Biomedical Engineering Reference
In-Depth Information
4
Pharmacological Treatment
of Cardiac Rhythm Disorders
To provide a comprehensive picture of pacing, this chapter
presents an overview of cardiac rhythm disorders with clini-
cal implications as well as basic information on pharmaco-
logical treatment options.
ion imbalance); endocrine causes (thyroid disease, adrenal
disease); vegetative nervous system status (carotid sinus syn-
drome, neurocardiogenic syncope); and others (pulmonary
embolism, intoxication).
Symptoms differ depending on the type of arrhythmia. In
bradycardia, they usually include fatigue, dizziness, vertigo,
muscle weakness, breathlessness, or fainting. When normal
generation of electric impulses is impaired, the heart is
unable to increase its activity during exercise. When the heart
rate is very slow or there are pauses in electric impulse gen-
eration of up to a few seconds, a short loss of consciousness
may occur. However, similar symptoms can be caused by
other diseases. In tachycardia, palpitation is the most fre-
quent symptom. It is an acutely perceived rapid heartbeat.
Tachycardia also present as bouts of regular palpitations with
a sudden onset and end. When there is concomitant involve-
ment of the coronary arteries, chest pain may occur.
The principle arrhythmogenic mechanisms [ 23 ] are
altered automaticity (enhanced normal automaticity, abnor-
mal automaticity), triggered activity (early or delayed after-
depolarization), and reentry. Enhanced automaticity is due to
accelerated depolarization in the cells of the sinoatrial node
or other cells of the conduction system, resulting in sinus
tachycardia or atrial tachycardia. In abnormal automaticity,
impulses are generated in the cells of the conduction system
outside the sinus node or even in myocardial cells. This
results in ectopic atrial tachycardia, accelerated idioventricu-
lar rhythm, or ventricular tachycardia. Triggered activity is
caused by an abnormal process of repolarization that leads to
further depolarization. The subsequent impulse is thus trig-
gered by the previous impulse.
Early after-depolarization occurs before the completion
of the previous repolarization, giving rise to a form of ven-
tricular tachycardia called Torsades de pointes. Delayed
after-depolarization occurs after the completion of the previ-
ous repolarization because of excessive intracellular concen-
tration of calcium cations. This results in ventricular
extrasystoles or some atrial and ventricular tachycardia.
4.1
Cardiac Rhythm Disorders
Cardiac rhythm disorders are generally referred to as arrhyth-
mias. They can result from abnormal impulse initiation,
abnormal impulse conduction, or a combination of both
(Fig 4.1 ). In addition to myocardial damage, a disorder can
be caused by extracardiac factors (changes in mineral or hor-
mone levels, alcohol intoxication, medication use, etc.).
Arrhythmias can be categorized according to heart rate as
bradycardia (a heart rate below 60 beats/min) and tachycar-
dia (three or more cardiac cycles above 100 beats/min, with
electrical activity of the heart arising from the same site).
Arrhythmias also can be categorized according to the ana-
tomic site of origin as sinus, supraventricular, and ventricular
arrhythmias [ 23, 25 ] . Sinus and supraventricular arrhythmias
originate above the branching of the bundle of His; ventricu-
lar arrhythmias arise from the ventricular myocardium. In
supraventricular arrhythmias, the shape of the QRS complex
on an electrocardiogram (ECG) is generally of normal width,
whereas in ventricular arrhythmias it is widened.
Arrhythmias can be of cardiac or noncardiac primary etiol-
ogy. Cardiac causes primarily include organic myocardial dam-
age (coronary artery disease, cardiomyopathy, hypertrophy,
inflammation, fibrosis, arrhythmogenic right ventricular dys-
plasia, congenital developmental defects with disorders of
impulse generation and conduction); hemodynamic causes
(congenital developmental defects with impaired hemodynam-
ics, acquired valvular heart disease, constrictive pericarditis,
ventricular septal defect); disorders due to medical intervention
(cardiac surgery, radiofrequency ablation); and cell membrane
disease (long QT syndrome and others). Noncardiac etiologies
include changes in the internal environment (hypoxia, anemia,
 
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