Clinical Pharmacology and Therapeutics

CHAPTER 32
CARDIAC DYSRHYTHMIAS
● Common dysrhythmias 217
● General principles of management 218
● Classification of anti-dysrhythmic drugs 218
● Cardiopulmonary resuscitation and cardiac arrest:
basic and advanced life support 218
● Treatment of other specific dysrhythmias 221
● Selected anti-dysrhythmic drugs 223
COMMON DYSRHYTHMIAS
SUPRAVENTRICULAR
ARISING FROM THE SINUS NODE
Sinus tachycardia
In sinus tachycardia, the rate is 100–150 beats per minute with
normal P-waves and PR interval. It may be physiological, for
example in response to exercise or anxiety, or pathological, for
example in response to pain, left ventricular failure, asthma,
thyrotoxicosis or iatrogenic causes (e.g. β-agonists). If pathological,
treatment is directed at the underlying cause.
Sinus bradycardia
In sinus bradycardia, the rate is less than 60 beats per minute
with normal complexes. This is common in athletes, in young
healthy individuals especially if they are physically fit, and
patients taking beta-blockers. It also occurs in patients with
raised intracranial pressure or sinoatrial (SA) node disease
(‘sick-sinus syndrome’), and is common during myocardial
infarction, especially inferior territory myocardial infarction,
since this area contains the SA node. It only requires treatment
if it causes or threatens haemodynamic compromise.
ATRIAL DYSRHYTHMIAS
Atrial fibrillation
The atrial rate in atrial fibrillation is around 350 beats per
minute, with variable AV conduction resulting in an irregular
pulse. If the AV node conducts rapidly, the ventricular
response is also rapid. Ventricular filling is consequently inadequate
and cardiac output falls. The method of treating atrial
fibrillation is either to convert it to sinus rhythm, or to slow
conduction through the AV node, slowing ventricular rate and
improving cardiac output even though the rhythm remains
abnormal.
Atrial flutter
Atrial flutter has a rate of 250–350 per minute and ventricular
conduction can be fixed (for example, an atrial rate of 300 per
minute with 3:1 block gives a ventricular rate of 100 per
minute) or variable.
NODAL AND OTHER SUPRAVENTRICULAR
DYSRHYTHMIAS
Atrioventricular block
• First degree: This consists of prolongation of the PR
interval.
• Second degree: There are two types, namely Mobitz I, in
which the PR interval lengthens progressively until a P-
wave fails to be conducted to the ventricles (Wenckebach
phenomenon), and Mobitz II, in which there is a constant
PR interval with variable failure to conduct to the
ventricles.
The importance of first- and second-degree block is that
either may presage complete (third-degree) heart block.
This is especially so in the case of Mobitz II block.
• Third degree: There is complete AV dissociation with
emergence of an idioventricular rhythm (usually around
50 per minute, although the rhythm may be slower, e.g.
30–40 per minute). Severe cerebral underperfusion with
syncope sometimes followed by convulsions
(Stokes–Adams attacks) often results.
SUPRAVENTRICULAR TACHYCARDIAS
Supraventricular tachycardia (SVT) leads to rapid, narrow
complex tachycardias at rates of approximately 150 per
minute. Not uncommonly in older patients the rapid rate leads
to failure of conduction in one or other bundle and ‘aberrant’
conduction with broad complexes because of the rate-dependent
bundle-branch block. This can be difficult to distinguish electrocardiographically
from ventricular tachycardia, treatment
of which is different in important respects. SVT can be intranodal
or extranodal.