Cardiac Excitation
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Cardiac Excitation Cardiac excitation Cellular contraction depends on action potentials Cardiac contraction depends on coordinated excitation, which depends on a pacemaker a conduction systems causing coordinated cellular contraction. The conduction systems: o Electrically specialized myocytes including: Sinoatrial (SA) node Atrioventricular (AV) node Bundle of His- right and left bundle branches Purkinje fibers o All have inherent excitability, but usually SA node determines rate of heart The conduction pathway is very sophisticated. Some special features include: Substantial atrial to ventricular delay. This allows the atria to completely empty their contents into the ventricles. This is achieved through a delay at the AV node, as the atria are electrically isolated from the ventricles apart from the AV node. Ventricular contraction begins at the apex of the heart, progressing from the apex to the base, and from the endocardium to the Epicardium. This is because contraction that squeezes blood towards the semilunar valves is more efficient that multi-directional squeezes. The left bundle branch provides electrical conduction to the chordae tendineae of the mitral valve through a short branch called the anteriosuperior left bundle branch. Electrical conductivity is also provided to the chordae tendineae of the tricuspid valve through the moderator band. This allows both atrioventricular valves to close before ventricular contraction.
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Cardiac Excitation
Cardiac excitation
Cellular contraction depends on action potentials
Cardiac contraction depends on coordinated excitation, which depends on a
pacemaker a conduction systems causing coordinated cellular contraction.
The conduction systems:
o Electrically specialized myocytes including:
Sinoatrial (SA) node
Atrioventricular (AV) node
Bundle of His- right and left bundle branches
Purkinje fibers
o All have inherent excitability, but usually SA node determines rate of heart
The conduction pathway is very sophisticated.
Some special features include:
Substantial atrial to ventricular delay.
This allows the atria to completely
empty their contents into the ventricles.This is achieved through a delay at the
AV node, as the atria are electrically
isolated from the ventricles apart from
the AV node.
Ventricular contraction begins at the
apex of the heart, progressing from the
apex to the base, and from the
endocardium to the Epicardium. This is
because contraction that squeezes
blood towards the semilunar valves is more efficient that multi-directional squeezes.
The left bundle branch provides electrical conduction to the chordae tendineae of the
mitral valve through a short branch called the anteriosuperior left bundle branch.
Electrical conductivity is also provided to the chordae tendineae of the tricuspid valve
through the moderator band. This allows both atrioventricular valves to close before
ventricular contraction.
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Action potentials and relation to cardiac muscle contraction
The cardiac action potential varies in shape in different regions.
Pacemaker cells are the cells within the SA and AV node, whereas non-pacemaker cells are the
atrial and ventricular myocytes, and cells within the Purkinje fibers.
Non-pacemaker cells
In non-pacemaker cells, the cardiac action potential looks as follows:
The phases of this cardiac potential, and the currents responsible for them are shown below:
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In the above picture, note that the absolute refractory period lasts from the fast upstroke to
the end of the plateau. The relative refractory period lasts from the end of the plateau to after
repolarization. This ensures a period of relaxation.
The Na+ activation and inactivation is time- and voltage-related. When inactivated, the H-gate
closes, and is only re-opened after repolarization. Hyperpol can reverse the inactivation of
Na+ channels in Phase 1.
This cardiac action potential causes the muscle fibers to contract and relax according to the
following relationship:
Pacemaker cells
Normally, the SA node in the right atrium is the cardiac
pacemaker. It is a group of specialized muscle cells that have
unstable resting membrane potential
The special thing about this cell is that there is no fast Na+
channel, and only the slow influx of Ca2+ allows the SA node to
perform its depolarization function.
The phases of the pacemaker cell are shown below:
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On details regarding action potentials in pacemaker
cells:
Slow depolarization is carried out in Phase 4
initially by “funny” currents, abbreviated toIF, which are slow, inward Na+ currents.
When the membrane potential reaches -50
mV, “transient” or T-type Ca2+ channels open.
When the membrane potential reaches -40
mV, “long-lasting” or L-type Ca2+ channels
open. This continues until the firing
threshold is reached. During this phase, K+
channels from Phase 3 are inactivated.
Phase 0 depolarization is primarily caused by
increased by Ca2+ conductance through the L-
type Ca2+ channels. The other two channels
from Phase 4 close. Because this movement
of Ca2+ into the cell isn’t rapid, the rate ofdepolarization is slow.
In Phase 3, K+ channels open, causinghyperpolarization. At the same time, L-type
Ca2+ channels become inactivated.
Autonomic control of the SA node
When parasympathetic fibers are stimulated, the membrane potential is hyperpolarized
and SA node pacemaker activity decreases. Conversely, sympathetic activity depolarizes
the membrane potential and causes increased SA node pacemaker activity.
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Electrocardiogram (ECG)
The magnitude of the voltages depends on the mass of tissues involved. Usually ventricles
have a greater mass of tissue than atria. The direction of the voltages is the ‘sum’ of thedepolarizing and repolarizing waves.
The recorded potential on the ECG depends on:
The size and voltage of each depolarizing element
The distance from the generator
The orientation: maximum when electrodes are parallel to the dipole, but zero when
perpendicular to dipole.
The designation of positive and negative electrodes is arbitrary: generally, positive deflections
are recorded as the depolarization wave reaches the positive electrode.
The ECG only records change transients, not the entire potential of cardiac tissue.
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Best depolarization recorded in Lead II, as it is parallel to depolarization wave in heart:
Ventricular repolarization occurs in reverse to depolarization of the heart: it spreads from
epicardial to endocardial regions instead of endocardial to epicardial like in the
depolarization wave. This is why the T wave is observed as a positive deflection, similar to the
QRS complex and P wave.
Note A very good .gif of the relationship between the ECG and conduction through the heart is
here: http://upload.wikimedia.org/wikipedia/commons/0/0b/ECG_Principle_fast.gif
Heart blocks
Partial
1st degree AV block:
All the impulses are slower than normal, and an unusually long PR interval.
2nd
degree AV block: Conducts some impulses but not others.
o Mobitz type I block (or Wenckebach block):
Gradual prolongation of the PR interval
AV node fails completely
Skips ventricular depolarization
o Mobitz type II block
The P-R interval is constant
Every nth ventricular depolarization is missing
Complete
3rd degree AV block:
No impulses are conducted through.
The AV node block electrically severs the atria and ventricles.
Ventricles are driven by their own pacemaker (AV dissociation)
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