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PRINCIPLES OF
HUMAN PHYSIOLOGY
13
THIRD EDITION
Cindy L. Stanfield | William J. Germann
The Cardiovascular
System:
Cardiac Function
Part A
PowerPoint® Lecture Slides prepared by W.H. Preston, College of the Sequoias
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Anatomy of the Heart
• Four Chambers
•
Two atria
•
Two ventricles
• Valves
•
Atrioventricular
•
Semilunar
• Interventricular
septum
• Base
• Apex
Figure 13.1
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Path of Blood Flow
• Cardiovascular system = closed system
• Flow through systemic and pulmonary circuits is in
series
• Left ventricle  aorta  systemic circuit 
vena cavae  right atrium  right ventricle 
pulmonary artery  pulmonary circuit 
pulmonary veins  left atrium  left ventricle
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© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Path of Blood Flow
Figure 13.2
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© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Heart Location
Figure 13.5
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Ventricular Muscle
Figure 13.6
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Properties of Cardiac Muscle
• Cells are smaller than cells of skeletal muscle
• Cells demonstrate branching
• Striations are evident
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Properties of Cardiac Muscle
• Intercalated disks
•
Gap junctions
• Cause heart to contract as a unit
•
Desmosomes
• Resist stress
• Atria and ventricles
•
Copyright
Separate units
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Properties of Cardiac Muscle
• Aerobic muscle
• No cell division after infancy—growth
by hypertrophy
• 99% contractile cells (for pumping)
• 1% autorhythmic cells (set pace)
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© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Function of Cardiac Muscle
• Rhythmic contraction and relaxation generates
heart pumping action
• Contraction pushes blood out of heart into
vasculature
• Relaxation allows heart to fill with blood
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© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Heartbeat
• Wave of contraction through cardiac muscle
• Atria contract as a unit
• Ventricles contract as a unit
• Atrial contraction precedes ventricle contraction
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Valves and Unidirectional Blood Flow
• Pressure within chambers of heart vary with
heartbeat cycle
• Pressure difference drives blood flow
•
High pressure to low pressure
• Normal direction of flow
•
Atria to ventricles
•
Ventricles to arteries
• Valves prevent backward flow of blood
• All valves open passively based on pressure
gradient
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Atrioventricular Valve Action
Figure 13.7
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Semilunar Valve Action
Figure 13.8
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Autorhythmic Cells
Location
SA Node
AV Node
Bundle of His
Purkinje Fibers
Firing Rate at Rest
70-80 APs/min*
40-60 APs/min
20-40 APs/min
20-40 APs/min
• Cardiac cells are linked by gap junctions
• Fastest depolarizing cells control other cells
• Fastest cells = pacemaker = set rate for rest of
heart
* action potentials per minute
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Cardiac Electrical Connections
Figure 13.9
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Conduction System of Heart
Figure 13.10
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Pathway of Depolarization
Figure 13.11
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Electrical Activity: Pacemaker Cell
Figure 13.12
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Electrical Activity: Pacemaker Cell
Table 13.1
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Electrical Activity: Contractile Cell
Figure 13.13
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Electrical Activity: Contractile Cell
Table 13.2
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Cardiac Cycle
Isovolumetric
contraction
Ventricular
ejection
Atrial contraction
Isovolumetric
relaxation
Ventricular filling
Ventricular
filling
Systole
Left atrium
Right atrium
Right
ventricle
Early diastole
Mid-to-late
diastole
Left ventricle
Phase
1
2
3
4
1
Atrioventricular valves
Open
Closed
Open
Aortic and pulmonary
(semilunar) valves
Closed
Open
Closed
Figure 13.18
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© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Ventricular Systole
• Isovolumetric ventricular contraction
•
AV and aortic valves closed
•
Ventricular pressure increases until it exceeds
atrial pressure
• Ventricular ejection
Copyright
•
Aortic valve opens
•
Blood moves from ventricle to aorta
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
•
AV valve opens
•
Blood moves from atria to ventricle
•
Passive until atrium contracts
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Ventricular Pressure
Figure 13.19
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Aortic Pressure
Figure 13.20
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Ventricular Volume
Copyright
•
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
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Figure 13.21
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
Copyright
•
Louder dubb
•
Semilunar valves close simultaneously
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
•
Extrinsic—neural and hormonal
•
Intrinsic—autoregulation
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
•
Rest: parasympathetic dominates, HR = 75
•
Excitement: sympathetic takes over, HR increases
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
•
Copyright
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
•
Copyright
Thyroid hormones, insulin and glucagon increase
force of contraction
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Sympathetic Effects on Contractility
• Increased
sympathetic activity
•
Increased
epinephrine
release
•
Increases
strength of
contraction
•
Increases rate of
contraction
•
Increases rate of
relaxation
Figure 13.27
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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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Influencing Stroke Volume
Venous return
Sympathetic
activity or
Epinephrine
Ventricle
End-diastolic
volume
Contractility
Arterial pressure
(afterload)
Stroke volume
Figure 13.30
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Influencing Stroke Volume
Venous return
Ventricle
End-diastolic
volume
Stroke volume
Figure 13.30, step 1
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Influencing Stroke Volume
Venous return
Sympathetic
activity or
Epinephrine
Ventricle
End-diastolic
volume
Contractility
Stroke volume
Figure 13.30, step 2
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Influencing Stroke Volume
Venous return
Sympathetic
activity or
Epinephrine
Ventricle
End-diastolic
volume
Contractility
Arterial pressure
(afterload)
Stroke volume
Figure 13.30, step 3
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Regulation of Cardiac Output
Figure 13.31
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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