section 2 electrophysiology of the heart

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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)General descriptionResting potential: -90mv (-

85-95mv)

Action Potential

Phase 0: rapid

depolarization, 1-2msPhase 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

0

1

2

3

4



(2) Ionic bases of transmembrane

potentials

Resting potential: the equilibration potential of potassium

Action potential:

Phase 0, Na+ influx. The threshold

potential, -70 mvPhase 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 cellThe 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

A, Cardiac ventricular cell

B, Sinoatrial node cell

Transmembrane potential of thesinoatrial node cell

1)Maximal repolarization

(diastole) potential, ±70mv

2) Low amplitude and longduration of phase 0. It is not

so sharp as ventricle cell and

Purkinje cell.

3)No phase 1 and 2

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 , thetime 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 restingcondition.

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 0Fast 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 contractilitydecrease ± 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 adrenalglands ± binding with 1 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 nodeIncreased rate of diastole

depolarization ; increased

cardiac rate

Decreased rate of diastole

depolarization ; Decreased

cardiac rate

AV node Increase conduction rate Decreased conduction rate

Atrial muscle Increase strength of

contraction

Decreased strength of

contraction

Ventricular

muscleIncreased strength of

contraction No significant effect



IV The Normal ElectrocardiogramConcept: 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

section 2 electrophysiology of the heart

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