Cardiac arrhythmia management in the ICU · ICU Topics

In one line

Arrhythmia in ICU — 20% of patients. Unstable (hypotension, shock, ischaemia, heart failure, altered mental status) → immediate synchronised cardioversion (VT) or unsynchronised defibrillation (VF/pVT). Stable → identify and treat cause (electrolytes, ischaemia, sepsis, drugs). AF (#1): rate control (metoprolol, diltiazem) ± rhythm control (amiodarone, DC cardioversion); anticoagulate per CHA2DS2-VASc. Atrial flutter: same as AF; cardiovert at lower energy (50–100 J biphasic). SVT: vagal manoeuvres → adenosine 6→12→12 mg. VT/VF: defibrillate + amiodarone 300 mg (lidocaine alternative). Torsades: IV magnesium 2 g, stop QT-prolonging drugs, overdrive pacing. Bradycardia: atropine 0.5 mg → adrenaline/isoprenaline infusion → transcutaneous → transvenous pacing. Check K+ and Mg2+ FIRST.

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Cinematic ICU scene of a cardiac monitor showing atrial fibrillation degenerating into ventricular tachycardia, a 12-lead ECG printout and defibrillator pads on the crash trolley, clinical-blue lighting, no faces, no text — FigureThe arrhythmia in the ICU — the first decision is the haemodynamic stability, not the ECG diagnosis. The unstable → the immediate cardioversion or the defibrillation; the stable → the systematic diagnosis and the pharmacology.

ICU arrhythmia classification: AF, flutter, SVT, VT/VF, bradyarrhythmia and AV block — educational panel — FigureClassify first by haemodynamic stability, then by QRS width and regularity.

Arrhythmia mechanisms: re-entry, triggered activity, automaticity; ICU triggers including ischaemia, electrolytes, catecholamines, drugs — educational diagram — FigureFix reversible triggers — K, Mg, ischaemia, fever, inotropes — before stacking antiarrhythmics.

Arrhythmia management pathway: unstable cardioversion or defibrillation, stable rate versus rhythm control, ACLS shockable algorithm — clinical-blue infographic — FigureUnstable: electricity first. Stable: rate or rhythm control with electrolyte optimisation and trigger removal.

General approach — first principles

The first decision in any arrhythmia is NOT the ECG diagnosis — it is haemodynamic stability. This single decision bifurcates management: the unstable patient needs an electrical therapy immediately, regardless of rhythm; the stable patient has time for systematic diagnosis and pharmacological management. [1]

Universal arrhythmia algorithm

Step 1 — Assess haemodynamic stability

Unstable = ANY of: hypotension (SBP <90), acutely altered mental status, signs of shock (cold, mottled, oliguric), ischaemic chest pain, acute heart failure/pulmonary oedema. If unstable and tachyarrhythmia → immediate SYNCHRONISED cardioversion. If unstable and VF/pulseless VT → UNSYNCHRONISED defibrillation + CPR. Do NOT wait for IV access, drugs, bloods, or a 12-lead ECG.

Step 2 — 12-lead ECG + rhythm strip

In the stable patient, obtain a 12-lead ECG. Key questions: (a) Regular or irregular? (b) Narrow (<120 ms) or wide (>120 ms) QRS? (c) Is atrial activity visible (P waves, flutter waves, fibrillation)? (d) Rate? This 2×2 grid (regular/irregular × narrow/wide) generates the differential diagnosis.

Step 3 — Identify and treat the precipitant

POCKET-ACID mnemonic: Potassium/magnesium/calcium, Oxygen (hypoxia), Cardiac ischaemia, Ketoacidosis and other metabolic, EPS/drugs (inotropes, bronchodilators, QT-prolonging), Alcohol/sepsis/stress (catecholamine surge), Ischaemia/Infection, Dehydration/hypovolaemia. Send K+, Mg2+, Ca2+, troponin, VBG (lactate, K+), TFTs. Review the drug chart — inotropes, dopamine, dobutamine, milrinone, salbutamol, azoles, macrolides, antipsychotics all provoke arrhythmia.

Step 4 — Choose rate vs rhythm control

For AF/flutter: rate control is usually first-line (beta-blocker or diltiazem). Rhythm control (cardioversion, amiodarone) if: haemodynamically unstable, heart failure (tachycardia-induced cardiomyopathy), symptomatic despite rate control, or first presentation <48 h duration. EAST-AFNET 4: early rhythm control (within 1 year) improves outcomes in newly diagnosed AF.

Step 5 — Anticoagulation and long-term plan

Assess stroke risk (CHA2DS2-VASc) and bleeding risk (HAS-BLED). In ICU, balance against bleeding (recent surgery, coagulopathy, procedures). New-onset AF <48 h: anticoagulate if high risk. AF >48 h or unknown duration: anticoagulate for 3 weeks before AND 4 weeks after cardioversion (or TOE-guided). Involve cardiology for ablation/definitive management.

[1] [6]

Arrhythmia epidemiology in ICU

12–20%

ICU patients

Develop arrhythmia during admission

8–10%

New-onset AF

In medical/surgical ICU; up to 40% post-cardiac surgery

2–4×

Mortality risk

New-onset AF in septic shock increases mortality

50 J

Cardioversion energy

Atrial flutter — lower than AF (120–200 J)

[12]

Atrial fibrillation

AF is the commonest arrhythmia in ICU and a high-yield exam topic. New-onset AF in the ICU is not benign — it independently predicts longer ventilation, longer stay, stroke, and death. The intensivist's task is threefold: decide rate vs rhythm control, anticoagulate appropriately, and treat the precipitant. [1]

Pathophysiology and ICU triggers

AF is sustained by trigger firing (usually from the pulmonary vein ostia) and an arrhythmogenic substrate (atrial dilation and fibrosis). ICU patients have a surplus of both: catecholamine surges (sepsis, pain, agitation, inotropes), volume overload and atrial stretch, electrolyte depletion (K+, Mg2+ from diuresis and redistribution), hypoxia, acidosis, sympathetic withdrawal/withdrawal, and direct atrial injury (post-cardiotomy, central line/PA catheter irritation). [1]

[1]

Rate versus rhythm control

Rate control (first-line in most ICU AF)

Beta-blocker or non-DHP CCB

Beta-blocker: metoprolol 5 mg IV over 2 min, repeat q5 min × 3 (max 15 mg); OR esmolol 500 mcg/kg loading then 50–200 mcg/kg/min (short half-life — ideal to titrate in unstable/anaesthetised patients)
OR non-dihydropyridine CCB: diltiazem 0.25 mg/kg IV (≈20 mg) over 2 min, repeat 0.35 mg/kg after 15 min if needed, then infusion 5–15 mg/h. AVOID verapamil/diltiazem in HFrEF (negative inotrope)
OR digoxin 500 mcg IV over 30 min (additive with beta-blocker; slow onset 2–6 h; useful in HF/AF and when beta-blockers contraindicated). AVOID in renal failure, hypokalaemia, WPW
Target: HR <110 (lenient) or <80 (strict). RACE II: lenient is non-inferior and easier to achieve; strict reserved for ongoing symptoms or tachycardia-mediated cardiomyopathy
Caveat: rate control is harder in hyperadrenergic states (sepsis, post-op) — may need combination therapy or amiodarone

Rhythm control (cardioversion)

If unstable, HF, failed rate control, <48 h

Pharmacological: amiodarone 300 mg IV over 20–60 min, then 900 mg/24 h infusion. Useful in HF, structural disease, renal failure. Slower than electrical (6–24 h)
OR flecainide 2 mg/kg IV over 10 min (AVOID in structural/IHD — pro-arrhythmic)
OR ibutilide 1 mg IV over 10 min (QT prolongation — do NOT use if QTc >440 ms)
Electrical: synchronised DC cardioversion — AF: 120–200 J biphasic (escalating); flutter: 50–100 J. Sedate (propofol/ketamine + midazolam) if awake. Anterior–posterior pads more effective
EAST-AFNET 4 (NEJM 2020): early rhythm control within 1 year of diagnosis improved composite CV outcome (HR 0.79). Strengthens case for rhythm control in newly diagnosed AF

[1] [4] [7]

Practical AF management in the ICU

1. Stabilise — is the patient unstable?

Hypotension/shock/ischaemia/HF → immediate synchronised DC cardioversion (200 J biphasic, escalating). Ensure sedation if awake. Pre-cardioversion anticoagulation is NOT a reason to delay if unstable.

2. Identify and correct precipitant

Check K+ (target >4.0), Mg2+ (>0.8), Ca2+. Treat hypoxia, sepsis, pain, agitation, withdraw inotrope if possible. Give K+/Mg2+ replacement even if borderline (magnesium potentiates rate control). Stop dopamine if causing the AF — switch to noradrenaline.

3. Rate control

Metoprolol 5 mg IV q5 min × 3 (avoid in severe asthma, decompensated HF with low EF). If HF/AF: diltiazem is safer (or digoxin/amiodarone). Target HR <110 (lenient) or <80 if HF/tachycardiomyopathy.

4. Rhythm control if indicated

Amiodarone 300 mg IV over 20–60 min, then 900 mg/24 h. OR synchronised DC cardioversion if AF duration <48 h (or TOE-guided to exclude LAA thrombus if >48 h/unknown).

5. Anticoagulate

CHA2DS2-VASc ≥2 in men (≥3 women) → anticoagulate. In ICU: therapeutic LMWH (enoxaparin 1 mg/kg BD, reduce for renal) or UFH (better if procedural/reversible). Switch to DOAC once stable and oral route restored. Hold anticoagulation only for active bleeding/procedures — NOT for rhythm control alone.

6. Long-term plan

Continue rate or rhythm control. Most new-onset ICU AF reverts within 48 h of treating the precipitant. Refer cardiology for ablation if recurrent/symptomatic. Initiate GDMT for HFrEF (beta-blocker, MRA, SGLT2i, ARNI — "four pillars") — these reduce AF.

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Anticoagulation in the ICU patient with AF

Anticoagulation decisions in ICU are harder than the outpatient CHA2DS2-VASc calculation because of competing bleeding risk (recent surgery, coagulopathy, central lines, planned procedures) and rapidly changing renal function. [1]

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CHA2DS2-VASc (stroke risk)

Score → anticoagulate if ≥2 (men) / ≥3 (women)

**C** — CHF/LV dysfunction (1)
**H** — Hypertension (1)
**A2** — Age ≥75 (2)
**D** — Diabetes (1)
**S2** — Stroke/TIA/thromboembolism (2)
**V** — Vascular disease (MI, PAD, aortic plaque) (1)
**A** — Age 65–74 (1)
**Sc** — Sex category female (1)
Score 0 (men) / 1 (women): omit. Score 1 (men) / 2 (women): consider. ≥2 (men) / ≥3 (women): anticoagulate.

HAS-BLED (bleeding risk)

≥3 = high bleeding risk — review/correct, not a reason to withhold

**H** — Hypertension (SBP >160) (1)
**A** — Abnormal renal/liver function (1 each)
**S** — Stroke history (1)
**B** — Bleeding history/predisposition (1)
**L** — Labile INR (not applicable to DOAC) (1)
**E** — Elderly (>65) (1)
**D** — Drugs (antiplatelet/NSAID) or alcohol excess (1)
A high score is NOT a reason to deny anticoagulation — it is a reason to correct modifiable factors (BP, NSAIDs, alcohol).

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Specific ICU scenarios in AF

Post-cardiac surgery AF (POAF): occurs in 30–40% of CABG/valve patients, peaks on day 2–3. Prophylaxis: amiodarone or beta-blocker (restore if withheld). Treat: rate control + anticoagulate (high stroke risk). Usually self-limited (<2 months) but anticoagulate for at least the perioperative period.
Sepsis-associated AF: reflects catecholamine surge + electrolyte loss. Correct the sepsis, replace Mg2+/K+, switch dopamine to noradrenaline. Beta-blockade in septic shock is contentious — esmolol (titratable) preferred if needed. AF usually reverts with recovery.
AF with HFrEF: AVOID diltiazem/verapamil (negative inotrope). Use digoxin, amiodarone, or a cardioselective beta-blocker (metoprolol/bisoprolol). Long-term: beta-blocker + MRA + SGLT2i + ARNI ("four pillars") reduce AF burden and mortality.
AF with WPW (pre-excited): AVOID AV-nodal blockers (adenosine, verapamil, diltiazem, digoxin, beta-blocker) — they preferentially block the AV node and allow unrestricted antegrade conduction down the accessory pathway → pre-excited AF → VF. Use synchronised cardioversion if unstable, or procainamide/flecainide/ibutilide if stable (block the accessory pathway).
Thyroid storm with AF: high-output, fast AF. Treat the storm (PTU, iodine, beta-blocker, steroids) — AF reverts with euthyroidism. Propranolol/esmolol preferred (blocks T4→T3 conversion). [1]

Atrial flutter

Atrial flutter is a macro-reentrant atrial tachycardia, classically around the cavotricuspid isthmus (typical, counterclockwise — "sawtooth" flutter waves at 300/min in inferior leads, 2:1 block → ventricular rate 150). Management mirrors AF in most respects, but with three key differences. [1]

[1]

Atrial flutter management

1. Identify typical flutter

Sawtooth flutter waves (best in II, III, aVF, V1) at ~300/min. Usually 2:1 AV block → ventricular rate ~150. If rate is exactly 150 with regular narrow complex — flutter until proven otherwise. Carotid sinus massage/adenosine (transient AV block) unmask the flutter waves.

2. Stability assessment

Unstable → synchronised DC cardioversion at 50–100 J biphasic. Stable → proceed to pharmacological management.

3. Rate control

Beta-blocker (metoprolol, esmolol) or diltiazem. Often inadequate — flutter circuits are robust. Add digoxin or consider amiodarone.

4. Rhythm control

Synchronised cardioversion 50–100 J (most reliable). OR ibutilide 1 mg IV (effective but QT-prolonging — do NOT use if QTc >440 ms). OR overdrive atrial pacing if a permanent pacemaker/atrial wire in situ (post-cardiac surgery).

5. Anticoagulation

Same as AF — CHA2DS2-VASc. Anticoagulate before/after cardioversion per AF rules.

6. Definitive cure

Cavotricuspid isthmus ablation is curative for typical flutter (success >90%) — refer for electrophysiology once the ICU insult resolves.

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Supraventricular tachycardia (SVT)

SVT refers to any tachycardia originating at or above the AV node. In practice the ICU SVT is AV nodal re-entrant tachycardia (AVNRT, ~60%) or AV re-entrant tachycardia (AVRT, e.g. WPW, ~30%), both presenting as a regular narrow-complex tachycardia at 150–250/min with no visible P waves. [1]

AVNRT (commonest SVT)

AV node has dual pathways

Mechanism: dual AV nodal pathways (slow and fast) form a re-entrant circuit within the AV node
ECG: regular narrow QRS at 150–250/min, P waves buried in QRS or pseudo R' in V1 / pseudo S in inferior leads (retrograde P)
No accessory pathway — antegrade AND retrograde via AV node
Cardiac arrest risk: low. Treat with AV-nodal blockade.

AVRT / WPW

Accessory pathway

Mechanism: accessory pathway connects atrium to ventricle (e.g. bundle of Kent in WPW) — re-entry via AV node + pathway
Orthodromic AVRT: antegrade AV node, retrograde pathway → narrow QRS, regular
Antidromic AVRT: antegrade pathway → WIDE QRS (looks like VT) — dangerous
WPW with AF: chaotic broad irregular QRS — DO NOT give adenosine/CCB/digoxin (risk of VF). Cardiovert or use procainamide/flecainide.

SVT termination — the adenosine protocol

1. Vagal manoeuvres (first-line, stable)

Modified Valsalva: forceful expiration against closed glottis for 15 s while semi-recumbent, then reposition supine with passive leg raise (or cough, carotid sinus massage if no bruits). Terminates ~25% of AVNRT. Establish IV access and run a continuous ECG strip during the manoeuvre.

2. Adenosine 6 mg rapid IV bolus

Draw up 6 mg, follow IMMEDIATELY with a 20 mL saline flush via a large proximal vein (antecubital fossa). Warn the patient: "you will feel a sense of doom, chest tightness, flushing — this lasts 10–15 s". Run continuous ECG. Adenosine half-life <10 s — speed of administration is critical.

3. Adenosine 12 mg if no response

If 6 mg fails to terminate, give 12 mg by the same rapid technique after 1–2 min. Use a 3-way tap or dual-syringe push technique to ensure the bolus reaches the heart in <5 s.

4. Adenosine 12 mg — second attempt

A second 12 mg dose can be given if the first 12 mg produced partial AV block but no termination. Maximum single dose 12 mg. Some patients need higher doses (18–24 mg) or are adenosine-resistant.

5. If adenosine fails or contraindicated

Verapamil 5 mg IV over 2 min (AVOID in HFrEF, broad-complex tachy, WPW). OR diltiazem. OR metoprolol 5 mg IV. OR amiodarone 300 mg IV if HF/structural disease. Synchronised DC cardioversion 50–100 J if unstable.

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Adenosine — pharmacology and safety

Mechanism: agonist at A1 receptors in the AV node → transient complete AV block (3–10 s).
Onset/offset: seconds (half-life <10 s) — administer via proximal IV with rapid saline flush.
Contraindications: asthma/COPD with severe bronchospasm (A2B receptors cause bronchoconstriction), 2nd/3rd-degree AV block, sick sinus syndrome, denervated transplanted heart (exaggerated response), WPW with AF (may precipitate VF by preferentially blocking AV node).
Important diagnostic use: in a stable regular broad-complex tachycardia of uncertain origin, adenosine can be used diagnostically — if it terminates the rhythm it was SVT with aberrancy; if it transiently reveals underlying VT it confirms VT. BUT this should only be done with full resuscitation facilities, as adenosine in true VT can degenerate to VF.
Interactions: dipyridamole potentiates adenosine (reduce dose); methylxanthines (theophylline, caffeine) antagonise it (increase dose); carbamazepine increases AV block risk.

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Ventricular arrhythmias

Ventricular arrhythmias in ICU are nearly always secondary — ischaemia, electrolyte derangement, drug toxicity, or the substrate of structural heart disease (post-MI scar, cardiomyopathy). The intensivist must distinguish monomorphic VT (single reentrant circuit, uniform QRS) from polymorphic VT (multiple foci, varying QRS axis), and from VF (disorganised, no identifiable QRS). [1]

Monomorphic vs polymorphic VT

Monomorphic VT

Uniform, regular wide QRS

Regular, wide (>120 ms) QRS at 100–250/min, uniform morphology
Mechanism: scar-related reentry (post-MI, cardiomyopathy, ARVC) OR bundle branch reentry OR idiopathic (RVOT, fascicular)
AV dissociation, capture beats, fusion beats = pathognomonic (but often absent)
Stable: amiodarone 150 mg IV over 10 min, then infusion 900 mg/24h. Alternatives: procainamide, lidocaine. Unstable: synchronised cardioversion 100 J escalating.
Prognosis depends on substrate — post-MI scar VT ablation/ICD often indicated.

Polymorphic VT

Varying QRS morphology — ask: is QT long?

Irregular, rapidly varying QRS morphology/axis at 200–300/min
Two forms by QT: (1) **Torsades de Pointes** — prolonged QTc (>440 m / >460 f), twisting QRS around baseline, bradycardia-dependent. (2) **Normal-QT polymorphic VT** — usually ischaemia-driven (acute MI), or catecholaminergic (CPVT)
Torsades treatment: IV magnesium 2 g, STOP all QT-prolonging drugs, correct K+ (>4.5), overdrive pacing / isoprenaline if bradycardia-dependent
Normal-QT polymorphic VT: treat ischaemia (PCI), beta-blockade, correct electrolytes. Often degenerates to VF — be ready to defibrillate.

[2]

Stable vs unstable VT

The defining decision in VT is haemodynamic stability: [1]

VT management algorithm

1. Is the patient pulseless?

NO pulse with VT = pulseless VT = cardiac arrest → UNSYNCHRONISED defibrillation 200 J biphasic immediately + CPR + ALS algorithm (adrenaline 1 mg q3–5 min, amiodarone 300 mg after 3rd shock).

2. Is the patient unstable (but with a pulse)?

Hypotension/shock/ischaemia/HF/altered mental status with a pulse → SYNCHRONISED DC cardioversion 100 J biphasic escalating (100→150→200 J). Sedate (propofol/ketamine + midazolam) if awake. Ensure the defibrillator is in SYNCH mode (syncs to R wave) — unsynchronised shock during the T wave can induce VF.

3. Stable VT — pharmacological termination

Amiodarone 150 mg IV over 10 min (then 1 mg/min × 6 h, then 0.5 mg/min). OR procainamide 20–50 mg/min until response/toxicity (hypotension, QRS widening 50%). OR lidocaine 1–1.5 mg/kg IV (repeat to 3 mg/kg). If fails → synchronised cardioversion.

4. Identify and treat the cause

Acute ischaemia → urgent PCI. Electrolytes → correct K+/Mg2+/Ca2+. Drug toxicity (digoxin, TCAs, cocaine) → specific antidotes. Long QT → stop offending drugs. Cardiomyopathy/scar → ICD referral.

5. Electrical storm — recurrent VT

≥3 episodes of VT/VF in 24 h. Treatment: beta-blockade (metoprolol/esmolol — most effective single agent), amiodarone + lidocaine infusion, deep sedation (propofol reduces sympathetic tone), correct K+/Mg2+, consider mechanical support (IABP/VA-ECMO) if cardiogenic. Ablation if scar-mediated.

[2] [6]

Amiodarone vs lidocaine for VT/VF

Amiodarone (first-line)

Class III (mixed I–IV)

Mechanism: blocks K+ channels (Class III) + Na+ (I) + beta (II) + Ca (IV) — broad-spectrum
Dose: cardiac arrest 300 mg IV after 3rd shock, 150 mg after 5th; stable VT 150 mg over 10 min then infusion
ALIVE trial (NEJM 2002): amiodarone superior to lidocaine for shock-resistant VF — survival to hospital 22.8% vs 12.0%
ARREST trial (NEJM 1999): amiodarone improved survival to hospital vs placebo in OHCA VF (44% vs 34%)
Acute SE: hypotension (solvent — give slowly), bradycardia. Chronic: pulmonary fibrosis, thyroid dysfunction, hepatitis, corneal deposits, photosensitivity, blue-grey skin, peripheral neuropathy. QT prolongation (low torsades risk as also blocks Ca).

Lidocaine (alternative)

Class Ib

Mechanism: fast Na+ channel blocker (binds inactivated channels — preferential in ischaemic tissue)
Dose: 1–1.5 mg/kg IV bolus, repeat 0.5–0.75 mg/kg q5–10 min to max 3 mg/kg, then infusion 1–4 mg/min
Most useful for ischaemic VT (binds preferentially to depolarised ischaemic myocardium)
SE: CNS — tinnitus, perioral tingling, seizures, altered mental state (dose-dependent). Avoid in severe hepatic disease, 2nd/3rd-degree block.
On the way out for cardiac arrest (amiodarone preferred) but still useful for ischaemic VT and amiodarone-intolerant patients.

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Torsades de Pointes

Torsades is polymorphic VT with prolonged QTc, classically with a twisting QRS axis around the baseline and bradycardia dependence (long-short initiating sequences, "pause-dependent"). It is the cardiac arrest rhythm you can actively cause and actively terminate. [1]

Torsades de Pointes — recognise and treat

Recognise

Polymorphic VT with QTc prolongation (>440 m / >460 f) on baseline ECG. Twisting QRS amplitude around isoelectric baseline. Often "pause-dependent" — long-short RR interval sequence precedes each episode (e.g. post-PVC pause). May be self-terminating or degenerate to VF.

IV magnesium sulphate 2 g over 10 min

FIRST-LINE and works even when serum Mg is normal — magnesium suppresses early afterdepolarisations (the trigger for torsades) by blocking Ca channels. Repeat 2 g if recurrent (up to 4–6 g total). Serum level is NOT a guide to efficacy.

STOP all QT-prolonging drugs

Review every drug: macrolides (erythro/clarithro/azithro), fluoroquinolones (moxifloxacin worst), antifungals (fluconazole), antipsychotics (haloperidol, droperidol, ziprasidone), methadone, antiarrhythmics (sotalol, amiodarone, quinidine, procainamide, ibutilide), TCAs, ondansetron. Use www.crediblemeds.org / www.qtdrugs.org for the full list. Stop one — stop them all.

Correct potassium aggressively

Target K+ >4.5 mmol/L (higher than usual — hypokalaemia prolongs QT and worsens torsades). Replace orally and IV.

Accelerate the heart rate (overdrive suppression)

Torsades is bradycardia-dependent — accelerating HR shortens QT and terminates the rhythm. Options: (a) isoprenaline infusion 1–4 mcg/min (if no ischaemia), (b) temporary pacing at 90–110 bpm (most reliable — transvenous if sustained), (c) atropine 0.5–1 mg (less reliable). Pacing rate should be set to keep QTc as short as possible.

If degenerates to VF — defibrillate

Unsynchronised 200 J biphasic + CPR + ALS. Torsades is a "shockable rhythm" if pulseless.

[2]

QTc thresholds and torsades risk

<440 ms

Male — normal

No action

<460 ms

Female — normal

No action

440–500

Borderline

Caution — review drugs

>500 ms

Prolonged

Stop offending drug, correct K+/Mg2+; torsades risk 1–5%

[2]

Channelopathies and inherited arrhythmia syndromes

Inherited arrhythmia syndromes that present in the ICU

Long QT syndrome (LQTS): congenital (KvLQT1/LQT1, HERG/LQT2, SCN5A/LQT3) or acquired (drugs, electrolytes). Present with syncope/torsades/Sudden death. Treat: beta-blockade (LQT1), avoid QT drugs, ICD for syncope despite beta-blocker.
Brugada syndrome: autosomal dominant (SCN5A loss of function). ECG: coved ST elevation V1–V3 (type 1). VF/sudden death risk. Treat: ICD, quinidine (blocks Ito), isoprenaline (for electrical storm). AVOID Class Ic drugs (flecainide — unmask the ECG but pro-arrhythmic), and treat fever aggressively (fever unmasks/worsens Brugada).
Catecholaminergic polymorphic VT (CPVT): normal QT, structurally normal heart, bidirectional/polymorphic VT with exertion/emotion. Treat: beta-blocker (nadolol), flecainide, left cardiac sympathetic denervation, ICD.
Arrhythmogenic RV cardiomyopathy (ARVC): fibrofatty replacement of RV → epsilon waves, VT with LBBB morphology. Treat: ICD, beta-blocker, ablation, sport restriction.

[1]

Bradyarrhythmias and AV block

Bradycardia in ICU spans the spectrum from benign sinus bradycardia (athlete, vasovagal, drugs) to life-threatening complete heart block. The key question is again stability: symptomatic bradycardia needs treatment; asymptomatic bradycardia needs monitoring and aetiology work-up. [1]

Classification of AV block

AV block grades — recognise on ECG

1st degree: PR >200 ms, all P conducted. Benign — observe, no pacing.
Mobitz I (Wenckebach) — 2nd degree type I: progressive PR prolongation until a P is not conducted, then cycle resets. Narrow QRS. Site: AV node. Usually benign (inferior MI, athletes, vagal, drugs). Treat the cause; pacing rarely needed.
Mobitz II — 2nd degree type II: PR constant, sudden non-conducted P. Usually WIDE QRS. Site: His-Purkinje. HIGH RISK of progression to complete heart block → permanent pacing indicated even if asymptomatic. Often anterior MI.
2:1 AV block: every other P blocked — could be type I or II (cannot tell from single ECG; wide QRS favours type II). Treat as Mobitz II if uncertain.
Complete (3rd degree) heart block: P waves and QRS independent, no relationship. Escape rhythm: junctional (narrow QRS, 40–60, stable) or ventricular (wide QRS, 20–40, unstable). Always needs pacing.
High-grade AV block: ≥2 consecutive non-conducted P — manage as Mobitz II/complete.

[1]

Bradycardia management algorithm

Symptomatic bradycardia — stepwise management

1. Recognise symptomatic bradycardia

HR <60 (often <40) with hypotension, shock, syncope, ischaemic chest pain, acute HF, or altered mental status due to low cardiac output. Asymptomatic bradycardia in an athlete or during sleep is NOT an emergency.

2. Atropine 500 mcg IV

500 mcg IV every 3–5 min, max 3 mg (6 doses). Mechanism: muscarinic blockade → removes vagal tone → accelerates sinus node and AV conduction. Works in: sinus bradycardia, 1st-degree block, Mobitz I, symptomatic bradycardia after inferior MI (vagally mediated). Ineffective in: Mobitz II, complete heart block (block is below AV node — no vagal input there), denervated transplanted heart (no vagal tone to block).

3. Catecholamine infusion

Adrenaline 2–10 mcg/min (start 2, titrate to HR >60 and SBP >90). OR dopamine 5–20 mcg/kg/min. OR isoprenaline 1–4 mcg/min (pure beta — increases HR but drops diastolic BP; useful for bradycardia-dependent torsades and beta-blocker overdose). Choice depends on BP: adrenaline/dopamine if hypotensive, isoprenaline if normotensive.

4. Specific antidotes

Beta-blocker overdose: glucagon 3–5 mg IV over 2 min, then infusion 2–5 mg/h (bypasses beta-receptor — activates adenylyl cyclase via glucagon receptor → cAMP). Calcium channel blocker overdose: calcium chloride 1 g IV (repeated), high-dose insulin/euglycaemia (1 U/kg then 0.5–1 U/kg/h with glucose), lipid emulsion in refractory cases. Digoxin toxicity: Digoxin Fab antibody fragments (DigiFab) — see toxicology topic.

5. Transcutaneous pacing (TCP)

External pacing pads (anterior–posterior or anterior–left lateral). Set rate 60–80, mA gradually above capture threshold (typically 40–80 mA). Always confirm ELECTRICAL capture (wide QRS after each pacing spike) AND MECHANICAL capture (palpable pulse matching paced rate). Bridge only — may be painful (sedate), unreliable in obese/emphysema.

6. Transvenous pacing (definitive bridge)

Semi-floating bipolar pacing wire via right IJV (or subclavian/femoral) into RV apex under fluoroscopy or ECG guidance. Set rate 60, output above capture threshold (typically 1–3 mA — the lower the capture threshold the more stable). Sensitivity set so the pacemaker senses intrinsic R waves. Indications: complete heart block, Mobitz II with symptoms, symptomatic bradycardia not responding to atropine/catecholamines, bradycardia-dependent torsades, post-cardiac arrest bradycardia. Permanent pacemaker for definitive treatment.

[6] [11]

Transcutaneous pacing (TCP)

Bridge only

Quick, non-invasive, can be done by any clinician
Pads anterior–posterior or anterior–left lateral. Set rate 60–80, mA above capture threshold
Often painful — sedate (ketamine/fentanyl/midazolam)
Capture unreliable in obesity, emphysema, large effusions
Use while arranging transvenous pacing — NEVER a destination therapy

Transvenous pacing (TVP)

Definitive temporary pacing

Bipolar wire via right IJV → RV apex (under fluoroscopy/echo or ECG guidance)
More reliable, less painful, allows patient mobility
Set rate 60, output 1–3 mA above threshold, sensitivity 1.5–2.5 mV
Risks: pneumothorax (IJV/subclavian), infection, myocardial perforation/tamponade, diaphragmatic pacing, lead displacement
Bridge to permanent pacemaker in complete heart block. Permanent pacemaker is the definitive treatment for symptomatic high-grade block.

Junctional rhythms

A junctional escape rhythm (narrow QRS, 40–60, no preceding P or retrograde P after QRS) is the AV node/junction protecting the heart when the sinus node fails or AV block prevents conduction. Junctional rhythm is rarely the primary problem — it is a marker of sinus node dysfunction, AV block, or drug effect (beta-blocker, CCB, digoxin). [1]

[1]

ACLS integration — shockable vs non-shockable rhythms

The full ALS algorithm is covered in the arrhythmia-cardiac-arrest topic. The arrhythmia-specific elements relevant here: [1]

Shockable rhythms

VF / pulseless VT

Unsynchronised defibrillation 200 J biphasic immediately + CPR
Adrenaline 1 mg IV q3–5 min (after 3rd shock)
Amiodarone 300 mg IV after 3rd shock, 150 mg after 5th (or lidocaine 100 mg if amiodarone unavailable)
Reversible causes: 4 Hs (hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia) and 4 Ts (tension pneumothorax, tamponade, thrombosis, toxins)

Non-shockable rhythms

Asystole / PEA

Adrenaline 1 mg IV q3–5 min immediately (do NOT wait for 3rd shock)
CPR 30:2 (or continuous if advanced airway)
NO defibrillation — rhythm is non-shockable
Identify and treat the reversible cause (4 Hs and 4 Ts) — this is the ONLY thing that works in PEA. Consider bedside ultrasound to find the cause (tamponade, RV dilatation in PE, empty hyperdynamic LV in hypovolaemia).

[6]

Synchronised cardioversion vs defibrillation — the exam distinction

Synchronised cardioversion: the shock is delivered TIMED to the R wave (avoiding the T wave — the vulnerable period when a shock can induce VF). Used for organised tachyarrhythmias WITH A QRS: unstable VT, AF, flutter, SVT. The machine must be in SYNCH mode — you will see a marker dot on each R wave.
Defibrillation: UNSYNCHRONISED shock delivered immediately, regardless of cardiac cycle. Used when there is NO QRS to synchronise to: VF and pulseless VT.
Pitfall: if you attempt synchronised cardioversion in VF, the machine will not find an R wave to sync to and will either refuse to fire or delay — wasting time. In VF/pulseless VT, always use UNSYNCHRONISED.
Pitfall: if you shock an organised tachyarrhythmia in UNSYNCHRONISED mode and the shock lands on the T wave, you can induce VF. Always confirm SYNCH mode for VT with a pulse, AF, flutter, SVT.

[1]

Antiarrhythmic pharmacology — the Vaughan-Williams classes

The intensivist must know the Vaughan-Williams classification, but also its limitations (most useful drugs are mixed class; the framework does not predict clinical utility). Learn by mechanism, indications, and key adverse effects. [1]

Class I — Na+ channel blockers

Use-dependent

**Ia** (quinidine, procainamide, disopyramide): prolong AP/QRS/QT. Procainamide: stable VT (20–50 mg/min). Torsades risk.
**Ib** (lidocaine, phenytoin, mexiletine): shorten AP, bind ischaemic tissue. Lidocaine: ischaemic VT (1–1.5 mg/kg).
**Ic** (flecainide, propafenone): marked QRS widening. AVOID in structural/IHD (CAST trial — increased mortality). Use for AF <48 h ("pill in the pocket") in structurally normal hearts.

Class II — Beta-blockers

AV nodal blockade

Metoprolol (IV/PO), esmolol (titratable IV, half-life 9 min), bisoprolol, atenolol, propranolol (also blocks T4→T3)
Indications: AF rate control, SVT, ischaemic VT, LQTS, CPVT, electrical storm, thyrotoxicosis, beta-blocker withdrawal
SE: bronchospasm, bradycardia, hypotension, worsening HFrEF (initially — long-term beneficial), masking hypoglycaemia, fatigue

Class III — K+ channel blockers

QT prolongation

**Amiodarone:** mixed I–IV. First-line for VT/VF, AF in HF/structural disease. Acute: hypotension. Chronic (months): pulmonary fibrosis (CT + Dlco at baseline and 6 monthly), hepatitis, thyroid (both hypo and hyper — check TFTs every 6 months), corneal microdeposits, blue-grey skin, photosensitivity, neuropathy. Half-life 50 days.
**Sotalol:** III + II. AF, VT. Torsades risk (pro-arrhythmic 2%) — start in monitored setting.
**Ibutilide:** IV only, AF/flutter cardioversion. High torsades risk — monitor 4 h post-dose.
**Dronedarone:** amiodarone analogue (no iodine). AF — but CONTRAINDICATED in HF (ATHENA, PALLAS — increased mortality).

Class IV — Ca channel blockers

Non-DHP — AV nodal blockade

Verapamil, diltiazem — slow AV node conduction
Indications: AF/flutter rate control (stable), SVT termination (verapamil 5 mg IV), rate control in HFrEF avoided (negative inotrope)
AVOID in: HFrEF, WPW with AF, broad-complex tachycardia (could be VT — CCB can cause VF/asystole), beta-blocker combination (severe bradycardia)

[2]

Special situations in ICU arrhythmia

Special situations — high-yield ICU scenarios

Post-cardiac surgery AF

30–40% of CABG/valve surgery, peaks day 2–3. Prophylaxis: continue/restart beta-blocker, or amiodarone in high-risk. Treat: rate control (beta-blocker/diltiazem) ± rhythm (amiodarone), anticoagulate (high stroke risk). Most resolves <2 months.

Sepsis-associated AF

Marker of illness severity — catecholamines, electrolyte loss, inflammation. Treat sepsis, replace Mg2+/K+, switch dopamine to noradrenaline, beta-blockade with caution (esmolol titratable). AF usually reverts with recovery. Anticoagulate if duration >48 h or high CHA2DS2-VASc.

Electrical (VT/VF) storm

≥3 episodes in 24 h. Combine: deep sedation (propofol/midazolam reduces sympathetic drive), beta-blockade (most effective single agent), amiodarone + lidocaine infusion, correct K+/Mg2+, ventilate/oxygenate, mechanical support (IABP/VA-ECMO) if cardiogenic. Urgent ablation if scar-mediated. Treat ischaemia (PCI).

Digoxin toxicity

Suspect in any patient on digoxin with arrhythmia (any rhythm — VT, AV block, atrial tachycardia with block, bradycardia), GI symptoms, visual disturbance (yellow-green halos), confusion. Potentiated by hypokalaemia, hypomagnesaemia, renal failure, amiodarone, verapamil. Treat: stop digoxin, correct K+, give Digoxin Fab antibody fragments (DigiFab) if life-threatening arrhythmia/K >5, lidocaine/phenytoin for VT (avoid CCB/beta-blocker), pacing for symptomatic bradycardia. Potassium >5 is itself a marker of toxicity (Na/K ATPase inhibition).

Beta-blocker / CCB overdose

Both present with bradycardia, hypotension, AV block. BB: glucagon 3–5 mg IV then infusion 2–5 mg/h (bypasses receptor), high-dose insulin/euglycaemia, lipid emulsion, pacing. CCB: calcium chloride 1 g IV (repeat), high-dose insulin/euglycaemia (1 U/kg then 0.5–1 U/kg/h), lipid emulsion. See toxicology topics for detail.

Acute coronary syndrome with VT/VF

No mortality difference. Rate control simpler and as effective in older patients with AF risk factors. Rhythm control reasonable in younger/symptomatic/HF.

Practice change

High-yield arrhythmia points for the CICM/FFICM exam

Unstable = immediate electrical therapy. Do NOT wait for drugs, bloods, or a 12-lead. Synchronised cardioversion for organised tachyarrhythmia with a pulse; unsynchronised defibrillation for VF/pulseless VT.
Check K+ and Mg2+ FIRST — correct before any antiarrhythmic (target K+ >4.0, Mg2+ >0.8; for torsades K+ >4.5). Hypokalaemia and hypomagnesaemia underlie most ICU arrhythmias.
AF rate control is first-line (metoprolol/diltiazem) in stable ICU AF; rhythm control (amiodarone/DC cardioversion) if unstable, HF, failed rate control, or first presentation <48 h (EAST-AFNET 4 supports early rhythm control in new AF).
RACE II: lenient rate control (HR <110) is non-inferior to strict (<80) and easier — but aim <80 in HF/tachycardiomyopathy.
VT/VF cardiac arrest: defibrillate 200 J biphasic + adrenaline 1 mg q3–5 min + amiodarone 300 mg after 3rd shock (150 mg after 5th). ALIVE: amiodarone beats lidocaine.
Torsades: IV magnesium 2 g FIRST (works even if Mg normal), STOP QT drugs, correct K+ to >4.5, overdrive pace/isoprenaline if bradycardia-dependent.
Bradycardia: atropine 500 mcg q3–5 min (max 3 mg) → adrenaline/dopamine infusion → transcutaneous then transvenous pacing. Atropine FAILS in Mobitz II and complete heart block (block is below AV node).
Beta-blocker overdose: glucagon 3–5 mg IV bypasses the blocked beta-receptor (acts on glucagon receptor → cAMP). CCB overdose: calcium chloride + high-dose insulin/euglycaemia + lipid emulsion.
Digoxin toxicity: any arrhythmia + GI/visual symptoms in a patient on digoxin → stop drug, correct K+, give DigiFab if life-threatening (especially if K+ >5).
SVT termination: vagal manoeuvres → adenosine 6→12→12 mg (rapid bolus via proximal IV with saline flush, continuous ECG). NEVER give adenosine in broad-complex tachy (could be VT → VF) or WPW with AF.
Atrial flutter: cardiovert at LOWER energy (50–100 J) than AF; rate control harder; anticoagulate per CHA2DS2-VASc (same stroke risk as AF); cavotricuspid isthmus ablation is curative.
Amiodarone IV causes hypotension (the solvent polysorbate, not the drug) — give slowly. Chronic toxicity: pulmonary fibrosis (CT + Dlco monitoring), thyroid (both directions), hepatitis, corneal deposits. Half-life 50 days.
Complete heart block: independent P and QRS; junctional escape (narrow, 40–60) is more stable than ventricular escape (wide, 20–40). Needs transvenous pacing → permanent pacemaker. Transcutaneous is only a bridge.
Mobitz II (constant PR, sudden dropped beat, wide QRS) is high-risk for progression to complete block — permanent pacing even if asymptomatic. Mobitz I (Wenckebach, progressive PR) is usually benign.
WPW with AF: irregular broad-complex tachy. AVOID adenosine/CCB/digoxin/beta-blocker (block AV node → unopposed accessory pathway conduction → VF). Cardiovert if unstable; procainamide/flecainide/ibutilide if stable.
CAST trial (1989): Class Ic drugs (flecainide/encainide) INCREASED mortality in post-MI patients despite suppressing PVCs. Never use Ic in structural/ischaemic heart disease.
Synchronised vs unsynchronised: SYNCH for any organised rhythm with a QRS (VT with pulse, AF, flutter, SVT); UNSYNCH for VF/pulseless VT. Shocking an organised rhythm unsynchronised on the T wave induces VF.
New-onset ICU AF is a marker of illness severity and independently worsens mortality — treat the precipitant (sepsis, hypoxia, electrolytes, inotrope excess), not just the rhythm.

[1]

Red flags

Critical arrhythmia points

Unstable = IMMEDIATE cardioversion/defibrillation — do NOT wait for drugs, bloods, or ECG. Synchronised for VT-with-pulse/AF/flutter/SVT; unsynchronised for VF/pulseless VT.
Check K+ and Mg2+ FIRST — correct before any antiarrhythmic (K+ >4.0, Mg2+ >0.8; torsades K+ >4.5).
Torsades: IV magnesium 2 g even if Mg is normal; STOP all QT-prolonging drugs (use crediblemeds.org); overdrive pace if bradycardia-dependent.
Adenosine is DANGEROUS in broad-complex tachycardia (could be VT — can cause VF) and in WPW with AF (preferential AV nodal block → unopposed accessory pathway → VF). Restrict to regular narrow-complex SVT.
Avoid verapamil/diltiazem in HFrEF — negative inotrope; may precipitate cardiac arrest. Use amiodarone or digoxin for rate control in HF.
Beta-blocker overdose: glucagon bypasses the blocked beta-receptor. CCB overdose: calcium + high-dose insulin + lipid emulsion.
Digoxin toxicity: any arrhythmia in a patient on digoxin — stop, check K+ (high K+ is a marker of severe toxicity), give DigiFab if life-threatening.
Complete heart block needs transvenous pacing — transcutaneous is only a bridge. Mobitz II also needs pacing (high progression risk).
WPW with AF: do NOT block the AV node (adenosine/CCB/digoxin/beta-blocker) — risk of VF. Cardiovert or use procainamide/flecainide.
Class Ic (flecainide, propafenone) CONTRAINDICATED in structural/ischaemic heart disease (CAST trial — increased mortality).
Synchronised cardioversion in VF/pVT will fail/delay — VF has no R wave to synchronise to. Use UNSYNCHRONISED for VF/pVT.
Electrical storm (≥3 VT/VF in 24 h): combine deep sedation + beta-blockade + amiodarone/lidocaine + correct electrolytes + mechanical support; refer for urgent ablation if scar-mediated.

[1]

References

[1]Hindricks G, Potpara T, Dagres N, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[2]Priori SG, Blomstrom-Lundqvist C, Mazzanti A, et al. Notum palmitoleoyl-protein carboxylesterase regulates Fas cell surface death receptor-mediated apoptosis via the Wnt signaling pathway in colon adenocarcinoma Bioengineered, 2021.PMID 34402722
[3]Roy D, Talajic M, Nattel S, et al. The relationship between self-harm and alexithymia: A systematic review and meta-analysis Scand J Psychol, 2020.PMID 32706131
[4]Kirchhof P, Camm AJ, Goette A, et al. Hydrostibination of Alkynes: A Radical Mechanism* Chemistry, 2020.PMID 32706129
[5]Dorian P, Cass D, Schwartz B, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure N Engl J Med, 2002.PMID 12124404
[6]Soar J, Perkins GD, Maconochie I, et al. Hierarchy and scaling behavior of multi-rank domain patterns in ferroelectric K(0.9)Na(0.1)NbO(3) strained films Nanotechnology, 2018.PMID 29185437
[7]Van Gelder IC, Groenveld HF, Crijns HJ, et al. Sudden cardiac death prediction and prevention: report from a National Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop Circulation, 2010.PMID 21147730
[8]Ezekowitz MD, Connolly HM, Eikelboom JW, et al. Antioxidant Supplementation in the Treatment of Neurotoxicity Induced by Platinum-Based Chemotherapeutics-A Review Int J Mol Sci, 2020.PMID 33092125
[9]January CT, Wann LS, Calkins H, et al. Surface plasmon assisted laser ablation of stainless steel Nanotechnology, 2019.PMID 30970328
[10]Kudenchuk PJ, Cobb LA, Copass MK, et al. Reproducibility and clinical utility of tendon palpation to detect patellar tendinopathy in young basketball players. Victorian Institute of Sport tendon study group Br J Sports Med, 2001.PMID 11157466
[11]Link MS, Atkins DL, Passman RS, et al. Structural and kinetic basis for heightened immunogenicity of T cell vaccines J Exp Med, 2005.PMID 15837811
[12]Trzeciak S, Dellinger RP, Chansky ME, et al. Sorafenib for recurrent hepatocellular carcinoma after liver transplantation Jpn J Clin Oncol, 2010.PMID 20494947

In one line

[1]

General approach — first principles

Universal arrhythmia algorithm

Step 1 — Assess haemodynamic stability

Step 2 — 12-lead ECG + rhythm strip

Step 3 — Identify and treat the precipitant

Step 4 — Choose rate vs rhythm control

Step 5 — Anticoagulation and long-term plan

[1] [6]

Arrhythmia epidemiology in ICU

12–20%

ICU patients

Develop arrhythmia during admission

8–10%

New-onset AF

In medical/surgical ICU; up to 40% post-cardiac surgery

2–4×

Mortality risk

New-onset AF in septic shock increases mortality

50 J

Cardioversion energy

Atrial flutter — lower than AF (120–200 J)

[12]

Atrial fibrillation

Pathophysiology and ICU triggers

[1]

Rate versus rhythm control

Rate control (first-line in most ICU AF)

Beta-blocker or non-DHP CCB

Beta-blocker: metoprolol 5 mg IV over 2 min, repeat q5 min × 3 (max 15 mg); OR esmolol 500 mcg/kg loading then 50–200 mcg/kg/min (short half-life — ideal to titrate in unstable/anaesthetised patients)
OR non-dihydropyridine CCB: diltiazem 0.25 mg/kg IV (≈20 mg) over 2 min, repeat 0.35 mg/kg after 15 min if needed, then infusion 5–15 mg/h. AVOID verapamil/diltiazem in HFrEF (negative inotrope)
OR digoxin 500 mcg IV over 30 min (additive with beta-blocker; slow onset 2–6 h; useful in HF/AF and when beta-blockers contraindicated). AVOID in renal failure, hypokalaemia, WPW
Target: HR <110 (lenient) or <80 (strict). RACE II: lenient is non-inferior and easier to achieve; strict reserved for ongoing symptoms or tachycardia-mediated cardiomyopathy
Caveat: rate control is harder in hyperadrenergic states (sepsis, post-op) — may need combination therapy or amiodarone

Rhythm control (cardioversion)

If unstable, HF, failed rate control, <48 h

Pharmacological: amiodarone 300 mg IV over 20–60 min, then 900 mg/24 h infusion. Useful in HF, structural disease, renal failure. Slower than electrical (6–24 h)
OR flecainide 2 mg/kg IV over 10 min (AVOID in structural/IHD — pro-arrhythmic)
OR ibutilide 1 mg IV over 10 min (QT prolongation — do NOT use if QTc >440 ms)
Electrical: synchronised DC cardioversion — AF: 120–200 J biphasic (escalating); flutter: 50–100 J. Sedate (propofol/ketamine + midazolam) if awake. Anterior–posterior pads more effective
EAST-AFNET 4 (NEJM 2020): early rhythm control within 1 year of diagnosis improved composite CV outcome (HR 0.79). Strengthens case for rhythm control in newly diagnosed AF

[1] [4] [7]

Practical AF management in the ICU

1. Stabilise — is the patient unstable?

2. Identify and correct precipitant

3. Rate control

Metoprolol 5 mg IV q5 min × 3 (avoid in severe asthma, decompensated HF with low EF). If HF/AF: diltiazem is safer (or digoxin/amiodarone). Target HR <110 (lenient) or <80 if HF/tachycardiomyopathy.

4. Rhythm control if indicated

Amiodarone 300 mg IV over 20–60 min, then 900 mg/24 h. OR synchronised DC cardioversion if AF duration <48 h (or TOE-guided to exclude LAA thrombus if >48 h/unknown).

5. Anticoagulate

6. Long-term plan

[1] [9]

Anticoagulation in the ICU patient with AF

[1]

CHA2DS2-VASc (stroke risk)

Score → anticoagulate if ≥2 (men) / ≥3 (women)

**C** — CHF/LV dysfunction (1)
**H** — Hypertension (1)
**A2** — Age ≥75 (2)
**D** — Diabetes (1)
**S2** — Stroke/TIA/thromboembolism (2)
**V** — Vascular disease (MI, PAD, aortic plaque) (1)
**A** — Age 65–74 (1)
**Sc** — Sex category female (1)
Score 0 (men) / 1 (women): omit. Score 1 (men) / 2 (women): consider. ≥2 (men) / ≥3 (women): anticoagulate.

HAS-BLED (bleeding risk)

≥3 = high bleeding risk — review/correct, not a reason to withhold

**H** — Hypertension (SBP >160) (1)
**A** — Abnormal renal/liver function (1 each)
**S** — Stroke history (1)
**B** — Bleeding history/predisposition (1)
**L** — Labile INR (not applicable to DOAC) (1)
**E** — Elderly (>65) (1)
**D** — Drugs (antiplatelet/NSAID) or alcohol excess (1)
A high score is NOT a reason to deny anticoagulation — it is a reason to correct modifiable factors (BP, NSAIDs, alcohol).

[1] [8]

Specific ICU scenarios in AF

Post-cardiac surgery AF (POAF): occurs in 30–40% of CABG/valve patients, peaks on day 2–3. Prophylaxis: amiodarone or beta-blocker (restore if withheld). Treat: rate control + anticoagulate (high stroke risk). Usually self-limited (<2 months) but anticoagulate for at least the perioperative period.
Sepsis-associated AF: reflects catecholamine surge + electrolyte loss. Correct the sepsis, replace Mg2+/K+, switch dopamine to noradrenaline. Beta-blockade in septic shock is contentious — esmolol (titratable) preferred if needed. AF usually reverts with recovery.
AF with HFrEF: AVOID diltiazem/verapamil (negative inotrope). Use digoxin, amiodarone, or a cardioselective beta-blocker (metoprolol/bisoprolol). Long-term: beta-blocker + MRA + SGLT2i + ARNI ("four pillars") reduce AF burden and mortality.
AF with WPW (pre-excited): AVOID AV-nodal blockers (adenosine, verapamil, diltiazem, digoxin, beta-blocker) — they preferentially block the AV node and allow unrestricted antegrade conduction down the accessory pathway → pre-excited AF → VF. Use synchronised cardioversion if unstable, or procainamide/flecainide/ibutilide if stable (block the accessory pathway).
Thyroid storm with AF: high-output, fast AF. Treat the storm (PTU, iodine, beta-blocker, steroids) — AF reverts with euthyroidism. Propranolol/esmolol preferred (blocks T4→T3 conversion). [1]

Atrial flutter

[1]

Atrial flutter management

1. Identify typical flutter

2. Stability assessment

Unstable → synchronised DC cardioversion at 50–100 J biphasic. Stable → proceed to pharmacological management.

3. Rate control

Beta-blocker (metoprolol, esmolol) or diltiazem. Often inadequate — flutter circuits are robust. Add digoxin or consider amiodarone.

4. Rhythm control

5. Anticoagulation

Same as AF — CHA2DS2-VASc. Anticoagulate before/after cardioversion per AF rules.

6. Definitive cure

Cavotricuspid isthmus ablation is curative for typical flutter (success >90%) — refer for electrophysiology once the ICU insult resolves.

[1]

Supraventricular tachycardia (SVT)

AVNRT (commonest SVT)

AV node has dual pathways

Mechanism: dual AV nodal pathways (slow and fast) form a re-entrant circuit within the AV node
ECG: regular narrow QRS at 150–250/min, P waves buried in QRS or pseudo R' in V1 / pseudo S in inferior leads (retrograde P)
No accessory pathway — antegrade AND retrograde via AV node
Cardiac arrest risk: low. Treat with AV-nodal blockade.

AVRT / WPW

Accessory pathway

Mechanism: accessory pathway connects atrium to ventricle (e.g. bundle of Kent in WPW) — re-entry via AV node + pathway
Orthodromic AVRT: antegrade AV node, retrograde pathway → narrow QRS, regular
Antidromic AVRT: antegrade pathway → WIDE QRS (looks like VT) — dangerous
WPW with AF: chaotic broad irregular QRS — DO NOT give adenosine/CCB/digoxin (risk of VF). Cardiovert or use procainamide/flecainide.

SVT termination — the adenosine protocol

1. Vagal manoeuvres (first-line, stable)

2. Adenosine 6 mg rapid IV bolus

3. Adenosine 12 mg if no response

If 6 mg fails to terminate, give 12 mg by the same rapid technique after 1–2 min. Use a 3-way tap or dual-syringe push technique to ensure the bolus reaches the heart in <5 s.

4. Adenosine 12 mg — second attempt

A second 12 mg dose can be given if the first 12 mg produced partial AV block but no termination. Maximum single dose 12 mg. Some patients need higher doses (18–24 mg) or are adenosine-resistant.

5. If adenosine fails or contraindicated

[9]

Adenosine — pharmacology and safety

Mechanism: agonist at A1 receptors in the AV node → transient complete AV block (3–10 s).
Onset/offset: seconds (half-life <10 s) — administer via proximal IV with rapid saline flush.
Contraindications: asthma/COPD with severe bronchospasm (A2B receptors cause bronchoconstriction), 2nd/3rd-degree AV block, sick sinus syndrome, denervated transplanted heart (exaggerated response), WPW with AF (may precipitate VF by preferentially blocking AV node).
Important diagnostic use: in a stable regular broad-complex tachycardia of uncertain origin, adenosine can be used diagnostically — if it terminates the rhythm it was SVT with aberrancy; if it transiently reveals underlying VT it confirms VT. BUT this should only be done with full resuscitation facilities, as adenosine in true VT can degenerate to VF.
Interactions: dipyridamole potentiates adenosine (reduce dose); methylxanthines (theophylline, caffeine) antagonise it (increase dose); carbamazepine increases AV block risk.

[1]

Ventricular arrhythmias

Monomorphic vs polymorphic VT

Monomorphic VT

Uniform, regular wide QRS

Regular, wide (>120 ms) QRS at 100–250/min, uniform morphology
Mechanism: scar-related reentry (post-MI, cardiomyopathy, ARVC) OR bundle branch reentry OR idiopathic (RVOT, fascicular)
AV dissociation, capture beats, fusion beats = pathognomonic (but often absent)
Stable: amiodarone 150 mg IV over 10 min, then infusion 900 mg/24h. Alternatives: procainamide, lidocaine. Unstable: synchronised cardioversion 100 J escalating.
Prognosis depends on substrate — post-MI scar VT ablation/ICD often indicated.

Polymorphic VT

Varying QRS morphology — ask: is QT long?

Irregular, rapidly varying QRS morphology/axis at 200–300/min
Two forms by QT: (1) **Torsades de Pointes** — prolonged QTc (>440 m / >460 f), twisting QRS around baseline, bradycardia-dependent. (2) **Normal-QT polymorphic VT** — usually ischaemia-driven (acute MI), or catecholaminergic (CPVT)
Torsades treatment: IV magnesium 2 g, STOP all QT-prolonging drugs, correct K+ (>4.5), overdrive pacing / isoprenaline if bradycardia-dependent
Normal-QT polymorphic VT: treat ischaemia (PCI), beta-blockade, correct electrolytes. Often degenerates to VF — be ready to defibrillate.

[2]

Stable vs unstable VT

The defining decision in VT is haemodynamic stability: [1]

VT management algorithm

1. Is the patient pulseless?

NO pulse with VT = pulseless VT = cardiac arrest → UNSYNCHRONISED defibrillation 200 J biphasic immediately + CPR + ALS algorithm (adrenaline 1 mg q3–5 min, amiodarone 300 mg after 3rd shock).

2. Is the patient unstable (but with a pulse)?

3. Stable VT — pharmacological termination

4. Identify and treat the cause

5. Electrical storm — recurrent VT

[2] [6]

Amiodarone vs lidocaine for VT/VF

Amiodarone (first-line)

Class III (mixed I–IV)

Mechanism: blocks K+ channels (Class III) + Na+ (I) + beta (II) + Ca (IV) — broad-spectrum
Dose: cardiac arrest 300 mg IV after 3rd shock, 150 mg after 5th; stable VT 150 mg over 10 min then infusion
ALIVE trial (NEJM 2002): amiodarone superior to lidocaine for shock-resistant VF — survival to hospital 22.8% vs 12.0%
ARREST trial (NEJM 1999): amiodarone improved survival to hospital vs placebo in OHCA VF (44% vs 34%)
Acute SE: hypotension (solvent — give slowly), bradycardia. Chronic: pulmonary fibrosis, thyroid dysfunction, hepatitis, corneal deposits, photosensitivity, blue-grey skin, peripheral neuropathy. QT prolongation (low torsades risk as also blocks Ca).

Lidocaine (alternative)

Class Ib

Mechanism: fast Na+ channel blocker (binds inactivated channels — preferential in ischaemic tissue)
Dose: 1–1.5 mg/kg IV bolus, repeat 0.5–0.75 mg/kg q5–10 min to max 3 mg/kg, then infusion 1–4 mg/min
Most useful for ischaemic VT (binds preferentially to depolarised ischaemic myocardium)
SE: CNS — tinnitus, perioral tingling, seizures, altered mental state (dose-dependent). Avoid in severe hepatic disease, 2nd/3rd-degree block.
On the way out for cardiac arrest (amiodarone preferred) but still useful for ischaemic VT and amiodarone-intolerant patients.

[5] [10]

Torsades de Pointes

Torsades de Pointes — recognise and treat

Recognise

IV magnesium sulphate 2 g over 10 min

STOP all QT-prolonging drugs

Correct potassium aggressively

Target K+ >4.5 mmol/L (higher than usual — hypokalaemia prolongs QT and worsens torsades). Replace orally and IV.

Accelerate the heart rate (overdrive suppression)

If degenerates to VF — defibrillate

Unsynchronised 200 J biphasic + CPR + ALS. Torsades is a "shockable rhythm" if pulseless.

[2]

QTc thresholds and torsades risk

<440 ms

Male — normal

No action

<460 ms

Female — normal

No action

440–500

Borderline

Caution — review drugs

>500 ms

Prolonged

Stop offending drug, correct K+/Mg2+; torsades risk 1–5%

[2]

Channelopathies and inherited arrhythmia syndromes

Inherited arrhythmia syndromes that present in the ICU

Long QT syndrome (LQTS): congenital (KvLQT1/LQT1, HERG/LQT2, SCN5A/LQT3) or acquired (drugs, electrolytes). Present with syncope/torsades/Sudden death. Treat: beta-blockade (LQT1), avoid QT drugs, ICD for syncope despite beta-blocker.
Brugada syndrome: autosomal dominant (SCN5A loss of function). ECG: coved ST elevation V1–V3 (type 1). VF/sudden death risk. Treat: ICD, quinidine (blocks Ito), isoprenaline (for electrical storm). AVOID Class Ic drugs (flecainide — unmask the ECG but pro-arrhythmic), and treat fever aggressively (fever unmasks/worsens Brugada).
Catecholaminergic polymorphic VT (CPVT): normal QT, structurally normal heart, bidirectional/polymorphic VT with exertion/emotion. Treat: beta-blocker (nadolol), flecainide, left cardiac sympathetic denervation, ICD.
Arrhythmogenic RV cardiomyopathy (ARVC): fibrofatty replacement of RV → epsilon waves, VT with LBBB morphology. Treat: ICD, beta-blocker, ablation, sport restriction.

[1]

Bradyarrhythmias and AV block

Classification of AV block

AV block grades — recognise on ECG

1st degree: PR >200 ms, all P conducted. Benign — observe, no pacing.
Mobitz I (Wenckebach) — 2nd degree type I: progressive PR prolongation until a P is not conducted, then cycle resets. Narrow QRS. Site: AV node. Usually benign (inferior MI, athletes, vagal, drugs). Treat the cause; pacing rarely needed.
Mobitz II — 2nd degree type II: PR constant, sudden non-conducted P. Usually WIDE QRS. Site: His-Purkinje. HIGH RISK of progression to complete heart block → permanent pacing indicated even if asymptomatic. Often anterior MI.
2:1 AV block: every other P blocked — could be type I or II (cannot tell from single ECG; wide QRS favours type II). Treat as Mobitz II if uncertain.
Complete (3rd degree) heart block: P waves and QRS independent, no relationship. Escape rhythm: junctional (narrow QRS, 40–60, stable) or ventricular (wide QRS, 20–40, unstable). Always needs pacing.
High-grade AV block: ≥2 consecutive non-conducted P — manage as Mobitz II/complete.

[1]

Bradycardia management algorithm

Symptomatic bradycardia — stepwise management

1. Recognise symptomatic bradycardia

2. Atropine 500 mcg IV

3. Catecholamine infusion

4. Specific antidotes

5. Transcutaneous pacing (TCP)

6. Transvenous pacing (definitive bridge)

[6] [11]

Transcutaneous pacing (TCP)

Bridge only

Quick, non-invasive, can be done by any clinician
Pads anterior–posterior or anterior–left lateral. Set rate 60–80, mA above capture threshold
Often painful — sedate (ketamine/fentanyl/midazolam)
Capture unreliable in obesity, emphysema, large effusions
Use while arranging transvenous pacing — NEVER a destination therapy

Transvenous pacing (TVP)

Definitive temporary pacing

Bipolar wire via right IJV → RV apex (under fluoroscopy/echo or ECG guidance)
More reliable, less painful, allows patient mobility
Set rate 60, output 1–3 mA above threshold, sensitivity 1.5–2.5 mV
Risks: pneumothorax (IJV/subclavian), infection, myocardial perforation/tamponade, diaphragmatic pacing, lead displacement
Bridge to permanent pacemaker in complete heart block. Permanent pacemaker is the definitive treatment for symptomatic high-grade block.

Junctional rhythms

[1]

ACLS integration — shockable vs non-shockable rhythms

The full ALS algorithm is covered in the arrhythmia-cardiac-arrest topic. The arrhythmia-specific elements relevant here: [1]

Shockable rhythms

VF / pulseless VT

Unsynchronised defibrillation 200 J biphasic immediately + CPR
Adrenaline 1 mg IV q3–5 min (after 3rd shock)
Amiodarone 300 mg IV after 3rd shock, 150 mg after 5th (or lidocaine 100 mg if amiodarone unavailable)
Reversible causes: 4 Hs (hypoxia, hypovolaemia, hypo/hyperkalaemia, hypothermia) and 4 Ts (tension pneumothorax, tamponade, thrombosis, toxins)

Non-shockable rhythms

Asystole / PEA

Adrenaline 1 mg IV q3–5 min immediately (do NOT wait for 3rd shock)
CPR 30:2 (or continuous if advanced airway)
NO defibrillation — rhythm is non-shockable
Identify and treat the reversible cause (4 Hs and 4 Ts) — this is the ONLY thing that works in PEA. Consider bedside ultrasound to find the cause (tamponade, RV dilatation in PE, empty hyperdynamic LV in hypovolaemia).

[6]

Synchronised cardioversion vs defibrillation — the exam distinction

Synchronised cardioversion: the shock is delivered TIMED to the R wave (avoiding the T wave — the vulnerable period when a shock can induce VF). Used for organised tachyarrhythmias WITH A QRS: unstable VT, AF, flutter, SVT. The machine must be in SYNCH mode — you will see a marker dot on each R wave.
Defibrillation: UNSYNCHRONISED shock delivered immediately, regardless of cardiac cycle. Used when there is NO QRS to synchronise to: VF and pulseless VT.
Pitfall: if you attempt synchronised cardioversion in VF, the machine will not find an R wave to sync to and will either refuse to fire or delay — wasting time. In VF/pulseless VT, always use UNSYNCHRONISED.
Pitfall: if you shock an organised tachyarrhythmia in UNSYNCHRONISED mode and the shock lands on the T wave, you can induce VF. Always confirm SYNCH mode for VT with a pulse, AF, flutter, SVT.

[1]

Antiarrhythmic pharmacology — the Vaughan-Williams classes

Class I — Na+ channel blockers

Use-dependent

**Ia** (quinidine, procainamide, disopyramide): prolong AP/QRS/QT. Procainamide: stable VT (20–50 mg/min). Torsades risk.
**Ib** (lidocaine, phenytoin, mexiletine): shorten AP, bind ischaemic tissue. Lidocaine: ischaemic VT (1–1.5 mg/kg).
**Ic** (flecainide, propafenone): marked QRS widening. AVOID in structural/IHD (CAST trial — increased mortality). Use for AF <48 h ("pill in the pocket") in structurally normal hearts.

Class II — Beta-blockers

AV nodal blockade

Metoprolol (IV/PO), esmolol (titratable IV, half-life 9 min), bisoprolol, atenolol, propranolol (also blocks T4→T3)
Indications: AF rate control, SVT, ischaemic VT, LQTS, CPVT, electrical storm, thyrotoxicosis, beta-blocker withdrawal
SE: bronchospasm, bradycardia, hypotension, worsening HFrEF (initially — long-term beneficial), masking hypoglycaemia, fatigue

Class III — K+ channel blockers

QT prolongation

**Amiodarone:** mixed I–IV. First-line for VT/VF, AF in HF/structural disease. Acute: hypotension. Chronic (months): pulmonary fibrosis (CT + Dlco at baseline and 6 monthly), hepatitis, thyroid (both hypo and hyper — check TFTs every 6 months), corneal microdeposits, blue-grey skin, photosensitivity, neuropathy. Half-life 50 days.
**Sotalol:** III + II. AF, VT. Torsades risk (pro-arrhythmic 2%) — start in monitored setting.
**Ibutilide:** IV only, AF/flutter cardioversion. High torsades risk — monitor 4 h post-dose.
**Dronedarone:** amiodarone analogue (no iodine). AF — but CONTRAINDICATED in HF (ATHENA, PALLAS — increased mortality).

Class IV — Ca channel blockers

Non-DHP — AV nodal blockade

Verapamil, diltiazem — slow AV node conduction
Indications: AF/flutter rate control (stable), SVT termination (verapamil 5 mg IV), rate control in HFrEF avoided (negative inotrope)
AVOID in: HFrEF, WPW with AF, broad-complex tachycardia (could be VT — CCB can cause VF/asystole), beta-blocker combination (severe bradycardia)

[2]

Special situations in ICU arrhythmia

Special situations — high-yield ICU scenarios

Post-cardiac surgery AF

Sepsis-associated AF

Electrical (VT/VF) storm

Digoxin toxicity

Beta-blocker / CCB overdose

Acute coronary syndrome with VT/VF

Practice change

Rate control is reasonable default for most stable AF

[1]

Exam practice

SAQ — New-onset AF in septic shock

10 minutes · 10 marks

[1]

SAQ — Torsades de Pointes

10 minutes · 10 marks

[1]

Clinical pearls

High-yield arrhythmia points for the CICM/FFICM exam

Unstable = immediate electrical therapy. Do NOT wait for drugs, bloods, or a 12-lead. Synchronised cardioversion for organised tachyarrhythmia with a pulse; unsynchronised defibrillation for VF/pulseless VT.
Check K+ and Mg2+ FIRST — correct before any antiarrhythmic (target K+ >4.0, Mg2+ >0.8; for torsades K+ >4.5). Hypokalaemia and hypomagnesaemia underlie most ICU arrhythmias.
AF rate control is first-line (metoprolol/diltiazem) in stable ICU AF; rhythm control (amiodarone/DC cardioversion) if unstable, HF, failed rate control, or first presentation <48 h (EAST-AFNET 4 supports early rhythm control in new AF).
RACE II: lenient rate control (HR <110) is non-inferior to strict (<80) and easier — but aim <80 in HF/tachycardiomyopathy.
VT/VF cardiac arrest: defibrillate 200 J biphasic + adrenaline 1 mg q3–5 min + amiodarone 300 mg after 3rd shock (150 mg after 5th). ALIVE: amiodarone beats lidocaine.
Torsades: IV magnesium 2 g FIRST (works even if Mg normal), STOP QT drugs, correct K+ to >4.5, overdrive pace/isoprenaline if bradycardia-dependent.
Bradycardia: atropine 500 mcg q3–5 min (max 3 mg) → adrenaline/dopamine infusion → transcutaneous then transvenous pacing. Atropine FAILS in Mobitz II and complete heart block (block is below AV node).
Beta-blocker overdose: glucagon 3–5 mg IV bypasses the blocked beta-receptor (acts on glucagon receptor → cAMP). CCB overdose: calcium chloride + high-dose insulin/euglycaemia + lipid emulsion.
Digoxin toxicity: any arrhythmia + GI/visual symptoms in a patient on digoxin → stop drug, correct K+, give DigiFab if life-threatening (especially if K+ >5).
SVT termination: vagal manoeuvres → adenosine 6→12→12 mg (rapid bolus via proximal IV with saline flush, continuous ECG). NEVER give adenosine in broad-complex tachy (could be VT → VF) or WPW with AF.
Atrial flutter: cardiovert at LOWER energy (50–100 J) than AF; rate control harder; anticoagulate per CHA2DS2-VASc (same stroke risk as AF); cavotricuspid isthmus ablation is curative.
Amiodarone IV causes hypotension (the solvent polysorbate, not the drug) — give slowly. Chronic toxicity: pulmonary fibrosis (CT + Dlco monitoring), thyroid (both directions), hepatitis, corneal deposits. Half-life 50 days.
Complete heart block: independent P and QRS; junctional escape (narrow, 40–60) is more stable than ventricular escape (wide, 20–40). Needs transvenous pacing → permanent pacemaker. Transcutaneous is only a bridge.
Mobitz II (constant PR, sudden dropped beat, wide QRS) is high-risk for progression to complete block — permanent pacing even if asymptomatic. Mobitz I (Wenckebach, progressive PR) is usually benign.
WPW with AF: irregular broad-complex tachy. AVOID adenosine/CCB/digoxin/beta-blocker (block AV node → unopposed accessory pathway conduction → VF). Cardiovert if unstable; procainamide/flecainide/ibutilide if stable.
CAST trial (1989): Class Ic drugs (flecainide/encainide) INCREASED mortality in post-MI patients despite suppressing PVCs. Never use Ic in structural/ischaemic heart disease.
Synchronised vs unsynchronised: SYNCH for any organised rhythm with a QRS (VT with pulse, AF, flutter, SVT); UNSYNCH for VF/pulseless VT. Shocking an organised rhythm unsynchronised on the T wave induces VF.
New-onset ICU AF is a marker of illness severity and independently worsens mortality — treat the precipitant (sepsis, hypoxia, electrolytes, inotrope excess), not just the rhythm.

[1]

Red flags

Critical arrhythmia points

Unstable = IMMEDIATE cardioversion/defibrillation — do NOT wait for drugs, bloods, or ECG. Synchronised for VT-with-pulse/AF/flutter/SVT; unsynchronised for VF/pulseless VT.
Check K+ and Mg2+ FIRST — correct before any antiarrhythmic (K+ >4.0, Mg2+ >0.8; torsades K+ >4.5).
Torsades: IV magnesium 2 g even if Mg is normal; STOP all QT-prolonging drugs (use crediblemeds.org); overdrive pace if bradycardia-dependent.
Adenosine is DANGEROUS in broad-complex tachycardia (could be VT — can cause VF) and in WPW with AF (preferential AV nodal block → unopposed accessory pathway → VF). Restrict to regular narrow-complex SVT.
Avoid verapamil/diltiazem in HFrEF — negative inotrope; may precipitate cardiac arrest. Use amiodarone or digoxin for rate control in HF.
Beta-blocker overdose: glucagon bypasses the blocked beta-receptor. CCB overdose: calcium + high-dose insulin + lipid emulsion.
Digoxin toxicity: any arrhythmia in a patient on digoxin — stop, check K+ (high K+ is a marker of severe toxicity), give DigiFab if life-threatening.
Complete heart block needs transvenous pacing — transcutaneous is only a bridge. Mobitz II also needs pacing (high progression risk).
WPW with AF: do NOT block the AV node (adenosine/CCB/digoxin/beta-blocker) — risk of VF. Cardiovert or use procainamide/flecainide.
Class Ic (flecainide, propafenone) CONTRAINDICATED in structural/ischaemic heart disease (CAST trial — increased mortality).
Synchronised cardioversion in VF/pVT will fail/delay — VF has no R wave to synchronise to. Use UNSYNCHRONISED for VF/pVT.
Electrical storm (≥3 VT/VF in 24 h): combine deep sedation + beta-blockade + amiodarone/lidocaine + correct electrolytes + mechanical support; refer for urgent ablation if scar-mediated.

[1]

References

[1]Hindricks G, Potpara T, Dagres N, et al. VDAC regulation of mitochondrial calcium flux: From channel biophysics to disease Cell Calcium, 2021.PMID 33529977
[2]Priori SG, Blomstrom-Lundqvist C, Mazzanti A, et al. Notum palmitoleoyl-protein carboxylesterase regulates Fas cell surface death receptor-mediated apoptosis via the Wnt signaling pathway in colon adenocarcinoma Bioengineered, 2021.PMID 34402722
[3]Roy D, Talajic M, Nattel S, et al. The relationship between self-harm and alexithymia: A systematic review and meta-analysis Scand J Psychol, 2020.PMID 32706131
[4]Kirchhof P, Camm AJ, Goette A, et al. Hydrostibination of Alkynes: A Radical Mechanism* Chemistry, 2020.PMID 32706129
[5]Dorian P, Cass D, Schwartz B, et al. Rapid measurement of B-type natriuretic peptide in the emergency diagnosis of heart failure N Engl J Med, 2002.PMID 12124404
[6]Soar J, Perkins GD, Maconochie I, et al. Hierarchy and scaling behavior of multi-rank domain patterns in ferroelectric K(0.9)Na(0.1)NbO(3) strained films Nanotechnology, 2018.PMID 29185437
[7]Van Gelder IC, Groenveld HF, Crijns HJ, et al. Sudden cardiac death prediction and prevention: report from a National Heart, Lung, and Blood Institute and Heart Rhythm Society Workshop Circulation, 2010.PMID 21147730
[8]Ezekowitz MD, Connolly HM, Eikelboom JW, et al. Antioxidant Supplementation in the Treatment of Neurotoxicity Induced by Platinum-Based Chemotherapeutics-A Review Int J Mol Sci, 2020.PMID 33092125
[9]January CT, Wann LS, Calkins H, et al. Surface plasmon assisted laser ablation of stainless steel Nanotechnology, 2019.PMID 30970328
[10]Kudenchuk PJ, Cobb LA, Copass MK, et al. Reproducibility and clinical utility of tendon palpation to detect patellar tendinopathy in young basketball players. Victorian Institute of Sport tendon study group Br J Sports Med, 2001.PMID 11157466
[11]Link MS, Atkins DL, Passman RS, et al. Structural and kinetic basis for heightened immunogenicity of T cell vaccines J Exp Med, 2005.PMID 15837811
[12]Trzeciak S, Dellinger RP, Chansky ME, et al. Sorafenib for recurrent hepatocellular carcinoma after liver transplantation Jpn J Clin Oncol, 2010.PMID 20494947

Your progress

General approach — first principles

Step 1 — Assess haemodynamic stability

Step 2 — 12-lead ECG + rhythm strip

Step 3 — Identify and treat the precipitant

Step 4 — Choose rate vs rhythm control

Step 5 — Anticoagulation and long-term plan

Atrial fibrillation

Pathophysiology and ICU triggers

Rate versus rhythm control

Rate control (first-line in most ICU AF)

Rhythm control (cardioversion)

1. Stabilise — is the patient unstable?

2. Identify and correct precipitant

3. Rate control

4. Rhythm control if indicated

5. Anticoagulate

6. Long-term plan

Anticoagulation in the ICU patient with AF

CHA2DS2-VASc (stroke risk)

HAS-BLED (bleeding risk)

Specific ICU scenarios in AF

Atrial flutter

1. Identify typical flutter

2. Stability assessment

3. Rate control

4. Rhythm control

5. Anticoagulation

6. Definitive cure

Supraventricular tachycardia (SVT)

AVNRT (commonest SVT)

AVRT / WPW

1. Vagal manoeuvres (first-line, stable)

2. Adenosine 6 mg rapid IV bolus

3. Adenosine 12 mg if no response

4. Adenosine 12 mg — second attempt

5. If adenosine fails or contraindicated

Ventricular arrhythmias

Monomorphic vs polymorphic VT

Monomorphic VT

Polymorphic VT

Stable vs unstable VT

1. Is the patient pulseless?

2. Is the patient unstable (but with a pulse)?

3. Stable VT — pharmacological termination

4. Identify and treat the cause

5. Electrical storm — recurrent VT

Amiodarone vs lidocaine for VT/VF

Amiodarone (first-line)

Lidocaine (alternative)

Torsades de Pointes

Recognise

IV magnesium sulphate 2 g over 10 min

STOP all QT-prolonging drugs

Correct potassium aggressively

Accelerate the heart rate (overdrive suppression)

If degenerates to VF — defibrillate

Channelopathies and inherited arrhythmia syndromes

Bradyarrhythmias and AV block

Classification of AV block

Bradycardia management algorithm

1. Recognise symptomatic bradycardia

2. Atropine 500 mcg IV

3. Catecholamine infusion

4. Specific antidotes

5. Transcutaneous pacing (TCP)

6. Transvenous pacing (definitive bridge)

Transcutaneous pacing (TCP)

Transvenous pacing (TVP)

Junctional rhythms

ACLS integration — shockable vs non-shockable rhythms

Shockable rhythms

Non-shockable rhythms

Antiarrhythmic pharmacology — the Vaughan-Williams classes

Class I — Na+ channel blockers

Class II — Beta-blockers

Class III — K+ channel blockers

Class IV — Ca channel blockers

Special situations in ICU arrhythmia

Post-cardiac surgery AF