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I. Excitability
II. Conductivity
III. Contractility
IV. Rhythmicity
Properties of the cardiac Muscle
I. Excitability (Irritability)
I. Excitability (Irritability):
= the ability of cardiac ms to respond to adequate
stimuli by generating an action potential
followed by a mechanical contraction.
Relation between the action potential
& the mechanical response
The mechanical response consists of contraction
(systole) & relaxation (diastole).
Duration of contraction:
0.2 sec in arial muscle, &
0.3 sec in ventricular muscle.
Relation between the action potential & the mechanical
response (continued)
Diastole begins at the end of the plateau.
2nd rapid repolarization is completed at about the
middle of diastole.
Action potential of different types of cardiac muscle
Action potential of ventricular muscle
Ventricular ms has a RMP of 90 mV. ( 85 to 95mV).
The trans-membranous AP overshoots to a potential of
( +20mV).
AP of ventricular muscle (continued)
Trans-membranous AP of ventricular ms is characterized
by presence of 5 phases.
Phase 0 = Rapid depolarization.
Phase 1 = Rapid repolarization/
1st rapid repolarization.
Phase 2 = A plateau.
Phase 3 = Slow repolarization/
2nd rapid repolarization.
Phase 4 = Complete repolarization.
1
AP of ventricular muscle 2
(continued) 0 3
4
Phase 0 = Rapid depolarization.
op fast Na+ channels Na+ influx.
Phase 1 = Rapid repolarization/ 1st rapid repolarization.
cls Na+ channels, K+ permeability, w Cl- influx.
Phase 2 = A plateau.
op slow Ca2+ channels (slow Ca2+ Na+ channels) Ca2+
influx, w slow op K+ channels.
Phase 3 = Slow repolarization/ 2nd rapid repolarization.
cls slow Ca2+ channels, w K+ permeability K+ efflux.
Phase 4 = Complete repolarization.
actv Na+ K+ pump 2K+ in/ 3Na+ out.
Excitability changes during the action potential:
Passes through 3 periods:
1. Absolute refractory period (ARP)
2. Relative refractory period (RRP)
3. Dangerous period (supranormal period)
Refractory Periods
1. Absolute refractory period (ARP):
The excitability of cardiac ms is completely lost
during this period, i.e. doesnt respond to 2nd stimulus.
V. long.
long
Occupies the whole period of systole.
Corresponds to the period of depolarization (phase 0),
& the first 2 phases of repolarization.
Ht cant be tetanized (continuous contraction), as its
ARP occupies the whole contraction phase.
2. Relative Refractory Period (RRP):
1. Cardiac Innervation:
Sympathetic NS excitability.
Parasympathetic NS (vagus) excitability.
2. Effect of ions concentration in ECF:
Ca2+ excitability.
K+ excitability.
3. Physical factors:
temperature excitability.
temperature excitability.
Factors affecting myocardial excitability (continued)
4. Blood flow:
Insufficient bl flow to cardiac ms excitability &
myocardial metabolism for 3 reasons:
(1) lack of O2,
(2) excess accumulation of CO2, &
(3) lack of sufficient food nutrients.
5. Chemical factors (drugs):
Digitalis excitability.
Properties of the cardiac Muscle
II. Conductivity
II. Conductivity:
= the ability of cardiac ms fibers to conduct the
cardiac impulses that are initiated in the SA-node
(the pacemaker of the heart).
The direction of the impulse:
The impulse is conducted:
1st Atrial spread
from SA-node conductive tissue
ventricles.
1. Cardiac Innervation:
Sympathetic NS conductivity.
Parasympathetic NS (vagus) conductivity.
2. Effect of ions concentration in ECF:
Ca2+ conductivity.
K+ conductivity.
3. Physical factors:
temperature conductivity.
temperature conductivity.
Factors affecting myocardial conductivity (continued)
4. Blood flow:
Insufficient bl flow to cardiac ms conductivity &
myocardial metabolism for 3 reasons:
(1) lack of O2,
(2) excess accumulation of CO2, &
(3) lack of sufficient food nutrients.
5. Chemical factors (drugs):
Digitalis conductivity.
Properties of the cardiac Muscle
III. Contractility
III. Contractility:
1. Cardiac innervation.
2. Oxygen supply.
3. Calcium & potassium ions concentration in ECF.
4. Physical factors.
5. Hormonal & chemical factors (drugs).
6. Mechanical factors.
Factors affecting myocardial contractility (continued)
1. Cardiac Innervation:
Sympathetic NS force of contraction.
Parasympathetic NS (vagus) atrial force of contraction
w no significant effect on ventricular ms.
Factors affecting myocardial contractility (continued)
2. Oxygen supply:
Hypoxia contractility.
3. Calcium & potassium ions concentration in
ECF:
Ca2+ contractility.
K+ contractility.
4. Physical factors:
Warming contractility.
Cooling contractility.
Factors affecting myocardial contractility (continued)
-ve inotropics:
(Acetylcholine, acidosis, ether, chloroform, some
bacterial toxins (e.g. diphtheria toxins), K+, )
Factors affecting myocardial contractility (continued)
6. Mechanical factors:
6-
Pacemaker Prepotential:
? Due to gradual state of depolarization:
Steady in K+ permeability
( K+ efflux), leading to
intracellular negativity.
Causing spontaneous leakage
of membrane to Na+ w/out
6-
stimulation.
(-60 mV to -55 mV).
Which causes op of voltage
gated transient Ca2+ channels,
leading to some Ca2+ influx.
(-40 mV).
Pacemaker Action potential (AP)
6-
Pacemaker Depolarization:
Opening of long lasting (fast) Ca2+ channels.
More Ca2+ influx till reaching the potential, i.e.
firing level point leading to depolarization.
Pacemaker Repolarization:
Opening of VG K+ channels.
K+ diffuses outward (efflux), (so +vity will go out of cell).
Pacemaker Hyperpolarization:
excessive K+ effllux,
(This will lead to hardship of K+ efflux in 2nd depolarization).
Ectopic pacemaker:
Pacemaker other than SA node:
If APs from SA node are prevented from reaching these areas,
these cells will generate pacemaker potentials.
Ca2+
in
L Ca2+ K+ out
b. Ach:
rhythmicity.
c. Hypoxia:
rhythmicity.
Remember:
Intrinsic rhythmicity of denervated SA- node is 90
impulses/min, while that of AV- node is 60
impulses/min.