Arrhythmias in the ICU

Contents

Overview

Arrhythmias occur in up to 30% of ICU patients and are associated with increased morbidity and mortality. They may be the primary presentation (acute MI, channelopathy), a direct complication of critical illness (electrolyte disturbance, hypoxia, sepsis), or iatrogenic (drug toxicity, central line placement). The first priority is always identifying and correcting the underlying cause before committing to antiarrhythmic therapy.

Atrial Fibrillation

New-onset AF is the most common arrhythmia in the ICU, occurring in 5–15% of all ICU admissions and up to 46% of patients with sepsis or following major cardiac surgery.

Pathophysiology

AF in critical illness is driven by multiple mechanisms: catecholamine excess, sympathetic nervous system activation, atrial stretch from volume overload, hypoxia-induced atrial ischaemia, inflammatory cytokines affecting ion channels, and electrolyte disturbances (hypokalaemia, hypomagnesaemia). These create a substrate of heterogeneous atrial conduction and refractoriness that facilitates re-entry.

Clinical Consequences

  • Haemodynamic compromise from loss of atrial kick (up to 25% of cardiac output in patients with poor LV compliance), rapid ventricular rate, and irregular rhythm
  • Thromboembolic risk (stroke): new-onset AF in critical illness confers a real but debated stroke risk — anticoagulation decisions must balance this against bleeding risk

Management

Step 1 — Identify and correct precipitants: electrolytes (K+ >4 mmol/L, Mg2+ >0.8 mmol/L), hypoxia, sepsis, volume status, pain, fever, thyrotoxicosis.

Step 2 — Rate vs rhythm control: The primary decision in haemodynamically stable patients.

Rate control: Target ventricular rate 60–100 bpm at rest.

  • IV beta-blocker (metoprolol 2.5–5 mg IV, repeat as needed; esmolol infusion for titration): preferred first-line in most patients. Avoid in severe LV dysfunction, bronchospasm, or significant bradycardia.
  • IV amiodarone 300 mg over 1 hour, then 900 mg over 24 hours: effective for rate control and may restore sinus rhythm. Preferred in haemodynamically compromised patients or severe LV dysfunction where beta-blockers are contraindicated.
  • IV digoxin 500 micrograms over 30 minutes: slow onset; suitable for rate control in patients who cannot tolerate beta-blockers or where rate at rest (not during activity) is the primary concern.

Rhythm control (cardioversion): Consider in patients with haemodynamically significant AF not responding to rate control, or when restoration of sinus rhythm is clinically important.

  • DC cardioversion: first-line for haemodynamically unstable AF requiring immediate treatment. Synchronised 200 J biphasic.
  • Pharmacological cardioversion: amiodarone is the most commonly used agent in critically ill patients. Flecainide and propafenone are effective in structurally normal hearts but are contraindicated in IHD, LV dysfunction, or HF.

Anticoagulation: Heparin or LMWH for new-onset AF in ICU in most patients where bleeding risk permits. Formal stroke risk stratification (CHA₂DS₂-VASc) and bleeding risk assessment (HAS-BLED) should inform long-term anticoagulation decisions.

AF After Cardiac Surgery

Post-operative AF (POAF) affects 30–40% of patients after CABG and up to 50% after combined CABG + valve surgery. It is driven by pericardial inflammation, surgical trauma, and sympathetic activation. Most episodes are self-limiting within 24–48 hours. Amiodarone (pre-operative and post-operative) and magnesium prophylaxis reduce incidence. Management follows standard principles.

Supraventricular Tachycardias

SVT (narrow complex tachycardia with a rate typically 150–250 bpm, paroxysmal onset) in the ICU usually represents AVNRT (AV nodal re-entrant tachycardia) or AVRT (AV re-entrant tachycardia using an accessory pathway).

Management

Vagal manoeuvres: Valsalva (modified — patient supine, legs raised after exhalation against resistance), carotid sinus massage. Effective in 25% of cases.

Adenosine: 6 mg rapid IV bolus through a large vein, followed by saline flush. If unsuccessful, 12 mg, then a further 12 mg. Adenosine blocks AV nodal conduction transiently, terminating re-entrant circuits through the AV node. It also unmasks underlying atrial arrhythmias (flutter, AF) if the tachycardia is not AVNRT/AVRT. Contraindicated in severe asthma, Wolff-Parkinson-White with AF (risk of ventricular fibrillation via accessory pathway).

DC cardioversion: Synchronised cardioversion for haemodynamically unstable SVT.

Atrial Flutter

Regular SVT at 150 bpm (with 2:1 AV block driving a flutter rate of 300 bpm). Vagal manoeuvres may transiently slow the rate, revealing the characteristic sawtooth flutter baseline (best seen in leads II, III, aVF). Management: rate control as for AF; DC cardioversion for haemodynamic compromise or failed rate control; atrial flutter ablation definitively in non-acute setting.

Ventricular Arrhythmias

Ventricular Tachycardia (VT)

VT is defined as three or more consecutive ventricular complexes at a rate >100 bpm, with broad QRS (>120 ms). It may be monomorphic (uniform morphology — scar-related re-entry) or polymorphic (varying morphology — myocardial ischaemia, channelopathy, QT prolongation).

Sustained VT (>30 seconds or haemodynamic compromise): Immediate DC cardioversion if unstable. If stable: IV amiodarone 300 mg over 20–60 minutes (preferred in structural heart disease), then infusion. Lidocaine 1–1.5 mg/kg IV is an alternative. Correct electrolytes (K+, Mg2+).

Non-sustained VT (<30 seconds, self-terminating): Investigate for cause. In the absence of structural heart disease, reassess and correct precipitants. In the presence of IHD or structural disease, specialist cardiology input is required.

Torsades de Pointes

A polymorphic VT associated with prolonged QTc, characterised by a twisting of the QRS axis around the isoelectric line. Usually self-terminating but can degenerate to VF.

Causes of prolonged QT in ICU: drugs (amiodarone, haloperidol, methadone, quinolones, azoles, many others), hypokalaemia, hypomagnesaemia, hypocalcaemia, bradycardia, hypothermia, hypothyroidism, congenital long QT syndrome.

Management: IV magnesium sulphate 2 g (8 mmol) IV over 10 minutes is first-line. Correct electrolytes. Stop QT-prolonging drugs. Temporary pacing to overdrive suppress (target rate 90–100 bpm) if recurrent or refractory.

Ventricular Fibrillation

VF is immediately life-threatening. Management follows ALS/ACLS guidelines: immediate defibrillation, CPR, adrenaline 1 mg IV every 3–5 minutes, amiodarone 300 mg IV after three shocks. Identify and treat reversible causes (4 Hs and 4 Ts).

Bradyarrhythmias

Sinus Bradycardia

Causes in ICU: hypothermia, hypothyroidism, raised intracranial pressure (Cushing's triad: bradycardia, hypertension, irregular respirations), vagal activation (suctioning, vomiting), beta-blockers, calcium channel blockers, digoxin, alpha-2 agonists (dexmedetomidine, clonidine), opioids.

Management: Treat the cause. If symptomatic or haemodynamically significant: atropine 500 micrograms IV (up to 3 mg); if ineffective, isoprenaline infusion (2–10 micrograms/min) or temporary pacing.

Heart Block

First-degree AV block (PR >200 ms): Usually benign. Identify cause.

Second-degree AV block:

  • Mobitz type I (Wenckebach): Progressive PR prolongation until a P wave is not conducted. Usually benign, nodal in origin.
  • Mobitz type II: Fixed PR interval with intermittent non-conducted P waves. More serious — infranodal; risk of progression to complete heart block.

Third-degree (complete) heart block: Complete AV dissociation. Ventricular rate is maintained by a slow escape rhythm (nodal 40–60 bpm, ventricular 20–40 bpm). Causes: inferior MI (often transient, vagally mediated), anterior MI (infranodal, serious), drug toxicity, Lyme disease, post-cardiac surgery. Requires urgent temporary pacing if haemodynamically significant.

Drug-Induced Arrhythmias

The ICU environment is replete with proarrhythmic drugs. Regular QTc monitoring is important:

Drug Arrhythmia risk
Amiodarone QT prolongation, bradycardia, torsades (rare)
Haloperidol QT prolongation, torsades
Methadone QT prolongation
Fluoroquinolones QT prolongation
Azole antifungals QT prolongation
Digoxin Brady-, tachy-, heart block in toxicity
Suxamethonium Bradycardia (muscarinic effect)
Dexmedetomidine Bradycardia, AV block

Target QTc <450 ms in men, <470 ms in women. A QTc >500 ms or increase of >60 ms from baseline warrants review and drug rationalisation.

General Principles of Management

  1. 12-lead ECG as the standard for diagnosis — a cardiac monitor alone is insufficient.
  2. Identify and correct reversible causes before antiarrhythmic drugs: hypoxia, electrolytes (K+, Mg2+, Ca2+), acid-base, volume, pain, fever, drugs.
  3. Haemodynamic stability determines urgency: unstable patients require immediate cardioversion; stable patients allow time for investigation and titrated pharmacological management.
  4. Antiarrhythmic drugs are not benign: all have proarrhythmic potential. Use the minimum effective agent.
  5. Electrolyte targets: K+ 4.0–4.5 mmol/L, Mg2+ >0.8 mmol/L — higher targets than standard normal ranges reduce arrhythmia burden.

Viva Questions

What are the causes of new-onset AF in a critically ill patient and how do you approach management?

New-onset AF in critical illness is almost always secondary to an identifiable precipitant. The most common causes are sepsis and systemic inflammation, catecholamine excess, hypoxia, electrolyte disturbances (hypokalaemia, hypomagnesaemia), volume overload causing atrial stretch, pain and agitation, and post-operative state — particularly following cardiac or thoracic surgery. Drug causes include catecholamines, theophylline, and, paradoxically, withdrawal of beta-blockers. The approach begins with identifying and treating these precipitants — correcting potassium above 4.0 mmol/L and magnesium above 0.8 mmol/L, optimising oxygenation, and addressing sepsis or pain. Once precipitants have been addressed, the rate-versus-rhythm decision follows. In haemodynamically stable patients, rate control is the primary aim — IV beta-blockers (metoprolol or esmolol) are first-line in most patients. IV amiodarone is preferred when beta-blockers are contraindicated (severe LV dysfunction, bronchospasm) or when rhythm control is also desirable. DC cardioversion is reserved for haemodynamically unstable patients or failed medical rate control. The majority of new-onset ICU AF resolves once the underlying illness improves, without the need for long-term antiarrhythmic therapy or anticoagulation, though formal assessment is required at or after hospital discharge.

How do you manage torsades de pointes in the ICU?

Torsades de pointes is a polymorphic ventricular tachycardia associated with QTc prolongation, recognisable by the twisting of the QRS complex around the isoelectric baseline. It is typically self-terminating but can degenerate to ventricular fibrillation. The immediate management is IV magnesium sulphate 2 g (8 mmol) over 10 minutes, which shortens the action potential and suppresses early afterdepolarisations — the cellular mechanism of torsades. The QTc-prolonging cause must be identified and removed: review the drug chart and stop or substitute offending agents (amiodarone, haloperidol, methadone, fluoroquinolones, azoles). Electrolyte abnormalities must be corrected aggressively — hypokalaemia, hypomagnesaemia, and hypocalcaemia all prolong the QT and must be addressed. Bradycardia worsens torsades by prolonging the action potential; if the heart rate is below 60 bpm, temporary pacing to overdrive suppress the arrhythmia at a rate of 90–100 bpm is appropriate. Isoprenaline infusion can also increase the ventricular rate in this setting. In hereditary long QT syndromes, beta-blockers are the cornerstone of prevention, and ICD implantation should be considered. If torsades degenerates to VF, standard defibrillation and ALS protocols apply.

A patient in the ICU develops a broad complex tachycardia at 180 bpm. How do you differentiate VT from SVT with aberrant conduction and why does it matter?

The distinction matters because VT is immediately life-threatening and requires different treatment from SVT with aberrant conduction. However, a broad complex tachycardia should always be treated as VT until proven otherwise — the consequences of misidentifying VT as SVT and administering a calcium channel blocker (verapamil) or adenosine to a patient with VT can be catastrophic. Clinical features that favour VT include: haemodynamic instability, absence of P waves, AV dissociation (P waves and QRS complexes occurring independently), fusion beats (QRS morphology intermediate between sinus and ventricular morphology), capture beats (normal QRS during the tachycardia), extreme axis deviation, and concordance (all QRS complexes in the chest leads pointing in the same direction — either all positive or all negative). Brugada's criteria and the Wellens algorithm provide systematic ECG-based approaches. A history of structural heart disease (previous MI, cardiomyopathy) strongly favours VT. If there is any diagnostic uncertainty and the patient is haemodynamically stable, amiodarone is the safest treatment option as it is effective in both VT and most SVTs. Adenosine can be used diagnostically in a stable patient — it terminates SVT and in VT either has no effect or transiently reveals underlying AV dissociation. DC cardioversion is the definitive treatment for haemodynamically unstable broad complex tachycardia regardless of the aetiology.