Pathophysiology and management of cardiac dysrrhythmias during anaesthesia - standard textbook answer

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Cardiac Dysrhythmias During Anaesthesia: Pathophysiology and Management

1. Introduction and Classification

Cardiac dysrhythmias are among the most frequent complications encountered during the perioperative period. They range from benign, transient disturbances requiring no intervention to life-threatening events demanding immediate treatment. Dysrhythmias represent alterations in cardiac electrical impulse initiation (abnormal automaticity, triggered activity) or conduction (re-entry, delay, or block), resulting in abnormal heart rate or rhythm and potentially compromised cardiac output.

Classification by QRS morphology and rate:

Category	Examples
Bradyarrhythmias	Sinus bradycardia, sick sinus syndrome, 1st/2nd/3rd degree AV block
Tachyarrhythmias - regular, narrow QRS	Sinus tachycardia, AVNRT, orthodromic AVRT, junctional tachycardia, atrial flutter
Tachyarrhythmias - irregular, narrow QRS	Atrial fibrillation, multifocal atrial tachycardia, frequent PACs
Tachyarrhythmias - regular, wide QRS	Monomorphic VT, antidromic AVRT, SVT with BBB
Tachyarrhythmias - irregular, wide QRS	Polymorphic VT, VF, frequent PVCs, irregular SVT with BBB

(Barash Clinical Anesthesia, Table 33-10)

2. Pathophysiological Mechanisms

2.1 Mechanisms of Arrhythmogenesis

Abnormal automaticity: Anaesthetic agents, electrolyte disturbances, hypoxia, and catecholamines can lower the threshold for spontaneous depolarisation in non-pacemaker cells, generating ectopic foci.

Re-entry: The most common mechanism. Requires two pathways with different conduction velocities and refractory periods. Conditions that slow conduction (ischaemia, hypercapnia) or create unidirectional block favour re-entrant circuits. This underlies AF, atrial flutter, AVNRT, AVRT, and most VT.

Triggered activity: Early afterdepolarisations (EADs) - favoured by bradycardia and QT prolongation - and delayed afterdepolarisations (DADs) - caused by intracellular calcium overload - generate arrhythmias particularly in the context of ischaemia or drug toxicity.

2.2 Anaesthesia-Specific Triggers

The perioperative period creates a unique milieu for arrhythmogenesis. Key triggering factors include:

Autonomic perturbations:

Laryngoscopy and intubation cause a sympathetic surge with catecholamine release, predisposing to tachyarrhythmias and PVCs
Surgical stimulation can produce both sympathetic (tachycardia, hypertension) and vagal (bradycardia, AV block) responses - particularly in ophthalmic surgery (oculocardiac reflex), carotid surgery, peritoneal traction, and anal dilatation

Hypoxia and hypercarbia:

Hypoxia directly depresses myocardial conduction and increases ectopic automaticity
Hypercarbia causes sympathoadrenal stimulation with associated tachycardia and sensitises the myocardium to catecholamine-induced arrhythmias

Electrolyte imbalances:

Hypokalaemia and hypomagnesaemia lower the arrhythmia threshold, prolong the QT interval, and predispose to TdP
Hypercalcaemia shortens the QT interval and increases risk of fatal dysrhythmia and sudden death
Hyperkalaemia causes progressive conduction slowing and can precipitate VF

Anaesthetic drug effects:

Halogenated agents (sevoflurane, desflurane): sensitise the myocardium to catecholamines to a modest degree; desflurane can cause sympathetic activation on initial administration
Propofol: can cause bradycardia and hypotension; prolonged infusions are particularly associated with arrhythmias in Brugada syndrome
Succinylcholine: can cause sinus bradycardia, junctional rhythms, or sinus arrest - particularly in children, with second doses, and after severe burns or denervation injuries (via hyperkalaemia-induced VF)
Neostigmine/anticholinesterases: muscarinic action can produce bradycardia and AV block unless co-administered with an anticholinergic
Opioids: reduce heart rate (vagally mediated) - beneficial in most contexts but can cause significant bradycardia
Ketamine: sympathomimetic, increases heart rate; arrhythmias are uncommon but possible
Local anaesthetics (LAST): sodium channel blockade at high plasma concentrations causes widened QRS, VT, and refractory VF; bupivacaine is the most cardiotoxic

Surgical factors:

Intrapericardial dissection, direct cardiac manipulation, and pneumonectomy all increase arrhythmia risk
Thoracic surgery carries 30-50% incidence of dysrhythmia in the first week, with 60-70% being AF; pneumonectomy (60%) > lobectomy (40%) > non-resection thoracotomy (30%)
Increased pulmonary vascular resistance post-lung-resection causes right heart strain, a key driver of post-thoracotomy atrial arrhythmias

Underlying cardiac disease:

Valvular disease, ischaemia, cardiomyopathy, congenital conduction abnormalities (LQTS, Brugada, WPW) all predispose to perioperative dysrhythmias
Beta-blocker withdrawal perioperatively causes catecholamine surge and increased arrhythmia risk

3. Recognition and Monitoring

All patients under anaesthesia require continuous ECG monitoring. Lead II is optimal for rhythm analysis (best P-wave visibility); lead V5 is best for detecting anterior ischaemia. A 12-lead ECG should be obtained if a significant new dysrhythmia develops. Haemodynamic monitoring (arterial line for high-risk cases) is essential because the clinical significance of any arrhythmia depends on whether it causes haemodynamic compromise.

Key questions on encountering an intraoperative arrhythmia:

Is the patient haemodynamically stable?
What is the QRS morphology - narrow or wide?
Is the rhythm regular or irregular?
Are P waves present and what is their relationship to QRS?
Is there a reversible cause (hypoxia, light anaesthesia, electrolyte problem, drug)?

4. Management

4.1 General Principles

The first priority is always treat reversible causes:

Correct hypoxia and hypercarbia (check ventilation and oxygenation)
Correct depth of anaesthesia (if too light - consider opioid/anaesthetic top-up)
Correct electrolytes: potassium, magnesium
Stop arrhythmogenic drugs if possible
Treat myocardial ischaemia if present

If the patient is haemodynamically unstable - hypotension, signs of low cardiac output, loss of pulse - proceed immediately to the relevant ACLS/ALS algorithm regardless of arrhythmia type.

4.2 Bradyarrhythmias

Sinus bradycardia and 1st/2nd-degree AV block:

Usually respond to reducing anaesthetic depth, treating hypoxia
Atropine 0.3-0.6 mg IV (repeated as needed up to 3 mg total)
Glycopyrrolate 0.2-0.4 mg IV (longer duration, no CNS penetration)
Ephedrine 5-10 mg IV for bradycardia with hypotension
Adrenaline (epinephrine) for refractory bradycardia

Complete (3rd-degree) AV block with haemodynamic compromise:

Transcutaneous pacing as immediate temporising measure
Transvenous/oesophageal pacing
Isoprenaline (isoproterenol) infusion if pacing unavailable (also first-line in Brugada arrhythmia: 1-2 mcg bolus, 0.15-2.0 mcg/min infusion)

Aminophylline is an alternative for symptomatic bradycardia unresponsive to atropine.

4.3 Supraventricular Tachyarrhythmias

Atrial fibrillation / Atrial flutter - new onset (haemodynamically stable):

Rate control with IV beta-blocker (metoprolol, esmolol) or non-dihydropyridine calcium channel blocker (diltiazem, verapamil) or digoxin
If duration <48 hours: chemical cardioversion can be considered - amiodarone, flecainide, dofetilide, propafenone, or ibutilide
If duration >48 hours or unknown: anticoagulation before cardioversion
Correct precipitants: electrolytes, pain, hypoxia, infection

AF with haemodynamic compromise:

Synchronised DC cardioversion (biphasic preferred)

Post-thoracotomy AF prophylaxis: Diltiazem is the most useful drug; beta-blockers are effective but caution in reactive airways disease (Miller's Anesthesia, 10e).

Regular narrow-complex SVT (AVNRT, orthodromic AVRT):

Vagal manoeuvres (Valsalva, carotid sinus massage - only if no carotid disease risk)
Adenosine 6 mg rapid IV bolus; if unsuccessful, 12 mg (dose should be halved if given via central line or if patient is on dipyridamole)
If refractory: verapamil, diltiazem, or beta-blockers
Synchronised cardioversion if unstable

4.4 WPW Syndrome (Accessory Pathway)

The crucial point is that in antidromic AVRT or AF with preexcitation (irregular wide-complex tachycardia, HR >200), AV nodal blocking agents are contraindicated:

Adenosine, verapamil, diltiazem, beta-blockers, and digoxin must NOT be given - they slow conduction through the AV node, forcing rapid antegrade conduction down the accessory pathway, which can precipitate VF.

Treatment: Procainamide IV (slows conduction in both the AV node and accessory pathway). DC cardioversion for haemodynamic instability or VF.

For stable orthodromic AVRT (narrow-complex regular tachycardia): vagal manoeuvres, adenosine, or AV nodal blockers are appropriate.

(Miller's Anesthesia, 10e, p. 4168-4169)

4.5 Ventricular Arrhythmias

Isolated PVCs (frequent):

Usually benign; treat the cause (correct hypoxia, electrolytes, light anaesthesia, ischaemia)
Lignocaine (lidocaine) 1-1.5 mg/kg IV bolus if frequent multifocal PVCs, runs, or R-on-T phenomenon
Beta-blocker if catecholamine-driven

Monomorphic VT (haemodynamically stable):

Amiodarone 150 mg IV over 10 min, then 1 mg/min infusion
Lignocaine (lidocaine) 1-1.5 mg/kg IV as alternative

Monomorphic VT (haemodynamically unstable or pulseless VT):

Immediate synchronised cardioversion (pulseless: defibrillation, then ACLS protocol)

Torsades de Pointes (TdP):

Magnesium sulphate 2 g IV over 5-10 min (first-line, regardless of magnesium level)
Correct underlying QT-prolonging drugs
In congenital LQTS: TdP is triggered by catecholamine surges - continue beta-blockers, avoid sympathetic stimulation, avoid QT-prolonging drugs. Manage: MgSO4, correct bradycardia (pacing at higher rate)
In acquired LQTS: TdP is triggered during bradycardia - temporary overdrive pacing is definitive

Ventricular fibrillation:

Immediate defibrillation (unsynchronised, 200 J biphasic)
CPR, adrenaline 1 mg IV every 3-5 min
Amiodarone 300 mg IV after 3rd shock
Follow ALS/ACLS algorithm

4.6 Local Anaesthetic Systemic Toxicity (LAST) - Arrhythmia

Stop local anaesthetic injection immediately
20% Intralipid (lipid emulsion therapy): 1.5 mL/kg IV bolus, then 0.25 mL/kg/min infusion
Avoid vasopressin, calcium channel blockers, beta-blockers
CPR if cardiac arrest; prolonged resuscitation may be needed
Avoid propofol as a substitute for Intralipid

(Barash Clinical Anesthesia, 9e)

4.7 Brugada Syndrome

Avoid drugs that unmask or worsen Brugada pattern: sodium channel blockers, excessive propofol infusions, fever
Treat arrhythmia: external defibrillation; stop precipitating agent
Isoproterenol infusion for electrical storm (suppresses the arrhythmia by increasing heart rate)
Correct hyperthermia and electrolytes (especially hyperkalaemia)
Postoperative ICU/cardiac monitoring

(Miller's Anesthesia, 10e, Box 29.5)

5. Key Drug Summary for Intraoperative Arrhythmias

Arrhythmia	First-line Drug(s)	Notes
Sinus bradycardia	Atropine, glycopyrrolate	Ephedrine if with hypotension
Complete AV block	Pacing; isoprenaline	Bridge to pacing
AF/flutter (rate control)	Diltiazem, beta-blocker, digoxin	Avoid AV-nodal blockers in WPW-AF
AF/flutter (chemical cardioversion)	Amiodarone, flecainide, ibutilide	Only if <48 h duration
SVT (AVNRT)	Adenosine 6-12 mg IV	Halve dose centrally or with dipyridamole
WPW + antidromic/AF	Procainamide	Contraindicated: adenosine, verapamil, digoxin
Stable VT	Amiodarone 150 mg IV; lignocaine
Pulseless VT/VF	Defibrillation + ACLS	Amiodarone 300 mg after 3rd shock
TdP	MgSO4 2 g IV	Correct QT prolongers; pacing for acquired LQTS
LAST	20% Intralipid (Lipid rescue)	Stop LA injection immediately
Brugada storm	Isoproterenol infusion	Defibrillate VF/VT
Post-thoracotomy AF	Diltiazem (prophylaxis)	Beta-blockers effective but caution in airway disease

6. Special Considerations

Oculocardiac reflex: Traction on extraocular muscles stimulates the trigeminal nerve, causing profound bradycardia and even asystole via a trigeminovagal reflex. Management: release traction, IV atropine; deeper anaesthesia or regional block (retrobulbar block) reduces the reflex
Laparoscopy/pneumoperitoneum: CO2 insufflation causes vagal stimulation, hypercarbia, and venous air embolism risk, all arrhythmogenic
Neuroaxial anaesthesia: High thoracic or cervical spinal block can cause profound bradycardia (T1-T4 cardioaccelerator fibre block) and hypotension; treated with atropine and vasopressors
Central venous catheter insertion: Wire advancement into the right heart stimulates PVCs and VT; withdraw the wire immediately
Malignant hyperthermia: Causes acidosis, hyperkalaemia, and VF; dantrolene + supportive care

Sources:

Miller's Anesthesia, 2-Volume Set, 10e - Chapters 29, 49
Barash, Cullen, and Stoelting's Clinical Anesthesia, 9e - Chapter 33
Sabiston Textbook of Surgery - Chapter 26 (Postoperative Arrhythmias)
Morgan and Mikhail's Clinical Anesthesiology, 7e

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