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Asystole and torsade de pointes are the two mechanisms underlying
syncope and Stokes-Adams attacks in patients with bradyarrhythmias
secondary to advanced atrioventricular block and sick sinus syndrome. The
abrupt development of complete atrioventricular block, especially at His-
bundle level, may result in a prolonged period of asystole because of a
slow and delayed response of the quiescent subsidiary ventricular
pacemaker. This prolonged period of asystole may result in syncope and
Stokes-Adams attack with a complete recovery of the consciousness once the
cardiac activity is resumed. Similarly, in sick sinus syndrome, the
syncope usually occurs when the tachyarrhythmia (atrial fibrillation,
atrial flutter or atrial tachycardia) terminates abruptly, resulting in an
abrupt marked decrease in heart rate, which, due to the underlying sinus
node disease, is slower than the normal range. Furthermore, the initiation
of cardiac activity after the abrupt termination of the tachyarrhythmia
may be preceded by a long period of asystole secondary to a markedly
prolonged recovery time of the diseased sinus node or a delayed initiation
of the pacing activity from a subsidiary pacemaker.
Torsade de pointes, a specific form of polymorphic ventricular
tachycardia, is a second frequent underlying cause of syncope and Stokes-
Adams attacks in patients with high-grade atrioventricular block and sick
sinus syndrome. Marked bradycardia caused by high-grade atrioventricular
block or sinus node disease may precipitate an episode of torsade de
pointes by prolonging the QT interval to a greater degree than expected
merely from the physiologically slowed heart rates [1]. This is of a
particular importance when heart rate slows abruptly because a sudden
decrease in heart rate, secondary to a sudden onset of high-grade
atrioventricular block in atrioventricular node disease or an abrupt
termination of a tachyarrhythmia in sick sinus syndrome, may create a
pause precipitating an episode of pause-dependent torsade de pointes. Due
its inability to maintain cardiac output, torsade de pointes may result in
loss of consciousness. However, most episodes of torsade de pointes
terminate spontaneously; therefore, patient regains consciousness but a
prolonged episode, like that of asystole, may result in sudden cardiac
death [2].
REFERENCES
1. Khan IA. Clinical and therapeutic aspects of congenital and
acquired long QT syndrome. Am J Med 2002;112(1):58-66.
2. Khan IA. Long QT syndrome: diagnosis and management. Am Heart J
2002;143(1):7-14.
Competing interests:
No competing interests
06 March 2002
Ijaz A. Khan
Assistant Professor of Medicine
Division of Cardiology, Creighton University School of Medicine, Omaha, NE 68131, USA
When speaking about bradycardias, it is worthwhile knowing what the
normal physiological mechanisms are inbuilt in the human heart that
actually act as reserves.
Physiologically the sinus node has an automaticity to beat
spontaneously at a rate of 70-80 bpm(Beats per minute). The AV node has an
automaticity to beat at a rate of 50-60 bpm, should the sinus node fail.
The ventricles have an automaticity to beat at a rate of 30-40 bpm, should
the AV node fail. What a wonderful piece of equipment the human heart
is!!!!
In pathological conditions when the sinus node is diseased, Sinus
Bradycardia occurs. When the sinus node is destroyed, the AV node take up
the job and produces a Nodal rhythm. When the AV node is destroyed, the
helpless ventricles decide to help themselves eventually, and produce an
Idioventricular rhythm(Broad complex). But if the sinus node is still
patent, it beats at its own pace irrespective of the idioventricular
rhythm producing the ECG picture of what is called a complete heart
block(Mobitz Type-III) where the P waves and QRS complexes beat at
different rates.
I hope the above explanation gives a logical and an easy way of
underatnding the genesis of the various bradyarrhythmias.
Mechanisms of syncope and Stokes-Adams attacks in bradyarrhythmia: Asystole and torsade de pointes
Asystole and torsade de pointes are the two mechanisms underlying
syncope and Stokes-Adams attacks in patients with bradyarrhythmias
secondary to advanced atrioventricular block and sick sinus syndrome. The
abrupt development of complete atrioventricular block, especially at His-
bundle level, may result in a prolonged period of asystole because of a
slow and delayed response of the quiescent subsidiary ventricular
pacemaker. This prolonged period of asystole may result in syncope and
Stokes-Adams attack with a complete recovery of the consciousness once the
cardiac activity is resumed. Similarly, in sick sinus syndrome, the
syncope usually occurs when the tachyarrhythmia (atrial fibrillation,
atrial flutter or atrial tachycardia) terminates abruptly, resulting in an
abrupt marked decrease in heart rate, which, due to the underlying sinus
node disease, is slower than the normal range. Furthermore, the initiation
of cardiac activity after the abrupt termination of the tachyarrhythmia
may be preceded by a long period of asystole secondary to a markedly
prolonged recovery time of the diseased sinus node or a delayed initiation
of the pacing activity from a subsidiary pacemaker.
Torsade de pointes, a specific form of polymorphic ventricular
tachycardia, is a second frequent underlying cause of syncope and Stokes-
Adams attacks in patients with high-grade atrioventricular block and sick
sinus syndrome. Marked bradycardia caused by high-grade atrioventricular
block or sinus node disease may precipitate an episode of torsade de
pointes by prolonging the QT interval to a greater degree than expected
merely from the physiologically slowed heart rates [1]. This is of a
particular importance when heart rate slows abruptly because a sudden
decrease in heart rate, secondary to a sudden onset of high-grade
atrioventricular block in atrioventricular node disease or an abrupt
termination of a tachyarrhythmia in sick sinus syndrome, may create a
pause precipitating an episode of pause-dependent torsade de pointes. Due
its inability to maintain cardiac output, torsade de pointes may result in
loss of consciousness. However, most episodes of torsade de pointes
terminate spontaneously; therefore, patient regains consciousness but a
prolonged episode, like that of asystole, may result in sudden cardiac
death [2].
REFERENCES
1. Khan IA. Clinical and therapeutic aspects of congenital and
acquired long QT syndrome. Am J Med 2002;112(1):58-66.
2. Khan IA. Long QT syndrome: diagnosis and management. Am Heart J
2002;143(1):7-14.
Competing interests: No competing interests