SMS 1053

Dr. Mohanad R. Alwan

II) Electrical properties i) Autorhythmicity

ii) Excitability
iii) Conductivity

 All

the cells of heart have an inherent ability to generate impulse SAN is the pacemaker of heart Rates of impulse generation SAN- 70 to 80/min AVN- 40 to 60/min Purkinje fibers- 15 to 40/min

 RMP

of SAN is -60mv (that of contractile cardiac fibers is 90mv) has a pre-potential, a spike,& a repolarization phase.

It

I)

Pre-potential or pacemaker potentialca2+channels ii) TMP changes from -60mv towards positivity

i) due to ca2+ influx through Transient (T-type) of

II) Spike potentiali) starts at threshold potential of -40mv ii) due to opening of voltage-gated Ca2+ channels (L-type or long-standing type) iii) potential peaks to +20mv

III) Repolarisationi) due to closure of Ca2+ channels and opening of K+ channels Significance of Pre-potential a) It is characteristic of tissues with automaticity b) It is prominent in SAN and AVN c) Alterations in pre-potential will alter the rate of impulse generation

Membrane potential of SA nodal cells

i) Autonomic nerve stimulation a) vagal stimulation decreases the slope of prepotential and reduces the rate of impulse generation b) sympathetic stimulation increases the slope and increases the impulse rate ii) Temperature iii) Hormones iv) Drugs v) Ionsa) K+ increased K+ in ecf decreased RMPhyperpolarisationreduced heart rate diastolic arrest

Vagal stimulation

Release of acetylcholine

Ach binds to M2 muscarinic receptor

subunit of G-protein act on K+ channels

Reduced cAMP

Opening of K + channels

Reduced Ca2+ influx

Decreased pre-potential slope

Sympathetic stimulation
Release of noradrenaline

Binds to 1 receptors
Increased cAMP
Opening of L-type Ca2+ channels

Increased Ca2+ influx Reduced pre-potential slope

Increased rate of impulse generation

 Ability

of excitable tissues to show change in potential when stimulated of cardiac muscle is 3-30ms

Chronaxie

TERMINOLOGY Excitation - definition: generation of action potentials - different from contraction

Contraction - definition: shortening of muscle cells - triggered by excitation

Properties of Cardiac Muscle

Excitation of the heart is triggered by electrical impulse rather than neural transmitters. Contraction of the heart is triggered by elevation of intracellular calcium influx.

Excitation
(Action Potentials)

[ Ca

++

]i

Contraction
(shortening)

Sequence of excitation
Sinus-Atrial node (SA node)

Atria
Atrial-ventricular node (AV node) Ventricles

0.09 0.00 0.19 0.03 0.16 0.17 0.19 0.18

0.22

0.21

0.18
0.21 0.20

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.

Excitability
(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

RMP: -90mv Phase 0- rapid influx of Na+ rising TMP to +20mv Phase 1- closure of Na+ channels Phase 2- plateau- opening of L-type Ca2+ channels Phase 3- Repolarisationclosure of Ca2+ channels & opening of K+ channels Phase 4- RMP

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

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.

RMP: -90mv Phase 0- rapid influx of Na+ rising TMP to +20mv Phase 1- closure of Na+ channels Phase 2- plateau- opening of L-type Ca2+ channels Phase 3- Repolarisationclosure of Ca2+ channels & opening of K+ channels Phase 4- RMP

1) 2) 3) 4) 5)

Nervous factors Hormones Drugs Ions- K+ acts by altering RMP and Na+ acts on amplitude of AP Temperature

SA Node Anterior bundle of bachman Middle bundle of wenkebach AV Node Bundle of His Right & left bundle branches Purkinje fibers Posterior bundle Of thorel

0.09 0.00 0.19 0.03 0.16 0.17 0.19 0.18

0.22

0.21

0.18
0.21 0.20

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

Factors affecting conductivity

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 Also: 1) Nervous stimulation 2) Hormones 3) Drugs 4) Ions 5) temperature

TISSUE Atrial muscle

Internodal tract

m/sec 0.3
1.0

AV Node Purkinje fibers

Ventricle muscle

0.05 1.5-4
1.0

Delay at A-V Node

Conduction speed in A-V node is slow (delay).
This delay allows time for the atria to finish contraction and empty their contents into the ventricles before ventricles start to contract.

A-V node is the only normal route that impulses from SA node are transmitted into ventricles.

Delay in transmission of impulses to ventricles by 0.13sec-( 0.09 at AVN & 0.04 at AV bundle) Causes of delayi) smaller size of fibers ii) smaller number of gap junctions iii) more negative RMP Significancea) atria contracts 0.1sec earlier than ventricle b) limits the number impulses transmitted to ventricles<230/min

 Function.. low

resistance connections small pores in the center of each gap junction allows ions and small peptides to flow from one cell to another action potential is propagated to adjacent muscle cells Heart behaves as a single motor unit

Conduction of Electrical Impulses in the Heart