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BRADYCARDIA & BRADYARRHYTHMIA - Complete Medicine Viva Guide

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PART 1: BRADYCARDIA

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1. Definition

• Bradycardia = heart rate < 60 beats/min (clinical/conventional definition)
• Based on large population studies of healthy individuals, the lower limit of normal resting heart rate is actually 50 beats/min (Braunwald's)
• For practical purposes, symptomatic bradycardia is defined as a rate < 50 beats/min with associated symptoms

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2. Physiological vs Pathological Bradycardia

• Increased stroke volume triggers baroreceptor reflex -> increased vagal tone
• Exercise training downregulates ion channels responsible for the "funny current" (If) that drives rhythmic sinus node depolarization (Guyton & Hall)

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3. Classification of Bradycardia

Sinus Node  →  AV Node  →  His-Purkinje System

1. Sinus node dysfunction - sinus bradycardia, sinus arrest, SA exit block, sick sinus syndrome
2. AV nodal block - 1st, 2nd (Mobitz I), 3rd degree at AV node
3. Infranodal block - Mobitz II, 2:1 block, complete heart block (His-Purkinje)

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4. ECG Recognition of Sinus Bradycardia

• Rate < 50 beats/min (Braunwald's) / < 60 beats/min (conventional)
• P waves are of normal contour, upright in leads I, II, aVF
• Every P wave followed by a QRS complex
• Constant PR interval > 120 ms
• Sinus arrhythmia often coexists

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5. Causes of Bradycardia

A. Physiological

• Athletes, vagal stimulation, sleep

B. Increased Vagal Tone (Neurally Mediated)

• Carotid sinus syndrome (hypersensitive baroreceptors - even mild neck pressure causes intense bradycardia, may cause cardiac standstill for 5-10 sec and syncope)
• Vasovagal syncope
• Inferior wall MI (vagal reflex from inferior wall)
• Raised intracranial pressure (Cushing reflex)
• Hemoperitoneum

C. Intrinsic Sinus Node Disease

• Sick sinus syndrome
• Fibrotic degeneration (elderly)
• Cardiomyopathies
• Post-cardiac surgery (Mustard/Senning repair for TGA, ASD repair, Fontan)

D. Drugs

• Beta-blockers (most common drug cause)
• Calcium channel blockers (diltiazem, verapamil)
• Digoxin
• Amiodarone
• Ivabradine

E. Metabolic / Systemic

• Hypothyroidism
• Hypothermia
• Hypoxia
• Hyperkalaemia
• Jaundice (bile salts)

F. Infections / Inflammatory

• Lyme disease (carditis)
• Myocarditis
• Chagas disease
• Rheumatic fever

G. Cardiac

• Acute inferior wall MI (AV nodal ischemia)
• Cardiac amyloidosis
• Sarcoidosis
• Post-cardiac transplant (atropine is ineffective - no vagal innervation)

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6. Clinical Features

Symptoms (when heart rate is insufficient for cardiac output):

• Dizziness, lightheadedness
• Syncope or near-syncope (Adams-Stokes attacks in complete heart block)
• Fatigue, exercise intolerance
• Dyspnea (reduced cardiac output)
• Chest pain (if ischemia occurs)
• Cognitive impairment (in elderly)
• Palpitations (escape beats)

Signs:

• Slow pulse (regular or irregular)
• Low BP (if haemodynamically compromised)
• S3 or S4 may be present
• Cannon A waves (complete heart block - atria contracting against closed TV)
• Variable S1 intensity (complete heart block)

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7. When Bradycardia Becomes Symptomatic

• Adequacy of escape rhythms
• Ventricular function
• Associated conditions (ischemia, heart failure)
• Duration and suddenness of onset

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8. Investigation

1. 12-lead ECG - identify the type of bradyarrhythmia
2. Holter monitoring (24-48 h) - detect intermittent bradycardia
3. Event recorder / Implantable loop recorder (ILR) - for infrequent syncope
4. Electrophysiology study (EPS) - localise block (A-H = AV node, H-V = His-Purkinje)
5. Carotid sinus massage - with ECG, identifies carotid sinus syndrome
6. Tilt table test - vasovagal syncope
7. Blood tests: TFTs (hypothyroidism), electrolytes (K+), drug levels, Lyme serology

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9. Management of Bradycardia

Acute (Emergency) Management

• Infranodal (His-Purkinje) AV block - can paradoxically worsen block
• Wide-complex escape rhythms
• Post-transplant (use isoproterenol)

Temporary Pacing Indications

• Haemodynamically unstable bradycardia not responding to drugs
• Anterior MI with new complete heart block or bifascicular block
• Post-cardiac surgery
• Drug toxicity with complete AV block
• Bridge to permanent pacemaker

• Transcutaneous pacing (emergency, uncomfortable, only temporary)
• Transvenous temporary pacing (more reliable, preferred in-hospital)

Permanent Pacemaker (PPM) Indications

• Symptomatic sinus node dysfunction
• Symptomatic AV block (2nd or 3rd degree)
• Post-MI: transient 2nd or 3rd degree AV block with bundle branch block
• Asymptomatic 3rd degree AV block with rate < 40 or pauses > 3 sec
• Chronotropic incompetence

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PART 2: BRADYARRHYTHMIAS (Detailed)

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1. Classification of Bradyarrhythmias

• Disorders of impulse formation (sinus node)
• Disorders of impulse conduction (AV/His-Purkinje)

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2. SINUS NODE DYSFUNCTION (SND)

A. Sinus Bradycardia

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B. Sinus Arrest (Sinus Pause)

• Sinus node fails to generate an impulse
• Results in absence of P wave on ECG
• Pause is NOT a multiple of the preceding P-P interval (distinguishes from SA exit block)
• A junctional or ventricular escape beat typically follows
• Causes: vagal stimulation, drugs, sick sinus syndrome

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C. Sinoatrial (SA) Exit Block

• Sinus node generates an impulse, but it fails to exit (conduct to the atria)
• Three degrees (analogous to AV block):
  • Type I SA exit block (Wenckebach): Progressive shortening of P-P intervals until one P wave is dropped; the cycle length of the pause is < 2x the preceding P-P interval
  • Type II SA exit block: Dropped P waves occur in a regular ratio (2:1, 3:1, 4:1) - the pause IS a multiple of the P-P interval
  • Type III / Complete SA block: No P waves (indistinguishable from sinus arrest)
• Causes: intrinsic SA node disease, vagal tone, drugs

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D. Sinus Arrhythmia

• Normal variation in sinus rate with respiration
• Respiratory sinus arrhythmia: Rate increases on inspiration (inhibition of vagal tone), decreases on expiration
• Variation < 5% in quiet breathing; up to 30% during deep breathing
• Entirely normal - most common in children and young adults
• Non-respiratory sinus arrhythmia: seen with digitalis toxicity

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E. Sick Sinus Syndrome (SSS) - "Sinus Node Disease"

1. Persistent spontaneous sinus bradycardia inappropriate for the physiological circumstance
2. Sinus arrest or SA exit block
3. Combinations of SA and AV conduction disturbances
4. Bradycardia-tachycardia (Tachy-Brady) syndrome - alternating paroxysms of rapid atrial tachyarrhythmias (usually AF, atrial flutter) and periods of slow atrial/ventricular rates

• Most common in older adults due to fibrotic degeneration
• Associated with: cardiomyopathies, connective tissue diseases, amyloidosis, sarcoidosis, myocarditis, certain drugs

• Post-tachycardia pauses: When the tachyarrhythmia (usually AF) terminates, the suppressed sinus node takes time to recover - resulting in excessive post-conversion pauses
• Also seen when AF alternates with periods of high-grade AV block causing bradycardia
• Commonly precipitated/worsened by beta-blockers or calcium channel blockers used to treat the tachycardia

• Sinus bradycardia; sinus pauses; SA block
• Post-tachycardia pauses (after AF)
• Escape beats (junctional or ventricular)
• Alternating fast and slow rates on Holter

• 24-h Holter (most useful)
• Event recorder / ILR (for infrequent episodes)
• EPS: sinus node recovery time (SNRT) - prolonged (> 1500 ms) is abnormal
• Intrinsic heart rate (IHR) after autonomic blockade - reduced in intrinsic SND

• Acute: Treat the specific rhythm (atropine for bradycardia, rate control for tachycardia)
• Long-term: Permanent pacemaker for symptomatic bradycardia + pharmacological therapy for the tachyarrhythmia component (note: drugs alone worsen bradycardia)
• Preferred pacemaker mode: AAI or DDD (rate-responsive AAIR/DDDR)

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3. AV CONDUCTION DISORDERS (HEART BLOCK)

• AV node (most common, usually benign)
• His bundle
• Bundle branches (infranodal - more serious)

• A-H interval prolonged = AV nodal block
• H-V interval prolonged = infranodal (His-Purkinje) block

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A. First-Degree AV Block

• PR interval > 200 ms (can be as long as 1000 ms!)
• Every P wave is followed by a QRS
• When PR > P-P interval: "skipped P waves" phenomenon
• If QRS is narrow: block is in AV node
• If QRS has BBB pattern: block may be AV nodal OR His-Purkinje (EPS needed)

• Normal variant (up to 2% of healthy young adults)
• Increased vagal tone
• Inferior MI
• Drugs (beta-blockers, CCBs, digoxin, amiodarone)
• Myocarditis, Lyme disease
• Rheumatic fever

• Usually asymptomatic, benign
• Can progress to higher-degree block if carotid massage applied or if atrial rate increases
• No treatment required; avoid nodal blocking agents

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B. Second-Degree AV Block

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Mobitz Type I (Wenckebach) Block

• Progressive lengthening of PR interval from beat to beat
• Until one P wave is suddenly blocked (dropped beat) - no QRS
• After the dropped beat, PR interval resets to shortest value and cycle repeats
• R-R intervals progressively shorten before the dropped beat (though the PR lengthens, the increments decrease each beat)
• The pause containing the dropped beat is less than 2x the preceding R-R interval
• Grouped beating (pairs, trios)

• The biggest increment in PR is in the 2nd beat of each cycle
• The greatest shortening of R-R is between 2nd and 3rd beat
• "Footprint" pattern on ladder diagram

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Mobitz Type II Block

• Fixed PR interval (same before and after blocked P)
• Sudden, unexpected dropped beat (no QRS) without preceding PR prolongation
• QRS is usually wide (BBB pattern) - block is infranodal
• May be associated with bundle branch block

• PR is constant; no progressive lengthening
• Block is infranodal (His bundle or below)
• More dangerous - higher risk of progression to complete heart block

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2:1 AV Block

• 2 P waves : 1 QRS (every other P wave blocked)
• Cannot distinguish between Mobitz I and II from a single strip (need longer strips, other clues)
• If QRS is narrow - more likely Mobitz I (AV nodal)
• If QRS is wide - more likely Mobitz II (infranodal)
• Carotid massage worsens Mobitz II (slows atrial rate - less conduction); atropine improves Mobitz I
• Requires further investigation

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High-Grade (Advanced) AV Block

• 2 or more consecutive P waves fail to conduct
• e.g., 3:1, 4:1 block
• Implies near-complete failure of AV conduction
• Usually requires pacing

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C. Third-Degree (Complete) AV Block

• P waves and QRS complexes are completely dissociated (P-P interval is regular, R-R interval is regular, but the two bear NO relationship to each other)
• Atrial rate > ventricular rate (always - because escape pacemakers are slower)
• Escape rhythm:
  • Junctional (nodal) escape: QRS narrow (< 120 ms), rate 40-60 bpm - block is in AV node (more benign)
  • Ventricular escape: QRS wide (> 120 ms), rate 20-40 bpm - block is infranodal (more dangerous, unstable, risk of asystole)
• Variable S1 intensity (AV dissociation - different PR relationships each beat)
• Cannon A waves in JVP (atrial contraction against closed tricuspid valve)

• Congenital complete heart block (associated with maternal anti-Ro/La antibodies, corrected TGA)
• Acquired:
  • Inferior MI (transient, often nodal - usually recovers)
  • Anterior MI (permanent, infranodal - serious)
  • Lyme disease (carditis)
  • Surgical/catheter trauma
  • Drugs (digoxin toxicity, beta-blockers, CCBs)
  • Sarcoidosis, amyloidosis
  • Fibrocalcific degeneration (Lenegre's/Lev's disease)
  • Post-TAVI (transcatheter aortic valve implantation)

• Adams-Stokes attacks (sudden syncope due to ventricular standstill before escape rhythm kicks in)
• Slow, regular pulse; wide pulse pressure (large stroke volume)
• Cannon A waves in JVP
• Variable S1 intensity
• S4 may be present
• Features of low cardiac output: dyspnea, angina, heart failure

• Acute: Atropine (if nodal block); avoid atropine in infranodal block (can worsen); dopamine/epinephrine infusion; temporary pacing (transcutaneous or transvenous)
• Definitive: Permanent pacemaker (DDD mode preferred in most; rate-responsive DDDR for active patients)
• Post-cardiac transplant: Isoproterenol (atropine is ineffective - no vagal innervation)

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4. AV DISSOCIATION

• NOT the same as complete heart block
• AV dissociation = atria and ventricles are driven by independent pacemakers (both independently beating) - but this is because the ventricular pacemaker has ACCELERATED (e.g., junctional tachycardia), not because of block
• In complete heart block: atria faster than ventricles
• In isorhythmic AV dissociation: rates similar
• In AV dissociation from accelerated ventricular rhythm: ventricle faster, captures occur when P waves find the AV node receptive

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5. LENEGRE'S DISEASE vs LEV'S DISEASE

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6. ECG COMPARISON TABLE - Summary

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7. MANAGEMENT ALGORITHM FOR BRADYARRHYTHMIA

BRADYARRHYTHMIA DETECTED
         |
    Is patient STABLE?
    /              \
  YES               NO
   |                 |
Identify type     Emergency:
of bradyarrhythmia Atropine 0.5-1mg IV
   |              Transcutaneous pacing
   |
   |---> Sinus bradycardia/SSS
   |       -> Treat cause, PPM if symptomatic
   |
   |---> 1st degree AV block
   |       -> Observe, no treatment
   |
   |---> Mobitz I (Wenckebach)
   |       -> Usually observe; PPM if symptomatic
   |
   |---> Mobitz II
   |       -> PPM (even if asymptomatic)
   |
   |---> Complete Heart Block
           -> Atropine if nodal, temporary pacing
           -> Permanent PPM

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8. PACEMAKER BASICS (for Viva)

• VVI: Ventricular pacing, ventricular sensing, inhibited - "demand pacing" - used in AF + CHB
• DDD: Dual-chamber, dual-sensing, dual-response - maintains AV synchrony - most physiological
• AAI: Atrial pacing - used in sick sinus syndrome with intact AV conduction
• VVIR/DDDR: Rate-responsive variants for active patients

• Symptomatic bradycardia (any cause)
• 3rd degree AV block (regardless of symptoms if rate < 40 or pauses > 3 sec)
• Mobitz II AV block (even asymptomatic)
• 2:1 AV block with wide QRS (infranodal)
• Symptomatic chronotropic incompetence
• Post-MI: transient 2nd or 3rd degree AV block with bundle branch block, or persistent symptomatic AV block

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9. SPECIAL SCENARIOS (High-Yield Viva Points)

Bradycardia in Acute Inferior MI

• Due to: RCA ischemia affecting AV node (+ increased vagal tone)
• Usually transient and reversible
• Usually nodal (narrow QRS escape)
• Responds to atropine
• Rarely needs pacing

Bradycardia in Acute Anterior MI

• Due to: LAD ischemia affecting bundle branches
• Usually infranodal (wide QRS escape)
• Does NOT respond to atropine (may worsen)
• Carries 4-6x higher in-hospital mortality (marker of extensive myocardial damage)
• Temporary pacing indicated
• Permanent pacing: even if transient 2nd/3rd degree AV block with bundle branch block

Post-Cardiac Transplant Bradycardia

• Denervated heart - no vagal supply
• Atropine is INEFFECTIVE (no muscarinic receptors to block)
• Isoproterenol is drug of choice (direct beta-1 agonist)
• May need pacemaker if persistent

Bradycardia in Lyme Disease

• Lyme carditis: spirochetal invasion of conduction tissue
• Any degree of AV block possible (can fluctuate rapidly)
• Usually temporary and reversible with antibiotics (doxycycline/amoxicillin)
• Monitor closely; temporary pacing for complete heart block

Drug-Induced Bradycardia

• Beta-blockers: Glucagon (0.5-5 mg IV) is specific antidote
• Digoxin toxicity: Digoxin-specific antibody fragments (Digibind/Fab)
• CCBs (verapamil/diltiazem): Calcium gluconate, glucagon, high-dose insulin

Hypersensitive Carotid Sinus Syndrome

• Baroreceptors in carotid sinus are excessively sensitive
• Even light pressure on the neck causes intense vagal discharge
• Can cause cardiac standstill for 5-10 seconds -> syncope
• Diagnosis: carotid sinus massage (with ECG, resuscitation equipment available!)
• Pause > 3 seconds = significant
• Treatment: PPM (DDD or VVI)

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10. AUTONOMIC / NEURALLY MEDIATED BRADYCARDIAS

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11. KEY DIFFERENTIALS IN VIVA

• Mobitz I: Progressive PR lengthening + narrow QRS + AV nodal location (benign, inferior MI)
• Mobitz II: Fixed PR + wide QRS + infranodal location + dangerous, needs PPM

• Can progress to complete heart block suddenly and unpredictably - risk of syncope and sudden death

• Atropine increases sinus rate; more impulses arrive at the blocked infranodal system -> paradoxically fewer conduct through -> worse bradycardia or asystole

• Sinus arrest: pause is NOT a multiple of P-P interval (node failed to fire)
• SA exit block (Type II): pause IS an exact multiple of P-P interval (node fired but impulse didn't exit)

• Part of sick sinus syndrome. Post-tachycardia suppression of sinus node -> long pauses after tachycardia terminates. Dangerous because drugs to treat tachycardia worsen bradycardia -> needs PPM + drug therapy

• Junctional escape rate 40-60 bpm (narrow QRS) = nodal block
• Ventricular escape rate 20-40 bpm (wide QRS) = infranodal block (more dangerous)

• His bundle electrogram (intracardiac EPS): A-H interval (AV node), H-V interval (His-Purkinje)

• Sudden syncope (brief LOC) due to transient cardiac standstill or very slow ventricular rate, classically in complete heart block. Characteristically: sudden fall without warning, rapid recovery, pallor followed by flushing

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12. QUICK RECALL: CAUSES OF PROLONGED PR (1st Degree AVB)

• D - Digoxin, Drugs (beta-blockers, CCBs, amiodarone)
• A - Athletic heart, Autonomic (high vagal tone)
• L - Lyme disease
• P - PR prolongation physiologic (athletes)
• I - Inferior MI, Inflammatory (myocarditis, RF)
• H - Hyperkalaemia, Hypomagnesaemia
• S - Surgery (cardiac)

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13. SUMMARY TABLE - Bradyarrhythmias at a Glance

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