CARDIOVASCULAR PHYSIOLOGY
Lecture 11
Current of Injury
When a region of the heart becomes ischemic or damaged, it quickly loses its
ability to maintain transmembrane ionic pumps leading to movement of positive
charge into the cells and the cells become depolarized. This causes the ischemic
region of the heart to become negative with respect to the rest of the heart. Thus,
a dipole is created and current flows between the pathologically depolarized and
the normally polarized areas even between heartbeats. This is called a current of
injury. The effect of current flow on ECG record is elevation of the ST segment in
ECG leads recorded with electrodes over the infarcted area. Some abnormalities
that can cause current of injury are:
(1) mechanical trauma, which sometimes makes the membranes remain so
permeable that full repolarization cannot take place.
(2) infectious processes that damage the muscle membranes.
(3) ischemia of heart muscle, which is the common cause of current of injury.
Effect myocardial infarction on ECG
During an acute myocardial infarction, the ECG evolves through three stages:
1.T wave peaking followed by T wave inversion (A and B, below).
2.ST segment elevation (C).Normally S-T segment is isoelectric (no current flow).
However, The abnormal current produced by infarction lead to deviation of ST
segment from the normal zero base line up or downward depending on direction
of current flow vector . Therefore, we had ST segment elevation in those leads
whose positive terminal facing the head of the projected vector. While we had
ST segment depression in those leads whose positive terminal facing the base of
the projected vector.
3. Appearance of new Q waves (D).When a region of myocardium dies, it becomes
electrically silent , thus it is no longer able to conduct an electrical current. As a
result, all of the electrical forces of the heart will be directed away from the area
of infarction. An electrode overlying the infarct will therefore record a deep
negative deflection, a Q wave.
Figure: Effect myocardial infarction on ECG.(A)T wave peaking ,(B) T wave
inversion, (C) ST segment elevation (D) Q wave.
(Note: Q waves usually appear within several hours of the onset of infarction,
but in some patients, they may take several days to evolve. The ST segment
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usually has returned to baseline by the time Q waves have appeared. Q waves
tend to persist for the lifetime of the patient).
Cardiac arrhythmias
The term arrhythmia (dysrhythmia) refers to any disturbance in the rate,
regularity, site of origin, or conduction of the cardiac electrical impulse. An
arrhythmia can be a single aberrant beat (or even a prolonged pause between
beats) or a sustained rhythm disturbance that can persist for the lifetime of the
patient.
The Five Basic Types of Arrhythmias
1. Abnormal rhythmicity of the pacemaker(arrhythmias of sinus origin).
2. Shift of the pacemaker from the SA node to another place in the heart (ectopic
rhythms).
3. Blocks at different points in the spread of the impulse through the heart.
4. Abnormal pathways of impulse transmission through the heart(reentrant
arrhythmias).
5.The electrical activity follows accessory conduction pathways that bypass the
normal ones, providing an electrical shortcut, or short circuit. These arrhythmias
are termed preexcitation syndromes.
Tachycardia
tachycardia, usually defined as heart rate faster than 100 beats /min.
ECG: is normal except the rate is fast.
Causes:
1.increased body temperature, the heart rate increases about 10 beats per
minute for each degree Fahrenheit increase in body temperature. increased
temperature increases the rate of metabolism of the sinus node, which in turn
directly increases its excitability of SA node.
2.stimulation of the heart by the sympathetic nerves, or toxic conditions of the
heart.
Bradycardia
bradycardia, defined as heart rate fewer than 60 beats/ min.
ECG: is normal except the rate is slow.
Causes:
1.Athlete’s heart, the athlete’s heart is larger and stronger than that of normal
person, which allows the athlete’s heart to pump a large stroke volume.
2.Vagal stimulation,as in carotid sinus syndrome ,which characterized by
increase sensitivity of the baroreceptors in the carotid sinus. Therefore, even
mild external pressure on the neck elicits a strong baroreceptor reflex, causing
intense vagal-acetylcholine effects on the heart, including extreme bradycardia.
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Sinus arrhythmia
In healthy young individuals breathing at a normal rate, the heart rate varies
with the phases of respiration: it accelerates during inspiration and de-celerates
during expiration, especially if the depth of breathing is increased. This sinus
arrhythmia is a normal phenomenon and is due primarily to fluctuations in
parasympathetic output to the heart. During inspiration, impulses in the vagi
from the stretch receptors in the lungs inhibit the cardioinhibitory area in the
medulla oblongata. The tonic vagal discharge that keeps the heart rate slow
decreases, and the heart rate rises.
Sinoatrial block
This condition is due to failure of impulse transmission from the sinus node into
the atrial muscle. ECG show sudden cessation of P waves.
Atrioventricular block
This condition characterized by either a decrease in the rate of impulse
conduction in A-V bundle or complete block of the impulse transmission
through A-V node or A-V bundle:
Causes
1. Ischemia of the A-V node or A-V bundle.
2. Compression of the A-V bundle by scar tissue.
3. Inflammation of the A-V node or bundle as in diphtheria or rheumatic fever.
4. Extreme stimulation of the heart by the vagus nerves.
First degree block( Prolonged P-R Interval)
The normal values for the PR interval range from 0.12–0.20 sec. If the PR
interval is longer than 0.20 sec , the condition is termed first-degree heart block.
ECG: normal a part from increased P-R interval to greater than 0.20 second.
Second-degree heart block
second-degree block, divided into two pattern
a.Wenckebach (Mobitz I) block, is almost always due to a block within the AV
node, the ECG show a progressive lengthening of the PR interval with each beat
and then suddenly a P wave that is not followed by a QRS complex.
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b. Mobitz type II block, usually is due to a block below the AV node in the His
bundle. It due to failure of conduction of some impulses through the AV node.
The ECG shows two or more normal beats with normal PR intervals and then a P
wave that is not followed by a QRS complex (a dropped beat). so we have a “2:1
rhythm” with the atria beating twice for every single beat of the ventricles. At
other times, rhythms of 3:2 or 3:1 .
Complete A-V block (third degree block).
This condition characterized by complete block of the impulse transmission
from the atria into the ventricles. The ventricles establish their own signal,
usually originating in the A-V node or A-V bundle.
ECG: P waves become dissociated from the QRS-T complexes. The P waves
marching across the rhythm strip at their usual rate (60 to 100 waves per minute) but
bearing no relationship to the QRS complexes that appear at a much slower escape
rate. The QRS complexes appear wide and bizarre.
Stokes-Adams Syndrome(Ventricular Escape).
In some patients with total A-V block, the block intermittent( comes and goes).
The duration of block may be a few seconds, a few minutes, a few hours, or even
weeks or longer before conduction returns. After each A-V block, the ventricles
often do not start their own beating until after a delay of 5 to 30 seconds. This
results from the phenomenon called overdrive suppression. However, after a few
seconds, certain area of A-V node or A-V bundle beyond the block, begins
discharging rhythmically at a rate of 15 to 40 times per minute and acting as the
pacemaker of the ventricles. This is called ventricular escape.
Bundle branch block
Bundle branch block is diagnosed by looking at the width and configuration of the
QRS complexes.
1.Right Bundle Branch Block
In right bundle branch block, conduction through the right bundle is obstructed. As a
result, right ventricular depolarization is delayed; it does not begin until the left
ventricle is almost fully depolarized. This causes two things to happen on the ECG:
1.The QRS complex widens beyond 0.12 seconds.
2.The wide QRS complex in lead V1 and V2 show a second R wave, called R', in
Meanwhile, in the left lateral leads overlying the left ventricle (I, AVL, V5, and V6),
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late right ventricular depolarization causes reciprocal late deep S waves to be
inscribed
2.Left Bundle Branch Block
In left bundle branch block, it is left ventricular depolarization that is delayed. Again,
there are two things to look for on the EKG:
1.The QRS complex to widen beyond 0.12 seconds
2.The QRS complex in the leads overlying the left ventricle (I, AVL, V5, and V6) will
either be broad on top or notched. Those leads overlying the right ventricle will show
reciprocal, broad, deep S waves.
Premature Contractions (extrasystole, ectopic beat)
A premature contraction is a contraction of the heart before the time that normal
contraction would have been expected.
Causes: premature contractions usually results from ectopic foci in the heart, the
most possible causes of ectopic foci are
(1). local areas of ischemia.
(2). small calcified plaques , which press on cardiac muscle and irritate them.
(3). toxic irritation of the A-V node, Purkinje system, or myocardium caused by
drugs, nicotine, or caffeine.
(4).Mechanical irritation during cardiac catheterization.
Premature Atrial beat
This condition due to an abnormal beat originated in an ectopic foci in the atria.
Premature atrial beat occur frequently in otherwise healthy people, like athletes,
or peoples with excess smoking, lack of sleep, ingestion of too much coffee,
alcoholism. In most cases these are of no consequence, although very frequent
atrial ectopic beats may herald the onset of atrial fibrillation.
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ECG: the P wave has a different morphology because the atria activate from an
abnormal site, the P-R interval is usually shortened, normal QRS complex, the
interval between the premature contraction and the next succeeding contraction
is slightly prolonged, which is called a compensatory pause.
Pulse Deficit: Premature atrial beat some time cause the ventricles to contract
with only small amount of blood so the stroke volume depressed or almost
absent. Therefore, the pulse wave passing to the peripheral arteries after a
premature contraction may be so weak that it cannot be felt in the radial artery.
Thus, a deficit in the number of radial pulses occurs when compared with the
actual number of contractions of the heart.
Premature Ventricular Contractions(PVCs)
This condition due to an abnormal beat originated in an ectopic foci in the
ventricule. PVCs may occur randomly or may alternate with normal sinus beats in a
regular pattern. If the ratio is one normal sinus beat to one PVC, the rhythm is called
bigeminy. Trigeminy refers to two normal sinus beats for every one PVC, and so on.
Isolated PVCs are common in normal hearts and they can result from factors as
cigarettes, coffee, lack of sleep, various mild toxic states, and emotional
irritability, and rarely require treatment. On the other hand, certain situations have
been identified in which PVCs appear to pose an increased risk for triggering
ventricular tachycardia, ventricular fibrillation, and death. These situations include:
frequent PVCs, any PVC occurring in the setting of an acute myocardial
infarction,and PVCs falling on the T wave of the previous beat, called the R-on-T
phenomenon. The T wave is a vulnerable period in the cardiac cycle, and a PVC
falling there appears to initiate a reentrant phenomenon which lead to serious
arrhythmia like ventricular tachycardia..
Figur:(A) PVC,the bigeminy rhythm,(B) R-on-T phenomenon and VTC
ECG: the ECG record of PVC characterized by
1.the QRS complex is usually considerably Prolonged, because the impulse is
conducted mainly through slowly conducting muscle of the ventricles, rather
than Purkinje system.
2.the QRS complex has a high voltage because normally both ventricles
depolarized nearly simultaneously so some of the currents of two ventricles
neutralize so decrease the net voltage. In case of PVC one entire ventricles is
depolarized ahead of the other; so that there is no such neutralization effect, this
causes large electrical potentials.
3. the T wave has an electrical potential polarity exactly opposite to that of the
QRS complex, because the slow conduction of the impulse through the cardiac
muscle causes the muscle fibers that depolarize first also to repolarize first.
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