Bradycardia and AV Blocks

Sinus Bradycardia (Normal Variant)

• Decreased automaticity of the sinoatrial (SA) node due to increased vagal tone or intrinsic sinus node dysfunction
• Enhanced parasympathetic activity via acetylcholine-mediated M2 receptor activation, increasing potassium conductance and hyperpolarizing the nodal membrane
• Reduced sympathetic drive or beta-blockade decreasing cAMP-dependent calcium channel opening
• Common in athletes and during sleep; benign unless associated with hypotension or symptoms

Pathological Bradycardia and AV Blocks

• SA node dysfunction (sick sinus syndrome): Fibrosis and degeneration of nodal tissue impairing pacemaker automaticity; may be intrinsic or secondary to infiltrative/inflammatory processes
• AV nodal conduction abnormalities: The AV node is the primary site of physiologic conduction delay (~100-120 ms), vulnerable to ischemia, inflammation, and medication effects due to its rich parasympathetic innervation and blood supply from the AV nodal artery (80% from RCA, 20% from LCx)
• Infranodal (His-Purkinje) conduction disease: Progressive fibrosis of the His bundle and bundle branches; less responsive to atropine given sympathetic predominance; carries higher risk of sudden progression to complete heart block
• Autonomic modulation: Increased vagal tone slows AV nodal conduction velocity and increases the effective refractory period through acetylcholine-mediated suppression of L-type calcium channel opening
• Structural disease: Acute ischemia/infarction causes inflammatory edema and necrosis; chronic processes include amyloidosis, sarcoidosis, chagas disease, and infiltrative cardiomyopathies

Medications (Most Common Modifiable Cause)

• Beta-blockers: Decrease SA node automaticity and slow AV nodal conduction
• Calcium channel blockers (diltiazem, verapamil): Impair L-type calcium influx in AV nodal cells
• Digoxin: Increases vagal tone and directly slows AV nodal conduction; toxicity is a classic cause of high-degree AV block
• Amiodarone: Direct negative chronotropic and dromotropic effects
• Cholinesterase inhibitors: Enhance acetylcholine-mediated bradycardia
• Ivabradine: Selective If channel inhibitor for SA node

Cardiac Ischemia and Infarction

• Inferior MI: RCA occlusion → AV nodal ischemia (AV block typically nodal, transient, responds to atropine)
• Anterior MI: LAD occlusion → septal infarction with His bundle/bundle branch damage (infranodal block, high risk of sudden complete heart block)

Degenerative Conduction Disease

• Age-related fibrosis of the conduction system (most common cause in elderly)
• Lev disease: Calcification of the fibrous skeleton (mitral and aortic annulus involvement)
• Lenegre disease: Progressive sclerosis of the bundle branches in younger patients

Infiltrative and Inflammatory Diseases

• Sarcoidosis: Granulomatous infiltration of the basal septum
• Amyloidosis (AL and ATTR subtypes): Deposition in conduction tissue
• Chagas disease (Trypanosoma cruzi): Myocarditis with fibrosis of the conduction system
• Rheumatoid arthritis: Inflammatory involvement of the conduction system
• Lyme disease (Borrelia burgdorferi): Spirochete invasion of the AV node; characteristic in endemic areas

Elevated Intracranial Pressure

• Vagal stimulation from increased ICP (classic in intracranial hemorrhage, head trauma)

Endocrine and Metabolic

• Hypothyroidism: Decreased metabolic rate and increased vagal sensitivity
• Hyperkalemia: Impairs AV nodal conduction

Infiltrative Cardiomyopathies

• Hemochromatosis, Fabry disease, storage diseases

Structural Heart Disease

• Myocardial infarction, cardiac surgery (AV node injury during valve replacement)

Congenital

• Congenital AV block: Associated with maternal anti-Ro/SSA and anti-La/SSB antibodies (lupus, Sjögren's syndrome); transplacental passage → fetal myocarditis and fibrosis

Autonomic Influences (Benign)

• Endurance athletes, sleep apnea, Valsalva maneuver

Asymptomatic Presentation

• Often an incidental finding on routine ECG (common in athletes, elderly with degenerative disease)
• No hemodynamic compromise despite abnormal conduction

Symptomatic Bradycardia (Insufficient Cardiac Output)

• Syncope/presyncope: Classic presenting symptom; due to inadequate cerebral perfusion during complete heart block or severe bradycardia; may have prodrome (palpitations, light-headedness) with nodal block, abrupt onset with infranodal block
• Dyspnea: From reduced cardiac output and pulmonary congestion; worsened by exertion
• Fatigue and exercise intolerance: Inability to increase heart rate appropriately with activity
• Palpitations: Sensation of skipped beats or irregular rhythm (common with second-degree block with dropped beats)
• Chest discomfort: Ischemia may precipitate blocks or occur concurrently (inferior MI)
• Acute decompensation: Heart failure exacerbation if chronic underlying disease present

Physical Examination Findings

• Bradypnea: Respiratory rate may be slow in severe cases
• Hypotension: Critical in symptomatic patients; may be orthostatic
• Irregular pulse: With second-degree AV blocks (irregular rhythm due to dropped beats)
• Cannon A waves: Seen in complete heart block when atrial contraction occurs against closed tricuspid valve during ventricular systole (pathognomonic finding)
• Variable S1 intensity: In complete heart block due to varying AV relationship at different cardiac cycles
• Signs of heart failure: Elevated JVP, hepatomegaly, peripheral edema (if chronic bradycardia leads to pump dysfunction)
• Hypothermia: May be present in severe bradycardia from metabolic suppression
• Neurological deficits: If syncope resulted in trauma

Specific Scenarios

• Inferior MI + bradycardia: Often accompanied by right ventricular infarction; consider need for RV pacing if AV block develops
• Lyme disease in endemic areas: May present with progressive AV block (first-degree → second-degree → complete), often in young patients without prior cardiac disease

12-Lead Electrocardiography (ECG) - Gold Standard

First-Degree AV Block

• Definition: PR interval >200 ms (>5 small squares) with 1:1 AV conduction
• Pathophysiology: Delay anywhere along AV conduction pathway but all atrial impulses conduct to ventricles
• Significance: Generally benign; nodal disease if PR >240 ms suggests more severe conduction delay
• Clinical note: May be incidental or associated with medications (digoxin, beta-blockers); rarely symptomatic

Second-Degree AV Block, Mobitz Type I (Wenckebach)

• Definition: Progressive PR interval prolongation until a P wave is blocked (dropped QRS), then cycle repeats
• ECG pattern: Repeating group of conducted beats followed by dropped beat; PR interval increases within the group
• Anatomical location: 90% occur at the AV node (nodal disease)
• Conduction properties: Longer cycle length after dropped beat (pause > PR interval increment)
• Clinical significance: Usually benign; rate remains adequate due to pauses; rarely progresses to complete block
• Response to atropine: Typically improves (nodal block responds to vagolytic)

Second-Degree AV Block, Mobitz Type II

• Definition: Sudden, unexpected dropped beat(s) without preceding PR prolongation
• ECG pattern: Fixed PR interval in conducted beats, then sudden blocked P wave without warning
• Anatomical location: His bundle or bundle branches (infranodal conduction disease)
• Conduction properties: May progress to 2:1, 3:1 conduction (multiple consecutive blocked beats)
• Clinical significance: HIGH RISK for sudden progression to complete heart block; requires urgent intervention
• Response to atropine: Does NOT improve (infranodal block is not vagally responsive)
• Distinguish from Mobitz I: No PR prolongation before dropped beat; narrower QRS complex exceptions exist

2:1 AV Block

• Definition: Every other P wave is conducted (alternating conducted and blocked P waves)
• Challenge: Cannot distinguish between Mobitz I and II by morphology alone since no PR prolongation sequence visible
• Discrimination strategies:
• Narrow QRS suggests nodal Mobitz I; wide QRS suggests infranodal Mobitz II
• Atropine or exercise: improvement suggests Mobitz I, no change suggests Mobitz II
• His bundle study: definitive but invasive
• Clinical approach: Treat as Mobitz II (higher risk) if wide QRS

High-Grade (Advanced) AV Block

• Definition: Multiple consecutive P waves blocked but not all; pattern of 3:1, 4:1, or variable conduction
• ECG appearance: Several blocked P waves in sequence before one is conducted
• Distinction from complete: Occasional AV conduction present (though rare)
• Symptoms: Usually symptomatic due to severe reduction in ventricular rate
• Prognosis: Intermediate between second-degree and complete block

Third-Degree (Complete) AV Block

• Definition: No AV conduction; complete dissociation between atrial and ventricular rhythms
• ECG findings:
• P waves march through QRS complexes at regular intervals
• QRS complexes at slower intrinsic rate (escape rhythm)
• No fixed PR relationship
• Narrow QRS (~60-80 bpm): nodal escape; wide QRS (~30-50 bpm): ventricular escape
• Anatomical implications:
• Nodal escape → nodal pacemaker takes over, relatively reliable
• Ventricular escape → unreliable, slow, with risk of prolonged asystole
• Acute presentation: Symptomatic with hypotension, altered mental status
• Chronic presentation: May be asymptomatic if escape rate adequate and stable

Sick Sinus Syndrome

• Definition: Constellation of SA node abnormalities; bradycardia-tachycardia syndrome if alternating slow and fast rates
• ECG findings:
• Sinus bradycardia
• SA node block (dropped P waves)
• Sinus pauses (>3 seconds is abnormal)
• Atrial fibrillation alternating with sinus bradycardia ("tachy-brady syndrome")
• Diagnosis criteria: Symptomatic bradycardia with documented rhythm abnormality

Additional Diagnostic Testing

Continuous ECG Monitoring (Holter, Event Monitor)

• Determines if bradycardia/block correlates with symptoms
• Documents frequency and duration of dysrhythmias
• Particularly useful for paroxysmal bradycardia/AV block
• Guideline: If symptomatic bradycardia/block not seen on initial ECG, ambulatory monitoring essential

Exercise Stress Testing

• Indicates whether bradycardia is appropriate (increases with exertion)
• Unmasks latent conduction disease that worsens with stress
• AV block developing with exercise suggests infranodal pathology and high risk

Electrophysiology Study (EPS)

• Invasive: Measures conduction intervals (AH interval = AV nodal conduction; HV interval = infranodal conduction)
• AH interval normal (<140 ms); HV interval prolonged (>55 ms): Infranodal disease
• Both prolonged: Combined disease
• Indications: Uncertain block location, evaluation of syncope, risk stratification
• Can assess pacemaker function and reserve, guide pacing decisions

Cardiac Imaging

• Echocardiography: Assess LV function, structural disease, infiltration
• Chest X-ray: Cardiomegaly, pulmonary congestion
• Cardiac MRI: Evaluate for infiltrative disease (sarcoidosis, amyloidosis), fibrosis pattern

Laboratory Studies

• Electrolytes: Hyperkalemia can cause AV block
• Thyroid function (TSH): Hypothyroidism-induced bradycardia
• Lyme serology: If endemic area and clinical suspicion
• Autoantibodies: Anti-Ro/SSA, anti-La/SSB if congenital AV block or connective tissue disease
• Troponin: Acute MI evaluation
• Drug levels: Digoxin toxicity (narrow therapeutic window)

Imaging Modalities for Specific Etiologies

• PET/FDG scan: Sarcoidosis cardiac involvement
• Chest CT: Lyme disease spirochete burden in endemic areas (research tool)

Asymptomatic Bradycardia/First-Degree AV Block

• Observation: No treatment required if asymptomatic with adequate rate
• Medication review: Discontinue offending agents (beta-blockers, calcium channel blockers, digoxin) if clinically feasible
• No pacemaker indicated: Unless progression documented or symptoms develop

Symptomatic Bradycardia (Sinus or SA Node Dysfunction)

Pharmacological Management

• Atropine 0.5-1 mg IV (nodal disease): First-line for acute symptomatic bradycardia
• Mechanism: Blocks muscarinic acetylcholine receptors, reducing parasympathetic brake
• Efficacy: High in nodal bradycardia (AV node-mediated), minimal in infranodal disease
• Caution: May precipitate tachycardia; risk of arrhythmias in acute MI

• Isoproterenol 1-4 mcg/min IV infusion: Beta-1 agonist
• Mechanism: Increases automaticity and AV nodal conduction
• Use: Temporizing measure before pacemaker insertion; useful in acute symptomatic bradycardia
• Disadvantage: Increases myocardial oxygen demand, risk of arrhythmias

• Epinephrine 2-10 mcg/min IV infusion: Alpha and beta agonist
• Alternative to isoproterenol; increases systemic vascular resistance in addition to inotropic effect
• Particularly useful if hypotension accompanies bradycardia

• Theophylline: Adenosine antagonist with weak chronotropic effects (rarely used)

Non-Pharmacological Management

• Pacemaker insertion: Definitive treatment for symptomatic bradycardia
• Indications:
• Symptomatic bradycardia unresponsive to drugs
• Sick sinus syndrome with symptomatic bradycardia
• Chronotropic incompetence (failure to increase heart rate with exercise)
• Any symptomatic bradycardia <40 bpm
• Temporary pacing: For acute symptomatic bradycardia/high-degree block pending permanent device
• Transcutaneous pacing: Non-invasive, used emergently
• Transvenous pacing: More comfortable, better long-term if prolonged support

Complications of the conduction disease itself

• Asystole and sudden cardiac death (emergency): infranodal block (Mobitz II, complete block with wide QRS) depends on an unreliable ventricular escape focus; if that focus fails, the result is prolonged asystole. Signaled by syncope without prodrome — the Stokes-Adams attack — or by long pauses on telemetry.
• Bradycardia-dependent polymorphic VT / torsades de pointes (emergency): long RR intervals prolong repolarization and permit early afterdepolarizations, especially with hypokalemia, hypomagnesemia, or QT-prolonging drugs. Signaled by pause-dependent ectopy and a long QT on the escape beats; treated with magnesium and rate support (pacing or isoproterenol) rather than more AV nodal blockade.
• Cardiogenic shock and pulmonary edema (emergency): fixed low rate with fixed stroke volume caps cardiac output; suggested by hypotension, cool extremities, altered mentation, rising lactate.
• Tachy-brady syndrome complications: the atrial fibrillation phase carries thromboembolic stroke risk, which is assessed by CHA₂DS₂-VASc and anticoagulated per the ACC/AHA/HRS atrial fibrillation guideline; rate control drugs then worsen the bradycardic phase, often forcing pacing.
• Trauma from syncope: head injury, hip fracture, motor vehicle crash.

Complications of treatment

• Atropine failure or harm: ineffective in infranodal block and in the denervated transplanted heart; in acute ischemia the induced tachycardia raises myocardial oxygen demand and can provoke ventricular arrhythmia.
• Catecholamine infusions (isoproterenol, epinephrine): ischemia and ventricular ectopy from increased demand and enhanced automaticity.
• Transcutaneous pacing: painful muscle capture and, critically, electrical spikes without mechanical capture — always confirm a pulse or arterial waveform, not just pacer artifact.
• Transvenous/permanent device placement: pneumothorax, pocket hematoma, lead dislodgement, RV perforation with tamponade (emergency — hypotension, pulsus paradoxus, JVD), and device infection/lead endocarditis (often Staphylococcus aureus), which per AHA guidance requires complete hardware extraction plus antibiotics, not antibiotics alone.
• Pacemaker syndrome: single-chamber ventricular pacing with retrograde atrial activation causes AV dyssynchrony — fatigue, dyspnea, cannon A waves; corrected by upgrading to dual-chamber pacing.
• Pacing-induced cardiomyopathy: high-burden RV apical pacing creates dyssynchronous activation and falling EF; ACC/AHA/HRS bradycardia guidance favors CRT or conduction-system pacing in such patients.

• The location of block, not the degree, drives management: nodal disease (Mobitz I, narrow QRS) is vagally modulated, atropine-responsive, and usually benign; infranodal disease (Mobitz II, wide QRS, prolonged HV interval) is atropine-*unresponsive* and can fail abruptly. Per the ACC/AHA/HRS bradycardia guideline, Mobitz II and third-degree block from non-reversible causes warrant a permanent pacemaker even if asymptomatic.
• Single best next step in the unstable patient: the AHA ACLS bradycardia algorithm sequence is atropine first, then — if no response — transcutaneous pacing and/or a chronotropic infusion (dopamine or epinephrine) as a bridge to transvenous or permanent pacing. Do not wait for a permanent device in a hypotensive patient.
• Buzzwords: progressive PR prolongation with grouped beating = Mobitz I (Wenckebach); unexpected dropped beat with a constant PR = Mobitz II; P waves marching through independent QRS complexes = third-degree block; cannon A waves with variable S1 = complete AV dissociation.
• The MI association examiners love: inferior MI (RCA, AV nodal artery) causes transient, atropine-responsive nodal block that rarely needs permanent pacing; anterior MI (LAD, septal branches) implies extensive septal necrosis with infranodal block and a far worse prognosis.
• Lyme carditis: young patient, endemic exposure, erythema migrans, high-grade AV block. Per IDSA/AAN/ACR Lyme disease guidance, treat with antibiotics (ceftriaxone for hospitalized high-grade block, doxycycline for milder disease) and use temporary pacing if needed — the block typically resolves, so a permanent pacemaker is the classic wrong answer.
• Always exclude reversible causes before implanting: drugs (beta blocker, non-dihydropyridine calcium channel blocker, digoxin, amiodarone), hyperkalemia, hypothyroidism, hypothermia, ischemia, elevated ICP. Digoxin toxicity with high-grade block calls for digoxin-specific antibody Fab fragments.
• Common distractors: asymptomatic sinus bradycardia or first-degree block in an athlete needs no workup and no pacemaker; atropine will not fix wide-complex infranodal block or the denervated transplanted heart (use isoproterenol/epinephrine and pacing); and pacer spikes on the monitor do not equal capture — confirm a pulse.
• Neonatal complete heart block points to maternal anti-Ro/SSA (and anti-La/SSB) antibodies from lupus or Sjögren syndrome.