1. Cardiovascular Physiology
Chapter 14b
Cardiovascular Physiology

2. Action Potentials in Cardiac Autorhythmic Cells
Pacemaker potential - no resting
-60mV drifts to -40 to action potential
Spread through connections to contractile fibers
If channels are permeable to both K+ and Na+ 20
Ca2+ channels close, K+ channels open
Ca2+ in
K+ out
Lots of Ca2+ channels open
–20
Membrane potential (mV)
Threshold
–40
Ca2+ in
Some Ca2+ channels open, If channels close
–60
If channels open
Net Na+ in
If channels open
Pacemaker potential
Action potential
K+ channels close
Time
Time
Time
(a) The pacemaker potential gradually becomes less negative until it reaches threshold, triggering an action potential.
(b) Ion movements during an action and pacemaker potential
(c) State of various ion channels
Figure 14-15

3. Action Potentials in Cardiac Autorhythmic Cells
PLAY
Interactive Physiology® Animation: Cardiovascular System: Cardiac Action Potential

4. Modulation of Heart Rate by the Autonomic Nervous System
Normal
Sympathetic stimulation
Normal
Parasympathetic stimulation 20 20
Membrane potential (mV)
–20
Membrane potential (mV)
–40
–60
–60
Depolarized
More rapid depolarization
Hyperpolarized
Slower depolarization
0.8
1.6
2.4
0.8
1.6
2.4
Time (sec)
Time (sec)
(a)
(b)
Figure 14-16

5. Action Potentials
Table 14-3

6. Electrical Conduction in Myocardial Cells
Membrane potential of autorhythmic cell
Membrane potential of contractile cell
Cells of SA node
Contractile cell
Intercalated disk with gap junctions
Depolarizations of autorhythmic cells rapidly spread to adjacent contractile cells through gap junctions.
Figure 14-17

7. Electrical Conduction in the Heart1 1
SA node depolarizes.
SA node
AV node 2 2
Electrical activity goes rapidly to AV node via internodal pathways. 3
Depolarization spreads more slowly across atria. Conduction slows through AV node.
THE CONDUCTING SYSTEM OF THE HEART 4
Depolarization moves rapidly through ventricular conducting system to the apex of the heart.
SA node 3
Internodal pathways 5
Depolarization wave spreads upward from the apex.
AV node
AV bundle 4
Bundle branches
Purkinje fibers 5
Figure 14-18

8. Electrical Conduction
SA node
Sets the pace of the heartbeat at 70 bpm
AV node (50 bpm) and Purkinje fibers (25-40 bpm) can act as pacemakers under some conditions
AV node
Routes the direction of electrical signals
Delays the transmission of action potentials

9. Einthoven’s Triangle Right arm Left arm I
Electrodes are attached to the skin surface. II
III
A lead consists of two electrodes, one positive and one negative.
Left leg
Figure 14-19

10. The Electrocardiogram
Three major waves: P wave, QRS complex, and T wave
Figure 14-20

11. Correlation between an ECG and electrical events in the heart
Electrical Activity
Correlation between an ECG and electrical events in the heart
START
P wave: atrial depolarization P
The end R
PQ or PR segment: conduction through AV node and AV bundle P T Q S P
Atria contract
T wave: ventricular repolarization
Repolarization
ELECTRICAL
EVENTS OF THE CARDIAC
CYCLE R P T Q S P
Q wave
ST segment Q R P
R wave R Q S
Ventricles contract R P Q P
S wave Q S
Figure 14-21

12. Electrical Activity Figure 14-21 (9 of 9)
P wave: atrial depolarization
START P
The end R
PQ or PR segment: conduction through AV node and AV bundle P T Q S P
Atria contract
T wave: ventricular repolarization
Repolarization
ELECTRICAL
EVENTS OF THE CARDIAC
CYCLE R P T Q S
Q wave P
ST segment Q R P
R wave R Q S
Ventricles contract R P Q P
S wave Q S
Figure (9 of 9)

13. Comparison of an ECG and a myocardial action potential
Electrical Activity
Comparison of an ECG and a myocardial action potential
1 mV
1 sec
(a) The electrocardiogram represents the summed electrical activity of all cells recorded from the surface of the body.
110 mV
1 sec
(b) The ventricular action potential is recorded from a single cell using an intracellular electrode. Notice that the voltage change is much greater when recorded intracellularly.
Figure 14-22

14. Normal and abnormal electrocardiograms
Electrical Activity
Normal and abnormal electrocardiograms
Figure 14-23

15. Mechanical events of the cardiac cycle1
Late diastole—both sets of chambers are relaxed and ventricles fill passively.
START 5
Isovolumic ventricular relaxation—as ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them closed. 2
Atrial systole—atrial contraction forces a small amount of additional blood into ventricles. S1 S2 3
Isovolumic ventricular contraction—first phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves. 4
Ventricular ejection— as ventricular pressure rises and exceeds pressure in the arteries, the semilunar valves open and blood is ejected.
Figure 14-24

16. Cardiac Cycle
PLAY
Interactive Physiology® Animation: Cardiovascular System: Cardiac Cycle

17. Left ventricular pressure-volume changes during one cardiac cycle
KEY
EDV = End-diastolic volume
Stroke volume
120 D
ESV = End-systolic volume
ESV 80 C
One cardiac cycle
Left ventricular pressure (mmHg) 40
EDV B A 65
100
135
Left ventricular volume (mL)
Figure 14-25

18. Wiggers Diagram Figure 14-26 Time (msec) 100 200 300 400 500 600 700
100
200
300
400
500
600
700
800
QRS complex
Electro- cardiogram (ECG)
QRS complex P T P
120 B 90
Aorta
Dicrotic notch
Pressure (mm Hg) A
Left venticular pressure 60 30
Left atrial pressure D C S1 S2
Heart sounds
135 E
Left ventricular volume (mL) 65 F
Atrial systole
Ventricular systole
Ventricular diastole
Atrial systole
Atrial systole
Isovolumic ventricular contraction
Ventricular systole
Early ventricular diastole
Late ventricular diastole
Atrial systole
Figure 14-26

19. Wiggers Diagram Figure 14-26 (13 of 13) Time (msec) 100 200 300 400
100
200
300
400
500
600
700
800
QRS complex
Electro- cardiogram (ECG)
QRS complex P T P
120 B 90
Aorta
Dicrotic notch
Pressure (mm Hg) A
Left venticular pressure 60 30
Left atrial pressure D C S1 S2
Heart sounds
135 E
Left ventricular volume (mL) 65 F
Atrial systole
Ventricular systole
Ventricular diastole
Atrial systole
Atrial systole
Isovolumic ventricular contraction
Ventricular systole
Early ventricular diastole
Late ventricular diastole
Atrial systole
Figure (13 of 13)

20. Stroke Volume and Cardiac Output
Amount of blood pumped by one ventricle during a contraction
EDV – ESV = stroke volume
Cardiac output
Volume of blood pumped by one ventricle in a given period of time
CO = HR  SV
Average = 5 L/min

21. Autonomic Neurotransmitters Alter Heart Rate
KEY
Integrating center
Cardiovascular control center in medulla oblongata
Efferent path
Effector
Tissue response
Sympathetic neurons (NE)
Parasympathetic neurons (Ach)
1-receptors of autorhythmic cells
Muscarinic receptors of autorhythmic cells
Na+ and Ca2+ influx
K+ efflux; Ca2+ influx
Hyperpolarizes cell and rate of depolarization
Rate of depolarization
Heart rate
Heart rate
Figure 14-27

22. Frank-Starling law states
Stroke Volume
Frank-Starling law states
Stroke volume increase as EDV (ending diastolic volume) increases – stretch -> more force
EDV is affected by venous return
Venous return is affected by
Skeletal muscle pump
Respiratory pump
Sympathetic innervation of vessels
Force of contraction is affected by
Stroke volume
Length of muscle fiber and contractility of heart

23. Length-force relationships in intact heart: a Starling curve
Stroke Volume
Length-force relationships in intact heart: a Starling curve
Figure 14-28

24. The effect of norepinepherine on contractility of the heart
Inotropic Effect
The effect of norepinepherine on contractility of the heart
Figure 14-29

25. Cardiac Output
PLAY
Interactive Physiology® Animation: Cardiovascular System: Cardiac Output

26. Catecholamines Modulate Cardiac Contraction
Epinephrine and norepinephrine
bind to
1-receptors
that activate
cAMP second messenger system
resulting in phosphorylation of
Voltage-gated Ca2+ channels
Phospholamban
Open time increases
Ca2+-ATPase on SR
Ca2+ entry from ECF
Ca2+ stores in SR
Ca2+ removed from cytosol faster
Shortens Ca-troponin binding time
Ca2+ released
KEY
SR = Sarcoplasmic reticulum
Shorter duration of contraction
ECF = Extracelllular fluid
More forceful contraction
Figure 14-30

27. Stroke Volume and Heart Rate Determine Cardiac Output
is a function of
Heart rate
Stroke volume
determined by
determined by
Rate of depolarization in autorhythmic cells
Force of contraction in ventricular myocardium
is influenced by
Decreases
Increases
increases
Contractility
End-diastolic volume
Sympathetic innervation and epinephrine
Due to parasympathetic innervation
which varies with
increases
Venous constriction
Venous return
aided by
Skeletal muscle pump
Respiratory pump
Figure 14-31

28. Cardiovascular system—anatomy review
Summary
Cardiovascular system—anatomy review
Pressure, volume, flow, and resistance
Pressure gradient, driving pressure, resistance, viscosity, flow rate, and velocity of flow
Cardiac muscle and the heart
Myocardium, autorhythmic cells, intercalated disks, pacemaker potential, and If channels
The heart as a pump
SA node, AV node, AV bundle, bundle branches, and Purkinje fibers

29. The heart as a pump (continued) The cardiac cycle
Summary
The heart as a pump (continued)
ECG, P wave, QRS complex, and T wave
The cardiac cycle
Systole, diastole, AV valves, first heart sound, isovolumic ventricular contraction, semilunar valves, second heart sound, and stroke volume
Cardiac output
Frank-Starling law, EDV, preload, contractility, inotropic effect, afterload, and ejection fraction