arrest. The electrocardiogram is likely to show asystole, severe
bradycardia or ventricular fibrillation. Occasionally narrow
complexes are present, but there is no detectable cardiac output
(‘electromechanical dissociation’). The doses given below are for
an average-sized adult. During the course of an arrest, other
rhythm disturbances are frequently encountered (e.g. sinus
bradycardia) and these are considered in the next section on
other specific dysrhythmias. If intravenous access cannot be
established, the administration of double doses of adrenaline
(or other drugs as appropriate) via an endotracheal tube can be
life-saving.
ASYSTOLE
Make sure ECG leads are attached properly and that the
rhythm is not ventricular fibrillation, which is sometimes mis-
taken for asystole if the fibrillation waves are of low amplitude.
If there is doubt, DC counter-shock (200 J). Once the diagnosis is
definite, administer adrenaline(otherwise known as epineph-
rine), 1 mg intravenously, followed by atropine, 3 mg intra-
venously. Further doses of adrenaline1 mg can be given every
three minutes as necessary. If P-waves (or other electrical activ-
ity) are present, but the intrinsic rate is slow or there is high
grade heart block, consider pacing.
VENTRICULAR FIBRILLATION
The following sequence is used until a rhythm (hopefully
sinus) is achieved that sustains a cardiac output. DC counter-
shock (200 J) is delivered as soon as a defibrillator is available
and then repeated (200 J, then 360 J) if necessary, followed by
adrenaline, 1 mg intravenously, and further defibrillation
(360 J) repeated as necessary. Consider varying the paddle
positions and also consider amiodarone300 mg, if ventricular
fibrillation persists. A further dose of 150 mg may be required
in refractory cases, followed by an infusion of 1 mg/min for
six hours and then 0.5 mg/min, to a maximum of 2 g.
Magnesium (8 mmol) is recommended for refractory VF
if there is a suspicion of hypomagnesaemia, e.g. patients
on potassium-losing diuretics. Lidocaineandprocainamide
are alternatives if amiodaroneis not available, but should
not be given in addition to amiodarone. During prolonged
resuscitation, adrenaline(1 mg i.v.) every three minutes is
recommended.
ELECTROMECHANICAL DISSOCIATION
When the pulse is absent, but the ECG shows QRS complexes,
this is known as electromechanical dissociation. It may be the
result of severe global damage to the left ventricle, in which
case the outlook is bleak. If it is caused by some potentially
reversible pathology such as hypovolaemia, pneumothorax,
pericardial tamponade or pulmonary embolus, volume
replacement or other specific measures may be dramatically
effective. If pulseless electrical activity is associated with a
bradycardia, atropine, 3 mg intravenously or 6 mg via the
endotracheal tube, should be given. High-dose adrenalineis
no longer recommended in this situation.
TREATMENT OF OTHER SPECIFIC
DYSRHYTHMIASTACHYDYSRHYTHMIASSUPRAVENTRICULAR
Atrial fibrillation
See also Figure 32.3, which outlines a useful algorithm for
the general treatment of tachydysrhythmias including atrial
fibrillation.
Patients who have not been in atrial fibrillation for too long
and in whom the left atrium is not irreversibly distended may
‘spontaneously’ revert to sinus rhythm. If this does not occur,
such patients benefit from elective DC cardioversion, follow-
ing which many remain in sinus rhythm. DC cardioversion is
unlikely to achieve or to maintain sinus rhythm in patients
with longstanding atrial fibrillation, or with atrial fibrillation
secondary to mitral stenosis, especially if the left atrium is sig-
nificantly enlarged; in such cases, it is quite acceptable to aim
for rate control rather than rhythm conversion. Indeed, trials
have demonstrated no difference in prognosis between
patients with atrial fibrillation treated with a rate control vs. a
rhythm control strategy, although patients who remain in atrial
fibrillation are more likely to be persistently symptomatic. The
main hazard of cardioversion is embolization of cerebral or
peripheral arteries from thrombus that may have accumulated
in the left atrial appendage. Patients should therefore be anti-
coagulated before elective cardioversion (usually for four to six
weeks) to prevent new and friable thrombus from accumulat-
ing and to permit any existing thrombus to organize, thereby
reducing the risk of embolization. An alternative is to perform
early cardioversion provided that transoesophageal echocar-
diography can be performed and shows no evidence of throm-
bus in the left atrial appendage. Anticoagulation is continued
for one month if the patient remains in sinus rhythm.
Anticoagulation should be continued long term if fibrillation
persists or intermittent episodes of dysrhythmia recur.Atrial flutter
Atrial flutter is treated with the same drugs as are effective in
atrial fibrillation, but tends to be more resistant to drug treat-
ment. However, it is very responsive to DC cardioversion. As
with atrial fibrillation, atrial flutter carries a risk of systemic
embolization.Paroxysmal supraventricular tachycardias
As discussed above, although supraventricular tachycardia is
generally a narrow complex QRS tachycardia, the presence of
rate-induced aberrant conduction can cause the QRS com-
plexes to be wide, thus making it difficult to distinguish from
ventricular tachycardia. Criteria exist for distinguishing broad
complex supraventricular and ventricular tachycardias, but
these are beyond the scope of this book, and in practice
are often difficult to apply precisely. Figure 32.3 thereforeTREATMENT OFOTHERSPECIFICDYSRHYTHMIAS 221