Supraventricular Arrhythmias

The curriculum asks for knowledge on (paraphrasing): narrow-complex tachycardias, atrial fibrillation, paroxysmal SVT, bradycardia and heart block.

Resources

Supraventricular tachyarrhythmias are those initiated ± maintained in atrial or AV-nodal tissue

Overall prevalence 2.25/1,000
Increased risk in:

Females (2x), except atrial flutter, where men carry a 2.5x increased incidence
>65yrs old (5x)

AF is the most common, followed by AVNRT, Flutter and AVRT

Perioperative

They are often paroxysmal although persistent supraventricular tachyarrhythmia is present in 2% of patients pre-operatively
Intra-operative dysrhythmia occurs in up to 29% of patients undergoing non-cardiac surgery
Post-operative arrhythmias tend to be supraventricular in origin, certainly following non-cardiac surgery

They most commonly arise in the 48-72hrs following surgery, possibly owing to sympathetic activity related to the inflammatory response
Persistent supraventricular tachyarrhythmia occurs in up to 6% of patients post-operatively

Haemodynamic instability
Perioperative MI
Heart failure
Progression to ventricular arrhythmia
Prolonged hospital stay
Stroke or other embolic phenomena, typically from AF

Patient factors	Anaesthetic factors	Physiological factors	Surgical factors
↑ Age	Cardiac depression → reflex sympathetic activation	Hypoxia	Pain
Existing coronary or cardiac disease HTN, IHD, CM, congenital cardiac dx	CVC/PA catheter	Hypovolaemia	Trauma
Respiratory disease e.g. OSA, COPD, pulmonary HTN	Excessive stimulation e.g. laryngoscopy	Electrolyte disturbance	Mediastinal manipulation
Endocrine: ↑T₄, ↓T₄, phaeo	Light planes of anaesthesia/inadequate analgesia	Hypo-/hyper-thermia	Infection
Malignancy	Drugs: volatile agents, ketamine, inotropes, suxamethonium, β-blockers	Hypo-/hyper-glycaemia	'SIRS'
Drugs: alcohol, caffeine, recreational	LA toxicity	Perioperative MI	Anaemia
Intracranial pathology e.g. SAH, raised ICP		Post-operative pulmonary complications

There are multiple classification systems and a mind-boggling array of different arrhythmias
I've gone for an anatomical slant and classified supraventricular tachyarrhythmias as arising from either:

The SA node e.g. sinus tachycardia
The atrial myocardium e.g. AF, atrial flutter, multifocal atrial tachycardia and focal atrial tachycardia
Around the AV node e.g. AVNRT, AVRT

The management steps described for each arrhythmia refer to haemodynamically stable patients
Haemodynamically unstable patients generally need DCCV as with any emergent tachycardia

A gradual onset, regular tachyarrhythmia with a ventricular rate >100bpm but at most '220-age' bpm
An appropriate autonomic response to stimulus, of which there are many aetiologies

ECG

Normal P-QRS relationship and morphology
P-wave positive in leads I, II, and aVF, and biphasic/negative in lead V₁

Management

Treatment is to manage the underlying cause(s)
May be transiently slowed by adenosine, but not terminated

An atrial re-entrant tachycardia, often arising at the cavotricuspid isthmus
Second commonest pathological supraventricular tachyarrhythmia
Leads to an atrial rate of 300bpm but a ventricular rate of 100-150bpm depending on whether there is 2:1 or 3:1 block
Characterised by 'sawtooth' P-waves on ECG

Management

In essence, is managed à la atrial fibrillation
Carries the same thromboembolic risk as AF

A sudden onset (over three or four beats), regular tachycardia

As opposed to sinus tachycardia which tends to arise over >30s

Originates at a discrete location within the LA or RA but outside of the sinus node

ECG

Normal P-QRS relationship but altered P wave appearance compared to the patient's normal sinus rhythm
There is a variable ventricular rate depending on the degree of AV nodal conduction, but typically 150-250bpm

Management

First line management is with β-blockers or calcium channel blockers
Second line agents include ibutilide, flecainide, propafenone or amiodarone
Patients may need catheter ablation for recurrent or refractory focal atrial tachycardia

An irregular supraventricular tachyarrhythmia, which is less common than its (uni)focal cousin
Classically arises in the elderly patient with concomitant (respiratory) infection, though is associated with other patient factors such as:

Respiratory disease e.g. COPD
Pulmonary hypertension
Coronary disease
Valvular heart disease
Hypomagnesaemia
Theophylline therapy

ECG

Characterised by changing P-wave morphology (>3 morphologies) prior to QRS complexes
Ventricular rate up to 150bpm
Progresses into other atrial arrhythmias e.g. AF

Management

Treat underlying cause(s) e.g. give some magnesium
β-blocker or calcium channel blocker to control the rate
Typically non-responsive to adenosine
Typically refractory to DCCV

Sudden onset regular tachycardia typically with a ventricular rate between 150-250bpm
Due to functional re-entrant circuit arising within the anterior and posterior inputs to the AV node, one of which conducts impulses rapidly and the other slowly
Commonest cause of palpitations in those with structurally normal hearts
Synonymous with 'SVT' as we know it

Leads to almost simultaneous atrial and ventricular activity, obscuring P waves within the QRS complex
ECG may therefore demonstrate no apparent atrial activity, or R' at the termination of the QRS
Rarely causes haemodynamic compromise
Terminated by adenosine

A re-entrant circuit develops through a band of congenitally abnormal myocardial fibres which connect the atria to the ventricles i.e. an accessory pathway

Wolff-Parkinson-White syndrome is the prime example

Can lead to three different arrhythmias:

Regular, narrow complex tachycardia i.e. orthodromic
Regular, broad complex tachycardia i.e. antidromic
Irregular broad complex tachycardia e.g. AF with rapid anterograde conduction via the accessory pathway

Orthodromic AVRT is managed as per the Resus Council algorithm e.g. vagal manoeuvres, adenosine etc.
Antidromic AVRT is difficult to distinguish from ventricular tachyarrhythmia

If in doubt, treat as VT
Otherwise, procainamide (1^st line), ibutilide or amiodarone can be used

Perioperative management of the patient with supraventricular arrhythmia

History and examination

Establish history of palpitations, SOB or pre-syncope
Chest pain or syncope is worrying and may indicate ventricular arrhythmia
Check for known triggers e.g. alcohol, caffeine
Establish existing treatments e.g. anti-arrhythmic drugs, previous ablations

Investigations

Bloods

FBC e.g. anaemia
U&E e.g. electrolyte issues
TFTs
LFTs

Consider CXR
12-lead ECG

Often normal
May show signs of pre-excitation or delta waves

ECG monitoring e.g. 24hr tape, Holter monitor

May identify structural abnormalities
Structural heart disease predisposes to supraventricular arrhythmia under anaesthesia

Optimisation

Address modifiable risk factors
Manage medical comorbidities
Tend to continue existing rate control e.g. β-blockers, non-DHP CCBs etc.
Consider need to manage perioperative anticoagulation

Ensure physiological aberrancies are addressed e.g. avoid hypoxia, electrolyte disturbance, inadequte analgesia/anaesthesia
Management is as per the tachycardia clinical incident page
A brief overview of options:

Treatment option	Examples
Non-pharmacological	Carotid sinus massage Modified valsalva manoeuvre
Electrolyte replacement	Potassium, target 4.5-5.5mmol/L Magnesium, target >1.0mmol/L
AV node blocker	Adenosine Tecadenoson
β-blocker	Esmolol 0.5mg/kg over 1 min, then 50-200μg/kg/min Metoprolol up to 5mg IV over 5-10mins Landiolol
Calcium channel blocker	Verapamil 5-10mg IV over 2mins Diltiazem 0.25mg/kg over 2mins, then 5-15mg/hr infusion
Amiodarone	300mg IV; duration of infusion depends on severity
Synchronised DCCV	Flutter/narrow-complex: 70-120J AF/broad complex: 120-150J

May need higher care monitoring e.g. on HDU or CCU if ongoing issues related to intra-operative dysrhythmia
Multi-modal analgesia to reduce risk of pain-related tachycardia
Multi-modal anti-emesis as dehydration and electrolyte imbalance from PONV may contribute to dysrhythmia
Liaise with surgical team about restarting normal anticoagulation