6- Cardiac Arrhythmia
Objectives:
1. List the types of arrhythmias.
2-Identify on ECG: ectopic beats, atrial & ventricular fibrillation, heart block
The causes of the cardiac arrhythmias are usually one or a combination of the
following abnormalities in the rhythmicity-conduction system of the heart:
1- Abnormal rhythmicity of the pacemaker.
2- Shift of the pacemaker from the sinus node to other parts of the heart.
3- Blocks at different points in the transmission of the impulse through the heart.
4- Abnormal pathways of impulse transmission through the heart.
5- Spontaneous generation of abnormal impulses in almost any part of the heart.
Types of arrhythmias
1- Abnormal sinus rhythms.
2- Conduction block.
3- Premature Contractions.
4- Paroxysmal tachycardia.
1-Abnormal sinus rhythms:
 Sinus Tachycardia.
 Sinus Bradycardia.
 Sinus Arrhythmia.
Tachycardia
The term "tachycardia" means fast heart rate, usually defined as faster than 100
beats per minute. The electrocardiogram is normal except that the rate of
heartbeat is increased. The general causes of tachycardia are: 1-Increased body
temperature,
2-Stimulation of the heart by the sympathetic nerves. See figure
22.
Figure (22): sinus tachycardia.
Bradycardia
The term "bradycardia" means a slow heart rate, usually defined as less than 60
beats per minute. Examples:
 Bradycardia in Athletes.
 Vagal Stimulation. In patients with carotid sinus syndrome; arteriosclerosis
of the carotid sinus causes excessive sensitivity of the baroreceptors
located in the arterial wall; as a result, mild pressure on the neck elicits a
strong baroreceptor reflex, causing intense vagal stimulation of the heart
and extreme bradycardia. Sometimes this reflex is so powerful that it stops
the heart. See figure (23).
Figure (23): Sinus bradycardia (Guyton & Hall 2006).
Sinus Arrhythmia
The heart rate is increased during inspiration and decreased during expiration. The
ECG is normal except that the number of the cycles varies with the two phases of
respiration. See figure (24).
Figure (24): Sinus arrhythmia.
2-Conduction block:
 Sinoatrial Block.
 Atrioventricular Block (Heart Block).
1. First Degree Heart Block.
2. Second Degree Heart Block.
3. Third Degree Heart Block.
Sinoatrial Block
The impulse from the sinus node is blocked before it enters the atrial
muscle. There is missed beat. Figure 25.
Figure (25): Sinoatrial nodal block (missed beat).
Atrioventricular block (Heart Block):
Heart block is caused by abnormality of impulse conduction in the AV node.
The causes of block are:
1- Ischemia of the A-V node by coronary insufficiency.
2- Compression of the A-V node by scar tissue or by calcification.
3- Inflammation of the A-V node, such as occur in rheumatic fever.
4- Extreme stimulation of the heart by the vagus nerves.
There are three types:
A- First degree: Prolonged P-R interval, The normal time between the beginning
of the P wave and the beginning of the QRS complex is 0.12 – 0.21 second.
When the P-R interval increases above 0.21 second, the P-R interval is said to be
prolonged and the patient is said to have first degree incomplete heart block.
B- Second degree: there are dropped beats of the ventricles. This condition is
called second degree incomplete heart block, one dropped beat as a result of
failure of conduction from the atria to the ventricles.
C- Third degree (Complete heart block): Conduction from the atria to the
ventricle is completely interrupted. Ventricular beats are independently of the
atrial beats. Ventricular rhythm is approximately 40 – 60 beats/ minute. It is
associated with bradycardia. Figure (26).
Figure (26): Atrioventricular (AV) node block (Fox, 2006).
In some patients with A-V block, suddenly no impulses are conducted from the
atria into ventricles for a period of time. The ventricles usually stop for 5 to 30
seconds. Because brain can not remain active for more than 4 to 5 seconds
without blood supply, most patients faint a few seconds after complete block
occurs. This period of fainting is known as the Stokes-Adams syndrome.
3-Premature Contractions:
A premature contraction is a contraction of the heart before the time that normal
contraction would have been expected. This condition is also called extrasystole,
premature beat, or ectopic beat. Most premature contractions result from ectopic
foci in the heart, The possible causes:
 Local areas of ischemia.
 Small calcified plaques at different points in the heart.
 Toxic irritation of the A-V node, Purkinje system, or myocardium caused
by drugs, nicotine, or caffeine. Mechanical initiation during cardiac
catheterization.
Premature Atrial Contractions
The P-wave of this beat occurs too soon in the heart cycle, and the P-R interval is
shortened, Also, the interval between the premature contraction and the next
succeeding contraction is slightly prolonged, which is called a compensatory
pause. Premature atrial contractions occur:
 In healthy people.
 In athletes.
 Mild toxic conditions resulting from; excess smoking, lack of sleep,
ingestion of too much coffee, alcoholism, and the use of various drugs.
Figure 27.
Figure (27): Atrial premature beat.
Premature Ventricular Contractions
Premature ventricular contractions (PVCs) cause specific effects in the electrocardiogram,
 The QRS complex is usually prolonged.
 The QRS complex has a high voltage.
 The T wave has a potential polarity opposite to that of the QRS complex.
Some PVCs result from factors such as cigarettes, coffee, lack of sleep, and
emotional irritability. Other PVCs originate from infracted or ischemic areas of
the heart. Figure 28.
Figure (28): Ventricular ectopic beats,
4-Paroxysmal tachycardia: The term "paroxysmal" means that the heart rate
usually becomes rapid in paroxysms, beginning suddenly and lasting for a few
seconds, a few minutes, a few hours, or much longer. Then the paroxysms
usually end suddenly as they begun. This phenomenon could be explained
according to Reentry phenomenon in that the impulse passes in one direction to
excite the cardiac muscle fibers, but if the impulse returns high up, it excites the
cardiac muscle fibers again.
Supra ventricular paroxysmal tachycardia: There is normal QRS complex, T
wave but missing P wave. there is a sudden increase in the rate of heartbeat from
about 95 to about 150 beats per minute.
A- Ventricular paroxysmal tachycardia: It is a series of ventricular premature
beats one after another without any normal beat. It is a serious condition because
it may change to ventricular fibrillation. See figure29.
Figure (29): Two types of paroxysmal tachycardia (Ganong's review of medical
physiology 20100)
5- Flutter and fibrillation:
1-Atrial flutter: The rate of contraction of atria 200-350 beat /minute, so the
amount of blood pumped by atria is slight. ECG show high rate of P wave, QRS
is less than P wave number, not all impulse pass AV node, so P: QRS is 2:1 or
3:1.
2-Atrial fibrillation: There is loss of systolic activity of atria but as 70% of the
blood passes from atria to ventricle passively. The patient will not be affected
during rest and the effect will appear during exercise where 30% of active systole
will be used. ECG show very rapid low voltage P wave (350-600 P
wave/minute). QRS normal in component, irregular and rapid (125-150
QRS/minute). See figure 30.
Figure (30): Atrial flutter and fibrillation (Ganong's review of medical physiology
2010).
3-Ventricular fibrillation: It seems to be produced by discharge of one or more
ectopic foci. The ventricle losses its contractile ability. It is very dangerous, death
can occur few minute after its occurrence. A strong high voltage electric current
(110 – 1000) volts (DC shock) passed through the ventricles for short interval can
stop fibrillation in which all action potential stop, and the heart remains quiescent
for 3 to 5 second, after which it begin to beat again. See figure 31.
Figure (31): Ventricular fibrillation & DC shock (Guyton & Hall 2006).
6-Effect of potassium concentration of blood on ECG:
Hyperkalemia is very dangerous, lethal because its effect on heart. Change in
ECG is tall peaked T wave. As plasma K level raises, paralysis of atria and
prolongation of QRS complex waves occur. The rest- membrane potential of
muscle fibers decreases as the extra cellular K concentration increase. The fiber
becomes unexcitable, heart stops in diastole. A decrease in the plasma K level
causes prolongation of PR interval, prominent U wave, T wave inversion.
Hypokalemia is a serious condition but it is not as rapidly fatal as hyperkalemia.
Figure (32).
Figure (32): Effect of Hyperkalemia and hypokalemia on ECG (Ganong's review
of medical physiology 2010).
7-Ischemic heart disease:
Myocardial ischemia may be detected by changes in the S-T segment of the
electrocardiogram. See figure 33.
Figure (33): Ischemic heart