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THE CARDIOVASCULAR SYSTEM: THE HEART
ANATOMY
1
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
2
HEART ANATOMY
3
Figure 18.1
COVERINGS OF THE HEART:
ANATOMY
• Pericardium – a double-walled sac around the
heart composed of:
1. A superficial fibrous pericardium
2. A deep two-layer serous pericardium
a. The parietal layer lines the internal surface of the
fibrous pericardium
b. The visceral layer or epicardium lines the surface of the
heart
• They are separated by the fluid-filled pericardial cavity
4
COVERINGS OF THE HEART:
PHYSIOLOGY
• The Function of 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
5
PERICARDIAL LAYERS OF THE
HEART
6
Figure 18.2
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
7
EXTERNAL HEART: MAJOR VESSELS
OF THE HEART (ANTERIOR VIEW)
• Vessels returning blood to the heart include:
1. Superior and inferior venae cavae
2. Right and left pulmonary veins
• Vessels conveying blood away from the heart
include:
1. Pulmonary trunk, which splits into right and left
pulmonary arteries
2. Ascending aorta (three branches) –
a. Brachiocephalic
b. Left common carotid
c. Subclavian arteries
8
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
9
EXTERNAL HEART: ANTERIOR VIEW
10
Figure 18.4b
EXTERNAL HEART: MAJOR VESSELS
OF THE HEART (POSTERIOR VIEW)
• Vessels returning blood to the heart include:
1. Right and left pulmonary veins
2. Superior and inferior venae cavae
• Vessels conveying blood away from the heart include:
1. Aorta
2. Right and left pulmonary arteries
11
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
12
EXTERNAL HEART: POSTERIOR
VIEW
13
Figure 18.4d
GROSS ANATOMY OF HEART:
FRONTAL SECTION
14
Figure 18.4e
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
15
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
16
MYOCARDIAL THICKNESS AND FUNCTION
Thickness of myocardium varies according to the function of the
chamber
Atria are thin walled, deliver blood to adjacent ventricles
Ventricle walls are much thicker and stronger
• right ventricle supplies blood to the lungs (little flow
resistance)
• left ventricle wall is the thickest to supply systemic circulation
17
THICKNESS OF CARDIAC WALLS
18
Myocardium of left ventricle is much thicker than the right.
ATRIAL SEPTAL DEFECT
19
VENTRICULAR SEPTAL DEFECT
20
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
21
PATHWAY OF BLOOD THROUGH
THE HEART AND LUNGS
22
Figure 18.5
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
23
CORONARY CIRCULATION:
ARTERIAL SUPPLY
24
Figure 18.7a
CORONARY CIRCULATION:
VENOUS SUPPLY
25
Figure 18.7b
HEART VALVES
• 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
26
HEART VALVES
• Semilunar valves prevent backflow of blood into the
ventricles
• Aortic semilunar valve lies between the left ventricle
and the aorta
• Pulmonary semilunar valve lies between the right
ventricle and pulmonary trunk
27
HEART VALVES
28
Figure 18.8a, b
HEART VALVES
29
Figure 18.8c, d
ATRIOVENTRICULAR VALVE
FUNCTION
30
Figure 18.9
SEMILUNAR VALVE FUNCTION
31
Figure 18.10
MITRAL VALVE PROLAPSE
32
MICROSCOPIC ANATOMY OF
HEART MUSCLE
• Cardiac muscle is striated, short, fat, branched, and interconnected
• The 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
33
InterActive Physiology®:
Cardiovascular System: Anatomy Review: The Heart
PLAY
MICROSCOPIC ANATOMY OF
HEART MUSCLE
34
Figure 18.11
18
THE CARDIOVASCULAR SYSTEM: THE HEART
PHYSIOLOGY
35
CARDIAC MUSCLE CONTRACTION
• Heart muscle:
• Is stimulated by nerves and is self-excitable (automaticity)
• Contracts as a unit
• Has a long (250 ms) absolute refractory period
• Cardiac muscle contraction is similar to skeletal muscle
contraction
36
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
37
PACEMAKER AND ACTION
POTENTIALS OF THE HEART
38
Figure 18.13
HEART PHYSIOLOGY: SEQUENCE
OF EXCITATION
• Sinoatrial (SA) node generates impulses about 75
times/minute
• Atrioventricular (AV) node delays the impulse
approximately 0.1 second
39
HEART PHYSIOLOGY: SEQUENCE
OF EXCITATION
• Impulse passes from atria to ventricles via the
atrioventricular bundle (bundle of His)
• AV bundle splits into two pathways in the interventricular
septum (bundle branches)
1. Bundle branches carry the impulse toward the apex of the
heart
2. Purkinje fibers carry the impulse to the heart apex and
ventricular walls
40
HEART PHYSIOLOGY: SEQUENCE
OF EXCITATION
41
Figure 18.14a
HEART EXCITATION RELATED TO
ECG
42
Figure 18.17
EXTRINSIC INNERVATION OF THE HEART
• Heart is stimulated by the
sympathetic
cardioacceleratory center
• Heart is inhibited by the
parasympathetic
cardioinhibitory center
43
Figure 18.15
ELECTROCARDIOGRAPHY
• Electrical activity is recorded by electrocardiogram (ECG)
• 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
44
InterActive Physiology®:
Cardiovascular System: Intrinsic Conduction System
PLAY
ELECTROCARDIOGRAPHY
45
Figure 18.16
HEART SOUNDS
• Heart sounds (lub-dup) are associated with closing of
heart valves
• First sound occurs as AV valves close and signifies beginning
of systole (contraction)
• Second sound occurs when SL valves close at the beginning of
ventricular diastole (relaxation)
46
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
47
PHASES OF THE CARDIAC CYCLE
• Ventricular filling – mid-to-late diastole
• Heart blood pressure is low as blood enters atria (passively) and flows into ventricles
• AV valves are open, then atrial systole occurs
48
PHASES OF THE CARDIAC CYCLE
• Ventricular systole (contraction)
• Atria relax
• Rising ventricular pressure results in closing of AV valves
• Isovolumetric contraction phase
• Ventricular ejection phase opens semilunar valves
49
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
50
InterActive Physiology®:
Cardiovascular System: Cardiac Cycle
PLAY
PHASES OF THE CARDIAC CYCLE
51
Figure 18.20
CARDIAC OUTPUT (CO) AND
RESERVE
• Cardiac Output 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
52
CARDIAC OUTPUT: EXAMPLE
• CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat)
• CO = 5250 ml/min (5.25 L/min)
53
REGULATION OF STROKE VOLUME
• 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
54
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
55
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
56
PRELOAD AND AFTERLOAD
57
Figure 18.21
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
58
EXTRINSIC FACTORS INFLUENCING
STROKE VOLUME
• Agents/factors that decrease contractility include:
• Acidosis
• Increased extracellular K+
• Calcium channel blockers
59
CONTRACTILITY AND NOREPINEPHRINE
• Sympathetic
stimulation releases
norepinephrine and
initiates a cyclic AMP
second-messenger
system
60
Figure 18.22
REGULATION OF HEART RATE
• Positive chronotropic factors increase heart rate
• Caffeine
• Negative chronotropic factors decrease heart rate
• Sedatives
61
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
• If the Vagus Nerver was cut, the heart would lose its
tone. Thus, increasing the heart rate by 25 beats
per minute.
62
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
63
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
64
InterActive Physiology®:
Cardiovascular System: Cardiac Output
PLAY
FACTORS INVOLVED IN REGULATION
OF CARDIAC OUTPUT
65
Figure 18.23
CONGESTIVE HEART FAILURE (CHF)
• Congestive heart failure (CHF) is caused by:
• Coronary atherosclerosis
• Persistent high blood pressure
• Multiple myocardial infarcts
• Dilated cardiomyopathy (DCM) – main pumping chambers of
the heart are dilated and contract poorly
66
DEVELOPMENTAL ASPECTS OF THE HEART
67
Figure 18.24
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
68
EXAMPLES OF CONGENITAL HEART
DEFECTS
69
Figure 18.25
AGE-RELATED CHANGES
AFFECTING THE HEART
• Sclerosis and thickening of valve flaps
• Decline in cardiac reserve
• Fibrosis of cardiac muscle
• Atherosclerosis
70
CONGESTIVE HEART FAILURE
• Causes of CHF
• coronary artery disease, hypertension, MI, valve
disorders, congenital defects
• Left side heart failure
• less effective pump so more blood remains in ventricle
• heart is overstretched & even more blood remains
• blood backs up into lungs as pulmonary edema
• suffocation & lack of oxygen to the tissues
• Right side failure
• fluid builds up in tissues as peripheral edema
71
CORONARY ARTERY DISEASE
• Heart muscle receiving
insufficient blood supply
• narrowing of vessels---
atherosclerosis, artery
spasm or clot
• atherosclerosis--smooth
muscle & fatty deposits
in walls of arteries
• Treatment
• drugs, bypass graft,
angioplasty, stent
72
CLINICAL PROBLEMS
• MI = myocardial infarction
• death of area of heart muscle from lack of O2
• replaced with scar tissue
• results depend on size & location of damage
• Blood clot
• use clot dissolving drugs streptokinase or t-PA &
heparin
• balloon angioplasty
• Angina pectoris
• heart pain from ischemia (lack of blood flow and
oxygen ) of cardiac muscle
73
BY-PASS GRAFT
74
PERCUTANEOUS TRANSLUMINAL CORONARY
ANGIOPLASTY
75
ARTIFICIAL HEART
76

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1 CARDIOVASCULAR SYSTEM.ppt

  • 1. THE CARDIOVASCULAR SYSTEM: THE HEART ANATOMY 1
  • 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 2
  • 4. COVERINGS OF THE HEART: ANATOMY • Pericardium – a double-walled sac around the heart composed of: 1. A superficial fibrous pericardium 2. A deep two-layer serous pericardium a. The parietal layer lines the internal surface of the fibrous pericardium b. The visceral layer or epicardium lines the surface of the heart • They are separated by the fluid-filled pericardial cavity 4
  • 5. COVERINGS OF THE HEART: PHYSIOLOGY • The Function of 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 5
  • 6. PERICARDIAL LAYERS OF THE HEART 6 Figure 18.2
  • 7. 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 7
  • 8. EXTERNAL HEART: MAJOR VESSELS OF THE HEART (ANTERIOR VIEW) • Vessels returning blood to the heart include: 1. Superior and inferior venae cavae 2. Right and left pulmonary veins • Vessels conveying blood away from the heart include: 1. Pulmonary trunk, which splits into right and left pulmonary arteries 2. Ascending aorta (three branches) – a. Brachiocephalic b. Left common carotid c. Subclavian arteries 8
  • 9. 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 9
  • 10. EXTERNAL HEART: ANTERIOR VIEW 10 Figure 18.4b
  • 11. EXTERNAL HEART: MAJOR VESSELS OF THE HEART (POSTERIOR VIEW) • Vessels returning blood to the heart include: 1. Right and left pulmonary veins 2. Superior and inferior venae cavae • Vessels conveying blood away from the heart include: 1. Aorta 2. Right and left pulmonary arteries 11
  • 12. 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 12
  • 14. GROSS ANATOMY OF HEART: FRONTAL SECTION 14 Figure 18.4e
  • 15. 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 15
  • 16. 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 16
  • 17. MYOCARDIAL THICKNESS AND FUNCTION Thickness of myocardium varies according to the function of the chamber Atria are thin walled, deliver blood to adjacent ventricles Ventricle walls are much thicker and stronger • right ventricle supplies blood to the lungs (little flow resistance) • left ventricle wall is the thickest to supply systemic circulation 17
  • 18. THICKNESS OF CARDIAC WALLS 18 Myocardium of left ventricle is much thicker than the right.
  • 21. 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 21
  • 22. PATHWAY OF BLOOD THROUGH THE HEART AND LUNGS 22 Figure 18.5
  • 23. 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 23
  • 26. HEART VALVES • 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 26
  • 27. HEART VALVES • Semilunar valves prevent backflow of blood into the ventricles • Aortic semilunar valve lies between the left ventricle and the aorta • Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk 27
  • 33. MICROSCOPIC ANATOMY OF HEART MUSCLE • Cardiac muscle is striated, short, fat, branched, and interconnected • The 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 33 InterActive Physiology®: Cardiovascular System: Anatomy Review: The Heart PLAY
  • 34. MICROSCOPIC ANATOMY OF HEART MUSCLE 34 Figure 18.11
  • 35. 18 THE CARDIOVASCULAR SYSTEM: THE HEART PHYSIOLOGY 35
  • 36. CARDIAC MUSCLE CONTRACTION • Heart muscle: • Is stimulated by nerves and is self-excitable (automaticity) • Contracts as a unit • Has a long (250 ms) absolute refractory period • Cardiac muscle contraction is similar to skeletal muscle contraction 36
  • 37. 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 37
  • 38. PACEMAKER AND ACTION POTENTIALS OF THE HEART 38 Figure 18.13
  • 39. HEART PHYSIOLOGY: SEQUENCE OF EXCITATION • Sinoatrial (SA) node generates impulses about 75 times/minute • Atrioventricular (AV) node delays the impulse approximately 0.1 second 39
  • 40. HEART PHYSIOLOGY: SEQUENCE OF EXCITATION • Impulse passes from atria to ventricles via the atrioventricular bundle (bundle of His) • AV bundle splits into two pathways in the interventricular septum (bundle branches) 1. Bundle branches carry the impulse toward the apex of the heart 2. Purkinje fibers carry the impulse to the heart apex and ventricular walls 40
  • 41. HEART PHYSIOLOGY: SEQUENCE OF EXCITATION 41 Figure 18.14a
  • 42. HEART EXCITATION RELATED TO ECG 42 Figure 18.17
  • 43. EXTRINSIC INNERVATION OF THE HEART • Heart is stimulated by the sympathetic cardioacceleratory center • Heart is inhibited by the parasympathetic cardioinhibitory center 43 Figure 18.15
  • 44. ELECTROCARDIOGRAPHY • Electrical activity is recorded by electrocardiogram (ECG) • 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 44 InterActive Physiology®: Cardiovascular System: Intrinsic Conduction System PLAY
  • 46. HEART SOUNDS • Heart sounds (lub-dup) are associated with closing of heart valves • First sound occurs as AV valves close and signifies beginning of systole (contraction) • Second sound occurs when SL valves close at the beginning of ventricular diastole (relaxation) 46
  • 47. 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 47
  • 48. PHASES OF THE CARDIAC CYCLE • Ventricular filling – mid-to-late diastole • Heart blood pressure is low as blood enters atria (passively) and flows into ventricles • AV valves are open, then atrial systole occurs 48
  • 49. PHASES OF THE CARDIAC CYCLE • Ventricular systole (contraction) • Atria relax • Rising ventricular pressure results in closing of AV valves • Isovolumetric contraction phase • Ventricular ejection phase opens semilunar valves 49
  • 50. 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 50 InterActive Physiology®: Cardiovascular System: Cardiac Cycle PLAY
  • 51. PHASES OF THE CARDIAC CYCLE 51 Figure 18.20
  • 52. CARDIAC OUTPUT (CO) AND RESERVE • Cardiac Output 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 52
  • 53. CARDIAC OUTPUT: EXAMPLE • CO (ml/min) = HR (75 beats/min) x SV (70 ml/beat) • CO = 5250 ml/min (5.25 L/min) 53
  • 54. REGULATION OF STROKE VOLUME • 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 54
  • 55. 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 55
  • 56. 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 56
  • 58. 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 58
  • 59. EXTRINSIC FACTORS INFLUENCING STROKE VOLUME • Agents/factors that decrease contractility include: • Acidosis • Increased extracellular K+ • Calcium channel blockers 59
  • 60. CONTRACTILITY AND NOREPINEPHRINE • Sympathetic stimulation releases norepinephrine and initiates a cyclic AMP second-messenger system 60 Figure 18.22
  • 61. REGULATION OF HEART RATE • Positive chronotropic factors increase heart rate • Caffeine • Negative chronotropic factors decrease heart rate • Sedatives 61
  • 62. 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 • If the Vagus Nerver was cut, the heart would lose its tone. Thus, increasing the heart rate by 25 beats per minute. 62
  • 63. 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 63
  • 64. 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 64 InterActive Physiology®: Cardiovascular System: Cardiac Output PLAY
  • 65. FACTORS INVOLVED IN REGULATION OF CARDIAC OUTPUT 65 Figure 18.23
  • 66. CONGESTIVE HEART FAILURE (CHF) • Congestive heart failure (CHF) is caused by: • Coronary atherosclerosis • Persistent high blood pressure • Multiple myocardial infarcts • Dilated cardiomyopathy (DCM) – main pumping chambers of the heart are dilated and contract poorly 66
  • 67. DEVELOPMENTAL ASPECTS OF THE HEART 67 Figure 18.24
  • 68. 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 68
  • 69. EXAMPLES OF CONGENITAL HEART DEFECTS 69 Figure 18.25
  • 70. AGE-RELATED CHANGES AFFECTING THE HEART • Sclerosis and thickening of valve flaps • Decline in cardiac reserve • Fibrosis of cardiac muscle • Atherosclerosis 70
  • 71. CONGESTIVE HEART FAILURE • Causes of CHF • coronary artery disease, hypertension, MI, valve disorders, congenital defects • Left side heart failure • less effective pump so more blood remains in ventricle • heart is overstretched & even more blood remains • blood backs up into lungs as pulmonary edema • suffocation & lack of oxygen to the tissues • Right side failure • fluid builds up in tissues as peripheral edema 71
  • 72. CORONARY ARTERY DISEASE • Heart muscle receiving insufficient blood supply • narrowing of vessels--- atherosclerosis, artery spasm or clot • atherosclerosis--smooth muscle & fatty deposits in walls of arteries • Treatment • drugs, bypass graft, angioplasty, stent 72
  • 73. CLINICAL PROBLEMS • MI = myocardial infarction • death of area of heart muscle from lack of O2 • replaced with scar tissue • results depend on size & location of damage • Blood clot • use clot dissolving drugs streptokinase or t-PA & heparin • balloon angioplasty • Angina pectoris • heart pain from ischemia (lack of blood flow and oxygen ) of cardiac muscle 73