Specific Interventions for Bradycardias

Specific interventions for bradycardias are listed below:

Atropine

Although this is the first-line treatment for symptomatic bradycardia, atropine will not always be effective. It competitively blocks the action of acetylcholine at muscarinic receptors thus blocking the action of the vagus nerve on the SA and AV nodes. High vagal tone is prominent in autonomic mediated bradycardia and may be a contributing factor in systemic illness and acute coronary syndromes. Atropine is very effective in the presence of high vagal tone but may have little effect on a fibrosed AV node or in most cases of drug toxicity (except organophosphates). In atropine resistant cases pacing and/or vasopressors may be required.

Atropine is effective in Mobitz type I heart block and third degree blocks with high nodal escape rhythms. It is less effective in bradycardias due to drug toxicity (except organophosphates), Mobitz type II block and third degree block with a low Purkinje or ventricular escape rhythm.

At doses below 0.5 mg it may paradoxically worsen bradycardia. A dose of 3 mg is thought to completely block the vagus nerve.

It must be remembered that atropine is not a short acting drug and has an elimination half life of 2 to 3 hours, thus side effects such as a dry mouth, blurred vision and resting tachycardia will be prolonged. Its use should be carefully considered, therefore, in self limiting situations such as transient brady-arrhythmias related to inferior AMI.

Learning bite

Atropine at a dose of 0.5mg is the first line treatment for most symptomatic bradycardias.

Inotropes

Following correction of hypoxia, hypovolaemia and ischaemia, atropine or temporary pacing may still be ineffective in treating bradycardia and/or its associated hypotension. In these cases it may be necessary to use an inotrope. The main choices are between isoprenaline and adrenaline.

• IsoprenalineThis acts mainly on beta-1 receptors and thus acts mainly as a positive chronotrope. It has a 60 to 90 minute duration of action. Because of its relatively long half life and the consequent difficulties in titration for optimum effect it has fallen out of favour for this situation. It also reduces systemic vascular resistance so may exacerbate hypotension especially in the presence of other vasodilator drugs such as calcium channel blockers. The usual starting dose is 5 mcg/min.

• AdrenalineThis is a non-selective adrenoreceptor agonist acting on beta and alpha receptors. It is potent and has a very rapid onset and offset (less than one minute). It is now the preferred inotrope for this indication. Infusions lasting more than a few hours can result in gut ischaemia and metabolic acidosis. Thus it should be seen as a temporising measure before transvenous pacing. The usual starting dose is 2-10 mcg/min

Pacing

Initial pacing, particularly if required urgently, is usually non-invasive and takes the form of percussion or transcutaneous pacing (see below). These are the most common pacing interventions used in the ED.

Transvenous pacing is usually indicated if percussion or transcutaneous pacing have been employed as a temporising measure and are commonly performed in in-patient settings (radiological screening is required) as is the placement of permanent implanted pacemakers.

Indications for non-invasive pacing

Any bradycardia causing haemodynamic compromise and unresponsive to atropine

Most common:

• Sinus node disease
• Second degree heart block (Mobitz type II)
• Junctional bradycardia
• Third degree heart block
• Ventricular pauses greater than 3 seconds

Percussion pacing (fist pacing)

This is most appropriate in the setting of ventricular standstill where there is evidence of P wave activity, used as an alternative to CPR. It can also be used for other bradycardias with haemodynamic compromise whilst attaching transcutaneous pacing pads.

It is performed by delivering firm blows over the precordium lateral to the left sternal edge. Position and firmness of blows can be adjusted to achieve capture and an appropriate threshold.

Transcutaneous pacing

Pacing pads can be rapidly applied and operated easily by medical and paramedical staff. This form of pacing can cause the patient discomfort due to chest wall muscle contraction. Pads are applied to the right sternal edge and apex (or in anterior-posterior positions). The pacing module is set on demand mode, an appropriate rate set and the pacing current increased until capture is achieved (a QRS complex following each pacing spike).