Section 2 Electrophysiology of the Heart
Two kinds of cardiac
cells
1, The working cells.
Special property:
contractility
2, Special conduction
system, including the
sinoatrial node,
atrioventricular node,
atrioventricular bundle
(bundle of His), and
Purkinje system.
Special property:
automaticity
I.
Transmembrane Potentials of Myocardial Cells
1. Transmembrane Potentials in Working Myocardial Cells
1
2
0
3
4
(1)General description
Resting potential: -90mv (85-95mv)
Action Potential
Phase 0: rapid
depolarization, 1-2ms
Phase 1: early rapid
repoarization, 10 ms
Phase 2: plateau, slow
repolarization, the
potential is around 0 mv.
100 – 150ms
Phase 3, late rapid
repolarization. 100 – 150
ms
Phase 4 resting potentials
(2) Ionic bases of transmembrane
potentials
Resting potential: the equilibration
potential of potassium
Action potential:
Phase 0, Na+ influx. The threshold
potential, -70 mv
Phase 1, K+ outward flow
Phase 2, Ca2+ inward flow and K+
outward flow
Phase 3, K+ outward flow
Phase 4, Na+ - K+ pump and Na + - Ca2 +
exchange
(primary and secondary active transport)
2. Transmembrane Potential of Rhythimic Cells
(1) Purkinje cell
The phases 0 – 3 are almost
the same with that of
ventricle cells.
At phase 4, the membrane
potential does not maintain
at a level, but depolarizes
automatically – the
automaticity
Mechanism: If, a kind of Na+ channel that is activated by the
hyperpolarization. It is not the same with the fast Na+ channel at phase 0.
It could be blocked by Cs but is not affected by TTX .
(2) The SA node cell
Transmembrane potential of the
sinoatrial node cell
1) Maximal repolarization
(diastole) potential, –70mv
2) Low amplitude and long
duration of phase 0. It is not
so sharp as ventricle cell and
Purkinje cell.
3) No phase 1 and 2
A, Cardiac ventricular cell
B, Sinoatrial node cell
4) Comparatively fast
spontaneous depolarization at
phase 4
Mechanism of the membrane potential
Phase 0, I Ca-L,
slow channel and
slow response cell
Phase 3, Ik, the
time dependent
channel, was
slowly inactivated
near the maximal
repolarization
potential (-60 mv)
Phase 4
Ik, ICa-T and If
ICa-T, activated at –50 mv during the repolarization and contribute to
the spontaneous deplorization during the Phase 4
Fast and slow response, rhythmic
and non-rhythmic cardiac
cells
1) Fast response, non –rhythmic
cells: working cells
2) Fast response, rhythmic cells:
cells in special conduction
system of A-V bundle and
Purkinje network.
3) Slow response, non-rhythmic
cells: cells in nodal area
4) Slow response rhythmic cells:
S-Anode, atrionodal area
(AN), nodal –His (NH)cells
II Electrical Properties of Cardiac Cells
Excitability, Conductivity and Automaticity
1. Excitability of Cardiac Muscle
(1) Factors determining the excitability
1) Resting potential or maximum diastole potential (rhythmic cell). Low
concentration of K+ outside the cell --- resting potential lower –
excitability lower
2) Threshold potential. High concentration of Ca2+ outside the cell –
threshold potential less negative – excitability lower
3) States of Na+ channel.
Resting state: close (could open at the threshold potential); activation
(open); inactivation (close, but could not open at any potential), this
state will transfer to resting state after a period of repolarization.
(2) Changes in excitability during an action potential
1) Effective refractory period, including:
A, Absolute refractory period, from the beginning of phase 0 to –60mv
of repolarization, no response to stimulus
State of Na+ channel, inactivation
B, Local potential period, form the –60mv to –55mg of phase 3, very
strong stimulus can elicit local response but not action potential
State of Na+ channel, most of them are inactivation
Common properties of A and B, from the beginning of phase 0 to –55mv
of phase 3, no action potential can be elicited, no matter how strong
the stimulus is – effective refractory period
2) Relative refractory period, from –60 mv to –80 mv of phase 3, a
stronger stimulus can elicit action potential, although the duration,
amplitude and slope of the upstroke is shorter and smaller
State of Na+ channel, part of them return to the resting state
3) Supernatural period
From –80 mv to –90 mv of phase 3, the excitability is higher than normal
Na+ state. Most of the Na+ channel have returned to the resting
condition.
The potential is higher than the resting potential
(3) Relationship between the excitability and contraction of myocardium
1) No tetanus in cardiac muscle, systole and diastole occur alternately. It
is very important for pumping blood to arteries.
2) Premature excitation, premature contraction and compensatory pause
Extra-stimulus – premature excitation – premature contraction –
compensatory pause
2. Automaticity (Autorhythmicity)
Concept: Some tissues or cells have the ability to produce spontaneous
rhythmic excitation without external stimulus.
(1) Different intrinsic rhythm of rhythmic cells
Purkinje fiber, 15 – 40 /min
Atrioventricular node 40 – 60 /min
Sinoatrial node 90 – 100 /min
Concept: normal pacemarker, latent pacemarker, ectopic pacemarker
(2) The mechanism that SA node controls the hearts rhythm (acts as
pacemaker) rather than the AV node and Purkinje fiber
1) The capture effect
2) Overdrive suppression
(3) Factors determining automaticity
1)Depolari
zation rate
of phase 4
2)Threshol
d potential
3)The
maximal
repolarizati
on
potential
3. Conductivity
(1) Pathways and characteristics of conduction in heart
Pathways: S-A node -- A-V node --- Bundle of His --- R.L. bundle
branches --- Purkinje network – ventricular muscles
Conductive speed of different cardiac muscles:
Atrial myocardium, 0.4m/s; nodal area of A-V junction, 0.02 m/s;
Purkinje network, 4m/s; ventricle myocardium, 1m/s
Characteristics
1) Delay in transmission at the A-V node (150 –200 ms) – sequence of
the atrial and ventricular contraction – physiological importance
2) Rapid transmission of impulses in the Purkinje system –
synchronize contraction of entire ventricles – physiological
importance
(2) Factors determining conductivity
1) Anatomical factors
A. Gap junction between working cells and functional atrial and
ventricular syncytium
B. Diameter of the cardiac cell – conductive resistance – conductivity
2) Physiological factors
A. Slope of depolarization and amplitude of phase 0
Fast and slow response cells
Factors that affect the depolarization rate of phase 0
B. Excitability of the adjacent unexcited membrane
III. Neural and humoral control of the cardiac function
1. Vagus nerve and acetylcholine (Ach)
Vagus nerve – release Ach from postganglionic fiber – M receptor on
cardiac cells - K+ channel permeability increase but Ca 2+ channel
permeability decrease
1) K+ channel permeability increase – resting potential (maximal
diastole potential) more negative – excitability decrease
2) On SA node cells, K+ channel permeability increase – the
depolarization velocity at phase 4 decrease + maximal diastole
potential more negative – automaticity decrease – heart rate decrease
--- Negative chronotropic action
3) Ca2+ channel permeability decrease – myocardial contractility
decrease – negative inotropic action
4) Ca2+ channel permeability decrease – depolarization rate of slow
response cells decrease – conductivity of these cell decrease –
negative dromotropic action
2. Effects of Sympathetic Nerve and catecholamine on the Properties of
Cardiac Muscle
Sympathetic nerve release norepinephrine from the postganglionic
endings; epinephrine and norepinephrine released from the adrenal
glands – binding with β1 receptor on cardiac cells – increase the Ca2+
channel permeability –
Increase the spontaneous depolarization rate at phase 4 – automaticity of
SA node cell rise – heart rate increase – Positive chronotropic action
Increase the depolarization rate (slope) and amplitude at phase 0 –
increase the conductivity of slow response cells – Positive dromotropic
action
Increase the Ca2+ concentration in plasma during excitation – myocardial
contractility increase -- positive inotropic action
Effect of autonomic nerve activity on the heart
Region affected
Sympathetic Nerve
Parasympathetic Nerve
SA node
Increased rate of diastole Decreased rate of diastole
depolarization ; increased depolarization ; Decreased
cardiac rate
cardiac rate
AV node
Increase conduction rate Decreased conduction rate
Atrial muscle
Increase strength of
contraction
Decreased strength of
contraction
Ventricular
muscle
Increased strength of
contraction
No significant effect
IV The Normal Electrocardiogram
Concept: The record of
potential fluctuations of
myocardial fibers at the
surface of the body
Waves of Normal ECG
1, The P wave, spread of
the depolarization wave
through the atria.
2, The QRS wave result
from the spread of the
depolarization wave
through the ventricles
3, The T wave represents
repolarization of
ventricular muscle
4, P-R internal, from the
beginning of the P wave to the
beginning of QRS wave,
represents the beginning of
contraction of atrium and the
beginning of contraction of
ventricle. 0.12 – 0.20 ms.
Atrial ventricular delay
5, Q-T internal: The duration
between the beginning of QRS
wave and the end of the T
wave, or the duration between
the beginning of contraction of
the ventricle and almost the
end of the contraction; or the
duration between the
beginning of depolarization
and the end of repolarization
6, P-R segment: The duration between the end of P wave and the
beginning of QRS wave
7, S-T segment: The duration between the end of QRS and the beginning
of T wave. All ventricles are in complete depolarization