Download The Cardiovascular System: Cardiac Function

PRINCIPLES OF
HUMAN PHYSIOLOGY
13
THIRD EDITION
Cindy L. Stanfield | William J. Germann
The Cardiovascular
System:
Cardiac Function
Part B
PowerPoint® Lecture Slides prepared by W.H. Preston, College of the Sequoias
Copyright © 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Aortic Pressure
Figure 13.20
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Ejection Fraction
Fraction of end-diastolic volume ejected during a
heartbeat
Ejection fraction =
stroke volume / end diastolic volume
= 70 mL / 130 mL = 0.54
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Sympathetic Effects: SA Potentials
Figure 13.25
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Factors Affecting Cardiac Output: Stroke Volume
Primary factors affecting stroke volume
• Ventricular contractility
• End-diastolic volume
• Afterload
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Intrinsic Control - Frank-Starling’s Law
Increase venous return
Increase strength of contraction
Increase stroke volume
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Starling’s Law
Figure 13.28
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
Starling’s Law
Figure 13.29
Copyright
© 2008 Pearson Education, Inc., publishing as Benjamin Cummings.
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.