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Heart Block

⚡ Severe Bradycardia - Management (UK ALS)

Step	What you do (OSCE/ALS wording)	Key notes / triggers
1) Recognise severity	🔍 Confirm bradycardia on monitor/ECG, check pulse + BP, assess symptoms.	🚨 Treat as unstable if any adverse features: shock, syncope, MI/ischaemia, acute HF.
2) Call for help + monitor	📞 Call resus team/senior help, attach defib/pacing pads, continuous ECG + SpO₂ + NIBP.	Have pacing ready early if high-grade AV block suspected.
3) ABCDE + access	🫁 ABCDE, oxygen only if hypoxic, 2 IV cannulas, take bloods (U&E, Mg, glucose, VBG/ABG if unwell).	Look for reversible causes: drug toxicity (β-blocker, digoxin, CCB), hyperkalaemia, hypoxia, MI.
4) ECG	📈 Get a 12-lead ECG (rhythm + PR/QRS, ischaemia, AV block).	High-risk ECG: Mobitz II, complete heart block, broad QRS escape, long pauses.
5) First-line drug	💉 Atropine 500 micrograms IV; repeat as needed to max 3 mg.	Less effective in infra-His block; avoid/seek specialist advice in transplanted heart.
6) If no response / unstable	⚡ Start transcutaneous pacing (with analgesia/sedation support) while preparing for definitive pacing.	Don’t delay pacing if high-grade AV block or recurrent syncope/shock.
7) If pacing not available / bridging	💧 Start an infusion per local protocol: adrenaline 2–10 micrograms/min OR isoprenaline 5 micrograms/min OR dopamine.	Use as a bridge to pacing; monitor for tachyarrhythmia/ischaemia.
8) Definitive management	🧑‍⚕️ Arrange temporary transvenous pacing ± permanent pacemaker; treat cause (MI pathway, stop culprit drugs, treat hyperkalaemia).	Complete heart block / Mobitz II usually needs pacing; document decisions + escalation.

⚡ Heart block (AV block) describes delayed or failed conduction from atria → ventricles. A slow heart rate - cunt QRS complexes can lead to low blood pressure and even shock. This may need emergent treatment. Exam focus: recognise the ECG pattern, assess stability, correct reversible causes, and escalate early for pacing when needed.

🧠 What “heart block” actually means

🔌 The AV node–His–Purkinje system is the only normal electrical bridge from atria to ventricles.
⛔ “Block” can be partial (delay or intermittent failure) or complete (no impulses conducted).
🫀 When ventricles don’t receive atrial impulses, they rely on an escape rhythm:
- ⬆️ Higher (junctional) escape → faster rate, usually narrow QRS.
- ⬇️ Lower (ventricular) escape → slower rate, usually wide QRS.

📊 First vs Second vs Third Degree AV Block (high-yield comparison)

Type	ECG hallmark	What you do (exam / ward)
1️⃣ First-degree AV block	PR > 200 ms, constant; every P followed by QRS	Usually observe ✅; review AV-nodal drugs; check U&E (K+/Mg), TFTs; treat underlying cause
2️⃣a 🔁 Mobitz I (Wenckebach)	Progressive PR prolongation → then dropped QRS	If stable: remove triggers/hold AV-nodal drugs, observe; if symptomatic/unstable: manage bradycardia + senior/cardiology review
2️⃣b ⚠️ Mobitz II	Fixed PR with intermittent dropped QRS (often wide QRS)	High-risk 🚨: urgent cardiology; prepare for pacing (often pacing-likely even if transient); treat instability per ALS (pacing preferred)
3️⃣ 🚑 Third-degree (complete) heart block	AV dissociation: P waves and QRS regular but independent; escape rhythm (narrow if high, wide if low)	Time-critical: ABCDE, stop causative drugs, treat reversible causes; atropine may help if nodal; isoprenaline/temporary pacing if needed → usually permanent pacemaker

🚨 Red flags that should make you escalate immediately

🧠 Syncope, recurrent presyncope, confusion
🫀 Hypotension, shock, chest pain, acute heart failure, ischaemic ECG changes
🧍 Very slow ventricular rate (especially < 40 bpm) or broad-complex escape rhythm
⚡ Mobitz II, high-grade AV block (multiple consecutive dropped beats), or complete heart block

🧩 Causes of AV block (exam-friendly table)

Category	Examples	Clues
❤️ Ischaemia / MI	Inferior MI (RCA → AV nodal branch), anterior MI (His–Purkinje damage)	Inferior MI block may respond to atropine and can be transient; anterior MI block is often extensive disease and higher risk.
💊 Drugs	β-blockers, verapamil/diltiazem, digoxin, amiodarone (and other antiarrhythmics)	Recent dose change, renal impairment (digoxin), bradycardia + hypotension.
🧓 Degenerative conduction disease	Fibrosis/sclerosis of the conduction system (age-related)	Older patient, bundle branch block, progressive conduction delay.
🦠 Infective / inflammatory	Myocarditis, endocarditis (peri-annular abscess), Lyme disease, diphtheria	Fever, raised inflammatory markers, new murmur, travel/tick exposure.
🧬 Infiltrative / metabolic	Sarcoid, amyloid, haemochromatosis; hyperkalaemia; hypothyroidism	Systemic features; abnormal K+ / thyroid; unexplained conduction disease.
🛠️ Post-procedure	TAVI, valve surgery, septal myectomy, ablation	New conduction delay after intervention.

🔎 Investigations (what to send in real life + OSCE)

📈 12-lead ECG + rhythm strip (confirm type of block; look for ischaemia).
🩺 Obs + perfusion: BP, mental status, cap refill; signs of heart failure.
🧪 Bloods: U&E (K+), Mg, Ca, glucose, FBC, CRP, TFTs; troponin if ACS suspected; digoxin level if relevant.
🖥️ Echocardiography if structural disease/MI suspected or ongoing instability.
🧷 Consider continuous monitoring / telemetry and cardiology review for unexplained or high-grade block.

⚡ Acute management of bradycardia due to AV block (UK ALS-style)

🚑 If unstable: treat as a peri-arrest bradycardia. Start with ABCDE + attach monitoring, then correct reversible causes while preparing for pacing.

Step	What you do	Why
1️⃣ Call for help	📞 Senior + cardiology; if peri-arrest, resus team/ALS response.	High-grade AV block can deteriorate rapidly.
2️⃣ Stabilise	🫁 Oxygen if hypoxic, IV access, fluids if shocked, treat pain, correct electrolytes.	Improve perfusion while definitive therapy is arranged.
3️⃣ Atropine (if appropriate)	💉 Atropine 500 micrograms IV, repeat to a maximum of 3 mg if needed.	May improve AV nodal block (often helpful in inferior MI / nodal disease).
4️⃣ If atropine fails / high-risk block	⚡ Prepare transcutaneous pacing early; consider isoprenaline infusion as a bridge if pacing not immediately available (specialist / local protocol).	In infranodal block, atropine may be ineffective; pacing prevents collapse.
5️⃣ Definitive treatment	🧷 Temporary pacing (wire) if needed → usually permanent pacemaker for persistent high-grade/complete AV block.	Prevents recurrence and improves long-term safety.

🧠 Teaching pearls (sounds clever in vivas)

🧬 Nodal vs infranodal block: nodal block is more likely to respond to atropine and has a narrow QRS; infranodal block is more dangerous and often needs pacing.
🫀 Why syncope happens: slow escape rhythms reduce cardiac output → cerebral hypoperfusion (Stokes–Adams attacks).
🧯 Reversible causes matter: hyperkalaemia, AV nodal drugs, and ischaemia are the “big three” to look for quickly.

⛔ Complete (Third-degree) Heart Block - exam-ready

🚨 Complete heart block can be a medical emergency requiring atropine and pacing. It is defined by complete failure of conduction between atria and ventricles, so the ventricles rely on an escape rhythm.

ℹ️ About

🔌 There is a complete failure of communication between atria and ventricles.
💓 Atria depolarise regularly (P waves), but do not stimulate the ventricles.
🫀 Ventricles beat at an intrinsic escape rate, often ~30–40 bpm if ventricular, faster if junctional.
📏 The higher the escape rhythm (closer to AV node), the faster the rate and the narrower the QRS.

📈 ECG features

Atrial rate: typically 60–100/min (sinus), independent of the ventricular rhythm (“dissociation”).
Ventricular rate: depends on escape focus:
- 🐢 Ventricular escape typically ~20–40/min (often wide QRS).
- ⚡ Junctional escape typically ~40–60/min (often narrow QRS).
Rhythm: atrial and ventricular rhythms are each regular but independent.
PR interval: no fixed PR relationship (by definition).
P waves: usually normal morphology (unless AF/atrial flutter etc.).
QRS: narrow suggests higher escape; wide suggests lower (infranodal) escape.
🧠 Note: If the atrial rhythm is atrial fibrillation, there are no P waves-you’ll see a slow regular escape rhythm with AV dissociation.

🧩 Causes

❤️ Inferior MI (RCA involvement affecting AV nodal blood supply) - can be transient.
🧱 Anterior MI - suggests extensive myocardial/conduction system damage; often more unstable.
💊 Medications: β-blockers, digoxin, rate-limiting calcium-channel blockers (verapamil/diltiazem), and some antiarrhythmics.
🧓 Degenerative fibrosis/sclerosis of conduction tissue (older adults).
🦠 Myocarditis, endocarditis (incl. peri-annular abscess), post-surgery, rheumatic fever.
🪲 Lyme disease, diphtheria (rare in UK but classic exam causes).

🩺 Clinical features

🚑 Acute: symptomatic bradycardia, low BP, shock, syncope (Stokes–Adams), acute heart failure.
🧍 Chronic: reduced exercise tolerance, fatigue, dizziness/presyncope.
🌊 JVP: cannon “a” waves can occur due to atrial contraction against a closed tricuspid valve.

🔎 Investigations

📈 ECG (diagnostic) + continuous monitoring.
🧪 U&E (K+), Mg/Ca, TFTs, glucose; troponin if ACS suspected; drug levels where relevant (e.g., digoxin).
🖥️ Echo if structural disease/MI suspected or ongoing instability.

💊 Management

🛟 ABCDE and resuscitation as needed; treat shock/ACS in parallel.
💉 Consider atropine, isoprenaline infusion (bridge), and temporary pacing (transcutaneous → transvenous) depending on stability and ECG features.
🧯 Treat reversible causes: stop AV nodal drugs, correct hyperkalaemia, manage MI/myocarditis/infection.
🧷 Most patients with persistent complete heart block will require a permanent pacemaker after specialist assessment.

📚 References (UK + core)

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