Practical Interpretation and Management of Arrhythmias

When interpreting arrhythmias a paper strip is often easier to read than an ECG monitor. Where this is not possible from the theatre monitor it may be possible to obtain a paper trace by connecting a defibrillator, most of which have a facility for printing a rhythm strip. The following basic points should be considered:

Examining an ECG strip:

1. What is the ventricular rate?
2. Is the QRS complex of normal duration or widened?
3. Is the QRS regular or irregular?
4. Are P waves present and are they normally shaped?

5. How is atrial activity related to ventricular activity?

1. What is the ventricular rate? Arrhythmias may be classified as fast or slow:

   • Tachyarrhythmias - rate greater than 100/min
   • Bradyarrhythmias - rate less than 60/min
   • Calculate approximate ventricular rate on a paper strip by counting the number of large squares between each QRS complex and dividing this number into 300 which will give the rate in beats/minute.

2. Is the QRS complex of normal duration or widened? Arrhythmias may be due to abnormal impulses arising from the:

   • atria = a supraventricular ryhthm
   • AV node = a nodal or junctional rhythm
   • or the ventricles = a ventricular arrhythmia

   Supraventricular and nodal rhythms arise from a focus above the ventricles. Since the ventricles still depolarise via the normal His-Purkinje system the QRS complexes are of normal width (< 0.1sec - 2.5 small squares) - and are therefore termed 'narrow complex' rhythms. Arrhythmias arising from the ventricles will be 'broad complex' with a QRS width of >0.1sec. The QRS complexes are widened in these patients since depolarisation is via the ventricular muscle rather than the His-Purkinje system and takes longer. In a few cases where there is an abnormal conduction pathway from atria to ventricles a supraventricular rhythm may have broad complexes. This is called 'aberrant conduction'.

3. Is the QRS regular or irregular?

   The presence of an irregular rhythm will tend to suggest ectopic beats (either atrial or ventricular), atrial fibrillation, atrial flutter with variable block or second degree heart block with variable block - see page 4.

4. Are there P waves present and are they normally shaped?

   The presence of P waves indicates that the atria have depolarised and gives a clue to the likely origin of the rhythm. Absent P waves associated with an irregular ventricular rhythm suggest atrial fibrillation whilst a saw tooth pattern of P waves is characteristic of atrial flutter. If the P waves are upright in leads II and AVF they have originated from the sinoatrial node. However, if the P waves are inverted in these leads, it indicates that the atria are being activated in a retrograde direction ie: the rhythm is junctional or ventricular.

5. How is atrial activity related to ventricular activity?

   Normally there will be one P wave per QRS complex. Any change in this ratio indicates a blockage to conduction at some point in the pathway from the atria to the ventricles. 

Classification of Arrhythmias

Arrhythmias may be divided into narrow complex and broad complex for the purpose of rapid recognition and management.

Narrow complex arrhythmias - arise above the bifurcation of the bundle of His. The QRS duration is less than 0.1s (2.5 small squares) duration

Broad complex arrhythmias - usually arise either from the ventricles or less commonly are conducted abnormally from a site above the ventricles so that delay occurs (this is called aberrant conduction). The QRS duration is greater than 0.1s (2.5 small squares).

Narrow Complex Rhythms:

• Sinus arrhythmia
• Sinus tachycardia
• Sinus bradycardia
• Junctional / AV nodal tachycardia
• Atrial tachycardia, atrial flutter
• Atrial fibrillation
• Atrial ectopics

Broad Complex Rhythms:

• Ventricular ectopics
• Ventricular tachycardia
• Supraventricular tachycardia with aberrant conduction
• Ventricular fibrillation 

Narrow Complex Arrhythmias

Sinus arrhythmia This is irregular spacing of normal complexes associated with respiration. There is a constant P-R interval with beat to beat change in the R-R interval. It is a normal finding especially in young people.

Sinus tachycardia

There is a rate greater than 100/min in adults. Normal P-QRS-T complexes are evident. Causes include:

• Inadequate depth of anaesthesia
• Pain / surgical stimulation
• Fever / sepsis
• Hypovolaemia
• Anaemia
• Heart failure
• Thyrotoxicosis
• Drugs eg atropine, ether, ketamine, catecholamines

Management: correction of any underlying cause where possible. Beta blockers may be useful if tachycardia causes myocardial ischaemia in patients with ischaemic heart disease, but should be avoided in asthma and used with caution in patients with heart failure.

Sinus bradycardia

This is defined as a heart rate of less then 60 beats/minute in an adult.

It may be normal in athletic patients and may also be due to vagal stimulation during surgery - see above.

Other causes include:

• Drugs eg; beta blockers, digoxin, anticholinesterase drugs, halothane, second dose of suxamethonium (occasionally first dose in children)
• Myocardial infarction
• Sick sinus syndrome
• Raised intracranial pressure
• Hypothyroidism
• Hypothermia

Management It is often not necessary to correct a sinus bradycardia in a fit young person, unless the rate is less than 45 - 50 beats per minute, and / or there is haemodynamic compromise. However consider:

• Correcting the underlying cause eg: stop the surgical stimulus
• Atropine up to 20 mcg/kg iv or glycopyrolate 10 mcg/kg iv. (Atropine works more rapidly and is usually given in doses of 300-400mcg and repeated if required).
• Patients on beta blockers may be resistant to atropine - occasionally an isoprenaline infusion may be required. Alternatively glucagon (2-10mg) can be used in addition to atropine.

Arrhythmias Due to Re-entry (Circular movement of electrical impulses).

These arrythmias occur where there is an anatomical branching and re-joining of a conduction pathway. Normally conduction would occur down both limbs equally. But if one limb is slower than the other, an impulse may pass normally down one limb but be blocked in the other. Where the pathways rejoin the impulse can then spread backwards up the abnormal pathway. If it arrives at a time when the first pathway is no longer refractory to activation it can pass right round the circuit repeatedly activating it and resulting in a tachycardia (figure 9.)

The classical example of this is the Wolf Parkinson White syndrome where there is a relatively large anatomical 'accessory' conduction pathway between the atria and the ventricles. This is called a 'macro re-entry' circuit. Other macro re-entry circuits can occur within the atrial and ventricular myocardium and are responsible for paroxysmal atrial flutter, atrial fibrillation and ventricular tachycardia. In junctional or AV nodal tachycardia there are 'micro re-entry'circuits within the AV node itself.

Junctional/AV Nodal Tachycardia

The term Supraventricular Tachycardia (SVT) applies to all tachyarrhythmias arising from a focus above the ventricles. However it is often used to describe junctional (AV nodal) tachycardias arising from micro re-entry circuits in or near the AV node, or as in the Wolf Parkinson White syndrome from an accessory conduction pathway between the atria and the ventricles. The ECG appearance is of a narrow complex tachycardia (QRS<0.1s ie 2.5 small squares of standard ECG paper), with a rate of 150 -200 bpm (figure 10).

The typical features seen on a 12 lead ECG taken when the patient is in sinus rhythm are:

• A short P-R interval
• A slurred upstroke on the R wave (the delta wave - best seen in V4)
• Inverted T waves in V2-5 are characteristic.

Management:

This arrhythmia may be associated with severe circulatory disturbance and needs to be managed as an emergency if it occurs during anaesthesia.

1. In the presence of hypotension, especially where the patient is anaesthetised in theatre, the first line treatment is synchronised direct current cardioversion with 200 - 360 joules.
2. Carotid Sinus Massage - this rarely converts to sinus rhythm but slows the rate and will reveal the underlying rhythm if there is any doubt. It is helpful in differentiating it from atrial flutter and fast atrial fibrillation. (The carotid sinus is a small dilatation of the proximal part of the internal carotid artery at the level of the superior border of the thyroid cartilage. It is vagally innervated and is involved in the control mechanism for causing a fall in heart rate and cardiac output in response to a rise in arterial pressure. Gentle pressure on the internal carotid artery at this level may result in a slowing of the heart rate and occasionally termination of a re-entry supraventricular tachycardia. It should NEVER be attempted on both sides at once as this may result in asystole and occlusion of the main arterial blood supply to the brain.) It is contra-indicated in patients with a history of cerebrovascular disease.
3. Adenosine - this slows AV conduction and is especially useful for terminating re-entry SVTs of the Wolf Parkinson White type. Give 3mg iv rapidly preferably via a central or large peripheral vein - followed by a saline flush. Further doses of 6mg and then 12mg may be given at 2 min intervals if there is no response to the first dose. The effects of adenosine last only 10 -15 seconds. It should be avoided in asthma.

4. Verapamil, beta blockers or other drugs such as amiodarone or flecainide may control the rate or convert to sinus rhythm.

   • Verapamil 5 -10mg iv slowly over 2 minutes. A further 5mg may be given after 10 minutes if required. Avoid giving concurrently with beta blockers as this may precipitate hypotension and asystole.
   • Beta blockers eg: propranolol 1 mg over 1 minute repeated if necessary at 2 minute intervals (maximum 5mg), or sotalol 100mg over 10 minutes repeated 6 hourly if neccesary. Esmolol - a relatively cardio-selective beta blocker with a very short duration of action may be given by infusion at 50 - 200 mcg/kg/minute.

Digoxin should be avoided - it facilitates conduction through the AV accessory pathway in the Wolf Parkinson White syndrome and may worsen the tachycardia. Note that atrial fibrillation in the presence of an accessory pathway may allow very rapid conduction which can degenerate to ventricular fibrillation. 

(Continued ...)

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