PERIOPERATIVE ARRHYTHMIAS - MD ANAESTHESIA THEORY EXAM ANSWER

PART I: PERIOPERATIVE ARRHYTHMIAS - AN OVERVIEW

Definition

Classification

• Preoperative arrhythmias (pre-existing or triggered by anxiety/pain)
• Intraoperative arrhythmias (most clinically significant)
• Postoperative arrhythmias (especially in the first 24-72 hrs)

• Tachyarrhythmias: Rate > 100/min
• Bradyarrhythmias: Rate < 60/min

• Supraventricular (SVT, AF, Atrial Flutter, AVNRT)
• Ventricular (PVCs, VT, VF, Accelerated idioventricular rhythm)
• Conduction defects (AV blocks, Bundle Branch Blocks)

Predisposing Factors / Causes (Mnemonic: HALT ME)

• Autonomic reflexes (oculocardiac reflex, vagal stimulation during bowel handling, peritoneal traction)
• Raised intracranial pressure (Cushing response - bradycardia + hypertension)
• Central venous catheter placement
• Volatile anaesthetic agents (halogenated agents sensitize myocardium to catecholamines)
• Inadequate anaesthesia during surgical stimulus

Common Perioperative Tachyarrhythmias

General Principles of Management of Intraoperative Arrhythmia

1. Check ABCs - Ensure adequate airway, oxygenation, ventilation
2. 12-lead ECG - Identify the rhythm
3. Treat reversible causes first (the "4Hs and 4Ts" of ACLS)
4. Is the patient haemodynamically stable?
   • Unstable (BP <90, signs of shock) → Immediate DC cardioversion
   • Stable → Pharmacological management
5. Follow Resuscitation Council/AHA peri-arrest guidelines
6. Involve cardiologist early for complex arrhythmias

PART II: MANAGEMENT OF ATRIAL FIBRILLATION - PERIOPERATIVE

Definition and Significance

• Incidence: 27-40% after cardiac and thoracic surgery (Barash Clinical Anaesthesia, 9e)
• Associated with: Increased morbidity, prolonged hospital stay, rehospitalization, healthcare costs, and reduced survival

Classification of Perioperative AF

Pathophysiology of PoAF

1. Inflammation: Elevated CRP, IL-6, postoperative leukocytosis - all predict PoAF. NSAIDs may reduce incidence via anti-inflammatory effect.
2. Oxidative stress: Perioperative oxidant stress at myocardial and systemic levels
3. Autonomic imbalance: Sympathetic surge during/after surgery
4. Atrial remodelling: Structural and electrical remodelling from pre-existing disease
5. Genetic predisposition: Polymorphisms on chromosome 4q25 (near PITX2c gene), GRK5, IL-6 gene, beta-1 adrenergic receptor gene (ADRB1 Arg389Gly)
6. Metabolic alterations: Ketone metabolism alterations in atrial tissue

Risk Factors for Perioperative AF

• Age >70 years
• Male sex
• Pre-existing structural heart disease (LVH, valvular disease, CCF)
• History of previous AF
• Hypertension, diabetes
• Obstructive sleep apnoea
• Elevated preoperative CRP/IL-6

• Cardiac surgery (CABG, valve surgery) - highest risk
• Thoracic surgery (pneumonectomy > lobectomy)
• Major abdominal/vascular surgery
• Cardiopulmonary bypass (CPB)

• Electrolyte imbalance (hypokalaemia, hypomagnasaemia)
• Sympathetic activation
• Fluid shifts
• Pericarditis (post-cardiac surgery)
• Pain, hypoxia

A. PREOPERATIVE MANAGEMENT OF AF

1. Assessment

• History: Duration of AF, symptoms (palpitations, dyspnoea, presyncope), prior episodes, current medications
• Examination: Heart rate, BP, signs of CCF
• Investigations:
  • 12-lead ECG
  • Echocardiography (LV function, LA size, valvular pathology, thrombus)
  • Thyroid function tests
  • Electrolytes, renal function
  • Holter monitor (if paroxysmal)

2. Pre-existing AF Coming for Surgery

• Is the AF permanent/long-standing or paroxysmal?
• Is ventricular rate controlled (target: 60-80 at rest, <110 during moderate exercise)?
• Is the patient on anticoagulation?

• Beta-blockers (metoprolol, atenolol) - first-line; continue perioperatively
• Rate-limiting calcium channel blockers (diltiazem, verapamil) - second-line
• Digoxin - useful in CCF; slow onset; continue perioperatively
• Amiodarone - for refractory cases; continue perioperatively

• Considered for symptomatic patients, younger patients, first episode
• Pharmacological: Flecainide (no structural HD), amiodarone, sotalol
• Electrical cardioversion (DC cardioversion) before elective surgery if needed

3. Anticoagulation Management

• Score 0 (male): No anticoagulation
• Score 1 (male) / 2 (female): Consider anticoagulation
• Score ≥2 (male) / ≥3 (female): Anticoagulation recommended

• Low bleeding risk surgery (cataract, endoscopy, dental): Continue warfarin/DOAC
• High bleeding risk surgery (major abdominal, cardiac, neurosurgery):
  • Warfarin: Stop 5 days before surgery; check INR <1.5 before proceeding
  • DOACs (rivaroxaban, apixaban, dabigatran): Stop 2-3 days before (longer if renal impairment)
  • Bridging therapy with LMWH: For high thromboembolic risk (CHA2DS2-VASc ≥5, mechanical valve, prior stroke)
  • Stop bridging LMWH 24 hrs before surgery
• Post-operative resumption: Restart anticoagulation as soon as haemostasis is secure (12-24 hrs for low risk, 48-72 hrs for high risk procedures)

4. Prophylaxis against New-Onset PoAF (Prior to Cardiac Surgery)

• Beta-blockers: Continue preoperative beta-blockers; most effective prophylaxis (Class I evidence)
• Amiodarone: Preoperative loading reduces PoAF incidence by ~50% in cardiac surgery
• Statins: May reduce PoAF via pleiotropic anti-inflammatory effects
• Magnesium supplementation: IV magnesium reduces PoAF incidence
• NSAIDs/Colchicine: May reduce post-pericardiotomy inflammation and PoAF

B. INTRAOPERATIVE MANAGEMENT OF NEW-ONSET AF

Haemodynamically Unstable AF:

• Immediate synchronised DC cardioversion: 120-200J (biphasic) or 200J (monophasic)
• Ensure adequate anaesthesia/analgesia before cardioversion

Haemodynamically Stable AF:

1. Rate control (ventricular rate <110/min):
   • IV Metoprolol (2.5-5 mg slow IV, repeat to max 15 mg)
   • IV Diltiazem (0.25 mg/kg over 2 min, then infusion 5-15 mg/hr)
   • IV Digoxin (0.5 mg loading, onset 1-2 hrs) - useful in CCF
   • IV Amiodarone (150 mg over 10 min, then 1 mg/min x 6 hrs)
2. Rhythm control (if AF <48 hrs duration - lower thrombus risk):
   • IV Amiodarone
   • Electrical cardioversion (after ruling out LA thrombus if >48 hrs)

C. POSTOPERATIVE MANAGEMENT OF PoAF

• Correct reversible triggers: Hypoxia, hypokalaemia, hypomagnasaemia, pain, hypovolaemia
• Rate control: Beta-blockers are first-line; diltiazem as alternative
• Rhythm control: Consider for persistent haemodynamically significant AF
• Anticoagulation: If AF lasts >48 hrs - initiate anticoagulation (heparin/LMWH then warfarin or DOAC) weighing bleeding risk
• TOE (Transesophageal Echo): Required before cardioversion if AF duration >48 hrs to exclude LA thrombus
• Electrolyte replacement: Target K+ >4.0 mmol/L and Mg2+ >0.9 mmol/L

PART III: COMMON BRADYARRHYTHMIAS IN THE PERIOPERATIVE PERIOD

Definition

Classification of Perioperative Bradyarrhythmias

• Sinus bradycardia
• Sinus arrest
• Sick Sinus Syndrome (SSS)

• First degree AV block
• Second degree AV block:
  • Mobitz Type I (Wenckebach)
  • Mobitz Type II
• Third degree (Complete) AV block
• Bundle Branch Blocks (LBBB, RBBB, Bifascicular, Trifascicular)

A. SINUS BRADYCARDIA

• Rate <60/min
• Normal P wave morphology and axis
• Normal PR interval
• 1:1 P:QRS relationship

• Physiological (athletes, vasovagal)
• Hypoxia (early response)
• Beta-blockers, digoxin (preoperative medications)
• Raised intracranial pressure (Cushing response)
• High spinal/epidural block (T1-T4 sympathetic blockade)
• Hypothyroidism
• Drugs: Neostigmine, succinylcholine, dexmedetomidine
• Vagal reflexes (oculocardiac reflex, bowel traction, cervical dilation, laparoscopy)
• Hypothermia

B. AV BLOCKS

First Degree AV Block

• ECG: PR interval >200 ms; all P waves conducted
• Usually benign; continue monitoring
• Caused by: Digoxin, beta-blockers, calcium channel blockers, myocarditis

Second Degree AV Block - Mobitz Type I (Wenckebach)

• ECG: Progressive lengthening of PR interval until P wave not conducted, then cycle resets
• Location: AV node (proximal)
• Usually benign; generally above His bundle
• Often drug-induced or vagally-mediated
• Does not usually require pacing unless symptomatic

Second Degree AV Block - Mobitz Type II

• ECG: Fixed PR interval; sudden non-conducted P waves (2:1, 3:1)
• Location: Below AV node (His-Purkinje)
• Dangerous - high risk of progression to complete heart block
• Requires preoperative pacemaker insertion

Third Degree (Complete) AV Block

• ECG: Complete dissociation between P waves and QRS complexes
• P rate > QRS rate; QRS is escape rhythm (narrow if junctional, wide if ventricular)
• Medical emergency - requires urgent pacing
• Perioperative causes: Inferior MI (AV node affected), cardiac surgery, trauma, drugs

C. BUNDLE BRANCH BLOCKS

D. VAGALLY-MEDIATED BRADYCARDIAS (REFLEXES)

E. DRUG-INDUCED PERIOPERATIVE BRADYARRHYTHMIAS

PART IV: MANAGEMENT OF PERIOPERATIVE BRADYARRHYTHMIAS

General Approach

• Is BP maintained? Is there end-organ perfusion?
• Symptoms: Syncope, chest pain, dyspnoea, altered consciousness

• Hypoxia: Increase FiO2, check airway
• Drug effects: Stop offending agent
• Electrolytes: Treat hyperkalaemia, correct Ca2+/Mg2+
• Vagal stimulus: Release surgical traction, lighten anaesthesia
• High spinal: IV fluids, vasopressors

Pharmacological Management

First Line: ATROPINE

• Dose: 0.5 mg IV bolus; repeat every 3-5 min; maximum dose 3 mg (total vagolytic dose)
• Mechanism: Muscarinic antagonist; accelerates SA node discharge; increases AV conduction
• Effective for: Sinus bradycardia, AV block at nodal level (Mobitz I, 3rd degree due to vagal causes), oculocardiac reflex
• Ineffective for: Infranodal blocks (Mobitz II, complete HB with wide escape) - may worsen by increasing atrial rate without improving ventricular rate
• Caution: Glaucoma, prostatic hypertrophy

Alternative: GLYCOPYRROLATE

• Dose: 0.2-0.4 mg IV (or 0.005 mg/kg)
• Synthetic quaternary ammonium compound; does not cross blood-brain barrier
• Advantages over atropine: No CNS effects (agitation, confusion), longer duration of action, less tachycardia
• Preferred in elderly, ICU patients

Second Line Agents:

• Isoprenaline (Isoproterenol): Non-selective beta-agonist; 2-20 mcg/min infusion; increases HR and contractility; useful for complete heart block as bridge to pacing
• Adrenaline (Epinephrine): 2-10 mcg/min infusion; for bradycardia associated with cardiac arrest or severe haemodynamic instability
• Dopamine: 2-10 mcg/kg/min; chronotropic and inotropic
• Glucagon: 3-5 mg IV bolus; used for beta-blocker or calcium channel blocker-induced bradycardia (increases cAMP independent of beta receptors)
• Aminophylline: Adenosine antagonist; useful for post-cardiac transplant bradycardia (transplant heart lacks vagal innervation; atropine ineffective)

Cardiac Pacing in Perioperative Bradyarrhythmias

Indications for Temporary Pacing (Preoperative)

• Symptomatic sinus bradycardia/SSS
• Complete (third degree) AV block
• Symptomatic Mobitz Type II AV block
• Alternating LBBB and RBBB
• New bifascicular block with prolonged PR (trifascicular block) + symptoms

• Asymptomatic Mobitz II with wide QRS
• Bifascicular block with unexplained syncope

• Isolated RBBB or LBBB (without advanced block)
• First degree or asymptomatic Wenckebach

Types of Perioperative Pacing

1. Transcutaneous pacing (TCP): Immediate non-invasive; large pads; rate 60-80/min; used as bridge; painful in conscious patients
2. Transvenous temporary pacing: Via internal jugular or subclavian; most reliable intraoperatively; rate 70-80/min
3. Permanent pacemaker (PPM): If patient has pre-existing indication per ACC/AHA guidelines
4. Transoesophageal pacing: Limited; only atrial pacing; used in selected cases

Pacemaker Management (Existing Pacemakers)

• Preoperative: Identify pacemaker type (VVI, DDD); determine pacemaker dependency
• Intraoperative concern: Electromagnetic interference (EMI) from surgical electrocautery can inhibit pacemaker output or cause asynchronous pacing
• Management:
  • Use bipolar diathermy whenever possible
  • If unipolar diathermy used: Place return pad away from pacemaker
  • Convert to asynchronous mode (VOO/DOO) for pacemaker-dependent patients before surgery
  • Magnet application (over pacemaker): Converts DDD to DOO (asynchronous) - removes sensing, prevents EMI inhibition
  • Have external pacing/defibrillation available
  • Reprogram pacemaker back to original settings post-operatively
• Per 2020 ASA guidelines, formal liaison with a cardiologist/device specialist is required for all patients with CIEDs (Cardiac Implantable Electronic Devices)

Summary Table: Bradyarrhythmia Management

VIVA QUESTIONS WITH ANSWERS

Section A: Perioperative Arrhythmias - General

4Hs: Hypoxia, Hypovolaemia, Hypo/Hyperkalaemia and metabolic disorders, Hypothermia 4Ts: Tension pneumothorax, Tamponade (cardiac), Toxins/drugs, Thrombosis (coronary/pulmonary)

Trigeminovagal reflex triggered by traction on extraocular muscles. The afferent limb is the ophthalmic branch of the trigeminal nerve; efferent limb is the vagus nerve. It results in sinus bradycardia, junctional rhythm, AV block, or ventricular fibrillation.

• Prevention: Retrobulbar block, avoid ketamine (which sensitises), premedication with IV atropine or glycopyrrolate
• Treatment: Immediately release traction; IV atropine 0.6 mg

Halothane sensitises the myocardium to catecholamines, lowers the threshold for ventricular arrhythmias. This is potentiated by hypercapnia. Mechanism involves beta-adrenergic receptor sensitisation and direct Na+/Ca2+ channel effects. The safe upper limit of adrenaline with halothane is 1.5 mcg/kg (compared to 7 mcg/kg with isoflurane).

A triad of bradycardia, hypotension, and vasodilatation caused by stimulation of ventricular C-fibre mechanoreceptors (afferent via vagus). Occurs in hypovolaemia, spinal anaesthesia, and haemorrhage. Treated with IV fluids, atropine, ephedrine.

Peaked T waves (earliest), widening of QRS, prolonged PR, loss of P waves, sine wave pattern, VF/asystole. Management: Calcium gluconate (membrane stabilisation), sodium bicarbonate, insulin-dextrose, salbutamol nebulisation, dialysis.

Section B: Atrial Fibrillation

New-onset AF occurring in the perioperative setting, most commonly after cardiac and thoracic surgery. Incidence is 27-40% after cardiac surgery (CABG, valve surgery). Associated with increased morbidity, hospital stay, healthcare costs, and reduced long-term survival.

Stroke risk stratification tool for AF. Score is calculated based on: CCF, Hypertension, Age ≥75 (2 pts), Diabetes, prior Stroke/TIA (2 pts), Vascular disease, Age 65-74, Sex (Female). Guides whether to initiate anticoagulation and whether bridging therapy is needed during perioperative anticoagulation interruption.

Bridging (LMWH) is considered when interruption of anticoagulation poses high thromboembolic risk:

• CHA2DS2-VASc score ≥5
• Prior stroke/TIA within 3 months
• Mechanical prosthetic heart valve
• Rheumatic mitral stenosis with AF LMWH stopped 24 hrs before surgery; restarted 24-72 hrs post-surgery.

A patient-directed approach for paroxysmal AF in otherwise healthy individuals: A single oral dose of flecainide (200-300 mg) or propafenone (450-600 mg) taken at onset of AF to restore sinus rhythm. Only used in patients without structural heart disease, significant LVH, or ischaemic heart disease.

• Ensure adequate oxygenation and ventilation
• Correct electrolytes (K+, Mg2+)
• If haemodynamically unstable (SBP <90, signs of organ hypoperfusion): Synchronised DC cardioversion immediately (120-200J biphasic) under adequate anaesthesia
• If stable: IV amiodarone 150 mg over 10 min, then 1 mg/min infusion
• Consider cardiology consult post-operatively

• Polymorphisms on chromosome 4q25 (near PITX2c transcription factor - involved in pulmonary myocardium development)
• ADRB1 Arg389Gly polymorphism (beta-1 adrenergic receptor)
• GRK5 polymorphisms (modulate beta-adrenergic signalling)
• IL-6 promoter SNP (-174G>C) - increased IL-6 → inflammation → PoAF
• LY96 (lymphocyte antigen 96) variant
• PAI-1 levels (independent predictor)

1. Continue preoperative beta-blockers (Class I)
2. Preoperative amiodarone loading (reduces PoAF by ~50%)
3. IV magnesium supplementation
4. Statins (anti-inflammatory pleiotropic effects)
5. NSAIDs/colchicine (reduce post-pericardiotomy syndrome)
6. Maintenance of electrolyte balance

Section C: Bradyarrhythmias

• Vagal reflexes (oculocardiac, Bezold-Jarisch, laryngoscopy, peritoneal traction)
• Drug-induced (neostigmine, succinylcholine second dose, dexmedetomidine, halothane, beta-blockers, digoxin)
• High spinal anaesthesia (T1-T4 sympathetic blockade)
• Hypoxia
• Raised ICP (Cushing response)
• Hypothermia
• AV block (pre-existing or new from ischaemia)
• Electrolyte abnormalities (hyperkalaemia)

• Mobitz I (Wenckebach): Progressive PR lengthening until a beat is dropped; occurs at AV node level; usually benign, often vagally mediated; does not require prophylactic pacing
• Mobitz II: Fixed PR interval, sudden non-conducted P waves; occurs below AV node (His-Purkinje); unpredictable progression to complete block; requires prophylactic pacemaker insertion before surgery

Atropine is a competitive muscarinic receptor antagonist. It blocks vagal (parasympathetic) effects on the SA node and AV node: increases SA node automaticity (rate), shortens AV nodal conduction time (decreases PR interval). Dose: 0.5 mg IV bolus, maximum 3 mg total (complete vagolytic dose). Doses <0.5 mg may cause paradoxical bradycardia due to central vagal stimulation.

The transplanted heart has no vagal innervation (the transplant procedure severs all efferent vagal fibres to the SA node). Atropine works by blocking vagal muscarinic receptors; without vagal innervation, there is no vagal tone to block. Use isoprenaline (direct beta-agonist), adrenaline, aminophylline (adenosine antagonist), or temporary pacing instead.

Trifascicular block = RBBB + LAHB (or LPHB) + prolonged PR interval (first degree AV block). It indicates disease in all three fascicles. Anaesthetic implications:

• High risk of progression to complete AV block under anaesthesia
• Pre-operative temporary transvenous pacing should be considered
• Intraoperative monitoring: 5-lead ECG, arterial line
• Avoid drugs that further depress conduction (high-dose beta-blockers, verapamil)
• Have external pacing readily available

• First dose: Usually transient sinus tachycardia (nicotinic stimulation)
• Second dose (especially in children): Marked bradycardia, junctional rhythm, or even asystole - due to muscarinic stimulation at SA node
• Prevention: Atropine 0.02 mg/kg IV before second dose (mandatory in children <2 years and adults receiving second dose within 5 minutes)

Spinal anaesthesia above T4 blocks the cardiac accelerator fibres (T1-T4 sympathetic innervation to the heart). This abolishes sympathetic tone to the SA node and AV node, leaving unopposed vagal tone, resulting in:

• Bradycardia (decreased HR)
• Hypotension (decreased SVR + decreased HR)
• In severe cases: Cardiac arrest (Bezold-Jarisch reflex from venous pooling) Management: IV fluids, IV atropine, IV ephedrine, IV adrenaline (epinephrine) if severe; position supine with legs elevated.

Applying a magnet over a permanent pacemaker converts it to asynchronous pacing mode (VOO or DOO) - fixed rate pacing regardless of sensing. This prevents electromagnetic interference (EMI) from surgical diathermy from inhibiting pacemaker output in pacemaker-dependent patients. The magnet should be removed after use of diathermy is complete. However, in ICD patients, magnet application suspends tachytherapy (anti-tachycardia pacing and shocks) - this is important to prevent inappropriate shocks intraoperatively.

Section D: Higher-Order Viva

Per 2020 ASA guidelines (and HRS/ASA Expert Consensus Statement), patients with CIEDs require:

1. Preoperative device interrogation within 6-12 months (within 3 months if pacemaker-dependent or ICD)
2. Assessment of pacemaker dependency
3. Decision on reprogramming vs. magnet use during surgery
4. Intraoperative monitoring: continuous ECG, external pacing/defibrillation available
5. Post-operative device interrogation before discharge

PoAF has a significant genetic basis. The most well-validated locus is on chromosome 4q25, near the PITX2c transcription factor gene (involved in pulmonary myocardium development - the sleeve of cardiomyocytes around pulmonary veins is the anatomic substrate for AF triggers). Other implicated genes include: GRK5 (modulates beta-1 AR signalling), ADRB1 (Arg389Gly variant), IL-6 promoter SNP (inflammation pathway), and LY96 (innate immune response). This polygenic predisposition combined with perioperative triggers (inflammation, sympathetic activation, oxidative stress) leads to PoAF.

In AF: loss of atrial "kick" (contributes 15-25% of ventricular filling), reduced diastolic filling time (fast rate), and irregular rhythm → variable stroke volume → reduced cardiac output. In mitral stenosis, the atrial kick is critical to maintain flow across the stenotic mitral valve. AF in MS causes:

• Loss of atrial kick → severe LV underfilling → pulmonary oedema
• Rapid ventricular rate → further reduced diastolic filling
• Potential for LA thrombus (dilated LA + AF) → systemic embolism Therefore MS + AF is a high-risk combination requiring aggressive rate control (HR 50-70/min), anticoagulation, and consideration of cardioversion.

Exam Tip: In theory papers, structure your answer as: Definition → Classification → Pathophysiology/Causes → Clinical Features → Management (Pre-op / Intra-op / Post-op) → Complications. In viva, always begin with the mechanism and relate it to clinical anaesthetic practice. Know drug doses precisely - examiners frequently ask about maximum atropine dose (3 mg), atropine dose for neostigmine reversal (1.2-1.8 mg with 2.5 mg neostigmine), and cardioversion energy (120-200J biphasic).