Download 14a+b_lect

THIRD EDITION
HUMAN PHYSIOLOGY
AN INTEGRATED APPROACH
Dee Unglaub Silverthorn, Ph.D.
Chapter 14
Cardiovascular Physiology
PowerPoint® Lecture Slide Presentation by
Dr. Howard D. Booth, Professor of Biology, Eastern Michigan University
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
About this Chapter
• Blood flow pumping & distribution
• Anatomy and histology of the heart
• Mechanism of cardiac contraction
• Heart beat sequence–how the pump works
• Regulators of heart beat and volume pumped
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The Heart
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The Heart
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Normal and Abnormal Chest X-Rays
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Overview of the Cardiosvascular System
• Heart and Blood vessels
• Products transported to sustain all cells
Table 14-1: Transport in the Cardiovascular System
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Circulation Reviewed
• Heart – "four chambered"
• Right atrium & ventricle
•
Pulmonary circuit
• Left atrium & ventricle
•
Systemic circuit
• Blood Vessels – "closed circulation"
• Arteries –from heart
• Capillaries– cell exchange
• Veins – to heart
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Circulation Reviewed
Figure 14-1: Overview of circulatory system anatomy
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Blood Flow: Pressure Changes
• Flows down a pressure gradient
• Highest at the heart (driving P), decreases over
distance
• Hydrostatic (really hydraulic) pressure in vessels
• Decreases 90% from aorta to vena cava
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Blood Flow: Pressure Changes
Figure 14-2 : Pressure gradient in the blood vessels
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Some Physic of Fluid Movement: Blood Flow
• Flow rate: (L/min)
• Flow velocity
= rate/C-S area of
vessel
• Resistance slows
flow
• Vessel diameter
• Blood viscosity
• Tube length
Figure 14-4 c: Pressure differences of static and flowing fluid
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Some Physic of Fluid Movement: Blood Flow
Figure 14-6: Flow rate versus velocity of flow
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Heart Structure
• Pericardium
• Chambers
• Coronary vessels
• Valves(one-way-flow)
• Myocardium
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Figure 14-7 g: ANATOMY SUMMARY: The Heart
Cardiac Muscle Cells:
• Autorhythmic
• Myocardial
• Intercalated discs
•
Desmosomes
•
Gap Junctions
• Fast signals
• Cell to cell
• Many mitochondria
• Large T tubes
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Figure 14-10: Cardiac muscle
Mechanism of Cardiac Muscle Excitation,
Contraction & Relaxation
Figure 14-11: Excitation-contraction coupling and relaxation in cardiac muscle
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Modulation of Contraction
• Graded Contraction: proportional to crossbridges
formed
• More [Ca++]: crossbridges, more force & speed
• Autonomic n & epinephrine modulation
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Modulation of Contraction
Figure 14-12: Modulation of cardiac contraction by catecholamines
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More Characteristics of Cardiac Muscle
Contraction
• Stretch-length relationship
•  stretch,  Ca++ entering
•  contraction force
• Long action potential
• Long refractory period
• No summation
• No tetanus
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More Characteristics of Cardiac Muscle
Contraction
Figure 14-13: Length-tension relationships in skeletal and cardiac muscle
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More Characteristics of Cardiac Muscle
Contraction
Figure 14-15c: Refractory periods and summation in skeletal and cardiac muscle
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Autorhythmic Cells: Initiation of Signals
• Pacemaker membrane potential
• I-f channels Na+ influx
• Ca++ channels – influx, to AP
• Slow K+ open – repolarization
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Autorhythmic Cells: Initiation of Signals
Figure 14-16: Action potentials in cardiac autorhythmic cells
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Sympathetic and Parasympathetic
• Sympathetic – speeds heart rate by  Ca++ & I-f
channel flow
• Parasympathetic – slows rate by  K+ efflux & 
Ca++ influx
Figure 14-17: Modulation of heart rate by the nervous system
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Coordinating the Pump: Electrical Signal Flow
• AP from autorhythmic cells in sinoatrial node
(SA)
• Spreads via gap junctions down internodal
pathways and across atrial myocardial cells
(atrial contraction starts)
• Pause – atrioventricular (AV) node delay
• AV node to bundles of His, branches & Purkinje
fibers
• Right and left ventricular contraction from apex
upward
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Coordinating the Pump: Electrical Signal Flow
Figure 14-18: Electrical conduction in myocardial cells
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Coordinating the Pump: Electrical Signal Flow
Figure 14-19a: Electrical
conduction in the heart
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Electrocardiogram (ECG):
Electrical Activity of the Heart
• Einthoven's
triangle
• P-Wave –
atria
• QRS- wave –
ventricles
• T-wave –
repolarization
Figure 14-20: Einthoven’s triangle
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Electrocardiogram (ECG):
Electrical Activity of the Heart
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Figure 14-21: The electrocardiogram
Electrocardiography (ECG)
•
Measures galvanically the electric activity of the heart
•
Well known and traditional, first measurements by
Augustus Waller using capillary electrometer (year
1887)
•
Very widely used method in clinical environment
•
Very high diagnostic value
2. Ventricular
depolarization
1. Atrial
depolarization
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3. Ventricular repolarization
12-Lead ECG measurement
•
Most widely used ECG measurement setup in clinical environment
•
Signal is measured non-invasively with 9 electrodes
•
Lots of measurement data and international reference databases
•
Well-known measurement and diagnosis practices
•
This particular method was adopted due to historical reasons, now it is already
rather obsolete
Einthoven leads: I, II & III
Goldberger augmented leads: VR, VL & VF
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Precordial leads: V1-V6
ECG Information Gained
• (Non-invasive)
• Heart Rate
• Signal conduction
• Heart tissue
• Conditions
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Figure 14-24: Normal and abnormal electrocardiograms
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Vectorcardiogram (VCG or EVCG)
• Instead of displaying the scalar amplitude
(ECG curve) the electric activation front is
measured and displayed as a vector (dipole
model)
 It has amplitude and direction
• Diagnosis is based on the curve that the point
of this vector draws in 2 or 3 dimensions
• The information content of the VCG signal is
roughly the same as 12-lead ECG system. The
advantage comes from the way how this
information is displayed
• A normal, scalar ECG curve can be formed
from this vector representation, although (for
practical reasons) transformation can be quite
complicated
• Plenty of different types of VCG systems are in
use
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Heart Cycle
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Figure 14-25: Mechanical events of the cardiac cycle
Heart Cycle:
Heart Chambers and the Beat Sequence
1. Late diastole: all chambers relax, filling with
blood
2. Atrial systole: atria contract, add 20% more
blood to ventricles
3. Isovolumic ventricular contraction: closes AV
valves ("lub"), builds pressure
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Heart Cycle: Finish and Around To the Start
4. Ventricular ejection: pushes open semi lunar
valves, blood forced out
5. Ventricular relaxation: aortic back flow slams
semi lunar valves shut ("dub")
AV valves open refilling starts – back to start of
cycle
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Summary of Heart Beat:
Electrical, Pressure and Chamber Volumes
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Figure 14-27: The Wiggers diagram
Regulators of the Heart: Reflex Controls of Rate
• Range: about 50 – near 200
• Typical resting: near 70
• AP conduction
• Muscle Contraction
• Parasympathetic slows
• Sympathetic speeds
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Regulators of the Heart: Reflex Controls of Rate
Figure 14-28: Reflex control of heart rate
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Cardiac Output: Heart Rate X Stroke Volume
• Around 5L :
(72 beats/m  70 ml/beat = 5040 ml)
• Rate: beats per minute
• Volume: ml per beat
• EDV - ESV
• Residual (about 50%)
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Deep Vein Thrombosis
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Clot
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Leg Swelling from Deep Vein Thrombosis
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Pulmonary Embolus
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Vena Caval Filter
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Cardiac Output: Heart Rate X Stroke Volume
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Figure 14-26: The Wiggers diagram
Left Ventricular
Pressure-Volume Loops
• Pressure-volume loop
plots LV pressure
against LV volume
through one complete
cardiac cycle
• Factors affecting:
– Preload
– Afterload
– Contractility
– IHSS
– Valvular problems
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Left Ventricular
Pressure-Volume Loops
•
KNOW:
1. When the mitral and aortic valves are open and
closed during each phase
2. When systole begins (B) and ends (D)
3. When diastole begins (D) and ends (B)
4. Diastolic filling occurs between points A and B
5. Ejection occurs between points C and D
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Left Ventricular
Pressure-Volume Loops
• Acute changes in
preload
– Increased preload:
• Filling increases
• SV increases
– Decreased preload:
• Filling decreases
• SV decreases
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*NOTE: the ventricle
empties to the same
end-systolic volume
after either an increase
or decrease in preload
Left Ventricular
Pressure-Volume Loops
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Left Ventricular
Pressure-Volume Loops
• Acute changes in
Afterload
– Increased afterload:
• Ventricle empties
less completely
• SV decreases
• Increase in BP
(shifts up and right)
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– Decreased afterload:
• Ventricle empties
more completely
• SV increases
• Decrease in BP
(shifts down and left)
Left Ventricular
Pressure-Volume Loops
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Left Ventricular
Pressure-Volume Loops
• Altered contractility
– Increased
contractility:
• Ventricle empties
more completely
• SV increases
• BP increases
(shifts up and left)
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– Decreased
contractility:
• Ventricle empties
less completely
• SV decreases
• BP decreases
(shifts down and right)
Left Ventricular
Pressure-Volume Loops
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Left Ventricular
Pressure-Volume Loops
• Summary of concepts:
– Alterations in preload: end-diastolic volume
increases or decreases, but the amount of blood
in the chamber at end-systole does not change
– Stroke volume falls: result of either an increase
in afterload or a decrease in contractility, the
volume of blood in the LV chamber increases
(chamber dilates)
– Stroke volume increases: result of a decrease in
afterload or an increase in contractility, the
volume of blood in the LV chamber decreases
(chamber shrinks)
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Left Ventricular
Pressure-Volume Loops
• A = Normal
• B = Mitral
stenosis
• C = Aortic stenosis
• D = mitral
regurgitation
(chronic)
• E = aortic
regurgitation
(chronic)
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Regulators of the Heart:
Factors Influencing Stroke Volume
• Starlings Law – stretch
• Force of contraction
• Venous return:
• Skeletal pumping
• Respiratory pumping
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Regulators of the Heart:
Factors Influencing Stroke Volume
Figure 14-29: Length-force relationships in the intact heart
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Regulators of the Heart:
Factors Influencing Stroke Volume
Figure 14-31: Factors that affect cardiac output
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Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Copyright © 2004 Pearson Education, Inc., publishing as Benjamin Cummings
Summary
• Anatomy and physiology of the Heart , its
chambers, muscles, valves, and its pacemaker
• Mechanism of cardiac muscle stimulation and
contraction
• Blood vessels and fluid flow down a pressure
gradient
• Electrical control of the beat sequence, and ECG
information
• Influence of beat rate and stroke volume by ANS
and hormones
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