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BRADYCARDIA - Complete Viva Notes

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Definition

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Physiology of the Sinus Node (SA Node)

• Intrinsic rate: 60-100 bpm
• Cells have a relatively higher resting membrane potential than atrial myocytes
• Phase 4 spontaneous depolarization (automaticity) - driven by "funny current" (If/I1 current via HCN4 channels), calcium influx (T-type and L-type), and decreased potassium conductance
• Phase 0 depolarization is mediated by calcium influx (L-type Ca2+ channels), NOT fast sodium channels (this explains why AV/SA node tissue is sensitive to calcium channel blockers)
• Subsidiary pacemakers take over if SA node fails:
  • AV junction: 40-60 bpm
  • His bundle/Purkinje: 20-40 bpm
  • Ventricular myocardium: 20-30 bpm (least reliable)

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Classification of Sinus Bradycardia

Physiologic (Benign)

• Well-trained athletes (vagal hypertonia)
• Sleep (normal HR can fall to 35-40 bpm in young adults; pauses up to 2 seconds are normal)
• Young healthy adults

Pathologic (Intrinsic SND)

• Idiopathic fibrosis/degeneration of SA node
• Post-cardiac surgery / post-ablation
• Post-cardiac transplant
• Ischemia/infarction of SA node (usually right coronary artery territory)
• Myocarditis, cardiomyopathy
• Infiltrative disease (sarcoidosis, amyloid, hemochromatosis)

Extrinsic (Reversible)

• Hypothyroidism (myxedema)
• Hypothermia
• Hypoxia
• Increased intracranial pressure
• Sleep apnea
• Lyme disease
• Myocarditis / COVID-19
• Gram-negative sepsis
• Vagal reflex (cough, pain, vomiting, Valsalva, carotid sinus stimulation, vasovagal syncope)
• Meningitis
• Ocular surgery (oculocardiac reflex)

• Beta-adrenergic blockers (including ophthalmic betaxolol drops for glaucoma)
• Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)
• Digoxin / cardiac glycosides
• Amiodarone, dronedarone, sotalol, flecainide, propafenone, procainamide
• Ivabradine (specific If/I1 current blocker)
• Clonidine, methyldopa
• Lithium
• Donepezil (cholinesterase inhibitor for Alzheimer's)
• Opioid analgesics, muscle relaxants, propofol
• SSRIs, tricyclic antidepressants, phenothiazines, phenytoin
• Cannabis, quinine

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Symptoms of Bradycardia

• Often asymptomatic (benign in athletes and during sleep)
• Fatigue, exercise intolerance, reduced effort tolerance
• Dizziness, pre-syncope, syncope (Stokes-Adams attacks)
• Palpitations (from compensatory escape rhythms)
• Chest pain, dyspnea (if cardiac output falls)
• Confusion, cognitive impairment (in the elderly)
• Sudden cardiac arrest (if reliable escape rhythm fails)

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ECG Features of Sinus Bradycardia

• Regular P waves (normal morphology, positive in II, aVF; negative in aVR)
• Heart rate < 60 bpm
• Each P wave followed by QRS (1:1 AV conduction)
• PR interval normal (0.12-0.20 sec)
• QRS normal duration (unless BBB coexists)

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Management of Sinus Bradycardia

• Cardiac output is inadequate
• Hemodynamic instability
• Arrhythmias result from the slow rate

• Atropine 0.5 mg IV (repeat if needed, max 3 mg total) - first line
  • Caution: lower doses (<0.5 mg) or subcutaneous route can cause paradoxical parasympathomimetic effect
• Isoprenaline (isoproterenol) IV infusion - beta-1 agonist
• Adrenaline (epinephrine) infusion 2-10 mcg/min
• Temporary transcutaneous or transvenous pacing if pharmacological measures fail

• Theophylline / aminophylline (adenosine blockade) - used in spinal cord injury, post-transplant
• Terbutaline (beta-2 agonist)

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BRADYARRHYTHMIAS - Complete Viva Notes

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Definition

1. Sinus node dysfunction (SND) - failure of SA node to generate or propagate impulses
2. Atrioventricular (AV) block - failure of conduction from atria to ventricles
3. Neurally/autonomically mediated bradyarrhythmias - Vagal overactivity

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PART 1: SINUS NODE DYSFUNCTION (SND)

Spectrum of SND - "Sick Sinus Syndrome"

1. Persistent sinus bradycardia - inappropriate for physiologic circumstances
2. Sinus pause/sinus arrest - failure of SA node to discharge, leading to atrial asystole with or without escape beats
3. SA exit block - SA node fires but impulse fails to exit and depolarize atria
4. Chronotropic incompetence (CI) - failure of heart rate to appropriately increase with exercise
5. Tachycardia-bradycardia syndrome (Tachy-Brady syndrome) - alternating tachyarrhythmias (usually AF/atrial flutter) and bradycardia

Sinus Pause / Sinus Arrest

• SA node fails to discharge
• Absent P wave for an interval NOT a multiple of the P-P cycle
• Distinguished from SA exit block by the pause duration
• Brief pauses are normal (especially in athletes and during sleep)
• Escape beats from AV junction or ventricles may occur
• Can cause presyncope/syncope if prolonged (Fuster's Heart)

Sinoatrial (SA) Exit Block

• 1st degree SA exit block: SA node fires but conduction to atria is slowed. NOT visible on ECG (SA node discharge not recorded on surface ECG).
• 2nd degree SA exit block - Type I (Wenckebach): P-P intervals progressively shorten before the pause; pause duration is LESS than 2 P-P cycles
• 2nd degree SA exit block - Type II: The pause equals an EXACT MULTIPLE (2x, 3x, 4x) of the basic P-P interval. Recognized on ECG as a pause equal to multiple of prior P-P intervals.
• 3rd degree SA exit block: Complete absence of P waves; very difficult to diagnose without sinus node electrograms

Tachycardia-Bradycardia Syndrome (Tachy-Brady Syndrome)

• Tachyarrhythmia (typically AF or atrial flutter) terminates with excessive post-conversion pause
• Can also occur during AF when rapid ventricular response alternates with periods of high-grade AV block
• Often worsened by/occurs as result of treatment with beta-blockers or calcium channel blockers
• Requires pacing + antiarrhythmic drug therapy (pacing for bradycardia, drugs for tachycardia)

Chronotropic Incompetence (CI)

• Failure to achieve 80% of age-predicted maximum heart rate (APMHR) during exercise
• Formula: APMHR = 220 - age
• Assessed by exercise treadmill testing (Bruce or modified Bruce protocol)
• Treated with rate-responsive pacemaker programming

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Investigations for SND

1. 12-lead ECG and rhythm strips - initial tool; identifies bradycardia, pauses, SA exit block
2. 24-72 hour Holter monitoring - correlates symptoms with rhythm; most practical for frequent symptoms
3. Event recorder / prolonged ambulatory monitoring - for infrequent symptoms
4. Implantable loop recorder (ILR) - subcutaneous device for symptoms occurring less than once per month; records for up to 3 years
5. Exercise treadmill testing - assesses chronotropic competence
6. Electrophysiology study (EPS) - limited utility for SND; NOT recommended as primary tool per recent guidelines; can measure:
   • Sinus Node Recovery Time (SNRT): longest pause after overdrive atrial pacing in excess of sinus cycle length
   • Sinoatrial Conduction Time (SACT)
7. Autonomic testing: Atropine and isoproterenol infusions; blunted tachycardic response suggests SND
8. Intrinsic heart rate (IHR): After autonomic blockade with atropine + propranolol; IHR = 117.2 - (0.53 x age); reduced IHR confirms intrinsic SND

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Pacemaker Indications for SND (ACC/AHA/HRS 2018 Guidelines)

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PART 2: ATRIOVENTRICULAR (AV) BLOCK (HEART BLOCK)

Definition

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Classification of AV Block

First-Degree AV Block

• Every atrial impulse is conducted - NO dropped beats
• PR interval > 0.20 sec (200 ms) in adults; can be up to 1.0 second
• Ventricular rate is regular
• If QRS is narrow: delay is almost always in the AV node (A-H interval prolonged)
• If QRS is wide (BBB pattern): delay may be in AV node OR His-Purkinje system (need His bundle electrogram to localize)
• Clinical significance: Usually benign; in elderly with bifascicular block, risk of progression to higher-degree block exists
• Carotid massage (vagal tone enhancement) can advance first-degree to Type I second-degree AV block

Second-Degree AV Block

Mobitz Type I (Wenckebach Block)

• Progressive lengthening of PR interval until one P wave is not conducted (dropped beat)
• After the dropped beat, the PR interval resets to its shortest value and the cycle repeats
• RR intervals shorten progressively before the dropped beat
• The pause containing the dropped beat is less than twice the shortest RR interval
• Site of block: Usually at the AV node (supra-Hisian)
• QRS is typically narrow (unless coexisting BBB)
• Prognosis: Usually benign; may be physiologic (vagal tone, athletes, inferior MI with Bezold-Jarisch reflex)
• Does NOT usually require pacing unless symptomatic

Mobitz Type II Block

• Constant PR interval (no progressive lengthening) followed by sudden, unexpected dropped beat
• When conducted, the PR interval stays the same
• QRS is usually wide (bundle branch block pattern), suggesting infra-Hisian block
• Site of block: Below the AV node, in the His bundle or bundle branches (infra-Hisian)
• Prognosis: Serious - high risk of progressing to complete heart block (third-degree); can be unpredictable and lead to syncope or sudden death
• Requires pacing in most cases even if asymptomatic

2:1 AV Block

• Every alternate P wave is not conducted (2 P waves for every 1 QRS)
• Cannot classify as Type I or Type II by surface ECG alone (need His bundle electrogram to distinguish)
• If QRS is narrow - likely AV nodal (Type I behavior)
• If QRS is wide - likely infra-Hisian (Type II behavior)

High-Grade (Advanced) AV Block

• Two or more consecutive non-conducted P waves
• Intermittent AV conduction still present (distinguishes it from complete heart block)
• Ventricular rhythm is irregular
• Causes: Acute coronary syndromes, rheumatic heart disease, autoimmune disorders, myocarditis, infiltrative cardiomyopathies
• Clinical presentation and outcomes indistinguishable from third-degree AV block

Third-Degree (Complete) AV Block

• No atrial activity is conducted to the ventricles
• Atria and ventricles beat independently (complete AV dissociation)
• Regular ventricular rate < 40 bpm (from escape pacemaker) - rate can be higher in congenital complete AV block
• Escape pacemaker location determines QRS width:
  • Junctional escape (narrow QRS): block at AV node level - more stable, faster rate
  • Ventricular escape (wide QRS): block below His bundle - unstable, slower, worse prognosis
• Atrial rate is faster than ventricular rate
• P waves "march through" QRS complexes with NO fixed relationship

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Paroxysmal AV Block

1. Vagally-mediated: Surge in vagal tone; typically benign; may cause syncope
2. Intrinsic (phase 4 dependent): AV block following premature beats or abrupt heart rate decrease; due to phase 4 depolarization and inexcitability in diseased His-Purkinje tissue; malignant - can cause recurrent syncope or sudden death; requires pacing
3. Idiopathic: No vagotonia or conduction system disease; may cause syncope but does NOT progress; possible role of adenosine

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AV Dissociation

1. AV block (ventricles are slower)
2. VA block (as in VT or ventricular pacing)
3. Isorhythmic AV dissociation - both pacemakers have similar rates; NO block in either direction
4. Slowing of primary rhythm + emergence of subsidiary pacemaker

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Causes of AV Block

Fibrosis/Degeneration

• Lev's disease: Fibrocalcific degeneration of the left side of the cardiac skeleton including the upper part of the bundle branches; age-related
• Lenegre's disease: Idiopathic progressive sclerosis/fibrosis of the His-Purkinje system in younger patients; genetic component; associated with SCN5A mutations

Ischemic

• Inferior MI (right coronary artery): AV block at the AV node level; usually Type I second-degree; generally transient (hours to days); narrow complex escape; Bezold-Jarisch reflex contributes
• Anterior MI (LAD): Block at infra-Hisian level (bundle branches); wide complex unstable escape; high mortality; requires pacing

Iatrogenic

• Cardiac surgery (especially valve surgery, VSD/ASD repair, TAVI/TAVR)
• Alcohol septal ablation (for HCM)
• Catheter ablation for AVNRT (< 1% risk)
• Radiation, chemotherapy

Drugs

• Beta-blockers, verapamil, diltiazem, digoxin

Infectious

• Lyme carditis (Borrelia burgdorferi) - important reversible cause; up to 3rd degree block; resolves with antibiotics
• Bacterial endocarditis with perivalvular abscess
• Viral myocarditis, Chagas' disease, toxoplasmosis, COVID-19

Infiltrative / Inflammatory

• Sarcoidosis (granulomas in conduction system)
• Amyloidosis
• Hemochromatosis
• Rheumatologic: SLE, RA, reactive arthritis (Reiter's syndrome), systemic sclerosis

Congenital

• Maternal Lupus (anti-Ro/SSA antibodies cross placenta and damage fetal AV node)
• Idiopathic congenital complete AV block
• Congenital heart defects (L-TGA, ASD, VSD)

Genetic / Neuromuscular

• Myotonic dystrophy (DM1 - DMPK gene, DM2 - CNBP gene)
• Kearns-Sayre syndrome (mitochondrial DNA deletion) - progressive ophthalmoplegia, retinitis pigmentosa, AV block
• Erb's muscular dystrophy (Emery-Dreifuss muscular dystrophy)
• SCN5A mutation (progressive cardiac conduction defect)

Endocrine

• Hypothyroidism, hypoadosteronism

Enhanced vagal tone

• Vasovagal syncope, carotid sinus hypersensitivity, sleep apnea

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Clinical Features of AV Block

• Stokes-Adams attacks: Sudden loss of consciousness due to transient complete heart block and asystole; the patient falls without warning, becomes pale or cyanotic, then flushes pink as cardiac output is restored; recovery is usually rapid (unlike seizures); can recur unpredictably

• Slow regular or irregular pulse
• Cannon "a" waves in the jugular venous pulse (JVP): when atria contract against closed tricuspid valve (during AV dissociation) - large, irregular, intermittent jugular pulsations
• Variable intensity of first heart sound (S1): Due to changing PR interval (loudest when PR is shortest; softest when PR is longest)
• "Bruit de Canon": Very loud S1 when PR interval is very short (atrium and ventricle contract nearly simultaneously) - seen in complete AV block when ventricular rate exceeds atrial rate briefly
• Second heart sound may split normally or paradoxically depending on ventricular activation pattern
• Signs of reduced cardiac output: hypotension, pulmonary edema

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Investigations for AV Block

1. 12-lead ECG - diagnoses and classifies most AV blocks
2. His bundle electrogram (EPS) - essential to distinguish supra-Hisian (AV node) from infra-Hisian (His-Purkinje) block; indispensable for 2:1 block; predicts risk of progression
   • A-H interval: AV nodal conduction (normal 60-125 ms)
   • H-V interval: His-Purkinje conduction (normal 35-55 ms); H-V > 100 ms indicates high risk
3. Holter/ambulatory monitoring: For paroxysmal or intermittent AV block
4. Exercise testing: AV block that worsens with exercise = infra-Hisian (sinister); AV block that improves with exercise = AV nodal (benign)
5. Lyme serology, thyroid function, electrolytes, toxicology screen (to exclude reversible causes)
6. Echocardiogram: Structural heart disease, LV function
7. Cardiac MRI: Sarcoidosis, cardiomyopathy, fibrosis

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Pacemaker Indications for AV Block (ACC/AHA/HRS Guidelines)

Definite Indications (Class I)

• Third-degree (complete) AV block - any anatomic site, symptomatic OR asymptomatic if:
  • Ventricular rate < 40 bpm while awake
  • Asystole ≥ 3.0 seconds
  • In setting of neuromuscular disease (e.g., myotonic dystrophy) even if asymptomatic
• Second-degree Mobitz Type II AV block with wide QRS (symptomatic OR asymptomatic)
• High-grade AV block (symptomatic)
• Symptomatic bradycardia from second-degree AV block (any type)
• Bifascicular block with intermittent third-degree or Type II second-degree AV block
• AV block from Lyme disease that is persistent

Key Distinctions for Viva

• In SND: Pacing indicated mainly when symptoms correlate with bradycardia
• In AV block: Pacing may be indicated EVEN WITHOUT SYMPTOMS if block is infra-Hisian (Mobitz Type II, complete heart block with wide QRS) due to risk of life-threatening asystole
• Congenital complete AV block in children: Pacing indicated if ventricular rate is very slow, QRS wide, exercise intolerance, or if systolic LV dysfunction develops

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Pacemaker Types

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Part 3: NEURALLY MEDIATED (AUTONOMIC) BRADYARRHYTHMIAS

Carotid Sinus Hypersensitivity (CSH)

• Exaggerated response to carotid sinus massage
• Cardioinhibitory response: Asystole > 3 seconds during carotid sinus massage
• Vasodepressor response: Systolic BP fall ≥ 50 mmHg without cardiac slowing
• Both can coexist in the same patient
• Diagnosis: Carotid sinus massage (with ECG and BP monitoring; avoid if carotid bruit present)
• Management: Cardioinhibitory type benefits from pacemaker implantation

Vasovagal Syncope (Neurocardiogenic Syncope)

• Most common cause of syncope in young healthy individuals
• Trigger: Prolonged standing, pain, emotional distress, heat, Valsalva
• Mechanism: Venous pooling → reduced ventricular filling → vigorous ventricular contraction → paradoxical activation of vagal afferents (Bezold-Jarisch reflex) → sudden bradycardia + hypotension
• Prodrome: Nausea, diaphoresis, warmth, visual dimming, pallor
• Tilt-table testing: Gold standard for diagnosis (60-70° for 20-45 min)
• Management:
  • Reassurance, avoiding triggers, hydration, salt loading
  • Physical counterpressure maneuvers (leg crossing, squatting)
  • Beta-blockers (limited evidence)
  • Fludrocortisone (volume expansion)
  • Midodrine (alpha-1 agonist, increases peripheral vascular resistance)
  • Dual-chamber pacing (for cardioinhibitory type with documented asystole)

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Bifascicular and Trifascicular Block

• Bifascicular block: Block in 2 of the 3 fascicles (RBBB + left anterior hemiblock is commonest; or RBBB + left posterior hemiblock)
• Trifascicular block: Evidence of disease in all 3 fascicles; classically described as bifascicular block + prolonged PR interval (first-degree AV block)
  • Caution: "Trifascicular AV block" is a misnomer - it does NOT mean third-degree block; it means disease/delay in all 3 fascicles
• Risk of progression to complete heart block is increased; EPS (H-V interval measurement) guides pacing decision

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Summary Table: Degrees of AV Block

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High-Yield Viva Points

1. Stokes-Adams attack = syncopal episode from complete heart block; sudden onset, no prodrome; patient flushes pink on recovery (not typical in vasovagal which has a prodrome and pallor)
2. Cannon a waves = hallmark of complete AV block; irregular large jugular pulsations when atria contract against closed tricuspid valve
3. Inferior MI → AV nodal block (reversible, Bezold-Jarisch reflex) vs Anterior MI → infra-Hisian block (irreversible, needs urgent pacing)
4. Wenckebach (Mobitz I) = narrower QRS, AV node, benign; Mobitz II = wide QRS, His-Purkinje, serious, requires pacing
5. Lev's disease = left-sided fibrocalcification (elderly); Lenegre's disease = idiopathic His-Purkinje fibrosis (younger)
6. Lyme disease is the single most common REVERSIBLE infective cause of high-degree AV block - treat with ceftriaxone/doxycycline; AV block usually resolves
7. Maternal SLE → anti-Ro/SSA antibodies → congenital complete AV block in baby
8. Kearns-Sayre syndrome = mitochondrial disease triad: progressive external ophthalmoplegia + pigmentary retinopathy + cardiac conduction block (needs prophylactic pacing)
9. Myotonic dystrophy = most common hereditary neuromuscular disease causing AV block; even asymptomatic patients with any degree of AV block on EPS may need pacing (unpredictable sudden death)
10. 2:1 AV block - cannot classify as Type I or II on surface ECG alone; narrow QRS suggests nodal (better), wide QRS suggests infra-Hisian (worse)
11. Atropine works for AV nodal block (Type I); may paradoxically worsen infra-Hisian (Type II/III) block by increasing sinus rate and exposing more non-conducted beats
12. Pacemaker syndrome = fatigue, hypotension, cannon a waves from VVI pacing with retrograde VA conduction - prevented by DDD pacing
13. Ivabradine = selective If (funny current/HCN4 channel) blocker; reduces HR without affecting contractility; can cause sinus bradycardia

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