ICU Map
ICU Medication MasterclassVF/pVT • PEA/asystole • Bradycardia • WCT • Torsades • Special causes

Cardiac Arrest & Peri-Arrest Pharmacology

Drug reasoning during cardiac arrest and peri-arrest instability: know which medications can help, which are merely optional, and which routine drugs distract from high-quality CPR, defibrillation and treatment of reversible causes.

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1

Keep high-quality CPR and defibrillation ahead of medication administration in shockable arrest.

2

Use epinephrine at the appropriate point without implying that vasopressors replace definitive arrest care.

3

Use amiodarone or lidocaine selectively for shock-refractory VF/pVT.

4

AHA 2025: routine calcium is not recommended, routine bicarbonate is not recommended, and routine magnesium is not recommended during undifferentiated adult cardiac arrest.

5

Choose procainamide/adenosine only in the stable wide-complex tachycardia phenotypes where they fit.

Cardiac Arrest & Post-Arrest

Full arrest and post-ROSC critical-care pathway.

Open →

Toxicology & Antidotes

Mechanism-specific poisoning pharmacology.

Open →
Core agents

Choose by physiology, not by habit

The table below is a selection framework. Open the individual monograph for exact dosing, preparation, renal/CRRT/IHD adjustment, interactions and evidence traceability.

Epinephrine
Potent Alpha-1, Beta-1, and Beta-2 Adrenergic Agonist
Core agent

ICU role: Core vasopressor in adult cardiac arrest and infusion/bolus therapy in selected peri-arrest states.

Choose: Use according to arrest rhythm/timing while uninterrupted CPR/defibrillation continue.
Hesitate: More epinephrine is not a substitute for correcting hypoxia, tamponade, tension PTX, thrombosis or other reversible causes.

Monitor: Rhythm, ROSC, BP after ROSC and perfusion.

Amiodarone
Class III Antiarrhythmic (Multi-Channel Blocker)
Core agent

ICU role: Antiarrhythmic option for VF/pVT unresponsive to defibrillation and selected stable ventricular arrhythmias.

Choose: Shock-refractory VF/pVT after defibrillation strategy; selected VT/electrical storm with specialist strategy.
Hesitate: Not a treatment for PEA/asystole and not first-line for classic torsades.

Monitor: ECG, BP, QT and hepatic effects with ongoing therapy.

Lidocaine IV
Class Ib antiarrhythmic
Core agent

ICU role: Alternative antiarrhythmic to amiodarone for shock-refractory VF/pVT and selected ventricular arrhythmias.

Choose: Reasonable alternative when amiodarone is unavailable/undesirable.
Hesitate: CNS toxicity accumulates with high exposure, hepatic dysfunction and low-flow states.

Monitor: ECG, neurologic status and hepatic perfusion.

Procainamide
Class IA Sodium-Channel Blocking Antiarrhythmic
Core agent

ICU role: Slow-infusion class IA agent for selected stable wide-complex tachycardia.

Choose: Stable regular monomorphic WCT when QT is not prolonged and significant HF/hypotension are absent.
Hesitate: Not a rapid arrest drug; stop for hypotension or major QRS widening.

Monitor: Continuous ECG/BP, QRS/QT and renal function.

Adenosine
Endogenous Purine Nucleoside / AV Nodal Blocking Agent
Core agent

ICU role: Ultra-short AV nodal blocker for regular narrow SVT and selected stable regular monomorphic WCT diagnosis/therapy.

Choose: When an AV-node-dependent rhythm is likely and the rhythm is regular.
Hesitate: Do not give for unstable, irregularly irregular or polymorphic WCT.

Monitor: Continuous ECG and resuscitation readiness.

Atropine
Anticholinergic / Competitive Muscarinic Receptor Antagonist
Core agent

ICU role: First-line medication for symptomatic bradycardia in appropriate adult peri-arrest algorithms.

Choose: Symptomatic bradycardia while preparing pacing/infusion strategies if ineffective.
Hesitate: Do not delay transcutaneous pacing/epinephrine/dopamine when atropine fails or high-grade block is unlikely to respond.

Monitor: HR, BP, rhythm and perfusion.

Magnesium Sulfate
Electrolyte / Multi-Mechanism Membrane & Neuromuscular Modulator
Core agent

ICU role: Treatment for torsades/long-QT polymorphic VT and selected electrolyte-driven arrhythmias.

Choose: Torsades or documented severe hypomagnesemia.
Hesitate: Routine magnesium in undifferentiated cardiac arrest is not recommended.

Monitor: Rhythm, Mg/K, BP and renal function.

Calcium Gluconate
Electrolyte / Cardiac Membrane Stabilizer
Core agent

ICU role: Membrane stabilization for hyperkalemia and selected calcium-channel blocker/toxicologic indications.

Choose: Hyperkalemic ECG toxicity or disease-specific indication.
Hesitate: Routine calcium in undifferentiated cardiac arrest is not recommended.

Monitor: ECG, ionized calcium and underlying cause.

Sodium Bicarbonate
Alkalinizing Agent / Buffer
Core agent

ICU role: Targeted therapy for sodium-channel blockade, severe hyperkalemia/acidemia contexts and selected poisonings.

Choose: Mechanism-specific indications such as TCA/sodium-channel toxicity.
Hesitate: Routine bicarbonate in undifferentiated cardiac arrest is not recommended.

Monitor: ABG/VBG, sodium, potassium, ECG/QRS and ventilation.

Clinical decision matrix

What changes the drug choice?

Witnessed VF persists after repeated high-quality shocks

Preferred reasoning: Continue CPR/defibrillation, give epinephrine according to algorithm and consider amiodarone or lidocaine for refractory VF/pVT.
Avoid: Stacking calcium, bicarbonate and magnesium without a specific indication.

Why: AHA 2025 supports amiodarone or lidocaine as optional antiarrhythmics but advises against routine calcium/bicarbonate/magnesium.

PEA with dialysis patient and sine-wave ECG immediately before arrest

Preferred reasoning: Treat presumed hyperkalemia aggressively, including IV calcium and potassium-shifting/removal strategies, while ACLS continues.
Avoid: Calling calcium 'routine arrest medication' and missing the mechanism.

Why: Calcium is appropriate for a specific hyperkalemic arrest mechanism even though routine use in undifferentiated arrest is not recommended.

Stable regular monomorphic WCT

Preferred reasoning: Use an AHA-supported stable-WCT strategy such as procainamide/amiodarone/sotalol as appropriate; adenosine may be considered if regular monomorphic and diagnosis is uncertain.
Avoid: Verapamil/diltiazem into undifferentiated WCT or adenosine into irregular/polymorphic WCT.

Why: Mechanism and stability determine the safe drug choices.

Polymorphic VT with long QT

Preferred reasoning: Defibrillate if unstable and give IV magnesium while removing QT triggers and correcting K.
Avoid: Routine amiodarone that may further prolong repolarization.

Why: Classic torsades is a repolarization problem, not generic monomorphic VT.

High-yield protocols

Mechanism-based sequences worth memorizing

Arrest medication checkpoint

  1. Rhythm + shock delivery/CPR first.
  2. Give epinephrine and antiarrhythmics only where the algorithm supports them.
  3. Search aggressively for Hs/Ts and use mechanism-specific therapies.
⚠️ A medication-rich resuscitation can still be a poor resuscitation if CPR, shocks or reversible causes are delayed.

Stable WCT

  1. Confirm stability; unstable WCT gets synchronized cardioversion.
  2. Define monomorphic versus polymorphic/irregular phenotype and QT status.
  3. Use the drug that fits the mechanism and stop if hypotension/conduction toxicity develops.
⚠️ Do not apply one antiarrhythmic to every wide-complex rhythm.
Organ failure & special settings

When standard pharmacology stops being standard

Toxicologic arrest
Priority: Use the specific antidote/physiology pathway in addition to ACLS.
Pitfall: Treating poison-induced arrest as if no mechanism-specific therapy exists.
Pregnancy
Priority: Use standard high-quality maternal resuscitation plus pregnancy-specific positioning and resuscitative-delivery planning.
Pitfall: Withholding indicated arrest medications solely because of pregnancy.
Post-ROSC hypotension
Priority: Switch from arrest dosing to targeted hemodynamic support and diagnose shock phenotype.
Pitfall: Continuing repeated arrest boluses after ROSC instead of controlled infusion/hemodynamic management.
Severe bradycardia/high-grade block
Priority: Prepare pacing early when atropine is unlikely or ineffective.
Pitfall: Repeating atropine while perfusion worsens.
Resident progression

R1 → R5 bedside cases

Recognition becomes selection, then organ-failure adjustment, competing physiology and senior-level prioritization.

R1

PEA

PEA arrest after severe hypoxemia; no shockable rhythm.

Show reasoning

High-quality CPR, epinephrine according to ALS algorithm, airway/oxygenation and aggressive treatment of the reversible cause. Amiodarone is not indicated for PEA.

R2

Shock-refractory VF

VF persists after multiple shocks and CPR cycles.

Show reasoning

Continue defibrillation/CPR and epinephrine; amiodarone or lidocaine may be considered for refractory VF/pVT.

R3

Hyperkalemic arrest

ESRD patient arrests after peaked T waves widened into a sine-wave pattern.

Show reasoning

Treat the mechanism: IV calcium for membrane stabilization plus insulin/glucose and definitive potassium removal while ACLS continues.

R4

Stable WCT with prolonged QT

Regular wide tachycardia but baseline QT is markedly prolonged and patient has severe HF.

Show reasoning

Procainamide is a poor choice because both prolonged QT and HF increase risk; use an alternative/electrical strategy guided by rhythm mechanism and stability.

R5

TCA arrest

Wide QRS, hypotension and ventricular arrhythmia after tricyclic overdose progressing to arrest.

Show reasoning

Standard ALS plus aggressive sodium bicarbonate therapy and ventilation/acid-base control for sodium-channel blockade; mechanism-specific treatment is crucial.

Full medication monograph

Epinephrine

Potent direct alpha/beta agonist for anaphylactic shock, cardiac arrest, post-cardiac arrest shock, and refractory septic shock — powerful inotrope and bronchodilator with transient hyperlactatemia.

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Amiodarone

Broad-spectrum antiarrhythmic used for shock-refractory cardiac arrest, stable ventricular arrhythmias, and rate/rhythm-related management of atrial fibrillation — notable for an extremely long half-life and cumulative multi-orga…

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Lidocaine IV

IV sodium-channel blocker used for refractory ventricular arrhythmias and as an alternative to amiodarone in shock-refractory VF/pVT.

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Procainamide

IV class IA antiarrhythmic that may be considered for stable monomorphic wide-complex tachycardia. It slows conduction and prolongs repolarization, so hypotension, QRS widening and QT prolongation limit use.

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Adenosine

Ultra-short-acting agent that transiently blocks AV nodal conduction to terminate AV-node-dependent reentrant SVT — its sub-10-second half-life makes the rapid-push-plus-immediate-flush administration technique as important as th…

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Atropine

Competitive muscarinic antagonist that blocks vagal parasympathetic tone at the SA and AV nodes, used as first-line for acute symptomatic sinus bradycardia (1 mg IV push q3–5m, max 3 mg) and in megadoses for organophosphate/choli…

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Magnesium Sulfate

Spans four genuinely distinct ICU indications — torsades de pointes, adjunctive severe asthma therapy, eclampsia/severe preeclampsia, and simple hypomagnesemia repletion — each with its own mechanism-relevant dosing; no single do…

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Calcium Gluconate

First-line cardiac membrane stabilizer for hyperkalemic ECG changes and definitive replacement therapy for symptomatic hypocalcemia — the single most important teaching point is that it stabilizes the myocardium without changing …

Dosing • renal/CRRT • toxicity • interactions →
Full medication monograph

Sodium Bicarbonate

A deliberately narrow-role buffer reserved for severe metabolic acidosis with concurrent AKI, sodium-channel-blocker toxicity, and select hyperkalemia with significant concurrent acidemia — explicitly NOT a routine therapy for la…

Dosing • renal/CRRT • toxicity • interactions →

Evidence & bedside-use boundary

This Masterclass teaches selection and reasoning. Exact dosing, concentration, infusion preparation, renal/hepatic/RRT adjustment and monitoring must be checked in the linked medication monograph and the institution's current formulary/protocol. Local resistance patterns and regulatory drug availability can change faster than a static teaching page.