Atrial Tachycardia and Atrial Flutter

This is due to an ectopic focus depolarising from anywhere within the atria. The atria contract faster than 150 bpm and P waves can be seen superimposed on the T waves of the preceding beats. The AV node conducts at a maximum rate of 200 bpm, therefore if the atrial rate is faster than this, AV block will occur. If the atrial rate is greater than 250 beats/min and there is no flat baseline between P waves, then the typical 'saw tooth ' pattern of atrial flutter waves will be seen.

Atrial tachycardia and flutter may occur with any kind of block:

Eg: 2:1, 3:1, or 4:1.

Atrial tachycardia is typically a paroxysmal arrhythmia, presenting with intermittent tachycardia and palpitations, and may be precipitated by anaesthesia and surgery. It is associated in particular with rheumatic valvular disease as well as ischaemic and hypertensive heart disease and may be seen with mitral valve prolapse. It may precede the onset of permanent atrial fibrillation. Atrial tachycardia with 2:1 block is characteristic of digitalis toxicity.

Management

• This arrhythmia is very sensitive to synchronised direct current cardioversion - there is a nearly 100% success rate. Therefore in the anaesthetised patient with any degree of cardiovascular compromise this should be the first line treatment.
• Carotid sinus massage and adenosine will slow AV conduction and reveal the underlying rhythm and block where there is doubt.
• Other drug treatment is as for atrial fibrillation. (see below).

Atrial Fibrillation

A common arrhythmia encountered in anaesthetic and surgical practice. There is chaotic and unco-ordinated atrial depolarisation, an absence of P waves on the ECG, with an irregular baseline and a completely irregular ventricular rate. Transmission of atrial activity to the ventricles via the AV node depends on the refractory period of the conducting tissue. In the absence of drug treatment or disease which slows conduction, the ventricular response rate will normally be rapid ie: 120 -200 beats/min.

Common causes of AF include:

• Ischaemia
• Myocardial disease/pericardial disease/mediastinitis
• Mitral valve disease
• Sepsis
• Electrolyte disturbance (particularly hypokalaemia or hypomagnesaemia)
• Thyrotoxicosis
• Thoracic surgery

Since contraction of the atria contributes up to 30% of the normal ventricular filling, the onset of AF may result in a significant fall in cardiac output. Fast AF may precipitate cardiac failure, pulmonary oedema and myocardial ischaemia. Systemic thrombo-embolism may occur if blood clots in the fibrillating atria and subsequently embolises into the circulation. There is a 4% risk per year of an embolic cerebro-vascular episode (CVE = stroke). The treatment of AF is aimed at the restoration of sinus rhythm whenever possible. Where this is not possible, the aim is control of the ventricular rate to <100/ minute and prevention of embolic complications. The management of this arrhythmia will vary depending on how long it has been present. In acute AF restoration of sinus rhythm is often possible, whereas in longstanding AF control of the ventricular rate is the usual aim of therapy.

Management:

1. Acute AF - Occuring in theatre or of recent onset (less than 48 hours):

   • Correction of precipitating factors where possible, especially correction of electrolyte disturbances.
   • Synchronised DC cardioversion - for recent onset AF. If AF has been present for more than several hours there is a risk of arterial embolisation unless the patient is anticoagulated. Shock at 200J then at 360J.
   • Digoxin can be used acutely to slow the ventricular rate - in the presence of a normal plasma potassium concentration. An intravenous loading dose of 500mcg in 100mls of saline over 20 minutes may be given and repeated at intervals of 4 - 8 hours if necessary until a total of 1 - 1.5mg has been given. This is contraindicated if the patient is already taking digoxin when lower doses are required. There is no evidence that digoxin is useful for converting AF to sinus rhythm or maintaining sinus rhythm once established.
   • Amiodarone may be used to restore sinus rhythm - it is especially useful in paroxysmal atrial fibrillation associated with critical illness, and where digoxin or beta blockers cannot be used. A loading dose of 300mg iv via a central vein is given over 1 hour and then followed by 900mg over 23 hours.
   • Verapamil 5 -10 mg slowly iv over 2 minutes can be used to control the ventricular rate. Where there is no impairment of left ventricular function or coronary artery disease, the subsequent administration of flecainide 50 - 100mg slowly iv may restore sinus rhythm. However flecainide should only be used where the arrhythmia is life threatening and no other options are open. It should be avoided if left ventricular function is poor or there is evidence of ischaemia.
   • Beta blockers are sometimes used to control the ventricular rate but may precipitate heart failure in the presence of an impaired myocardium, thyrotoxicosis or calcium channel blockers, and should be used with caution.

2. Chronic AF with a ventricular rate of greater than 100/min. Aim to control the ventricular rate to less than 100/minute. This allows time for adequate ventricular filling and helps maintain the cardiac output.

   • Digitalisation - if patient not already taking it. Consider extra digoxin if not fully loaded - beware signs of digoxin toxicity, nausea, anorexia, headache, visual disturbances etc, and arrhythmias especially ventricular ectopics and atrial tachycardia with 2:1 block.
   • Beta blockers or verapamil
   • Amiodarone

   When AF has been present for more than a few hours anticoagulation is necessary before DC cardioversion to prevent the risk of embolisation. Usually patients should be warfarinised for 3 weeks prior to elective DC cardioversion, with regular monitoring of their prothrombin time. An INR of 2 or more is a satisfactory value at which to proceed with cardioversion. Warfarin should then be continued for 4 weeks afterwards. Occasionally when a patient develops AF and is compromised by it, DC cardioversion has to be considered even where anticoagulation is contraindicated (eg recent surgery).

Atrial Ectopic Beats

An abnormal P wave is followed by a normal QRS complex. The P wave is not always easily visible on the ECG trace. The term 'ectopic' indicates that depolarisation originated in an abnormal place, ie not the SA node hence the abnormal shape of the P wave. If such a focus depolarises early the beat produced is called an extrasystole or premature contraction and may be followed by a compensatory pause. If the underlying SA node rate is slow, sometimes a focus in the atria takes over and the rhythm is described as an atrial escape, as it occurs after a small delay. Extrasystoles and escape beats have the same QRS appearance on the ECG, but extrasystoles occur early whereas escape beats occur late.

Causes:

• Often occur in normal hearts
• May occur with any heart disease
• Ischaemia, hypoxia
• Light anaesthesia
• Sepsis
• Shock
• Anaesthetic drugs are common causes

Management:

• Correction of any underlying cause.
• Specific treatment of atrial ectopic beats is unnecessary unless runs of atrial tachycardia occur - see above. 

Broad Complex Arrhythmias

Ventricular Ectopic Beats

Depolarisation spreads from a focus in the ventricles by an abnormal, and therefore slow, pathway so the QRS complex is wide and abnormal. The T wave is also abnormal in shape.

In the absence of structural heart disease these are usually benign. They may be related to associated abnormalities especially hypokalaemia. They are common during dental procedures and anal stretches particularly with halothane, or whenever there is raised CO2, light anaesthesia or no analgesia associated with halothane anaesthesia. In fit young patients under anaesthesia, they are often of little significance and respond readily to manipulation of the anaesthetic as described in 'first line management'. Small doses of intravenous beta blockers are very commonly effective in this situation.

However they may herald the onset of runs of ventricular tachycardia, and should be taken more seriously where:

• There is a bigeminal rhythm (one ectopic beat with every normal beat).
• If they occur in runs of 2 or more, or where there are more than 5/minute.
• Where they are multifocal (arising from different foci within the ventricles and hence having different shapes).
• Those where the R wave is superimposed on the T wave ('R on T' phenomenon).

The value of prophylactic treatment has been questioned as it is not known whether this influences the final outcome. However most would recommend treatment in the above four situations or where ventricular tachycardia has already occurred.

Management:

• Correction of any contributing causes identified with the anaesthetic ensuring adequate oxygenation, normocarbia and analgesia. A small dose of beta blocker is worth trying as mentioned above.
• If the underlying sinus rhythm is slow <50 bpm, then increasing this rate using intravenous atropine or glycopyrrolate may be effective as the ventricular ectopics may be a form of escape rhythm.
• Lignocaine is the drug of first choice. An initial loading dose of 50 - 100mg iv over 2 minutes is given followed by infusion of: 4mg/minute - for 30 minutes, then 2mg/minute - for 2 hours and then 1mg/minute. The dose should be reduced in the elderly, in liver disease and where there is bradycardia or hypotension.
• Alternatives include amiodarone 300mg iv (preferably via a central venous catheter) over 1 hour, followed by infusion of 900mg over 23 hours. Occasionally bretyllium or procainamide may be used.

Ventricular tachycardia

In this rhythm a focus in the ventricular muscle depolarises at high frequency. Excitation spreads through the ventricles by an abnormal pathway and therefore the QRS complexes are wide and abnormal.

The appearance is characterised by absent P waves, wide QRS complexes which may be slightly irregular or vary in shape.

VT is a serious, potentially life threatening arrhythmia. It may be triggered intraoperatively by:

• Hypoxia
• Hypotension
• Fluid overload
• Electrolyte imbalance (low K⁺, Mg²⁺ etc)
• Myocardial ischaemia
• Injection of adrenaline

Management:

• Synchronised direct current cardioversion is the first line treatment if the patient is haemodynamically unstable. This is safe and effective and will restore sinus rhythm in virtually 100% of cases. If the VT is pulseless or very rapid, synchronisation is unnecessary. But otherwise synchronisation is used to avoid a 'shock on T ' phenomenon which may initiate VF. If the patient lapses back into VT, drugs such as lignocaine or amiodarone may be given to sustain sinus rhythm.
• Lignocaine given as a 100mg bolus restores sinus rhythm in up to 60% and may be followed by a maintenance infusion as above.
• Verapamil is ineffective in ventricular tachycardia and may worsen hypotension and precipitate cardiac failure.

Other drugs which may be used if lignocaine fails:

• Amiodarone 300mg iv - via a central venous catheter over 1 hour followed by infusion of 900mg over 23 hours.
• Procainamide 100mg iv over 5 minutes followed by one or two further boluses before commencing infusion at 3mg/min.
• Mexiletine 100 - 250mg iv at 25mg/min followed by infusion 250mg over 1 hour, 125mg/hour for 2 hours, then 500mcg/min.
• Bretylium tosylate 400 - 500 mg diluted in 5% dextrose over 10 minutes
• Propranolol 0.5 - 1.0mg iv and repeated if necessary particularly if the underlying pathology is myocardial ischaemia or infarction.
• Sotalol 100mg iv over 5 minutes. This was shown to be better than lignocaine for acute termination of ventricular tachycardia.
• Overdrive pacing can be used to suppress VT by increasing the heart rate.

Supraventricular tachycardia with aberrant conduction

When there is abnormal conduction from the atria to the ventricles, a supraventricular tachycardia (SVT) may be broad complex as discussed above. This may occur for example if there is a bundle branch block. Sometimes the bundle branch block may be due to ischaemia and may only appear at high heart rates. SVTs may be due to an abnormal or accessory pathway (as in the Wolf Parkinson White syndrome), but during the tachycardia the complex is of normal width as conduction in the accessory pathway is retrograde, ie; it is the normal pathway that initiates the QRS complex. Adenosine may be used diagnostically to slow AV conduction and will often reveal the underlying rhythm if it arises from above the ventricles. In the case of SVT it may also result in conversion to sinus rhythm. In practice however the differentiation of the two is not important, and all such tachycardias should be treated as ventricular tachycardia if there is any doubt.

Ventricular Fibrillation

This results in cardiac arrest. There is chaotic and disorganised contraction of ventricular muscle and no QRS complexes can be identified on the ECG.

Management

Immediate direct current cardioversion as per established resuscitation protocol. ( Resuscitation from Cardiac Arrest, Update in Anaesthesia 1999;10:6).

(Continued ...)

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