Arrhythmias in Myocardial Infarction
Objectives
- To prevent sudden death and treat severe arrhythmias
immediately
- To prevent arrhythmias by treating the underlying
conditions
Causes of Arrhythmias
- Myocardial damage, ischaemia, and sympathetic stimulation are
associated with ventricular arrhythmias.
- Ejection failure causes supraventricular tachyarrhythmias and
atrial fibrillation.
- Vagal stimulation causes bradyarrhythmias and atrioventricular
(AV) conduction disturbances, especially in cases of
inferior-posterior wall infarction.
- Reperfusion often causes benign ventricular rhythm; however, it
also causes severe ventricular arrhythmias.
Ventricular Fibrillation
- Often occurs within 2 to 4 hours of infarction. After 12 hours,
a primary ventricular fibrillation is rare.
- An early ectopic beat may initiate ventricular fibrillation in
an ischaemic myocardium. Ectopic beats are not treated if cardiac
monitoring is effective.
- Treatment
- Acute ventricular fibrillation is treated by immediate
defibrillation starting with 200 joules. Prolonged ventricular
fibrillation frequently calls for cardiopulmonary resuscitation
(CPR).
- To prevent recurrence of fibrillation, lidocaine is given:
initially as bolus of 100 mg, which can be repeated if necessary.
Thereafter, a continuous infusion of 3 to 4 mg/min is given.
Amiodarone is a modern and more effective alternative to lidocaine:
infuse a 150 to 300 mg bolus in 20 minutes. Thereafter infusion at
800 to 1200 mg/24 hours.
- A beta-blocker is usually added to the therapy.
Ventricular Tachycardia
- More than three ectopic beats and a heart rate over 120 beats
per minute.
- Brief, spontaneously ending bursts are seen in over 50% of
patients with infarction during the first two days. They occur
mainly 8 to 14 hours after, not immediately after the infarction,
as does ventricular fibrillation.
- Ventricular tachycardia (VT) leads to haemodynamic collapse or
ventricular fibrillation. The severity depends on the duration,
variability, frequency, and timing of tachycardia.
- Ventricular tachycardia may be monomorphic or polymorphic.
- Treatment
- Beta-blocker
- Lidocaine boluses and infusion as in ventricular fibrillation,
if haemodynamics compromise. Amiodarone may be a better
alternative.
- If necessary, synchronized cardioversion shock with 50 joules
is performed.
- Late in infarction, ventricular tachycardia is, like
ventricular fibrillation, a serious problem that requires further
examination.
Ventricular Ectopic Beats
- Occur in nearly all patients with painful MI
- May cause complications if they are frequent (more than 5/min),
are variable, or occur concomitantly with an early T wave
- Treatment is usually not necessary if cardiac monitoring is
effective. A beta-blocker may be indicated. Potassium level should
be kept above 4.0.
Idioventricular Rhythm
Idioventricular rhythm is an arrhythmia often associated with
MI. In the reperfusion phase, it may even indicate that
thrombolysis has been successful. The frequency is often 70 to 80
beats per minute and drug therapy is not necessary.
Supraventricular Tachyarrhythmias
- Atrial fibrillation in a patient with infarction is often
associated with cardiac insufficiency and it worsens the prognosis.
Atrial fibrillation increases the risk of stroke, which is why low
molecular weight (LMW) heparin and warfarin therapy are
indicated.
- Atrial fibrillation is often associated with the thrombosis of
the right coronary artery or the circumflex branch: reperfusion
also often restores the rhythm.
- Atrial function is important in MI. In cardiac insufficiency,
rapid atrial fibrillation requires active direct current (DC)
cardioversion. Often, the achieved sinus rhythm does not remain. In
such a case, haemodynamics must be stabilised (oxygenation,
treatment of pulmonary oedema, controlling of ventricular response
with a beta-blocker and digitalis) after which spontaneous reversal
of the rhythm is waited for. The effect of the beta-blocker is seen
rapidly but that of digitalis not before several hours. Rapid
ventricular response may be controlled even if cardiac
insufficiency is present: the benefit often outweighs the
disadvantage.
- Selective beta-blockers are best suited for maintaining the
achieved sinus rhythm.
- Intravenous amiodarone will not reduce the contraction of the
myocardium. It is effective in prophylaxis of atrial fibrillation
(together with a beta-blocker) and it may be used in cardioversion
of atrial fibrillation and/or slowing down the ventricular
response.
- Ibutilide is a new class III drug with a single indication:
treatment of atrial fibrillation and flutter. There are limited
data on its use in patients with infarction.
- Note: A broad QRS complex tachycardia in a patient with
infarction must always be treated as a ventricular
tachycardia.
Bradyarrhythmias
- A strong vagal reaction in the early stages of infarction may
lead to a circulatory collapse.
- Posteroinferior wall infarction is often associated with a
functional atrioventricular block. The QRS complex is narrow and
the heart rhythm is 50 to 60 even in cases of a total block. A
pacemaker is rarely needed.
- In anterior wall infarction, the proximal conduction system may
be blocked: the QRS complex is wide, the substituting rhythm is
slow (30-40), the patient is in a poor condition, and pacing is
necessary. Prognosis is poor even with pacing.
- Drug treatment
- Atropine 0.5 mg i.v., repeated as necessary, for treatment of
functional bradycardia.
Pacemaker
- In anterior wall infarction, pacing is indicated if there is a
2nd or 3rd degree block. Pacing should be anticipated in case of a
trifascicular block, alternating right and left bundle branch
block, or if an extensive infarction is associated with left
anterior hemi-block (LAFB) or left posterior hemi-block
(LPFB).
- Posteroinferior wall infarction associated with a 3rd degree
atrioventricular (AV) block requires pacing if bradycardia is
detrimental to haemodynamics and not responsive to treatment with
atropine.
- Sinus bradycardia may be temporarily controlled with i.v.
atropine.