principles of human physiology third edition cindy l. stanfield | william j. germann powerpoint ®...

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


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


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


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


Ventricular Pressure

Figure 13.19


Aortic Pressure

Figure 13.20


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


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


Ejection Fraction

Fraction of end-diastolic volume ejected during a heartbeat

Ejection fraction = stroke volume / end diastolic volume

= 70 mL / 130 mL = 0.54


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


Heart Sounds

Figure 13.22


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


Regulation of Cardiac Output

• Regulate heart rate and stroke volume

• Extrinsic and intrinsic regulation

• Extrinsic—neural and hormonal

• Intrinsic—autoregulation


Autonomic Inputs to Heart

Figure 13.23


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


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


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


Sympathetic Effects: SA Potentials

Figure 13.25


Factors Affecting Cardiac Output: Stroke Volume

Primary factors affecting stroke volume

• Ventricular contractility

• End-diastolic volume

• Afterload


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


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


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


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


Intrinsic Control - Frank-Starling’s Law

Increase venous return

Increase strength of contraction

Increase stroke volume


Starling’s Law

Figure 13.28


Starling’s Law

Figure 13.29


Factors Affecting End-Diastolic Volume

• End-diastolic pressure = preload

• Filling time

• Atrial pressure

• Central venous pressure

• Afterload = pressure in aorta during ejection


Factors Influencing Stroke Volume

Figure 13.30

Stroke volume

End-diastolicvolume

Venous return

Contractility Arterial pressure(afterload)

Sympatheticactivity orEpinephrine

Ventricle



Figure 13.30, step 1

Stroke volume

End-diastolicvolume

Venous return

Ventricle




Stroke volume

End-diastolicvolume

Venous return

Contractility


Ventricle




Stroke volume

End-diastolicvolume

Venous return

Contractility Arterial pressure(afterload)


Ventricle


Regulation of Cardiac Output

Figure 13.31

principles of human physiology third edition cindy l. stanfield | william j. germann powerpoint ®...

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