SA node)

124. Cardiopathologies Congestive Heart Failure
Chronic situation caused by atherosclerosis myocardial infarcts, and/or high diastolic pressure.
Results in hypertrophy of the myocardium which reduces its effectiveness which then enhances hypertrophy.
If LEFT side fails, then Pulmonary Congestion because the blood can’t flow back as fast to the heart from the lungs causing edema and then suffocation.

125. Cardiopathologies Congenitial Defects Septal defects
Patent ductus arteriosis
Coarctation of aorta

129. Cardiopathologies Age-related changes sclerosis of valve flaps
Fibrosis of myocardium
Atherosclerosis
Reduction in cardiac output

130. Circulatory Shock
Circulatory shock – any condition in which blood vessels are inadequately filled and blood cannot circulate normally
Results in inadequate blood flow to meet tissue needs
Three types include:
Hypovolemic shock – results from large-scale blood loss
Vascular shock – poor circulation resulting from extreme vasodilation
Cardiogenic shock – the heart cannot sustain adequate circulation

131. Alterations in Blood Pressure
Hypotension – low BP in which systolic pressure is below 100 mm Hg
Hypertension – condition of sustained elevated arterial pressure of 140/90 or higher
Transient elevations are normal and can be caused by fever, physical exertion, and emotional upset
Chronic elevation is a major cause of heart failure, vascular disease, renal failure, and stroke (cerebrovascular accident)

132. Hypotension
Orthostatic hypotension – temporary low BP and dizziness when suddenly rising from a sitting or reclining position
Chronic hypotension – hint of poor nutrition and warning sign for Addison’s disease
Acute hypotension – important sign of circulatory shock
Threat to patients undergoing surgery and those in intensive care units

133. Hypertension
Primary or essential hypertension – risk factors in primary hypertension include diet, obesity, age, race, heredity, stress, and smoking
Secondary hypertension – due to identifiable disorders, including excessive renin secretion, arteriosclerosis, and endocrine disorders

134. Aneurysm A weakening of the arteries and subsequent bursting
Due to hypertension or arteriosclerosis
Generally affect cerebral arteries, aorta, and renal arteries

135. Cardiopathologies

138. Capillary with red blood cells.
SEM x5140