Pharmacology for Anaesthesia and Intensive Care

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14 Anti-arrhythmics

Arrhythmias
Tachyarrhythmias
These may originate fromenhanced automaticitywhere the resting potential
of contractile tissue loses its stability and may reach its threshold for depolari-
zation before that of the SA node. This is seen during ischaemia and hypo-
kalaemia.
Ischaemic myocardium may result in oscillations of the membrane potential.
Theseafter-potentialsmay reach the threshold potential and precipitate tach-
yarrhythmias.
Re-entryorcircusmechanisms describe how an ectopic focus may originate, lead-
ing to tachyarrhythmias (Figure14.2).

Bradyarrhythmias
These are due to failure of conduction from the SA node to surrounding tissue.
Second- and third-degree block becomes clinically significant. Atropine,βstimula-
tion or pacing may be required.

Classification of anti-arrhythmics
Traditionally anti-arrhythmics have been classified according to the Vaughan–
Williams classification. However, it does not include digoxin and more recently intro-
duced drugs such as adenosine. In addition, individual agents do not fall neatly into
one category, e.g. sotalol has class I, II and III activity.
Anti-arrhythmics may also be divided on the basis of their clinical use in the
treatment of:

0

30

60

90

0 100 200 300 400 Time (msec)

4

3

2

1

0

(a) (b)

Membrane potential (mV)

Figure 14.1.Action potentials of (a) pacemaker and (b) contractile tissue.
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