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Chapter 4
BLOOD
CIRCULATION
Key points in this unit:
1.the action potential of the ventricular
muscle and the action potential of the
pacemaker cells.
2.electrophysiological properties of
cardiac muscle.
1.Physiology
of the heart
Function of heart
Pumping
Endocrine
atrial natriuretic
peptide(ANP,心房钠尿肽)
brain natriuretic
peptide(BNP,脑钠尿肽)
General process of
excitation and contraction
of cardiac muscle
• Initiation of action
potential in sinoatrial node
• Conduction of action
potential along specialized
conductive system
• Excitation-contraction
coupling
• Muscle contraction
+30
0
细
胞
内
电
位
(
除
极
化
复
极
化
mV
)
阈电位
-55
后电位
-70
静息电位
0
2
4
6
8
10
12
时间(ms)
神经或骨骼肌AP
心室肌AP
1.1 Action potentials in cardiac muscle
Two major types of cardiac muscle:
Working cardiac muscle cell:
atrial and ventricular
muscle cells
non-autorhythmic cardiac
cell
Specialized excitatory
and conductive muscle:
sinoatrial (SA) node,
Purkinje fiber
autorhythmic cardiac
cell
1.1.1 AP of ventricular muscle
Phase 0: rapid depolarization
-90mV-+30mV
Phase1: early phase of
rapid repolarization
+30mV-+10mV
Phase2: the plateau or slow
phase of repolarization
+10-0mV
Phase3: late phase of rapid
repolarization
0mV-90mV
Phase4: resting phase
-90mV
Mechanism
K+
Phase 0:
Na+
influx
K+,Ca2+,Na+
Phase 1: K+ outflux
Phase 2: K+ outflux,
Ca2+ and Na+ influx
Phase 3: K+ outflux
Phase 4: Na+ - K+ pump
Ca2+ pump
Na+ - Ca2 exchanger
Na+
K+
Phase2 needs 100-150ms.
the main cause of long duration of
cardiac action potential.
the main characteristic which differs
from the action potential in nervous
fiber or skeletal muscle.
resting potential
maximal repolarization
potential
working cells phase4
stable
autorhythmic cells phase4
spontaneous depolarization
1.1.2 AP of Purkinje cell
quite similar to that of working cells except
spontaneous depolarization during phase 4.
Phase 4:
内向电流
If (inward current, caused
by Na+ influx) increases
outward current ( caused by
K+ outflux) decreases
gradually.
If
1.1.3 AP of the P cell of SA node
Phase 0: Ca2+ influx
Slow response cell
Phase 3: K+ outflux
Phase 4: fast spontaneous depolarization
ICa
0
3
IK
4
IK, If, ICa
IK decreases
If increases
ICa-T
outflow of K+ inflow of Na+
outflow of K+ < inflow of Na+
2. Electrophysiological
Characteristics of cardiac muscle
2.1 Excitability
2.1.1 Factors affecting excitability
o Level of RP ↓ :→ excitability ↓
o Level of TP:↑→ excitability ↓
o States of sodium channel:
resting state: excitability is normal
activated state: Na+ diffuse in
inactivated state: excitability is zero
2.1.2 Excitability changes:
o Effective refractory period (ERP ):
Any strong stimulus fails to elicit an AP.
Cause: The sodium channels are at inactivated state and
so the excitability is zero.
ERP is nearly 100-250ms.
Significance:
the heart can not be
tetanized.
the heart can
ERP
eject and fill continually.
ARP:phase0---phase3 -55mV
ERP
LRP:phase0---phase3 -60mV
o Relative refractory period
phase3 -60-- -80mV
Effective stimulus is suprathreshold stimulus.
Cause: the most sodium channels are at resting
state but their opening ability are not good as
normal, so the excitability is lower than
normal.
o Supranormal period
phase3 -80-- -90mV
subthreshold stimulus can elicit an AP.
Cause: the sodium channels are at resting state and the
distance between the resting potential and the
threshold potential is nearer, so the excitability is
better than normal.
2.1.3 Extrasystole and compensatory pause
①extrasystole (期前收缩)
premature systole
②compensatory pause
(代偿间歇)
①
②
ERP
After ERP, a stimulus can
evoke a extrasystole.
compensatory pause:
a S-A node AP meets the
ERP of extrasystole.
2. 2 Autorhythmicity
the ability that the cardiac muscle can
generate an action potential by itself.
Index: frequency of AP
SA node
AV node
left,right bundle branch
terminal Purkinje cells
(beats/min)
50
100
40
25
Natural pacemaker: the pacemaker which can
control the activity of the heart under normal
condition.(SA node)
Latent pacemaker: the pacemaker which doesn’t
show its autorhythmicity under normal
condition. (other rhythmic regions of the heart)
Ectopic pacemaker: from latent pacemaker
① autorhythmicity of latent pacemaker
increases
② autorhythmicity of SA node decreases
③ severe conduction block
Why can SA node be natural pacemaker?
① Preoccupation(抢先抑制): SA node
autorhythmicity is much higher than latent
pacemakers and elicit excitations before they
finish phase 4.
② Overdrive suppression(超速抑制):The higher
rate pacemaker suppresses the
autorhythmicity of the lower rate pacemakers
Factors affecting Autorhythmicity
o Velocity of spontaneous depolarization:
↑(b to a)→autorhythmicity
o Threshold potential:
(TP2 to TP1)→ autorhythmicity ↑
o Maximum repolarization potential
(d to a)→ autorhythmicity ↑
2.3 Conductivity
2.3.1Specialized conducting system
SA node
preferential pathway
(优势通路)
AV node
AV bundle
right and left bundle branch
terminal Purkinje fibers
传导最慢 纤维最小,缝
隙连接少,慢反应细胞
0.1s
synchronization
contraction
2.3.2 Factors affecting conduction velocity
Rate and amplitude of phase0 depolarization:
local current↑→ conduction↑
rate and number of Na+or Ca2+ influx
level of resting potential
concentration and potential gradient of Na+, Ca2+
Structure of cardiac muscle:
diameter↑→ local current↑→conduction↑
number of intercalated disc (gap junction)
Excitability of the adjacent region:
↑→conduction ↑
2.3.3 Spread of cardiac impulse
Electrocardiogram (ECG)
With an electrocardiogragh, electrical
activity of the heart can be recorded
from the surface of the body.
When a large number of cells are
simultaneously depolarizing or
repolarizing, large voltages are
observed on ECG.
• Normal ECG
P wave : depolarization of the
atria.
PQ(PR) interval:
from the onset of atrial
excitation to the onset of Q
QRS complex:
depolarization of the
ventricles.
S-T segment : from the end
of QRS complex to the
onset of T wave (plateau)
T wave : repolarization
of the ventricles.
Q-T interval :
from the onset of QRS
complex to the end of the T
wave. (AP duration)
+30
反极化
0
细
胞
内
电
位
(
除
极
化
复
极
化
mV
) -55
阈电位
e
-70
a
b
2
c
4
静息电位
f
d
6
时间(ms)
8
10
12
14
• Cardiac muscle as a syncytium
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