# Types - 1st degree heart block - 2nd degree heart block - 3rd degree heart block ### 1st degree heart block - misnomer - conduction delay but not a block ![[Pasted image 20260527120125.png]] - ECG features - 1:1 P to QRS (P wave always followed by a QRS) - PR interval >0.2s (>5 small squares) but constant - Causes - vagal stimulation - high vagal tone (young patients, athletes, sleep) - inferior MI - abnormalities of AV node - age-related fibrosis (Lev/Lenegre) - AV nodal blockers - beta blocker, CCB, digoxin, amiodarone - Rare - myocarditis, digoxin toxicity, idiopathic fibrosis or underlying structural - No treatment required if asymptomatic - Withhold contributing drugs only if symptomatic or PR markedly prolonged (>0.3ms) - Good to know: Pseudo-pacemaker syndrome - Marked first degree block PR >0.3ms - Symptoms attributable to AV dyssynchrony - IIa pacing indication ### 2nd degree heart block ##### Morbitz Type I (Wenckebach) ![[Pasted image 20260527120241.png]] - Impaired conduction in ==AV node== (rarely infranodel) - Atrial impulses to ventricles is intermittently blocked -> atrial rate is greater than ventricular rate - ECG features - progressive increase in PR interval until a dropped QRS complex occurs - AV conduction recovers after this - Anatomical pathology is above the His bundle -> no intervention needed if asymptomatic - Causes - Inferior MI - AV nodal blockers - beta blocker, CCB, digoxin - high vagal tone (athletes, young patients - up to 5% of healthy young adult during sleep) - myocarditis - Nearly always normal in healthy individuals - May progress to complete heart block in patients with underlying heart disease - Treatment - No treatment required if asymptomatic and healthy - In haemodynamically compromised patients, - Atropine 0.5-1mg q3-5min IV to max dose of 3mg (will respond to atropine in most cases) - Isoprenaline/Adrenaline/Dopaine - pacing rarely required ##### Morbitz Type II AV block ![[Pasted image 20260527120312.png]] - Due to intermittent failure of AV conduction at the His bundle or bundle branches (i.e. infranodal almost always) - QRS is wide if block is infra-Hisian (~70%) - Narrow if intra-Hisian (~30%) - Almost always due to underlying cardiac disease - ACS involving left coronary artery - Idiopathic fibrosis of bundle branches - ECG features - PR interval remains constant but there is irregular intermittent failure of P-wave conduction (Atrial rate greater than ventricular rate) - Regular atrial rhythm (P-P interval) - PR usually prolonged but constant - QRS may be narrow or widened - Usually symptomatic - Canon A waves on JVP (AF has lack of A waves) - More likely to be associated with stroke, Stokes-Adams attack (syncope), slow ventricular rate and sudden death - Can progress to complete heart block (unpredictable) - Treatment - In haemodynamically compromised patients, - Pacing (transcutaneous/transvenous) - Isoprenaline/Adrenaline/Dopamine - Isoprenaline 20-40mcg IV bolus -> 0.5-20mcg/min (same dose as adrenaline) - Atropine 0.5 mg IV max 3mg (60% respond to atropine - may paradoxically worsen the block ratio by increasing atrial rate without improving infranodal conduction) - May still be tried but only while pacing is being set up ##### 2:1 AV block - Cannot be classified as Mobitz I vs II from a 2:1 strip in isolation — there is only one conducted PR to assess. - Clues to site of block: - Narrow QRS, normal PR on conducted beats, improves with atropine/exercise, worsens with carotid sinus massage = likely nodal (Mobitz I behaviour). - Wide QRS or BBB, worsens with atropine/exercise, improves with vagal manoeuvres = likely infranodal (Mobitz II behaviour, treat as such). - If in doubt, treat as Mobitz II and admit for monitoring. ##### High-grade (advanced) AV block - ≥2 consecutive non-conducted P waves with some preserved AV conduction (e.g. 3:1, 4:1). Treat as Mobitz II equivalent: monitored bed, pads on, cardiology, pacing pathway. ### 3rd degree (complete) heart block ![[Pasted image 20260527120339.png]] - complete blockade of A-V conduction - Causes - Degenerative/Idiopathic age-related fibrosis (Lev/Lenegre, most common) - Inferior MI - usually nodal, will usually resolve spontaneously within 7 days - Anterior MI - usually infranodal due to necrosis of His-Purkinje, worse prognosis - Drugs - digoxin, beta-blockers, CCBs, amiodarone - Myocardial fibrosis - Cardiac sarcoid and amyloid (consider in younger patients or atypical features) - Subsidiary pacemakers arise - His bundle -> Narrow QRS without any P waves - Left/right bundle branches -> Widen QRS with bundle branch block patterns - Also seen in up to 8% of inferior MI (often transient in such cases) - Can be associated with Sick Sinus Syndrome, Mobitz II block and transient second-degree block with new bundle branch or fascicular block - ECG features - AV dissociation - QRS may be narrow or widened depending on the block level - Ventricular escape pacemaker is at 20-50/min - Management - same as above (atropine rarely effective) - Pacing - Fist pacing if nothing else available - 60bpm - Transcutaneous pacing starting at 100mA and titrating up above capture - Transvenous pacing if resistant to isoprenaline, failure of transcutaneous pacing - PPM ultimately - Treat reversible causes (see below) - Note: Never treat third-degree heart block with ventricular escape beats using lignocaine or any agent that suppresses ventricular escape rhythms as this will suppress the already slow heart rate, resulting in reduced cardiac output ##### Reversible-cause specifics - Beta-blocker toxicity - high-dose glucagon (5–10 mg IV bolus, infusion 2–10 mg/h) - high-dose insulin euglycaemia therapy (HIET) - IV lipid emulsion if cardiac arrest from lipid-soluble agent. - CCB toxicity - calcium gluconate 10% 30 mL IV (or chloride 10 mL central) - HIET (insulin 1 unit/kg bolus then 0.5–1 unit/kg/h with dextrose to maintain euglycaemia) - vasopressors. - Digoxin toxicity - digoxin-specific Fab fragments (DigiFab) - dose by ingested amount, serum level, or - empirically 5 vials acute / 2 vials chronic. - No need to avoid calcium ("stone heart" — disputed but historical caution). - Correct K+. - BRASH syndrome (Bradycardia, Renal failure, AV-blocker, Shock, Hyperkalaemia) - synergistic bradycardia from AV-nodal blocker plus AKI plus hyperkalaemia - Treat K+ aggressively (calcium, insulin/dextrose, salbutamol, dialysis) - volume resuscitate - vasopressors. - Pacing often fails until K+ corrected. - Hyperkalaemia - calcium gluconate 10% 30 mL IV first if any ECG change (peaked T, wide QRS, sine wave) - insulin/dextrose - salbutamol - sodium bicarb if acidotic - dialysis if severe/anuric (eTG Toxicology, 2024). ![[Pasted image 20260527122150.png]]