Transcript Chapter 14b

Chapter 14b
Cardiovascular
Physiology
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
Membrane potential (mV)
0
Ca2+ in
K+ out
–20
–40
Lots of Ca2+
channels
open
Threshold
Some Ca2+
channels open,
If channels close
Ca2+ in
–60
Net Na+ in
Pacemaker
potential
If channels
open
Action
potential
Time
(a) The pacemaker potential
gradually becomes less negative
until it reaches threshold,
triggering an action potential.
Time
(b) Ion movements during an action
and pacemaker potential
If channels
open
K+ channels close
Time
(c) State of various ion channels
Figure 14-15
Action Potentials in Cardiac Autorhythmic Cells
PLAY
Interactive Physiology® Animation: Cardiovascular
System: Cardiac Action Potential
Sympathetic stimulation
Normal
Membrane potential (mV)
Membrane potential (mV)
Modulation of Heart Rate by the Autonomic Nervous
System
20
0
–20
–40
–60
Depolarized
Normal
0
–60
More rapid depolarization
0.8
1.6
Hyperpolarized
2.4
Slower depolarization
0.8
Time (sec)
(a)
Parasympathetic stimulation
20
1.6
2.4
Time (sec)
(b)
Figure 14-16
Action Potentials
Table 14-3
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
Electrical Conduction in the Heart
1
1 SA node depolarizes.
SA node
AV node
2 Electrical activity goes
rapidly to AV node via
internodal pathways.
2
3 Depolarization spreads
more slowly across
atria. Conduction slows
through AV node.
THE CONDUCTING SYSTEM
OF THE HEART
SA node
3
Internodal
pathways
4 Depolarization moves
rapidly through ventricular
conducting system to the
apex of the heart.
5
Depolarization wave
spreads upward from
the apex.
AV node
4
AV bundle
Bundle
branches
Purkinje
fibers
5
Figure 14-18
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
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
The Electrocardiogram
• Three major waves: P wave, QRS complex,
and T wave
Figure 14-20
Electrical Activity
• Correlation between an ECG and electrical
events in the heart
P wave: atrial
depolarization
START
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
Q S
Atria contract
T wave:
ventricular
repolarization
Repolarization
R
ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
T
P
Q S
P
ST segment
Q wave
Q
R
R wave
P
R
Q S
R
Ventricles contract
P
Q
S wave
P
Q S
Figure 14-21
Electrical Activity
START
P wave: atrial
depolarization
P
The end
R
P
PQ or PR segment:
conduction through
AV node and AV
bundle
T
P
QS
Atria contract
T wave:
ventricular
repolarization
R
T
P
Repolarization ELECTRICAL
EVENTS
OF THE
CARDIAC
CYCLE
QS
P
ST segment
R
Q wave
Q
R wave
R
P
QS
R
Ventricles contract
P
Q
P
S wave
QS
Figure 14-21 (9 of 9)
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
Electrical Activity
• Normal and abnormal electrocardiograms
Figure 14-23
Mechanical Events
• Mechanical events of the cardiac cycle
1
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.
3
Isovolumic ventricular
contraction—first phase of
ventricular contraction pushes AV
valves closed but does not create
enough pressure to open semilunar
valves.
S1
S2
4
Ventricular ejection—
as ventricular pressure
rises and exceeds pressure
in the arteries, the semilunar
valves open and blood is
ejected.
Figure 14-24
Cardiac Cycle
PLAY
Interactive Physiology® Animation: Cardiovascular
System: Cardiac Cycle
Cardiac Cycle
• Left ventricular pressure-volume changes
during one cardiac cycle
Stroke volume
120
Left ventricular pressure (mmHg)
KEY
EDV = End-diastolic
volume
ESV = End-systolic
volume
ESV
D
80
C
One
cardiac
cycle
40
B
EDV
A
0
65
100
Left ventricular volume (mL)
135
Figure 14-25
Wiggers Diagram
Time (msec)
0
Electrocardiogram
(ECG)
100
200
300
400
500
600
700
800
QRS
complex
QRS
complex
P
T
P
120
B
90
Pressure
(mm Hg)
Dicrotic notch
A
60
Left
venticular
pressure
30
Left atrial
pressure
0
D
C
S1
Heart sounds
135
S2
E
Left
ventricular
volume (mL)
F
65
Atrial
systole
Atrial
systole
Ventricular
systole
Ventricular
diastole
Isovolumic Ventricular
Early
Late
ventricular
systole
ventricular ventricular
contraction
diastole
diastole
Atrial
systole
Atrial
systole
Figure 14-26
Wiggers Diagram
Time (msec)
0
Electrocardiogram
(ECG)
100
200
300
400
500
600
700
800
QRS
complex
QRS
complex
P
T
P
120
B
90
Dicrotic notch
A
Pressure
(mm Hg)
60
Left
venticular
pressure
30
Left atrial
pressure
0
D
C
S1
Heart sounds
135
S2
E
Left
ventricular
volume (mL)
F
65
Atrial
systole
Atrial
systole
Ventricular
systole
Ventricular
diastole
Isovolumic Ventricular
Early
Late
ventricular
systole
ventricular ventricular
contraction
diastole
diastole
Atrial
systole
Atrial
systole
Figure 14-26 (13 of 13)
Stroke Volume and Cardiac Output
• Stroke volume
• 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
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
Rate of depolarization
Hyperpolarizes cell and
rate of depolarization
Heart rate
Heart rate
Figure 14-27
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
Stroke Volume
• Length-force relationships in intact heart: a
Starling curve
Figure 14-28
Inotropic Effect
• The effect of norepinepherine on contractility
of the heart
Figure 14-29
Cardiac Output
PLAY
Interactive Physiology® Animation: Cardiovascular
System: Cardiac Output
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
KEY
Ca2+ stores in SR
Ca2+ released
Ca2+ removed from cytosol faster
Shortens Ca-troponin
binding time
SR = Sarcoplasmic
reticulum
ECF = Extracelllular
fluid
More forceful
contraction
Shorter
duration
of contraction
Figure 14-30
Stroke Volume and Heart Rate Determine Cardiac
Output
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
Due to
parasympathetic
innervation
Increases
increases
Contractility
Sympathetic
innervation and
epinephrine
increases
End-diastolic
volume
which varies with
Venous constriction
Venous return
aided by
Skeletal muscle
pump
Respiratory
pump
Figure 14-31
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
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