Adjacent Myocardial Cells Are Joined End To End at Structures Called Intercalated Discs

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Adjacent myocardial cells are joined end to end at structures called intercalated discs

Within an intercalated disc there are two types of membrane junctions.


A. Desmosomes . B. Gap –junctions
Desmosomes is type of a mechanical junction that hold cells together.
Gap –junction allow ions to flow from one cell directly into the next cell making the action
potentials
Properties of the cardiac muscle:
1. Syncytium.
2. Automaticity and Rhythmicity.
3. Excitability and Conductivity.
4. Contractility.
(1) Syncytium
The myocardium contracts as if it is a single Functional unit.
(2) Autorhythmicity
Automaticity: The ability of the heart to initiate its own contraction independent of external
stimuli. i. e., Automatic generation of cardiac impulse (the property of self-excitation).
Rhythmicity: The regular generation of action potentials (cardiac impulse). i.e., the heart
can beat regularly.
(3) Excitability and conductivity
In the pacemaking cells of the heart, the pacemaker potential (also called the pacemaker
current) is the slow, positive increase in voltage across the cell's membrane (the membrane
potential) that occurs between the end of one action potential and the beginning of the
next action potential.
1. Sinus node (SA node)
2. Internodal pathways.
3. The AV node ( impulse delay).
4. The AV bundle (bundle of His).
5. The left and right bundles of purkinje fibers.
SA node as the pacemaker of the heart:
- The highest rate of impulse generation is in the SAN [≈(100-110) / min], therefore the SAN
is considered as the pacemaker of the heart.
- The AV node is a secondary pacemaker (40 to 60 /minute).
- The Purkinje system is a tertiary pacemaker (15 and 40).
Q: What causes the SA node fire spontaneously?
A:
- Although the SA node discharges at an intrinsic rhythmical rate of 100-110 times per
minute but the pulse rate averages 70 or 80 times per minute, this is because of the effect
of vagal tone.
- the high Na+ ions concentration in the ECF as well as the negative electrical charge inside
the resting sinus nodal fibers, the positive Na+ ions outside the fibers tend to leak to the
inside, rising the membrane potential up to a threshed to fire an action potential.
Factors Affecting Heart Rate

Atrial excitation
An action potential originating in the S-A node spread rapidly throughout both atria primarily
from cell to cell via gap junction
Inter-atrial pathway:
Extends from the S-A node within the right atrium to the left atrium.
Inter- nodal pathway:
- The A-V node is the only point of electrical contact between the atria and ventricles
because atria are separated by non-conductive fibrous tissue.
- The action potential is conducted relatively slowly through the A-V node. This slowness
allows time for emptying blood of atria & ventricular filling. The impulse is delayed about
0.12sec [the A-V nodal delay]
Ventricular –excitation:
After the A-V nodal delay the impulse travels rapidly down the septum to the right and left
branches of the bundle of Hiss and throughout the ventricular myocardium via the purkinje
fibers.
1. Ventricles, atria, and the Purkinje system
■ have stable resting membrane potentials of about −90 millivolts (mV). This value
approaches the K+ equilibrium potential.
■Action potentials are of long duration, especially in Purkinje fibers, where they last 300
milliseconds (msec).
a. Phase 0
■ is the upstroke of the action potential.
■ is caused by a transient increase in Na+ conductance. This increase results in an inward
Na+ current that depolarizes the membrane.
■At the peak of the action potential, the membrane potential approaches the Na+
equilibrium potential.
b. Phase 1
■ Is a brief period of initial repolarization.
■ Initial repolarization is caused by an outward current, in part because of the movement
of K+ ions out of the cell and in part because of a decrease in Na+ conductance.
c. Phase 2
■ is the plateau of the action potential.
■is caused by a transient increase in Ca2+ conductance, which results in an inward Ca2+
current, and by an increase in K+ conductance.
■During phase 2, outward and inward currents are approximately equal, so the membrane
potential is stable at the plateau level.
d. Phase 3
■ is repolarization.
■ During phase 3, Ca2+ conductance decreases, and K+ conductance increases and
therefore predominates.
■ The high K+ conductance results in a large outward K+ current (IK), which hyperpolarizes
the membrane back toward the K+ equilibrium potential.
e. Phase 4
■is the resting membrane potential.
■is a period during which inward and outward currents are equal and the membrane
potential approaches the K+ equilibrium potential.

• Phase 0 (upstroke): initial rapid depolarization (Na+ influx).


• Phase 1 (partial repolarization): K+ efflux (K+ outflow)
• Phase 2 (plateau): prolonged plateau is due to slower and prolonged opening of the
voltage-gated Ca+2 channels with Ca+2 influx.
• Phase 3 (rapid repolarization): by (K+ efflux).
• Phase 4 (complete repolarization): by Na-K pump.
Phases of excitability during the action potential:
Refractory period:
(1) Absolute refractory period (ARP)
- It is the interval during which no action potential can be produced
- It coincides with phases 0-2 & about half of phase 3
- It coincides with whole period of systole & beginning of diastole
- Therefore, tetanus & wave summation cannot occur in cardiac muscle (safety feature)
(2) Relative Refractory Period (RRP)
- It is the interval during which a second action potential can be produced
- So that, a stimulus with higher intensity is needed to produce an action potential ==> Early
premature contraction
- It coincides with 2nd half of phase 3 till phase 4 (shortly before complete repolarization)
- It coincides with first half of diastole

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