chapter 18 heart.ppt
- 1. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 The Cardiovascular System: The Heart Part A
- 2. 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
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- 9. 9 Heart Covering • Pericardial physiology • Protects and anchors heart • Prevents overfilling Figure 19.2
- 10. 10 Heart Covering • Pericardial anatomy • Fibrous pericardium • Serous pericardium (separated by pericardial cavity) • Epicardium (visceral layer) Figure 19.2
- 11. 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. 12 • 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 External Heart: Major Vessels of the Heart (Anterior View)
- 13. 13 • Arteries – right and left coronary (in atrioventricular groove), marginal, circumflex, and anterior interventricular • Veins – small cardiac vein, anterior cardiac vein, and great cardiac vein External Heart: Vessels that Supply/Drain the Heart (Anterior View)
- 14. 14 External Heart: Anterior View Figure 19.4b
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- 17. 17 • 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 External Heart: Major Vessels of the Heart (Posterior View)
- 18. 18 • 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 External Heart: Vessels that Supply/Drain the Heart (Posterior View)
- 19. 19 External Heart: Posterior View Figure 19.4d
- 20. 20 Gross Anatomy of Heart: Frontal Section
- 21. 21 Gross Anatomy of Heart: Frontal Section Figure 19.4e
- 22. 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. 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
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- 25. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 The Cardiovascular System: The Heart Part B
- 26. 26 Pathway of Blood through the Heart and Lungs Figure 19.5
- 29. 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
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- 35. 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
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- 38. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 The Cardiovascular System: The Heart Histology & Microanatomy
- 39. 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. 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. 41 • Autorhythmic • Myocardial Characteristics: • Intercalated discs • Desmosomes • Gap Junctions • Fast signals • Cell to cell • Many mitochondria • Large T tubes Cardiac Muscle Cells: Figure 14-10: Cardiac muscle
- 42. 42 Cardiac Muscle Cells: Figure 14-10: Cardiac muscle
- 43. 43 Microscopic Heart Muscle Anatomy Figure 19.11b
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- 46. 46 Ions
- 47. 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. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 The Cardiovascular System: The Heart Electrophysiology
- 50. 50 * Purkinje fibers 100X
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- 54. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings
- 55. 55 Heart Physiology: Intrinsic Conduction System Figure 19.13
- 56. 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. 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. 58 Heart Physiology: Sequence of Excitation Figure 19.14a
- 59. 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
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- 62. 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. 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. 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. 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. 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. 67 Phases of the Cardiac Cycle Figure 19.19a
- 68. 68 Phases of the Cardiac Cycle Figure 19.19b
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- 70. 70 Heart Sounds • Heart sounds (lub- dup) are associated with closing of heart valves Figure 19.20
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- 74. 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. 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. 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. 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. 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. 79 Preload and Afterload Figure 19.21
- 80. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 The Cardiovascular System: The Heart Part D
- 81. 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. 82 Contractility and Norepinephrine • Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system Figure 19.22
- 83. 83 • 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 Regulation of Heart Rate: Autonomic Nervous System
- 84. 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. 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. 86 Factors Involved in Regulation of Cardiac Output
- 87. 87 Factors Involved in Regulation of Cardiac Output
- 88. 88 Factors Involved in Regulation of Cardiac Output
- 89. 89 Factors Involved in Regulation of Cardiac Output
- 90. 90 Factors Involved in Regulation of Cardiac Output
- 91. 91 Developmental Aspects of the Heart • Embryonic heart chambers • Sinus venous • Atrium • Ventricle • Bulbus cordis Figure 19.24
- 92. 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
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- 96. 96 Normal Heart Sound Mitral valve prolapse
- 97. Human Anatomy & Physiology FIFTH EDITION Elaine N. Marieb PowerPoint® Lecture Slide Presentation by Vince Austin Copyright © 2003 Pearson Education, Inc. publishing as Benjamin Cummings Chapter 19 Pathologies Part D
- 98. 98 Endocarditis-symptoms • Fever • Chills • Weakness • Fatigue • Aching joints and muscles • Night sweats • Shortness of breath • 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
- 99. 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. 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.
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- 102. 102 Age-Related Changes Affecting the Heart • Sclerosis and thickening of valve flaps • Decline in cardiac reserve • Fibrosis of cardiac muscle • Atherosclerosis
- 103. 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. 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. 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. 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. 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.
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- 110. 110 Illust.
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- 120. 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.
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- 122. 122 Cardiopathologies • Valvular Stenosis • Stiffening of valves constrict opening to next vessel. • Increases cardiac workload • Valve replacement if needed.
- 123. 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. 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. 125 Cardiopathologies • Congenitial Defects • Septal defects • Patent ductus arteriosis • Coarctation of aorta
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- 129. 129 Cardiopathologies • Age-related changes • sclerosis of valve flaps • Fibrosis of myocardium • Atherosclerosis • Reduction in cardiac output
- 130. 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. 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. 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. 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. 134 Aneurysm • A weakening of the arteries and subsequent bursting • Due to hypertension or arteriosclerosis • Generally affect cerebral arteries, aorta, and renal arteries
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- 138. 138 Capillary with red blood cells. SEM x5140