principles of human physiology third edition cindy l. stanfield | william j. germann powerpoint ®...
TRANSCRIPT
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PRINCIPLES OFHUMAN PHYSIOLOGY
THIRD EDITION
Cindy L. Stanfield | William J. Germann
PowerPoint® Lecture Slides prepared by W.H. Preston, College of the Sequoias
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
13
Part B
The Cardiovascular System:
Cardiac Function
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Cardiac Cycle
Figure 13.18
Ventricularfilling
Ventricular filling
Mid-to-latediastole
Atrial contraction
Isovolumetriccontraction
Ventricularejection
Isovolumetricrelaxation
Left atrium
Right atrium
Rightventricle
Left ventricle
Systole
Early diastole
OpenAtrioventricular valves
Aortic and pulmonary(semilunar) valves
Phase
Open
OpenClosed
ClosedClosed
1 2 3 4 1
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Ventricular Systole
• Isovolumetric ventricular contraction
• AV and aortic valves closed
• Ventricular pressure increases until it exceeds atrial pressure
• Ventricular ejection
• Aortic valve opens
• Blood moves from ventricle to aorta
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Ventricular Diastole
• Isovolumetric ventricular relaxation
• Ventricle muscle relaxes so that pressure is less than aorta
• Aortic valve closes
• Pressure in ventricle continues dropping until it is less than atrial pressure
• Ventricular filling
• AV valve opens
• Blood moves from atria to ventricle
• Passive until atrium contracts
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Ventricular Pressure
Figure 13.19
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Aortic Pressure
Figure 13.20
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Figure 13.21
Ventricular Volume
• EDV = end-diastolic volume, volume of blood in ventricle at the end of diastole
• ESV = end systolic volume, volume of blood in ventricle at the end of systole
• SV = stroke volume, volume of blood ejected from ventricle each cycle.
• SV = EDV -ESV
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Stroke Volume
Volume of blood ejected by the ventricle each beat
Stroke volume = end diastolic volume – end systolic volume =
130 mL – 60 mL = 70 mL
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Ejection Fraction
Fraction of end-diastolic volume ejected during a heartbeat
Ejection fraction = stroke volume / end diastolic volume
= 70 mL / 130 mL = 0.54
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Heart Sounds
• Due to turbulent flow when valves close
• First heart sound
• Soft lubb
• AV valves close simultaneously
• Second heart sound
• Louder dubb
• Semilunar valves close simultaneously
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Heart Sounds
Figure 13.22
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Cardiac Output
Volume of blood pumped by each ventricle per minute
• Cardiac output = CO = SV x HR
• Average CO = 5 liters/min at rest
• Average blood volume = 5.5 liters
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Regulation of Cardiac Output
• Regulate heart rate and stroke volume
• Extrinsic and intrinsic regulation
• Extrinsic—neural and hormonal
• Intrinsic—autoregulation
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Autonomic Inputs to Heart
Figure 13.23
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Heart Rate - Determined by SA Node Firing Rate
• SA node intrinsic firing rate = 100/min
• No extrinsic control on heart, HR = 100
• SA node under control of ANS and hormones
• Rest: parasympathetic dominates, HR = 75
• Excitement: sympathetic takes over, HR increases
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Effects of Sympathetic Activity on Heart Rate
Increased sympathetic activity (nerves or epinephrine)
Beta 1 receptors in SA node
Increase open state of If and calcium channels
Increase rate of spontaneous depolarization
Increase heart rate
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Effects of Parasympathetic Activity on Heart Rate
Increased parasympathetic activity (vagus nerve)
Muscarinic Cholinergic Receptors in SA Node
Increase open state of K channels and closed state of calcium channels
Decrease rate of spontaneous depolarization and hyperpolarize cell
Decrease heart rate
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Sympathetic Effects: SA Potentials
Figure 13.25
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Factors Affecting Cardiac Output: Stroke Volume
Primary factors affecting stroke volume
• Ventricular contractility
• End-diastolic volume
• Afterload
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Stroke Volume
• Ventricles never completely empty of blood
• More forceful contraction will expel more blood
• Extrinsic controls of SV
• Sympathetic drive to ventricular muscle fibers
• Hormonal control
• Intrinsic controls of SV
• Changes in EDV
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Extrinsic Control of Stroke Volume
• Sympathetic innervation of contractile cells
• Cardiac nerves
• NE binds to 1 adrenergic receptors
• Increases cardiac contractility
• Parasympathetic innervation of contractile cells
• Not significant
• Hormones
• Thyroid hormones, insulin and glucagon increase force of contraction
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Figure 13.27
Sympathetic Effects on Contractility
• Increased sympathetic activity
• Increased epinephrine release
• Increases strength of contraction
• Increases rate of contraction
• Increases rate of relaxation
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Principle of Frank-Starling’s Law
• Increased EDV stretches muscle fibers
• Fibers closer to optimum length
• Optimum length = greater strength of contraction
• Result = Increased SV
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Intrinsic Control - Frank-Starling’s Law
Increase venous return
Increase strength of contraction
Increase stroke volume
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Starling’s Law
Figure 13.28
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Starling’s Law
Figure 13.29
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Factors Affecting End-Diastolic Volume
• End-diastolic pressure = preload
• Filling time
• Atrial pressure
• Central venous pressure
• Afterload = pressure in aorta during ejection
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Factors Influencing Stroke Volume
Figure 13.30
Stroke volume
End-diastolicvolume
Venous return
Contractility Arterial pressure(afterload)
Sympatheticactivity orEpinephrine
Ventricle
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Factors Influencing Stroke Volume
Figure 13.30, step 1
Stroke volume
End-diastolicvolume
Venous return
Ventricle
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Factors Influencing Stroke Volume
Figure 13.30, step 2
Stroke volume
End-diastolicvolume
Venous return
Contractility
Sympatheticactivity orEpinephrine
Ventricle
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Factors Influencing Stroke Volume
Figure 13.30, step 3
Stroke volume
End-diastolicvolume
Venous return
Contractility Arterial pressure(afterload)
Sympatheticactivity orEpinephrine
Ventricle
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Regulation of Cardiac Output
Figure 13.31