Bradyarrhythmias & Heart Block in ICU

Quick Answer

Bradyarrhythmias are rhythm disturbances characterised by a heart rate less than 60 bpm, caused by dysfunction of the sinoatrial (SA) node, atrioventricular (AV) node, or His-Purkinje conduction system. Haemodynamic instability with symptomatic bradycardia is a medical emergency requiring immediate intervention.

Key Emergency Actions:

1. Atropine 0.5-1 mg IV (max 3 mg) - first-line for symptomatic bradycardia
2. Transcutaneous pacing - immediate if atropine fails or complete heart block
3. Transvenous pacing - definitive temporary pacing for refractory cases
4. Isoprenaline infusion (1-10 mcg/min) - bridge to pacing

Critical Distinctions:

• Narrow QRS escape (junctional, 40-60 bpm): More stable, may respond to atropine
• Wide QRS escape (ventricular, less than 40 bpm): Unstable, atropine often ineffective, urgent pacing required

ICU Mortality: Complete heart block 10-25%; drug-induced bradycardia 5-15%

Must-Know Facts:

• Atropine is contraindicated in infranodal block (may worsen block by increasing atrial rate)
• Post-MI AV block: Inferior MI = AV nodal, better prognosis; Anterior MI = infranodal, high mortality
• Transvenous pacing via right internal jugular is preferred (shortest, straightest path)

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CICM Exam Focus

Written Exam (SAQ)

Common SAQ Stems:

• "A 68-year-old patient on Day 2 post-anterior STEMI develops complete heart block. Outline your assessment and management."
• "A patient presents with symptomatic bradycardia following beta-blocker overdose. Describe your approach."
• "Discuss the indications for temporary and permanent pacing in critically ill patients."
• "Compare and contrast transcutaneous and transvenous pacing."

Expected Depth:

• Systematic approach to bradycardia (ANZCOR/AHA algorithm)
• Differentiation between nodal vs infranodal block (ECG features, escape rhythm characteristics)
• Drug pharmacology (atropine, isoprenaline, adrenaline, aminophylline)
• Pacing indications, techniques, complications
• Post-MI heart block prognosis (anterior vs inferior)
• Drug-induced bradycardia specific antidotes

Viva Voce

Expected Discussion Areas:

• Pathophysiology of SA and AV nodal dysfunction
• Temporary pacing techniques (TCP vs TVP) and complications
• Permanent pacemaker indications (ACC/AHA Class I, IIa)
• Post-operative heart block management
• Electrolyte and drug-induced bradycardia
• Troubleshooting pacemaker malfunction

Examiner Expectations:

• Safe, systematic approach to haemodynamically unstable patient
• Knowledge of pacing thresholds, settings, complications
• Evidence-based decision-making (cite guidelines)
• Indigenous health awareness (remote retrieval challenges)

Hot Case

Typical Presentations:

• Post-cardiac surgery patient with complete heart block and epicardial pacing wires
• Patient with transvenous pacing wire and failure to capture
• Beta-blocker/CCB overdose with symptomatic bradycardia

Common Mistakes

1. Giving atropine for infranodal (wide QRS) block - ineffective and may worsen
2. Inadequate TCP settings (current too low, failure to capture)
3. Not recognising pacemaker malfunction patterns
4. Delaying pacing in haemodynamically unstable complete heart block
5. Not considering reversible causes before permanent pacing

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Key Points

Must-Know Facts

1. Bradycardia Definition: Heart rate less than 60 bpm; clinically significant when symptomatic or haemodynamically compromising (PMID: 29146516)

2. SA Node Dysfunction (Sick Sinus Syndrome): Includes sinus bradycardia, sinus pauses greater than 3 seconds, sinoatrial exit block, tachy-brady syndrome; intrinsic rate declines with age (PMID: 34185046)

3. AV Block Classification:

   • First-degree: PR greater than 200 ms, all P waves conducted
   • Second-degree Mobitz I (Wenckebach): Progressive PR prolongation then dropped beat (AV node level)
   • Second-degree Mobitz II: Fixed PR interval with sudden non-conducted P waves (infranodal - dangerous)
   • Third-degree (Complete): Complete AV dissociation, independent atrial and ventricular rhythms (PMID: 29146516)

4. Escape Rhythm Localisation:

   • Junctional escape (AV node/His bundle): Narrow QRS, 40-60 bpm, more stable
   • Ventricular escape (below His): Wide QRS, less than 40 bpm, unreliable, high risk of asystole (PMID: 34185046)

5. Atropine Pharmacology: Muscarinic (M2) receptor antagonist, increases SA node automaticity and AV nodal conduction; ineffective for infranodal block; dose 0.5-1 mg IV, max 3 mg (PMID: 26547456)

6. Isoprenaline: Non-selective beta-agonist, increases automaticity of all pacemaker cells (SA, AV, His-Purkinje); dose 1-10 mcg/min IV; bridge to pacing (PMID: 18439613)

7. Transcutaneous Pacing (TCP): Immediate, non-invasive; painful (requires sedation/analgesia); not reliable long-term; settings: demand mode, rate 60-80 bpm, current titrated to capture (typically 50-200 mA) (PMID: 8556295)

8. Transvenous Pacing (TVP): Definitive temporary pacing; preferred access right internal jugular vein (shortest path); VVI mode standard; typical settings rate 60-80 bpm, output 2-3x threshold (PMID: 3873236)

9. Post-MI Heart Block Prognosis:

   • Inferior MI: AV nodal ischaemia (RCA), often transient (48-72h), good prognosis, rarely needs permanent pacing
   • Anterior MI: Infranodal (LAD - septal perforators), indicates extensive myocardial damage, high mortality (70-80% without pacing), usually requires permanent pacemaker (PMID: 24573958, 30063141)

10. Permanent Pacemaker Class I Indications (ACC/AHA/HRS 2018):

    • Symptomatic sinus node dysfunction
    • Symptomatic chronotropic incompetence
    • Third-degree AV block
    • Symptomatic second-degree Mobitz II AV block
    • Alternating bundle branch block
    • Post-MI persistent AV block greater than 7 days (PMID: 29554191)

Memory Aids

Mnemonic - PACE for Bradycardia Management:

• Pacemaker (temporary/permanent indications)
• Atropine first (if nodal level block)
• Chronotropes (isoprenaline, adrenaline, dopamine)
• Electrolytes and drugs (reversible causes)

Mobitz I vs II:

• Mobitz I (Wenckebach): "Longer, longer, longer, DROP - then you have a Wenckebach" (progressive PR prolongation)
• Mobitz II: "All the same, then sudden drop" (constant PR, sudden non-conduction)

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Classification

Anatomical Classification of Bradyarrhythmias

Sinus Node Dysfunction (Sick Sinus Syndrome)

Definition: Intrinsic inability of the SA node to generate adequate heart rate for physiological needs (PMID: 34185046).

Subtypes:

1. Sinus Bradycardia: Sinus rhythm less than 60 bpm (less than 50 bpm considered pathological in adults)
2. Sinus Arrest/Pause: Absence of P waves for greater than 2.0 seconds (pathological if greater than 3.0 seconds)
3. Sinoatrial Exit Block: Regular PP intervals with sudden missed P wave (no progressive shortening)
4. Tachy-Brady Syndrome: Alternating tachycardia (usually AF) and bradycardia
5. Chronotropic Incompetence: Inability to increase HR appropriately with exercise (less than 80% predicted maximal HR)

First-Degree AV Block

Definition: Prolonged PR interval greater than 200 ms with 1:1 AV conduction (PMID: 29146516).

ECG Features:

• PR interval greater than 200 ms (up to 0.40 seconds in some cases)
• Every P wave followed by QRS
• Constant PR interval

Clinical Significance:

• Usually benign, asymptomatic
• May indicate underlying conduction disease or drug effect
• Rarely requires intervention alone
• Associated conditions: Athletes, vagotonia, drugs (beta-blockers, digoxin, CCBs), inferior MI, myocarditis

Second-Degree AV Block

Mobitz Type I (Wenckebach)

Definition: Progressive prolongation of PR interval until a P wave fails to conduct (PMID: 29146516).

ECG Features:

• Progressive PR prolongation with each beat
• Greatest PR increment in second beat of cycle
• RR intervals progressively shorten before dropped beat
• QRS usually narrow (block at AV node)
• Pause less than 2x the preceding RR interval

Pathophysiology:

• Block at AV node level (decremental conduction)
• Often due to increased vagal tone, ischaemia (inferior MI), drugs

Clinical Significance:

• Usually benign, especially in athletes
• May progress in setting of anterior MI (poor prognosis)
• Rarely requires pacing unless symptomatic

Mobitz Type II

Definition: Intermittent non-conduction of P waves without preceding PR prolongation (PMID: 29146516).

ECG Features:

• Constant PR interval before conducted beats
• Sudden non-conducted P wave
• Often associated with wide QRS (bundle branch block pattern)
• May have fixed conduction ratios (2:1, 3:1)

Pathophysiology:

• Block below AV node (His bundle or bundle branches)
• Indicates structural conduction system disease
• High risk of progression to complete heart block

Clinical Significance:

• Always pathological - requires urgent evaluation
• Pacing usually indicated even if asymptomatic
• Common causes: anterior MI, degenerative conduction disease, post-cardiac surgery

2:1 AV Block

Challenge: Cannot differentiate Mobitz I vs II from single ECG.

Clues to Location:

Third-Degree (Complete) AV Block

Definition: Complete failure of AV conduction with independent atrial and ventricular rhythms (AV dissociation) (PMID: 29146516).

ECG Features:

• Regular P waves at one rate
• Regular QRS complexes at different (slower) rate
• No relationship between P waves and QRS complexes
• Escape rhythm determines QRS morphology and rate

Escape Rhythm Classification:

Clinical Significance:

• Medical emergency if symptomatic
• Always requires evaluation for reversible causes
• Permanent pacing indicated for most causes
• Wide QRS escape = more unstable, higher risk of asystole

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Pathophysiology

Normal Cardiac Conduction

Conduction System Hierarchy:

1. SA Node: Primary pacemaker, intrinsic rate 60-100 bpm
2. AV Node: Secondary pacemaker, intrinsic rate 40-60 bpm, provides physiological delay
3. His Bundle: Tertiary pacemaker, intrinsic rate 30-40 bpm
4. Bundle Branches: Quaternary, intrinsic rate 20-30 bpm
5. Purkinje Fibres: Lowest automaticity, rate less than 20 bpm

Ion Channel Physiology:

SA Node Automaticity:

• Slow diastolic depolarisation (Phase 4) via:
  • Hyperpolarisation-activated cyclic nucleotide-gated (HCN) channels (If "funny current")
  • L-type Ca2+ channels
  • Na+/Ca2+ exchanger
• Sympathetic activation: Beta-1 receptors → cAMP → increased If → faster depolarisation
• Parasympathetic activation: M2 receptors → Gi → decreased cAMP + activated IKACh → slower depolarisation, hyperpolarisation

AV Node Conduction:

• Calcium-dependent slow-response tissue (L-type Ca2+ channels)
• Decremental conduction (progressive slowing with rapid rates)
• Controlled by autonomic input (vagal tone slows, sympathetic accelerates)

SA Node Dysfunction Mechanisms

Intrinsic Causes:

1. Fibrosis: Age-related replacement of nodal cells with fibrous tissue
2. Ischaemia: SA nodal artery (branch of RCA in 55%, LCx in 45%) occlusion
3. Infiltrative: Amyloidosis, sarcoidosis, haemochromatosis
4. Inflammatory: Myocarditis, rheumatic heart disease
5. Genetic: SCN5A, HCN4 mutations (familial sick sinus syndrome)

Extrinsic Causes:

1. Drugs: Beta-blockers, calcium channel blockers, digoxin, antiarrhythmics (amiodarone, sotalol, flecainide)
2. Electrolytes: Hyperkalaemia, hypokalaemia
3. Hypothyroidism: Decreased metabolic rate, reduced sympathetic tone
4. Hypothermia: Direct effect on ion channel kinetics
5. Increased intracranial pressure: Cushing reflex (bradycardia with hypertension)
6. Obstructive sleep apnoea: Vagal surges during apnoeic episodes

AV Nodal Block Mechanisms

Level of Block Determines Prognosis:

AV Node Level (Supra-Hisian):

• Vagal tone excess
• Drug effects (beta-blockers, CCBs, digoxin)
• Inferior MI (RCA supplies AV node in 90%)
• Myocarditis
• Usually reversible
• Junctional escape (40-60 bpm) - more reliable

His Bundle Level (Intra-Hisian):

• Infiltrative disease
• Calcific degeneration
• Surgical/procedural trauma
• May be reversible
• Variable escape reliability

Infranodal Level (Infra-Hisian):

• Anterior MI (LAD - septal perforators supply bundle branches)
• Degenerative (Lev's disease - fibrous skeleton calcification; Lenègre's disease - idiopathic fibrosis)
• Post-cardiac surgery, TAVI (PMID: 26688003)
• Usually irreversible
• Ventricular escape (less than 40 bpm) - unreliable

Post-MI Heart Block Pathophysiology

Inferior MI

Blood Supply: Right coronary artery (RCA) supplies:

• AV node (90% of patients)
• SA node (55% of patients)
• Inferior wall, posterior wall, RV

Mechanism of AV Block:

• AV nodal ischaemia (not necrosis)
• Adenosine and vagal reflex (Bezold-Jarisch reflex)
• Usually reversible within 48-72 hours
• Narrow QRS escape (junctional)

Prognosis:

• Hospital mortality 5-10%
• AV block usually transient
• Permanent pacing rarely required (less than 5%)

Anterior MI

Blood Supply: Left anterior descending (LAD) artery supplies:

• Anterior wall, apex
• Ventricular septum (septal perforators)
• Bundle branches, distal His bundle

Mechanism of AV Block:

• Extensive myocardial necrosis (usually greater than 40% of LV)
• Infarction of bundle branches (bilateral BBB → complete block)
• Sudden onset, wide QRS escape
• Often preceded by new bundle branch block

Prognosis:

• Hospital mortality 50-80% (reflects extent of infarction)
• AV block often persists
• Indicates massive myocardial damage
• Survivors usually require permanent pacing (PMID: 24573958, 30063141)

Haemodynamic Consequences of Bradycardia

Cardiac Output = Heart Rate × Stroke Volume

Compensatory Mechanisms:

1. Increased stroke volume (Frank-Starling mechanism)
2. Increased sympathetic tone (vasoconstriction, inotropy)
3. Ventricular hypertrophy (chronic)

Decompensation Occurs When:

• HR too slow to maintain CO despite maximum SV
• Underlying cardiac disease limits compensation
• Irregular rhythm prevents coordinated AV contraction
• Loss of AV synchrony (cannon A waves, reduced CO by 15-25%)

Clinical Effects of Haemodynamic Compromise:

• Hypotension, syncope
• Reduced coronary perfusion (coronary flow occurs mainly in diastole, but also depends on adequate MAP)
• Cerebral hypoperfusion
• Renal hypoperfusion (AKI)
• Mesenteric ischaemia

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Aetiology

Intrinsic Causes

Drug-Induced Bradycardia (PMID: 24632433)

Electrolyte Abnormalities

Infectious/Inflammatory Causes

Other Causes

• Hypothyroidism: Decreased metabolic rate, reduced sympathetic tone
• Hypothermia: J waves (Osborn waves), progressive bradycardia below 32°C
• Increased ICP: Cushing response (bradycardia + hypertension + irregular breathing)
• Obstructive Sleep Apnoea: Vagal surges during apnoea
• Spinal Cord Injury (above T6): Loss of sympathetic innervation to heart
• Carotid Sinus Hypersensitivity: Exaggerated vagal response to carotid pressure

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Clinical Assessment

History

Presenting Symptoms:

• Syncope/pre-syncope (Stokes-Adams attacks)
• Dizziness, light-headedness
• Fatigue, exercise intolerance
• Dyspnoea on exertion
• Chest pain (reduced coronary perfusion)
• Confusion (cerebral hypoperfusion)
• Palpitations (awareness of slow/irregular rhythm)

Focused History:

• Timing: Sudden onset vs gradual, associated activities
• Previous episodes: Frequency, duration
• Medications: Beta-blockers, CCBs, digoxin, antiarrhythmics
• Cardiac history: Known CAD, previous MI, cardiomyopathy, valve disease, prior arrhythmias
• Recent surgery/procedures: Cardiac surgery, TAVI, ablation
• Comorbidities: Thyroid disease, renal disease, sleep apnoea
• Travel history: Lyme disease endemic areas, Chagas (Latin America)

Physical Examination

General:

• Level of consciousness (GCS)
• Skin perfusion (colour, temperature, CRT)
• Respiratory distress

Cardiovascular:

• Heart rate and regularity: Confirm bradycardia, assess regularity
• Blood pressure: Hypotension indicates haemodynamic compromise
• JVP:
  • Cannon A waves (AV dissociation - atria contracting against closed tricuspid)
  • Elevated JVP (RV failure)
• Heart sounds:
  • Variable S1 intensity (AV dissociation)
  • S3/S4 (heart failure)
  • Murmurs (valvular disease)
• Peripheral pulses: Rate, volume, character

Assessment of Haemodynamic Stability:

Identifying Escape Rhythm Type

Narrow QRS Escape (Junctional):

• QRS less than 120 ms
• Rate 40-60 bpm
• More stable, responds to atropine
• Indicates block at AV nodal level

Wide QRS Escape (Ventricular):

• QRS greater than 120 ms
• Rate less than 40 bpm
• Unstable, unreliable
• Atropine often ineffective
• Indicates infranodal block
• Urgent pacing required

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Investigations

Electrocardiogram (ECG)

Systematic Analysis:

1. Rate: Calculate atrial rate (P waves) and ventricular rate (QRS) separately
2. Rhythm: Regular vs irregular, relationship between P waves and QRS
3. P waves: Morphology, regularity, P:QRS ratio
4. PR interval: Measure in consecutive beats, note progression
5. QRS width: Narrow (less than 120 ms) vs wide (greater than 120 ms)
6. ST/T changes: Ischaemia, electrolyte abnormalities
7. QT interval: Prolongation (drugs, electrolytes)

ECG Patterns by Diagnosis:

Laboratory Investigations

Essential Tests:

• Electrolytes: K+, Ca2+, Mg2+ (causes of bradycardia and arrhythmias)
• Drug levels: Digoxin (therapeutic 0.8-2.0 ng/mL, toxic greater than 2.0), antiarrhythmics
• Troponin: Myocardial ischaemia/infarction
• Thyroid function: TSH, fT4 (hypothyroidism)
• Urea/creatinine: Renal function (drug clearance, hyperkalaemia)
• Full blood count: Infection, anaemia
• ABG/VBG: Metabolic status, lactate (hypoperfusion)

Specific Tests if Indicated:

• Lyme serology: If travel history to endemic areas
• Autoantibodies: ANA, anti-Ro/La (if congenital heart block, SLE suspected)
• Cardiac MRI: Infiltrative disease (sarcoid, amyloid), myocarditis

Imaging

Chest X-Ray:

• Cardiomegaly
• Pulmonary oedema
• Pacemaker/ICD position (if present)

Echocardiography:

• LV function (cardiomyopathy)
• Valvular disease
• Pericardial effusion
• Structural abnormalities (septal defects, infiltrative disease)
• Regional wall motion abnormalities (ischaemia)

Advanced Electrophysiology

Invasive EP Study (rarely performed acutely, more for chronic evaluation):

• HV interval measurement (normal 35-55 ms; prolonged greater than 100 ms indicates infranodal disease)
• Block localisation (intra-Hisian vs infra-Hisian)
• Sinus node recovery time

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Pharmacological Management

Atropine

Mechanism: Muscarinic (M2) receptor antagonist; blocks parasympathetic (vagal) input to SA and AV nodes; increases SA node automaticity and AV nodal conduction velocity (PMID: 17679615).

Indications:

• Symptomatic sinus bradycardia
• AV block at nodal level (narrow QRS escape)
• First-line drug therapy for symptomatic bradycardia (ANZCOR, AHA)

Contraindications/Limitations:

• Infranodal block (wide QRS escape): Atropine increases atrial rate without improving conduction → may worsen block, increase haemodynamic compromise
• Denervated heart (cardiac transplant): No vagal input to block
• Anticholinergic toxicity: Already present

Dosing:

• Adult: 0.5-1 mg IV bolus, repeat every 3-5 minutes
• Maximum dose: 3 mg (full vagolysis)
• Paediatric: 20 mcg/kg (minimum 100 mcg, maximum 600 mcg single dose)

Adverse Effects:

• Tachycardia, increased myocardial oxygen demand
• Urinary retention, dry mouth
• Pupil dilation (blurred vision)
• Delirium (especially elderly)
• Paradoxical bradycardia with low doses (less than 0.5 mg) - central vagal stimulation

Isoprenaline (Isoproterenol)

Mechanism: Non-selective beta-adrenergic agonist (beta-1 and beta-2); increases automaticity of all pacemaker tissues (SA node, AV node, His-Purkinje, ventricular myocardium); positive chronotropic and dromotropic effects (PMID: 18439613).

Indications:

• Refractory symptomatic bradycardia after atropine failure
• Bridge to pacing (transcutaneous or transvenous)
• Infranodal block (where atropine ineffective)
• Torsades de Pointes (increases heart rate, shortens QT)
• Post-cardiac transplant bradycardia

Dosing:

• Infusion: 1-10 mcg/min IV, titrate to effect
• Prepare: 1 mg in 250 mL D5W = 4 mcg/mL
• Start low, increase every 2-5 minutes as needed

Adverse Effects:

• Tachyarrhythmias (VT, VF) - especially in ischaemic heart
• Increased myocardial oxygen demand → ischaemia
• Hypotension (beta-2 vasodilation)
• Anxiety, tremor

Cautions:

• Use with extreme caution in CAD/acute MI (increases oxygen demand)
• Monitor for ventricular arrhythmias
• Avoid in digoxin toxicity (increases ectopy)

Adrenaline (Epinephrine)

Mechanism: Non-selective adrenergic agonist (alpha and beta); at low doses, beta effects predominate with increased HR; at higher doses, alpha vasoconstriction also significant.

Indications:

• Symptomatic bradycardia unresponsive to atropine
• Alternative to isoprenaline (especially if hypotensive)
• Cardiac arrest with bradycardia/asystole (ANZCOR)

Dosing:

• Infusion for bradycardia: 2-10 mcg/min IV
• Cardiac arrest: 1 mg IV every 3-5 minutes

Advantages over Isoprenaline:

• Alpha-1 effect provides vasoconstrictive support for hypotensive patients
• More readily available in most ICUs

Aminophylline/Theophylline

Mechanism: Methylxanthine; adenosine receptor antagonist (A1, A2a); phosphodiesterase inhibitor (increases cAMP); enhances catecholamine release; reverses adenosine-mediated AV block (PMID: 16713939, 23801896).

Indications:

• Adenosine-mediated bradycardia
• Drug-refractory sinus bradycardia
• Heart transplant bradycardia (denervated heart - adenosine mechanism important)
• Inferior MI with vagally-mediated bradycardia
• Theophylline can be used for chronic bradycardia (limited evidence)

Evidence: Pinheiro meta-analysis (PMID: 23801896) - aminophylline may increase HR in some forms of symptomatic bradycardia, but limited high-quality evidence.

Dosing:

• Aminophylline: 250 mg IV over 15-20 minutes, then infusion 0.5-0.7 mg/kg/hr
• Target serum level: 10-20 mg/L (55-110 micromol/L)

Adverse Effects:

• Nausea, vomiting
• Arrhythmias (particularly at toxic levels)
• Seizures (at toxic levels)
• Drug interactions (CYP1A2 metabolism)

Monitoring:

• Serum theophylline levels (narrow therapeutic index)
• ECG for tachyarrhythmias

Dopamine

Mechanism: Dose-dependent effects; at 5-10 mcg/kg/min, beta-1 effects predominate (increased HR, inotropy); at higher doses, alpha effects cause vasoconstriction.

Indications:

• Symptomatic bradycardia with hypotension (combined chronotropic and pressor effect)
• Alternative to isoprenaline/adrenaline

Dosing:

• For bradycardia: 5-20 mcg/kg/min IV infusion

Limitations:

• Less reliable chronotropic effect than isoprenaline
• May cause significant vasoconstriction at higher doses

Glucagon

Mechanism: Glucagon receptor agonist → activates adenylyl cyclase → increases cAMP → positive chronotropic and inotropic effects independent of beta-receptors (PMID: 25124663).

Indications:

• Beta-blocker overdose/toxicity (first-line antidote)
• Calcium channel blocker toxicity (second-line after calcium)

Dosing:

• Loading: 5-10 mg IV bolus over 1-2 minutes
• Infusion: 2-5 mg/hour (or 50-150 mcg/kg/hr)
• Effect within 1-3 minutes; duration 10-15 minutes (requires infusion for sustained effect)

Adverse Effects:

• Nausea, vomiting (common - consider antiemetic)
• Hyperglycaemia
• Hypokalaemia (from intracellular shift)

Calcium (for CCB/Hyperkalaemia)

Indications:

• Calcium channel blocker toxicity
• Hyperkalaemia with ECG changes
• Hypermagnesaemia

Dosing:

• Calcium chloride 10%: 10-20 mL (1-2 g) IV over 5-10 minutes (contains 272 mg elemental calcium per 10 mL)
• Calcium gluconate 10%: 30-60 mL IV (contains 93 mg elemental calcium per 10 mL)
• Repeat as needed; may require infusion for CCB toxicity

Caution: Calcium chloride via central line only (tissue necrosis if extravasation); gluconate safer for peripheral access.

High-Dose Insulin Euglycaemic Therapy (HIET)

Mechanism: High-dose insulin improves cardiac contractility and conduction in CCB/beta-blocker toxicity via increased glucose transport, enhanced cardiac metabolism, and direct inotropic effects (PMID: 28463086).

Indications:

• Refractory hypotension/bradycardia from beta-blocker or CCB overdose

Dosing:

• Insulin bolus: 1 unit/kg IV
• Insulin infusion: 0.5-1 unit/kg/hr (may increase to 10 units/kg/hr)
• Dextrose 50%: 25 g IV bolus, then infusion to maintain BGL 8-12 mmol/L
• Potassium: Monitor closely, supplement to maintain 3.5-4.5 mmol/L

Digoxin-Specific Antibody Fragments (DigiFab)

Mechanism: Binds and neutralises free digoxin (PMID: 33970999).

Indications:

• Life-threatening digoxin toxicity (ventricular arrhythmias, haemodynamically significant bradycardia, K+ greater than 5.5 mmol/L)

Dosing (based on digoxin level or estimated ingestion):

• Each 40 mg vial binds approximately 0.5 mg digoxin
• Known level: Number of vials = [Digoxin level (ng/mL) × Weight (kg)] / 100
• Unknown ingestion: 10-20 vials empirically for life-threatening toxicity

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Temporary Pacing

Indications for Temporary Pacing (PMID: 21435707)

Class I (Definitely Required):

• Symptomatic bradycardia unresponsive to drugs
• Haemodynamically unstable complete heart block
• Mobitz II AV block with haemodynamic compromise
• Asystole or symptomatic pauses greater than 3 seconds
• Alternating bundle branch block (impending complete heart block)
• New bundle branch block with first-degree AV block post-MI
• Bridge to permanent pacing

Class IIa (Reasonable):

• Asymptomatic complete heart block with escape less than 40 bpm
• Asymptomatic Mobitz II AV block
• Overdrive pacing for drug-refractory ventricular tachycardia

Class III (Not Indicated):

• Asymptomatic sinus bradycardia
• Asymptomatic first-degree AV block
• Asymptomatic Mobitz I (Wenckebach) AV block

Transcutaneous Pacing (TCP)

Mechanism: External electrical stimulation via large adhesive electrodes; depolarises myocardium through chest wall (PMID: 8556295).

Equipment:

• Defibrillator/pacing unit with TCP capability
• Large adhesive pacing electrodes (anterior-posterior placement preferred)

Technique:

1. Apply electrodes: Anterior (left parasternal or apex) and posterior (left infrascapular)
2. Connect to pacing unit
3. Set mode: Demand (VVI) - senses native rhythm, only paces when needed
4. Set rate: 60-80 bpm (or as clinically indicated)
5. Increase current: Start at 0 mA, increase in 10 mA increments until electrical capture
   • Typical capture threshold: 50-100 mA (range 40-200 mA)
6. Confirm mechanical capture: Palpable pulse with pacing, improved BP
7. Set safety margin: 10-20% above threshold

Signs of Capture:

• Pacing spike followed by wide QRS complex
• Palpable pulse coinciding with paced beats
• Blood pressure improvement

Troubleshooting TCP Failure:

Limitations of TCP:

• Painful: Requires sedation/analgesia (fentanyl, ketamine, propofol)
• Unreliable capture: Especially with chest wall oedema, obesity, pericardial effusion
• Not definitive: Bridge only; must plan for transvenous pacing
• Causes muscle contraction: Difficult to assess peripheral pulses

Advantages:

• Immediate (no procedural delay)
• Non-invasive
• Can be initiated by nursing staff in emergencies
• Minimal training required

Transvenous Pacing (TVP)

Mechanism: Direct endocardial stimulation via temporary pacing wire positioned in right ventricle (PMID: 3873236, 15867130).

Equipment:

• Temporary pacing wire (balloon-tipped or non-balloon)
• Introducer sheath (usually 6 French)
• Temporary pacing generator
• Sterile supplies for central line insertion
• ECG monitoring
• Fluoroscopy (ideal) or bedside echocardiography

Vascular Access (in order of preference):

Preferred Access: Right internal jugular vein (RIJ) provides the most direct path to RV apex (PMID: 26826175).

Technique (RIJ Approach):

1. Preparation:

   • Patient supine, slight Trendelenburg if tolerated
   • Sterile drape, ultrasound-guided access
   • Have TCP running as backup

2. Vascular Access:

   • Ultrasound-guided IJ puncture
   • Insert 6 French sheath

3. Wire Insertion:

   • Advance balloon-tipped pacing wire through sheath
   • Inflate balloon when wire in SVC (reduces arrhythmia risk)
   • Advance with fluoroscopy or ECG guidance

4. Positioning:

   • Fluoroscopy guidance (gold standard):
     • RAO view: Wire should curve toward apex
     • LAO view: Wire tip should be anterior (RV) not posterior (coronary sinus)
   • ECG guidance (if no fluoroscopy):
     • Connect V lead to distal electrode of pacing wire
     • Current of injury (ST elevation) when wire contacts endocardium
   • Echocardiography guidance:
     • Visualise wire in RV apex

5. Testing and Settings:

   • Sensing threshold: Decrease sensitivity until sensing lost; set at half this value
   • Capture threshold: Decrease output until capture lost; set output at 2-3× this value
   • Typical capture threshold: 0.5-1.0 mA (accept up to 2 mA)
   • Settings: VVI mode, rate 60-80 bpm, output 2-3× threshold

6. Secure Wire:

   • Suture sheath to skin
   • Document insertion depth
   • Secure connections

7. Confirmation:

   • CXR for wire position (RV apex) and to exclude pneumothorax
   • Continuous ECG monitoring
   • Daily threshold checks

Complications of TVP (PMID: 22203695):

Epicardial Pacing

Setting: Post-cardiac surgery patients with temporary epicardial wires placed intraoperatively.

Wire Positions:

• Usually atrial and ventricular wires placed
• Allows AAI, VVI, or DDD pacing

Management:

• Connect to external pacing box
• Test thresholds daily (epicardial thresholds often higher than transvenous)
• Typical output: 10-20 mA (higher than TVP)
• Remove when no longer needed (usually 5-7 days post-op)

Complications:

• Wire fracture during removal (rare, usually of no consequence)
• Bleeding from wire site
• Infection
• Rare: coronary graft damage during removal

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Transvenous Pacing Settings

Pacing Modes (NBG Code)

Nomenclature: 3-5 letter code describing pacemaker function

Common Temporary Pacing Modes:

VVI Mode (Standard for Temporary Pacing):

• Paces ventricle when no native ventricular activity sensed
• Inhibits pacing when native QRS sensed
• Maintains minimum ventricular rate

Setting Pacing Parameters

Rate:

• Default: 60-80 bpm
• May increase for higher output states (sepsis, fever)
• Avoid very high rates (ischaemia risk)

Output (mA):

• Threshold testing: Decrease output until capture lost
• Accept threshold: Less than 2 mA (ideally less than 1 mA)
• Set output: 2-3× threshold (usually 3-6 mA for TVP)
• High threshold suggests poor lead position, fibrosis, or metabolic abnormalities

Sensitivity (mV):

• Sensing threshold testing: Decrease sensitivity until oversensing occurs
• Set sensitivity: 2-3 mV typically (half the sensed R wave)
• Too sensitive: May sense T waves or noise (inhibits pacing when needed)
• Too insensitive: May not sense native QRS (competition with pacing)

AV Delay (if DDD mode):

• Typical: 150-200 ms
• Allows atrial contraction before ventricular pacing

Troubleshooting Pacemaker Malfunction

Failure to Pace (No pacing spike on ECG):

Failure to Capture (Pacing spike but no QRS):

Failure to Sense (Pacing when native rhythm present):

ECG Patterns of Malfunction:

• Undersensing: Pacing spikes falling in native QRS or T wave
• Oversensing: Long pauses (pacemaker inhibited by noise)
• No capture: Pacing spikes not followed by QRS

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Permanent Pacemaker Indications

ACC/AHA/HRS 2018 Guidelines (PMID: 29554191, 29146516)

Class I Indications (Pacing Indicated)

Sinus Node Dysfunction:

• Symptomatic sinus bradycardia (syncope, near-syncope, dizziness, HF symptoms)
• Symptomatic chronotropic incompetence
• Symptomatic sinus pauses

AV Block:

• Third-degree (complete) AV block
• Second-degree Mobitz II AV block
• Advanced AV block (2:1 or greater)
• Symptomatic second-degree AV block (regardless of type)
• AV block post-ablation (intentional or unintentional)
• AV block from drug therapy that is required and cannot be stopped

Post-MI:

• Persistent AV block greater than 7 days post-MI
• Transient complete or Mobitz II AV block with residual bundle branch block

Post-Cardiac Surgery/TAVI:

• Complete AV block not expected to resolve (greater than 7 days)
• Mobitz II AV block not expected to resolve

Class IIa Indications (Pacing Reasonable)

• Sinus node dysfunction with HR less than 40 bpm but unclear symptom-rhythm correlation
• First-degree AV block with symptoms attributable to AV dyssynchrony
• Lamin A/C gene mutation with any degree of AV block
• Asymptomatic complete heart block with escape less than 40 bpm or escape rhythm below AV node
• Asymptomatic Mobitz II AV block with narrow QRS
• 1:1 or 2:1 AV block at infranodal level (HV greater than 100 ms)

Class III Indications (Pacing Not Indicated)

• Asymptomatic first-degree AV block
• Asymptomatic Mobitz I AV block at AV nodal level
• AV block expected to resolve (e.g., drug-induced, post-operative, Lyme disease)
• Sinus bradycardia or pauses during sleep without symptoms

Pacemaker Types for Permanent Implantation

Evidence for Pacing Modes

DAVID Trial (PMID: 10362203): Minimise RV pacing in patients with reduced EF - backup VVI at 40 bpm superior to DDD 70 bpm.

MOST Trial (PMID: 19038685): DDDR vs VVIR in sinus node dysfunction - DDDR reduced AF and improved QoL, but no mortality difference.

Toff Meta-Analysis (PMID: 16714861): Physiological pacing (DDD) associated with reduced AF and trends toward reduced stroke and mortality compared to ventricular pacing alone.

Key Principles:

• Maintain AV synchrony when possible (DDD preferred)
• Minimise unnecessary RV pacing (programming)
• Rate-response for chronotropic incompetence

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Post-MI AV Block

Inferior MI and AV Block (PMID: 24573958, 27050531)

Incidence: 10-20% of inferior MIs develop some degree of AV block.

Blood Supply Anatomy:

• AV node supplied by AV nodal artery (branch of RCA in 90%, LCx in 10%)
• Inferior MI typically involves RCA occlusion

Characteristics:

Management:

1. Monitor closely (telemetry/ICU)
2. Atropine for symptomatic bradycardia (usually effective)
3. Temporary pacing if haemodynamically unstable or atropine-refractory
4. Observe for recovery (most resolve within 5-7 days)
5. Permanent pacing only if persistent greater than 7 days with symptoms

Anterior MI and AV Block (PMID: 24573958, 30063141)

Incidence: 5-10% of anterior MIs develop AV block.

Blood Supply Anatomy:

• Bundle branches supplied by septal perforators of LAD
• His bundle supplied by both AV nodal artery and septal perforators
• Anterior MI with AV block indicates extensive septal/anterior wall necrosis

Characteristics:

Management:

1. Immediate temporary pacing (TVP or TCP as bridge)
2. Do not rely on atropine (ineffective for infranodal block)
3. Consider prophylactic temporary pacing for new bifascicular block with first-degree AV block post-anterior MI
4. Permanent pacing indicated for survivors with persistent block
5. Address underlying cardiogenic shock/LV dysfunction (likely severe)

Prophylactic Temporary Pacing Post-Anterior MI (consider for high-risk patients):

• New bifascicular block (RBBB + LAFB or LPFB)
• Alternating bundle branch block
• Bifascicular block with first-degree AV block
• Mobitz II AV block

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Drug-Induced Bradycardia Management

Beta-Blocker Toxicity (PMID: 23454621)

Mechanism: Competitive antagonism of beta-adrenergic receptors → decreased cAMP → reduced SA/AV node automaticity and conduction.

Clinical Features:

• Sinus bradycardia, AV block
• Hypotension
• Hypoglycaemia (masked symptoms, impaired gluconeogenesis)
• Bronchospasm (beta-2 blockade)
• Reduced consciousness
• Seizures (especially propranolol - lipophilic, CNS penetration)

Management Protocol:

1. Supportive Care:

• IV access, monitoring
• Activated charcoal if recent ingestion (less than 1 hour)
• IV fluids (crystalloid boluses)

2. Atropine:

• 0.5-1 mg IV, repeat every 3-5 minutes (max 3 mg)
• Often ineffective in severe toxicity

3. Glucagon (First-line specific antidote):

• Mechanism: Bypasses beta-receptor to activate adenylyl cyclase
• Dose: 5-10 mg IV bolus, followed by 2-5 mg/hr infusion
• Onset: 1-3 minutes
• Side effects: Vomiting (give antiemetic), hyperglycaemia

4. High-Dose Insulin Euglycaemic Therapy:

• Insulin 1 unit/kg bolus, then 0.5-1 unit/kg/hr infusion
• Dextrose to maintain glucose 8-12 mmol/L
• Monitor K+ (hypokalaemia risk)

5. Catecholamines:

• Isoprenaline 1-10 mcg/min (chronotropic)
• Adrenaline 2-10 mcg/min (if hypotensive)
• Noradrenaline for refractory hypotension

6. Calcium (limited evidence):

• Calcium chloride 1-2 g IV (may have modest benefit)

7. Lipid Emulsion Therapy (for lipophilic agents like propranolol):

• Intralipid 20%: 1.5 mL/kg bolus, then 0.25 mL/kg/min infusion

8. Temporary Pacing:

• For refractory bradycardia

9. ECMO/Mechanical Support:

• For refractory cardiogenic shock

Calcium Channel Blocker Toxicity (PMID: 18048762, 28463086)

Mechanism: L-type calcium channel blockade → reduced cardiac contractility, SA/AV node depression, vasodilation.

Clinical Features:

• Bradycardia, AV block
• Hypotension (vasodilation + negative inotropy)
• Hyperglycaemia (insulin secretion impaired - calcium-dependent)
• Metabolic acidosis (tissue hypoperfusion)
• Pulmonary oedema (cardiogenic)
• Seizures, coma (severe)

Management Protocol:

1. Supportive Care:

• IV access, monitoring
• Activated charcoal if less than 1-2 hours
• Whole bowel irrigation for sustained-release preparations
• IV fluids cautiously (may worsen pulmonary oedema)

2. Atropine:

• 0.5-1 mg IV (often ineffective)

3. Calcium (First-line specific antidote):

• Mechanism: Increases extracellular calcium to overcome channel blockade
• Dose: Calcium chloride 10% 10-20 mL IV (1-2 g) every 10-20 minutes
• Infusion: 0.2-0.4 mL/kg/hr
• Target: Ionised calcium 2.0-2.5 mmol/L
• May require massive doses (10+ grams)

4. High-Dose Insulin Euglycaemic Therapy (First-line for haemodynamic instability):

• Mechanism: Improves cardiac metabolism, inotropy, vasodilation
• Dose: Insulin 1 unit/kg bolus, then 0.5-1 unit/kg/hr (up to 10 units/kg/hr in refractory cases)
• Dextrose: Maintain glucose 8-12 mmol/L
• Potassium: Monitor and supplement
• Onset of effect: May take 15-60 minutes

5. Glucagon:

• Second-line (less effective than for beta-blockers)
• 5-10 mg IV bolus, then 2-5 mg/hr infusion

6. Catecholamines:

• Noradrenaline for hypotension
• Adrenaline or dobutamine for inotropy
• High doses often required (receptor downregulation)

7. Lipid Emulsion:

• Consider for lipophilic CCBs (verapamil, diltiazem)
• Intralipid 20%: 1.5 mL/kg bolus, then 0.25 mL/kg/min

8. Temporary Pacing:

• For refractory bradycardia (may have poor capture due to negative inotropy)

9. Methylene Blue:

• For refractory vasoplegia
• 1-2 mg/kg IV

10. ECMO/VA-ECMO:

• For refractory cardiogenic shock (PMID: 28463086)
• Early consideration in severe toxicity

Digoxin Toxicity (PMID: 9596004, 33970999)

Mechanism: Na+/K+-ATPase inhibition → increased intracellular calcium → enhanced vagal tone → SA/AV nodal depression + increased automaticity of ectopic pacemakers.

Clinical Features:

• Bradycardia, AV block (especially with hypokalaemia)
• Characteristic arrhythmias:
  • Atrial tachycardia with block
  • Accelerated junctional rhythm
  • Bidirectional VT (pathognomonic)
  • Regularised AF (junctional rhythm in AF)
• Nausea, vomiting, abdominal pain
• Visual disturbances (yellow-green halos, photophobia)
• Confusion, weakness

Risk Factors for Toxicity:

• Renal impairment (reduced clearance)
• Hypokalaemia (increases toxicity at same level)
• Hypercalcaemia
• Hypomagnesaemia
• Drug interactions (amiodarone, verapamil, quinidine)
• Elderly, low body weight

Management Protocol:

1. Supportive Care:

• IV access, monitoring
• Activated charcoal if less than 1 hour
• Correct electrolytes (especially K+ - but cautiously)

2. Electrolyte Management:

• Hypokalaemia: Correct to 4.0-5.0 mmol/L (potentiates toxicity)
• Caution: Do not give calcium (may precipitate "stone heart")
• Magnesium: 2 g IV if low or for ventricular arrhythmias

3. Digoxin-Specific Antibody Fragments (DigiFab):

• Indications:
  • Life-threatening arrhythmias (VT, VF, high-grade AV block)
  • Haemodynamically significant bradycardia
  • K+ greater than 5.5 mmol/L (indicates severe poisoning)
  • Ingestion greater than 10 mg (adult) or greater than 4 mg (child)
  • Digoxin level greater than 15 ng/mL at any time or greater than 10 ng/mL at 6 hours
• Dosing: Each 40 mg vial binds 0.5 mg digoxin
  • "Known ingestion: vials = (dose ingested × 0.8) / 0.5"
  • "Known level: vials = [level (ng/mL) × weight (kg)] / 100"
  • "Empiric life-threatening: 10-20 vials"
• Response: Usually within 30-60 minutes
• Monitoring: Level will rise post-DigiFab (measures bound + free), but free digoxin falls

4. Bradycardia Management:

• Atropine 0.5-1 mg IV (often effective for vagal-mediated)
• Avoid isoprenaline (increases ectopy)
• Temporary pacing if refractory (may have increased irritability)

5. Tachyarrhythmia Management:

• Magnesium 2 g IV
• Lidocaine for VT
• Avoid DC cardioversion if possible (may precipitate VF)
• If cardioversion essential, use lowest effective energy

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Australian/NZ Context

ANZCOR Guidelines (PMID: 32078917, 26542571)

ANZCOR Guideline 11.10 - Bradycardia:

Algorithm for Adult Bradycardia:

1. Assess for signs of compromise (altered LOC, hypotension, chest pain, acute HF)
2. If compromised:
   • Atropine 0.5 mg IV (repeat to max 3 mg)
   • Transcutaneous pacing if atropine ineffective
   • Adrenaline infusion 2-10 mcg/min or isoprenaline 1-10 mcg/min
   • Transvenous pacing for definitive management
3. If stable:
   • Search for and treat reversible causes
   • Monitor, observe
   • Consider cardiology/electrophysiology referral

Key ANZCOR Principles:

• Treat the patient, not the rhythm
• Haemodynamic compromise dictates urgency
• Atropine first-line for nodal-level block
• TCP as immediate intervention; TVP for definitive temporary pacing

Remote and Rural Considerations

Challenges in Australian Context:

• Geographic isolation - long retrieval times
• Limited access to interventional cardiology
• Lack of fluoroscopy for TVP positioning
• Telemedicine support for complex decisions

Remote Temporary Pacing:

• TCP may be only option in remote settings
• Consider blind TVP insertion with ECG guidance if experienced
• Coordinate with retrieval services (RFDS, state retrieval)
• Telemedicine consultation with tertiary centre

Retrieval Considerations:

• TCP in place for transport if unstable
• Ensure adequate sedation/analgesia
• Continuous monitoring during retrieval
• Isoprenaline/adrenaline infusion running

State-Based Retrieval Services:

• NSW: NSW Ambulance Retrieval, CareFlight, NETS (paediatric)
• VIC: Adult Retrieval Victoria (ARV), PIPER
• QLD: Retrieval Services Queensland (RSQ)
• WA: Royal Flying Doctor Service (RFDS) Western Operations
• SA: MedSTAR
• NT: CareFlight, RFDS Central Operations

Indigenous Health Considerations (PMID: 22722715, 27884807)

Epidemiology:

• Aboriginal and Torres Strait Islander peoples have higher rates of:
  • Ischaemic heart disease (2-3× higher rates)
  • Rheumatic heart disease (still endemic in remote communities)
  • Cardiomyopathy
  • Diabetes and CKD (complicating factors)
• Younger age at presentation for cardiac disease
• Higher complication rates

Barriers to Care:

• Geographic isolation
• Delayed presentation
• Limited access to specialist services
• Cultural and language barriers
• Health literacy challenges
• Distrust of healthcare system (historical trauma)

Cultural Safety in ICU:

• Involve Aboriginal Health Workers (AHWs) / Aboriginal Liaison Officers (ALOs)
• Respect family involvement in decision-making (extended family may be involved)
• Understand "sorry business"
• cultural obligations may affect attendance/decisions
• Allow for traditional healing practices alongside Western medicine
• Use interpreters for non-English speakers
• Consider gender preferences for staff

Māori Health Considerations (New Zealand):

• Higher cardiovascular disease rates
• Rheumatic heart disease more prevalent
• Whānau (extended family) involvement essential
• Tikanga Māori (cultural practices) must be respected
• Māori Health Workers involvement
• Te Tiriti o Waitangi obligations

Practical Considerations:

• Allow for larger family groups in ICU
• Flexible visiting hours
• Family meetings with cultural support
• Consider transfer to tertiary centre closer to community if stable
• Ensure follow-up arranged with appropriate community support

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SAQ Practice

SAQ 1: Post-Anterior MI Complete Heart Block

Time Allocation: 10 minutes Total Marks: 15

Stem:

A 62-year-old male is admitted to your ICU on Day 2 following an anterior STEMI treated with primary PCI to a proximal LAD occlusion. Peak troponin was 45,000 ng/L. This morning he becomes unresponsive for 30 seconds and the monitor shows the following rhythm:

• Atrial rate: 85 bpm (regular P waves)
• Ventricular rate: 32 bpm (wide QRS complexes, independent of P waves)
• QRS duration: 160 ms
• Blood pressure: 75/50 mmHg

Question 1.1 (5 marks) Describe the rhythm abnormality and explain its pathophysiology in the context of anterior STEMI.

Question 1.2 (5 marks) Outline your immediate management of this patient.

Question 1.3 (5 marks) What is the prognosis for this patient, and what are the indications for permanent pacing?

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Model Answer

Question 1.1 (5 marks)

Rhythm Description (2 marks):

• Complete (third-degree) AV block with AV dissociation
• Regular atrial activity at 85 bpm (P waves)
• Independent wide QRS complexes at 32 bpm (ventricular escape rhythm)
• No relationship between P waves and QRS complexes
• Wide QRS (160 ms) indicates infranodal (ventricular) escape focus

Pathophysiology (3 marks):

• Anterior STEMI involves LAD territory, which supplies the interventricular septum via septal perforators
• Septal perforators supply the bundle branches (right bundle, left anterior and posterior fascicles) and distal His bundle
• Extensive anterior/septal infarction causes bilateral bundle branch necrosis → complete infranodal block
• Peak troponin of 45,000 ng/L indicates massive myocardial necrosis (likely greater than 40% LV involvement)
• Wide QRS escape indicates the escape focus is ventricular (below bundle branch bifurcation), which is unreliable (rate less than 40 bpm)
• Unlike inferior MI (AV nodal ischaemia, often reversible), anterior MI AV block is due to structural necrosis and is usually irreversible

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Question 1.2 (5 marks)

Immediate Management (ABCDE approach):

Airway/Breathing (1 mark):

• High-flow oxygen
• Prepare for intubation if GCS remains low or deteriorates
• Avoid hypoxia (exacerbates myocardial ischaemia)

Circulation - Immediate Rhythm Management (2 marks):

• Atropine 0.5-1 mg IV - but likely to be ineffective (infranodal block does not respond to vagolytic agents)
• Transcutaneous pacing immediately while preparing for TVP:
  • Apply pads (anterior-posterior)
  • Demand mode, rate 60-80 bpm
  • Increase current until capture (typically 50-100 mA)
  • Confirm mechanical capture with pulse, BP
  • Provide sedation/analgesia (fentanyl, midazolam, or ketamine)
• Isoprenaline infusion 1-10 mcg/min as bridge (caution: may increase myocardial oxygen demand in acute MI)
• Alternative: Adrenaline infusion 2-10 mcg/min

Definitive Pacing (1 mark):

• Transvenous pacing as soon as possible
• Right internal jugular approach preferred
• VVI mode, rate 60-80 bpm, output 2-3× threshold
• If unsuccessful/unavailable, continue TCP

Haemodynamic Support (1 mark):

• IV fluid bolus if not overloaded (but caution with extensive LV damage)
• Consider vasopressor support (noradrenaline) if BP remains low despite pacing
• Assess for cardiogenic shock (may need inotropic support, IABP, or mechanical support)

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Question 1.3 (5 marks)

Prognosis (2 marks):

• Very poor prognosis: In-hospital mortality 50-80% for complete heart block complicating anterior MI
• High mortality reflects extent of myocardial damage rather than the block itself
• Cardiogenic shock likely (massive LV infarction)
• Even with successful pacing, high risk of pump failure
• Survivors have reduced LV function and heart failure risk

Indications for Permanent Pacing (2 marks):

Per ACC/AHA/HRS 2018 Guidelines (Class I indications):

• Persistent AV block greater than 7 days post-MI
• Transient complete or Mobitz II AV block with associated bundle branch block (even if block resolves)

In this patient:

• Infranodal block due to necrosis is unlikely to resolve
• If patient survives acute phase and block persists beyond 7 days → permanent pacemaker indicated
• DDD pacing preferred (maintains AV synchrony for optimising cardiac output)

Additional Considerations (1 mark):

• If severe LV dysfunction (EF less than 35%), may need ICD with pacing capability or CRT-D rather than standard pacemaker
• Optimisation of heart failure therapy
• Cardiac rehabilitation
• Address secondary prevention

---

Common Mistakes:

• Giving atropine repeatedly when block is infranodal (waste of time, delays pacing)
• Not recognising wide QRS escape as unstable/dangerous
• Delaying pacing in haemodynamically unstable patient
• Confusing prognosis of anterior vs inferior MI AV block

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SAQ 2: Drug-Induced Bradycardia

Time Allocation: 10 minutes Total Marks: 15

Stem:

A 45-year-old female with a history of hypertension and anxiety is brought to the Emergency Department after being found unresponsive by her husband. She has a history of depression and her medications include verapamil SR 240 mg daily and citalopram 20 mg daily. Empty medication bottles were found at the scene.

On Arrival:

• GCS: 10 (E2V3M5)
• HR: 38 bpm
• BP: 65/40 mmHg
• RR: 12
• SpO2: 94% on room air
• Temperature: 36.2°C
• BSL: 14.5 mmol/L

ECG: Sinus bradycardia, rate 38 bpm, PR 280 ms, QRS 110 ms, QTc 480 ms

Question 2.1 (5 marks) What is the most likely toxicological diagnosis? List the key clinical and ECG features supporting this diagnosis.

Question 2.2 (6 marks) Outline your management priorities for this patient, including specific antidotes and their dosing.

Question 2.3 (4 marks) The patient remains hypotensive despite initial treatment. What additional interventions would you consider?

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Model Answer

Question 2.1 (5 marks)

Most Likely Diagnosis (1 mark):

• Calcium channel blocker (verapamil) toxicity/overdose

Clinical Features Supporting Diagnosis (2 marks):

• Bradycardia (HR 38 bpm) - verapamil blocks L-type calcium channels in SA and AV nodes
• Hypotension (BP 65/40 mmHg) - negative inotropy + vasodilation
• Altered consciousness (GCS 10) - cerebral hypoperfusion
• Hyperglycaemia (BSL 14.5 mmol/L) - calcium-dependent insulin secretion impaired (characteristic of CCB toxicity, contrasts with beta-blocker which causes hypoglycaemia)
• History of verapamil prescription and empty medication bottles
• Sustained-release preparation (SR) - prolonged toxicity expected

ECG Features (2 marks):

• Sinus bradycardia (38 bpm) - SA node depression
• First-degree AV block (PR 280 ms) - AV nodal conduction slowing
• Normal-ish QRS (110 ms) - CCB does not significantly affect sodium channels (unlike Class I antiarrhythmics)
• Prolonged QTc (480 ms) - may be due to concomitant citalopram effect

Note: Must exclude beta-blocker co-ingestion (similar bradycardia/hypotension, but causes hypoglycaemia, not hyperglycaemia)

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Question 2.2 (6 marks)

Immediate Resuscitation (1 mark):

• High-flow oxygen
• IV access × 2 (large bore)
• Continuous cardiac monitoring
• Arterial line for BP monitoring
• Prepare for intubation if GCS deteriorates

GI Decontamination (1 mark):

• Activated charcoal 50 g orally/via NGT if airway protected (within 1-2 hours of ingestion)
• Whole bowel irrigation with polyethylene glycol (PEG) 1-2 L/hr for sustained-release verapamil - continues until clear rectal effluent

Specific Antidotes (3 marks):

1. Calcium (first-line):

• Calcium chloride 10%: 10-20 mL (1-2 g) IV bolus over 5 minutes
• Repeat every 15-20 minutes as needed
• Consider calcium infusion: 0.2-0.4 mL/kg/hr (10-20 mL/hr of 10% CaCl)
• Target ionised calcium 2.0-2.5 mmol/L (may need supraphysiological levels)
• Use central access for calcium chloride (caustic if extravasation)

2. High-Dose Insulin Euglycaemic Therapy (HIET) (first-line for haemodynamic instability):

• Insulin: 1 unit/kg IV bolus, then 0.5-1 unit/kg/hr infusion
• Dextrose 50%: 25 g IV bolus, then infusion to maintain BSL 8-12 mmol/L
• Monitor and supplement potassium (target K+ 3.5-4.5 mmol/L)
• May increase insulin up to 10 units/kg/hr in refractory cases
• Effect may take 15-60 minutes to manifest

3. Glucagon (second-line):

• 5-10 mg IV bolus, then 2-5 mg/hr infusion
• Less effective for CCB than beta-blocker toxicity
• Side effects: vomiting - pre-treat with antiemetic

Vasopressor Support (1 mark):

• Noradrenaline infusion for hypotension
• High doses often required (receptor downregulation/desensitisation)
• Start 0.1 mcg/kg/min, titrate to MAP greater than 65 mmHg

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Question 2.3 (4 marks)

Refractory Hypotension Management:

1. Escalate HIET (1 mark):

• Increase insulin infusion up to 10 units/kg/hr
• Ensure adequate dextrose supplementation

2. Lipid Emulsion Therapy (1 mark):

• Intralipid 20%: 1.5 mL/kg IV bolus over 1 minute
• Follow with infusion 0.25-0.5 mL/kg/min for 30-60 minutes
• Repeat bolus if cardiovascular instability persists
• Mechanism: "Lipid sink" for lipophilic drugs (verapamil moderately lipophilic)

3. Methylene Blue (0.5 mark):

• For refractory vasoplegic shock
• 1-2 mg/kg IV over 5 minutes
• Inhibits NO-mediated vasodilation
• May repeat after 1 hour if needed

4. Temporary Pacing (0.5 mark):

• Transcutaneous pacing if profound bradycardia
• Transvenous pacing for definitive management
• Note: Capture may be difficult due to negative inotropy

5. VA-ECMO/Mechanical Support (1 mark):

• For refractory cardiogenic shock
• Early consideration in severe CCB toxicity
• Provides both circulatory and respiratory support
• Bridge to recovery (CCB eventually metabolised/cleared)
• Contact ECMO centre early in severe poisoning

---

Common Mistakes:

• Not recognising hyperglycaemia as a clue to CCB (vs beta-blocker) toxicity
• Underdosing calcium or insulin
• Not considering whole bowel irrigation for SR preparations
• Delaying ECMO consultation in refractory shock

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Hot Case Scenarios

Hot Case 1: Post-Cardiac Surgery Complete Heart Block

Setting: Cardiac ICU Bed 12 Duration: 20 minutes (10 min assessment + 10 min discussion) Equipment: Ventilator, monitors, IV pumps, epicardial pacing wires, charts available

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Actor/Simulator Briefing (Not given to candidate):

Patient Details:

• Age: 71 years
• Gender: Male
• Admission diagnosis: Day 3 post-aortic valve replacement for severe aortic stenosis
• Aboriginal Australian from remote Northern Territory community

History:

• Severe calcific aortic stenosis, NYHA III
• Hypertension, type 2 diabetes, CKD stage 3
• Uneventful surgery, AV block noted intraoperatively - epicardial pacing wires placed
• Extubated Day 1, doing well until this morning

Current Problem:

• Pacing suddenly not capturing
• HR dropped to 28 bpm with syncope
• Currently being paced at 80 bpm with intermittent capture

Examination Findings:

• General: Elderly Aboriginal man, appears anxious, dry skin
• Airway: Patent, speaking in short sentences
• Breathing: RR 20, SpO2 96% on 2L NC, bilateral clear
• Circulation: HR varies 28-80 depending on capture, BP 95/60, cool peripheries, CRT 4s, JVP visible 3 cm above sternal angle, sternotomy wound healing well
• Disability: GCS 15 now (was 3 during syncopal episode), pupils equal and reactive
• Exposure: Temp 37.2°C, epicardial wires on chest wall, foot ulcer with dressing (diabetic)

Charts/Data Available:

• Pacing threshold yesterday: 3 mA (was 1 mA Day 1)
• Current output: 10 mA, capture intermittent
• K+: 3.2 mmol/L (yesterday 4.1)
• Mg2+: 0.6 mmol/L
• Creatinine: 180 (baseline 150)
• No fever

Current Management:

• Epicardial VVI pacing: rate 80, output 10 mA - intermittent capture
• Ramipril 2.5 mg, bisoprolol 2.5 mg, aspirin, atorvastatin
• Insulin sliding scale, heparin prophylaxis

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Candidate Task:

"You are the ICU registrar. This is Mr. Williams, a 71-year-old Aboriginal man from a remote community, Day 3 post-aortic valve replacement. He has epicardial pacing wires in place. The nurse is concerned that his pacing is not working properly and he has had an episode of syncope. Please assess the patient and present your findings to the consultant."

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Expected Performance:

Assessment Phase (10 minutes) - 15 marks

History from Nurse/Patient (3 marks):

• Timeline of events (sudden syncope, pacing issues)
• Pacing history (thresholds trending up)
• Medications (bisoprolol could contribute)
• Electrolytes (identify hypokalaemia, hypomagnesaemia)
• Symptoms before syncope (nil, sudden)

Examination (10 marks):

• Airway: Patent, no stridor
• Breathing: Clear, no pulmonary oedema
• Circulation:
  • Note variable HR with intermittent capture
  • Cool peripheries, delayed CRT (low output state)
  • JVP assessment
  • Heart sounds (mechanical click, no failure)
  • Surgical wound inspection
• Disability: Now alert (had syncopal episode - Stokes-Adams attack)
• Exposure: Temperature, diabetic foot (infection source?)
• Device Review:
  • Check pacing connections
  • Review threshold trends
  • Assess pacing capture on monitor

One-Minute Summary (2 marks):

"This is Mr. Williams, a 71-year-old Aboriginal man from a remote NT community, Day 3 post-aortic valve replacement. He has presented with syncope due to intermittent pacing failure from elevated epicardial pacing thresholds. He has underlying complete heart block requiring pacing. Current issues are: (1) Rising capture thresholds with intermittent loss of capture causing haemodynamic instability; (2) Electrolyte abnormalities - hypokalaemia and hypomagnesaemia likely contributing; (3) Dependence on pacing with underlying ventricular escape rate of 28 bpm. Immediate plan is to maximise current output, correct electrolytes urgently, and prepare for transvenous pacing if epicardial capture not reliable."

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Discussion Phase (10 minutes) - 15 marks

Opening Question: "What are your immediate management priorities?"

Expected Answer (3 marks):

1. Optimise epicardial pacing: Increase output to maximum (usually 20-25 mA), ensure connections secure
2. Prepare backup pacing: Have TCP pads applied and ready; prepare for TVP insertion
3. Correct electrolytes urgently:
   • IV potassium 40 mmol over 2-4 hours (aim K+ greater than 4.0)
   • IV magnesium 10-20 mmol over 1 hour (aim Mg greater than 0.8)
4. Review medications: Hold bisoprolol, consider if contributing

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Follow-up Question 1: "The epicardial pacing threshold is now 18 mA and capture is marginal even at maximum output. What are your options?"

Expected Answer (3 marks):

• Transcutaneous pacing as immediate backup (apply pads now)
• Transvenous pacing - definitive temporary measure:
  • Right internal jugular approach
  • 6 French sheath, balloon-tipped wire
  • Position in RV apex with fluoroscopy or ECG guidance
  • Set VVI 70-80, output 2-3× threshold
• Consider alternative epicardial wire if second wire available (atrial wire sometimes works in ventricle)
• Isoprenaline infusion (1-5 mcg/min) as bridge - but caution post-cardiac surgery (arrhythmia risk)

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Follow-up Question 2: "The AV block has now persisted for 3 days. What are the options regarding permanent pacing?"

Expected Answer (3 marks):

• Post-operative AV block may resolve up to 7-10 days
• If persists beyond 7 days → permanent pacemaker indicated (ACC/AHA Class I)
• TAVI-related AV block has higher permanent pacing rates (12-25%), valve surgery lower (3-5%)
• In this case:
  • Monitor for recovery with TVP in place
  • Daily assessment of native rhythm (turn off pacing briefly to assess escape)
  • If no recovery by Day 7-10, plan for permanent pacemaker (likely DDD)
• Cultural considerations: Discuss with patient and whānau/family, involve Aboriginal Liaison Officer, consider preference for transfer closer to home community if stable

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Follow-up Question 3: "Mr. Williams's family has arrived from his remote community. How would you approach the family meeting?"

Expected Answer (3 marks):

• Preparation:

  • Involve Aboriginal Liaison Officer/Aboriginal Health Worker
  • Ensure interpreter if needed (not a family member for complex discussions)
  • Identify decision-makers (may be extended family involved)
  • Private, comfortable space

• Meeting Structure:

  • Introductions, cultural acknowledgement
  • Explore their understanding of his condition
  • Explain the situation clearly (avoid jargon): "His heart's electrical system was affected by the surgery. Right now, we're using wires to keep his heart beating properly."
  • Explain options: "We're hoping his heart will start working on its own in the next few days. If not, he may need a small device put under his skin to help his heart beat."
  • Address concerns, allow questions
  • Discuss logistics (he may need to stay in tertiary centre for permanent pacemaker)
  • Follow-up arrangements

• Cultural Safety:

  • Respect for cultural obligations (sorry business, etc.)
  • Acknowledge importance of connection to country
  • Plan for eventual return to community with appropriate follow-up

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Follow-up Question 4: "What complications can occur with transvenous pacing, and how would you monitor for them?"

Expected Answer (3 marks):

• Procedural complications:

  • Arrhythmias (VT/VF during insertion - keep defib ready)
  • Pneumothorax (if subclavian) - CXR post-insertion
  • Haemothorax
  • Air embolism
  • Arterial puncture

• In-situ complications:

  • "Lead displacement (10-20%): Loss of capture, change in paced QRS morphology"
  • "Perforation/tamponade (1-2%): Hypotension, raised JVP, muffled sounds, pulsus paradoxus"
  • Infection (increases with duration, 5-15% at 5-7 days)
  • Thrombosis
  • Diaphragmatic stimulation (hiccups with pacing)

• Monitoring:

  • Daily threshold checks
  • Daily CXR to confirm position
  • Observation for tamponade signs
  • Sterile dressing changes
  • Remove as soon as permanent solution in place

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Marking Criteria (Total 30 marks):

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Hot Case 2: Beta-Blocker Overdose with Refractory Bradycardia

Setting: ICU Bed 6 Duration: 20 minutes Equipment: Monitors, infusion pumps, TCP pads in place, CVL

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Patient Details:

• Age: 35 years
• Gender: Female
• Admission diagnosis: Intentional propranolol overdose (estimated 4 g)
• Day 0 (admitted 6 hours ago)

Current Status:

• Intubated and ventilated
• HR 42 bpm on TCP at 80 mA (only intermittent capture)
• BP 75/45 mmHg
• On glucagon infusion 5 mg/hr, noradrenaline 0.5 mcg/kg/min
• BSL 3.8 mmol/L

Key Findings:

• Wide QRS on native beats (140 ms)
• Lactate 6.5 mmol/L
• K+ 5.2 mmol/L
• pH 7.24, BE -10

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Expected Discussion Points:

1. Recognition: Severe beta-blocker toxicity with cardiogenic shock
2. Failed TCP: Need for TVP or alternative strategies
3. Escalation: HIET initiation, dose escalation
4. Lipid emulsion: Indication for propranolol (lipophilic)
5. ECMO consideration: Early discussion with ECMO centre
6. Psychiatric management: Safety assessment when recovered

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Viva Scenarios

Viva Scenario 1: Pathophysiology and Acute Management of Complete Heart Block

Stem: "A 70-year-old man collapses at home. Paramedics find him with GCS 3, HR 25 bpm, BP 60/40 mmHg. ECG shows complete heart block with a wide QRS escape rhythm at 25 bpm. He has regained consciousness with transcutaneous pacing in place, rate 70, output 120 mA."

Duration: 12 minutes (2 min reading + 10 min discussion)

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Opening Question: "Describe the pathophysiology of complete heart block and explain why this patient has a wide QRS escape."

Expected Answer (3-4 minutes):

Complete Heart Block Pathophysiology:

• Complete failure of conduction from atria to ventricles
• Atria and ventricles beat independently (AV dissociation)
• Atrial rate determined by SA node (usually 60-100 bpm)
• Ventricular rate determined by escape focus (location dictates rate and QRS width)

Levels of Block and Escape Rhythms:

• Block can be at AV node, His bundle, or bundle branches
• AV nodal block: Junctional escape (narrow QRS, 40-60 bpm) - more reliable
• Infranodal block (His bundle/bundle branches): Ventricular escape (wide QRS, less than 40 bpm) - unreliable

Why Wide QRS in This Patient:

• Escape focus is below the bifurcation of the bundle of His
• Ventricular myocardium depolarises via cell-to-cell conduction (not specialised conducting tissue)
• This is slow → wide QRS (greater than 120 ms)
• Escape rate is low (25 bpm) because ventricular cells have lowest automaticity
• Critical point: Wide QRS escape is haemodynamically unstable and prone to asystole

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Follow-up Question 1: "What are the causes of complete heart block?"

Expected Answer (2 minutes):

Causes (broad categories):

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Follow-up Question 2: "Transcutaneous pacing is maintaining his rhythm. What are your next steps?"

Expected Answer (2 minutes):

Immediate Priorities:

1. Confirm capture: Mechanical capture with palpable pulse, not just electrical

2. Sedate/analgesia: TCP is very painful (fentanyl, propofol/midazolam)

3. Investigate cause:

   • ECG (12-lead when possible - look for ischaemia)
   • Electrolytes (K+, Ca2+, Mg2+)
   • Drug history and levels (digoxin)
   • Troponin
   • Renal function, thyroid function
   • Lyme serology if endemic area travel

4. Plan definitive pacing:

   • Transvenous pacing - definitive temporary measure
   • RIJ approach preferred
   • VVI mode, rate 60-70 bpm

5. Assess for reversible causes:

   • Correct hyperkalaemia
   • Stop offending drugs
   • If MI → reperfusion
   • If Lyme → antibiotics

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Follow-up Question 3: "You have successfully inserted a transvenous pacing wire. How do you set it up and what are appropriate settings?"

Expected Answer (2 minutes):

Setup:

• Connect pacing wire to external generator
• Ensure correct polarity (negative to tip/distal electrode)

Initial Settings:

• Mode: VVI (ventricular pacing, ventricular sensing, inhibited)
• Rate: 60-70 bpm (or 70-80 if higher output needed)
• Output: Start at 5 mA, assess capture

Threshold Testing:

• Capture threshold: Decrease output until capture lost; accept if less than 2 mA
• Set output at 2-3× threshold (e.g., if threshold 1 mA, set output 2-3 mA)
• Sensing threshold: Decrease sensitivity until oversensing; set at 2-3 mV typically

Monitoring:

• Continuous ECG - pacing spike followed by wide QRS
• Confirm haemodynamic improvement
• Daily threshold checks (may rise over time due to fibrosis)
• CXR for position confirmation

Warning Signs of Problems:

• Loss of capture (spikes without QRS) → increase output, reposition
• Undersensing (pacing into native rhythm) → increase sensitivity
• Oversensing (pauses, inhibited pacing) → decrease sensitivity

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Follow-up Question 4: "When would you consider permanent pacing for this patient?"

Expected Answer (2 minutes):

Indications for Permanent Pacing (ACC/AHA/HRS 2018):

Class I (Pacing Indicated):

• Complete heart block (regardless of symptoms) with:
  • Symptomatic bradycardia
  • Ventricular escape less than 40 bpm
  • Wide QRS escape
  • Post-MI persistent greater than 7 days
• Symptomatic Mobitz II AV block

In This Patient:

• If no reversible cause identified: Permanent pacemaker indicated
• If reversible cause (e.g., drug toxicity, Lyme, acute MI): Observe for recovery with TVP, pacing only if block persists
• Post-MI: Persist 7 days → permanent pacing

Timing:

• Once acute reversible causes excluded
• Usually within hospital admission
• Dual-chamber (DDD) preferred if sinus node function intact

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Viva Scenario 2: Drug-Induced Bradycardia and Specific Antidotes

Stem: "A 58-year-old man with atrial fibrillation on digoxin 250 mcg daily and diltiazem SR 240 mg daily presents with lethargy, nausea, and visual disturbances. HR 34 bpm, BP 85/55 mmHg. ECG shows slow AF with prominent U waves and inverted T waves. Digoxin level is 4.2 ng/mL (therapeutic less than 2.0). K+ is 2.8 mmol/L."

Duration: 12 minutes

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Opening Question: "What is the diagnosis and what are the key clinical and laboratory features?"

Expected Answer (2 minutes):

Diagnosis: Digoxin toxicity compounded by hypokalaemia and diltiazem

Clinical Features:

• Cardiovascular: Bradycardia (HR 34), hypotension
• GI: Nausea (common early symptom)
• Neurological: Lethargy
• Visual: Visual disturbances (yellow-green halos - xanthopsia, photophobia)

ECG Features of Digoxin Toxicity:

• Bradycardia (enhanced vagal tone)
• Various arrhythmias possible:
  • Slow AF (seen here)
  • AV block
  • Accelerated junctional rhythm
  • Atrial tachycardia with block
  • Bidirectional VT (pathognomonic)

Laboratory:

• Digoxin level 4.2 ng/mL (toxic greater than 2.0)
• Hypokalaemia (K+ 2.8) - potentiates toxicity even at therapeutic levels
• U waves on ECG consistent with hypokalaemia

Contributing Factors:

• Diltiazem increases digoxin levels (P-glycoprotein inhibition)
• Hypokalaemia increases binding of digoxin to Na+/K+-ATPase

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Follow-up Question 1: "How does digoxin cause toxicity at the cellular level?"

Expected Answer (2 minutes):

Mechanism of Action and Toxicity:

Normal Action:

• Digoxin inhibits Na+/K+-ATPase pump
• Increased intracellular Na+ → reduced Na+/Ca2+ exchanger activity → increased intracellular Ca2+
• Increased Ca2+ → positive inotropy

Toxicity:

• Excessive Na+/K+-ATPase inhibition →:

  • Intracellular K+ depletion
  • Excessive intracellular Ca2+

• Electrophysiological Effects:

  • Enhanced vagal tone → SA node depression, AV nodal slowing → bradycardia, AV block
  • Increased automaticity of Purkinje fibres → ectopic rhythms (VT, bidirectional VT)
  • Delayed afterdepolarisations (DADs) from Ca2+ overload → triggered arrhythmias

Hypokalaemia Effect:

• Potentiates toxicity because:
  • K+ normally competes with digoxin for binding site on Na+/K+-ATPase
  • Low extracellular K+ → increased digoxin binding → more inhibition
  • Can have toxicity at "therapeutic" digoxin levels if K+ low

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Follow-up Question 2: "Outline your management of this patient."

Expected Answer (3 minutes):

Immediate Management:

1. Monitoring and Resuscitation:

• Cardiac monitoring (high risk of arrhythmias)
• IV access
• Have defibrillator ready

2. Withhold Offending Agents:

• Stop digoxin and diltiazem

3. Electrolyte Correction:

• Potassium replacement:
  • IV K+ 40 mmol over 2-4 hours (max 20 mmol/hr via peripheral)
  • Target K+ 4.0-5.0 mmol/L
  • Check Mg2+ and replace if low
• CAUTION with K+ in severe toxicity: If already hyperkalaemic from massive ingestion, K+ may worsen toxicity; check level first

4. Bradycardia Management:

• Atropine 0.5-1 mg IV - often effective (vagally mediated)
• Temporary pacing if refractory (caution: may trigger arrhythmias)

5. DigiFab (Digoxin-Specific Antibody Fragments):

Indications:

• Life-threatening arrhythmias (VT, VF)
• Haemodynamically significant bradycardia refractory to atropine
• K+ greater than 5.5 mmol/L (indicates severe poisoning)
• Ingestion greater than 10 mg
• Level greater than 15 ng/mL at any time

This Patient: Symptomatic bradycardia, hypotension, level 4.2 - consider DigiFab if no response to atropine and K+ replacement

Dosing:

• Each 40 mg vial binds 0.5 mg digoxin
• Based on level: Vials = [Digoxin level (ng/mL) × Weight (kg)] / 100
• Empiric: 10 vials for severe toxicity

6. Avoid:

• Calcium (risk of "stone heart")
• Cardioversion unless life-threatening (low energy if required - 10-25 J)

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Follow-up Question 3: "The patient develops bidirectional ventricular tachycardia. What is this and how do you manage it?"

Expected Answer (2 minutes):

Bidirectional VT:

• Definition: Wide complex tachycardia with alternating QRS axis (beat-to-beat axis change)
• Pathognomonic of digoxin toxicity (or catecholaminergic polymorphic VT)
• Mechanism: DAD-triggered activity from two different foci in the ventricles

Management:

• Immediate DigiFab if not already given (life-threatening arrhythmia)
• Magnesium sulfate 2 g IV over 10 minutes (stabilises membranes)
• Correct hypokalaemia
• Avoid DC cardioversion if possible (may precipitate VF)
• If unstable: Low-energy cardioversion (10-25 J)
• Lidocaine for ongoing VT (if DigiFab not immediately available)
• Avoid amiodarone (may worsen)

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Follow-up Question 4: "After DigiFab, the digoxin level comes back as 8.5 ng/mL. How do you interpret this?"

Expected Answer (1 minute):

Interpretation:

• Post-DigiFab, measured digoxin level rises because assays measure total digoxin (bound + free)
• DigiFab binds free digoxin → inactive Fab-digoxin complex → still detected by assay
• Free (active) digoxin has actually decreased - which is why patient improved
• Do NOT treat based on this elevated level
• Monitor clinically - symptoms, HR, rhythm
• True free digoxin levels available in specialised labs (rarely needed)
• Fab-digoxin complex renally excreted over 3-5 days