When should flecainide be held in the Intensive Care Unit (ICU)?

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Last updated: December 15, 2025View editorial policy

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When to Hold Flecainide in the ICU

Flecainide should be held in the ICU for patients with structural heart disease (particularly ischemic heart disease or prior MI), heart failure, renal impairment, conduction abnormalities, hemodynamic instability, and electrolyte disturbances—particularly hypokalemia.

Critical Contraindications and High-Risk Scenarios

Structural Heart Disease and Ischemia

  • Flecainide is absolutely contraindicated in patients with ischemia, prior myocardial infarction, and should be avoided in patients with other structural heart diseases 1
  • The CAST trial demonstrated increased mortality among post-MI patients treated with sodium channel blockers, establishing this as a firm contraindication 1
  • Use only in patients without structural heart disease or ischemic heart disease 1

Heart Failure

  • Hold flecainide in patients with congestive heart failure, as it can worsen cardiac function 2
  • The drug has negative inotropic effects that can precipitate or worsen heart failure 3
  • Caution is required even in mild CHF, as elimination may be slower 4

Renal Dysfunction

  • Flecainide accumulation occurs with acute kidney injury and chronic renal impairment, leading to toxicity 5, 6
  • Approximately 27% of flecainide is excreted unchanged in urine, making renal function critical for drug clearance 4
  • Plasma elimination is markedly slower in end-stage renal disease and somewhat slower in moderate renal failure 4
  • Dosage reduction is mandatory in severe renal disease 4
  • Toxic levels (>1.50 μg/mL) can develop rapidly in AKI, even with normal dosing 5

Conduction System Abnormalities

  • Hold in patients with:
    • Sinus node dysfunction or pre-existing sinus node disease 2
    • AV block or infranodal conduction disease 1
    • Bundle-branch block 1, 2
    • Brugada syndrome 1
  • Flecainide slows conduction throughout the myocardium and specialized conduction system 2
  • Sodium channel blockers increase pacing thresholds and defibrillation energy requirements, potentially causing loss of capture in paced patients 1

Electrolyte Disturbances

  • Hypokalemia significantly increases the risk of flecainide toxicity and proarrhythmia 5
  • Correct potassium levels before continuing flecainide therapy
  • Alkaline urinary conditions may decrease flecainide elimination 4

Proarrhythmic Risk

  • Hold if QRS widening is observed, as this indicates toxicity 5, 3
  • Flecainide can convert atrial fibrillation to atrial flutter with 1:1 AV conduction, creating wide QRS complexes that mimic ventricular tachycardia 1
  • Risk of sustained monomorphic ventricular tachycardia, particularly with Class IC drugs 1
  • Can accelerate ventricular rate during AF 1

ICU-Specific Considerations

Hemodynamic Instability

  • Hold flecainide in any patient with hypotension or cardiogenic shock 5
  • The drug's negative inotropic effects can worsen hemodynamic compromise 3

Sepsis and Critical Illness

  • Acute kidney injury from sepsis or other critical illness can rapidly lead to flecainide accumulation 5
  • Monitor renal function closely in critically ill patients on flecainide

Drug Interactions in the ICU

  • Flecainide is metabolized by CYP2D6; inhibitors (quinidine, fluoxetine, tricyclics) increase plasma concentrations 1
  • Avoid combining with other Class IA, IC, or III antiarrhythmics, which may exacerbate cardiac toxicity 1

Management of Suspected Toxicity

Recognition

  • Wide complex tachycardia in a patient on flecainide should raise immediate suspicion for toxicity 5
  • QRS widening is a key electrocardiographic finding 5, 3
  • Altered mental status may accompany severe toxicity 5

Treatment

  • Intravenous sodium bicarbonate (1-2 mEq/kg boluses) is the treatment of choice for flecainide toxicity 1, 6
  • Target arterial pH >7.45, similar to tricyclic antidepressant toxicity 1
  • Hemodialysis is not effective for removing unchanged flecainide 4

Common Pitfalls to Avoid

  • Do not assume normal renal function in ICU patients—even mild AKI can cause accumulation 5, 6
  • Do not mistake flecainide-induced atrial flutter with 1:1 conduction for ventricular tachycardia—this can lead to inappropriate treatment 1
  • Do not continue flecainide in patients requiring pacemakers or ICDs without checking device function, as increased pacing thresholds may cause loss of capture 1
  • Do not overlook hypokalemia, which dramatically increases toxicity risk 5

References

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Research

Flecainide: a new antiarrhythmic drug.

Clinical cardiology, 1986

Research

Safety of flecainide.

Drug safety, 2012

Research

Metabolism of flecainide.

The American journal of cardiology, 1984

Research

The Case of Flecainide Toxicity: What to Look for and How to Treat.

The Journal of emergency medicine, 2020

Research

Flecainide toxicity in renal failure.

Proceedings (Baylor University. Medical Center), 2018

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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