Ilyas K. Colombowala, MD, FACC, FHRS
Cardiac Electrophysiology · Houston, TX · colombowala.com
EP Staff Education

Emergency

Code Drugs and ACLS in the EP Lab

What's on the crash cart, what's in the room, and what's drawn up before the case for what kind of patient. ACLS adapted to the EP-lab context — where pacing wires, ablation catheters, anticoagulation, and ongoing sedation all change the equation.

Indications

  • ▸Cardiac arrest in the EP lab — PEA, asystole, VF, or pulseless VT
  • ▸Pre-arrest deterioration: severe bradycardia, profound hypotension, sustained VT with hemodynamic compromise
  • ▸Severe vagal reaction: rate < 30 with hypotension
  • ▸Bronchospasm or anaphylaxis during sedation or contrast

Equipment / drugs

  • ▸Crash cart with defibrillator/AED, intubation supplies, and full ACLS drug tray within arm's reach of the table
  • ▸Pressor infusions (norepinephrine, epinephrine drips) preassembled and primed for high-risk cases
  • ▸Reversal agents per anticoagulant in use (protamine, idarucizumab, andexanet, 4F-PCC)
  • ▸Sedation reversal: flumazenil (for benzodiazepines), naloxone (for opioids)
  • ▸External pacing pads on every EP-lab patient before the case starts

Pitfalls

  • ▸Forgetting that an ablation catheter, sheath, or pacing wire is INSIDE the heart during a code — pause ablation, defibrillate with pads, manage carefully
  • ▸Defibrillating through an active intracardiac sheath without considering current path — pads should be in standard anterolateral position
  • ▸Atropine for vagal bradycardia from pacing-test-induced hypotension — usually works, but watch for SVT precipitation in dual-AV-nodal patients
  • ▸Epinephrine boluses in patients with structural heart disease, IHD, or active ablation — proarrhythmic; use the smallest effective dose
  • ▸Treating sedation hypotension with pressors first when fluid and lighter sedation would do — over-treating is its own complication

Before the case: standard setup

Every EP-lab patient gets the same baseline setup, regardless of acuity:

  • External defibrillator pads placed before the case starts. Anterolateral position by default; antero-posterior if pads will be in the field. Connected to the defibrillator and tested.
  • Crash cart in the room or immediately outside, drug tray current and dated.
  • At least one large-bore IV in addition to the procedural sheath access.
  • Arterial line for any case where hemodynamic monitoring matters (most ablations, all VT cases).
  • Pressors drawn up for higher-risk cases — phenylephrine 100 µg/mL syringes, epinephrine 1:10,000 ready, norepinephrine drip primed.
  • Reversal agents appropriate to the anticoagulant in use, stocked and located.

Knowing where everything lives means the team doesn’t waste seconds during the event.

ACLS adapted to the EP lab

Standard ACLS algorithms apply with two layers of adaptation:

  1. There are catheters in the heart. Most arrests in the lab occur with a sheath in the right atrium, a mapping catheter in the LA or LV, sometimes a deflectable in the coronary sinus, and possibly a pacing wire in the RV. Decisions about ablation energy, defibrillation vector, and catheter removal all interact.
  2. The patient is anticoagulated. Most cases use uninterrupted DOAC or therapeutic heparin throughout. Any arrest carries a tamponade-until-proven-otherwise corollary.

Shockable rhythms (VF, pulseless VT)

  • Defibrillate at 200 J biphasic (or device-appropriate maximum). Pads in standard position. Pause ablation if active before the shock; some operators briefly retract the ablation catheter from heart contact to avoid energy-delivery-related injury during the shock (debated, institutionally variable).
  • CPR between shocks per standard ACLS — 30:2 if not intubated, continuous compressions if intubated. Person doing compressions should be positioned to clear the catheters.
  • Epinephrine 1 mg IV every 3–5 minutes per ACLS, given between shocks not during.
  • Amiodarone 300 mg IV bolus after second or third shock if VF/pulseless VT persists, then 150 mg IV at 3–5 minutes if needed.
  • Consider reversible causes the moment ROSC is achieved or refractory persists — particularly tamponade (ICE!), pulmonary embolism, hyperkalemia.

Non-shockable rhythms (PEA, asystole)

  • Recognize the trigger. PEA in the EP lab is tamponade until proven otherwise. Check ICE immediately.
  • CPR + epinephrine 1 mg IV every 3–5 minutes per ACLS.
  • Don’t shock asystole. It does not respond to defibrillation.
  • Consider reversible causes (“the H’s and T’s”) with EP-lab specificity:
    • Tamponade — ICE, pericardiocentesis
    • Hypoxia — airway, intubate if not already
    • Toxin/drug effect — sedation overdose (reverse), anesthetic effect, recent ablation energy
    • Hyperkalemia — particularly post-RF energy delivery in some niche scenarios; calcium, bicarb, glucose-insulin
    • PE — TEE if available; thrombolysis is a high-bar decision

Severe bradycardia (rate < 40 with hypotension)

  • Atropine 0.5–1 mg IV — first line for vagal-mediated bradycardia
  • Pacing — transcutaneous if external pads are already placed (often the case in the EP lab); transvenous if longer-term needed. Wire pacing is usually faster if a catheter is already in the heart
  • Epinephrine drip 2–10 µg/min, titrate to MAP > 65 — bridge to pacing or pacer placement
  • Dopamine drip 5–20 µg/kg/min is an alternative — both work; team familiarity matters more than choice

Severe hypotension without arrhythmia

  • Fluid bolus 500 mL crystalloid wide open — first move
  • Light up sedation if over-sedated — propofol off, midazolam reversal with flumazenil if appropriate, naloxone if opioid-heavy
  • Pressor if MAP < 65 despite fluid — phenylephrine 100 µg IV bolus repeated, or start norepinephrine drip
  • Echo / ICE — rule out tamponade, new wall motion abnormality, mechanical complication
  • Consider anaphylaxis if rash, bronchospasm, or recent contrast — IM epinephrine 0.3–0.5 mg, IV fluid, steroids

Specific drug notes

Epinephrine

The default ACLS pressor. 1 mg IV every 3–5 minutes during arrest. For severe but non-arrest hypotension, 10–100 µg pushes are titratable.

In the EP lab, epinephrine is proarrhythmic — it can precipitate VT in a patient with structural heart disease, IHD, or ongoing ablation substrate. Use the smallest effective dose. In a patient who just had a successful ablation, post-arrest epinephrine may trigger the very rhythm you just treated.

Amiodarone

300 mg IV bolus for refractory VF/pulseless VT, followed by 150 mg if needed. After ROSC, consider an infusion (1 mg/min × 6 hours, then 0.5 mg/min × 18 hours).

Avoid if QT is already prolonged. Common transient hypotension with rapid push — slow it down.

Atropine

0.5–1 mg IV for vagal bradycardia. Repeat every 3–5 minutes up to 3 mg total. Watch for SVT precipitation in patients with dual AV nodal pathways.

Generally not effective for AV-block bradycardia where the block is below the AV node (Mobitz II, complete heart block) — pacing is the answer there.

Adenosine

6 mg → 12 mg → 12 mg IV push for narrow-complex regular tachycardia or as a diagnostic tool. Run with fast saline flush. Warn the patient about transient awful feeling (chest pressure, doom) — sedated patients tolerate this better.

Contraindicated in pre-excited AFib (can precipitate VF), severe asthma (bronchospasm), or known sensitivity. Caffeine and theophylline blunt the effect.

Lidocaine

100 mg IV bolus (or 1–1.5 mg/kg) is an alternative to amiodarone in shock-refractory VF/VT, particularly in ischemic substrate. Has fallen out of fashion compared to amiodarone but remains in the ACLS algorithm and is reasonable when amiodarone is contraindicated or unavailable.

Magnesium sulfate

2 g IV for torsades de pointes — first-line. Also reasonable in refractory VF with prolonged QT.

Calcium chloride / gluconate

For known or suspected hyperkalemia, calcium-channel-blocker toxicity, or severe beta-blocker toxicity. 10% calcium chloride 1 g IV via central line preferred (peripheral irritation), or calcium gluconate 1–3 g IV peripherally.

Reversal agents

  • Protamine for unfractionated heparin — 1 mg per 100 units heparin given in the last 2 hours, max 50 mg per dose, slow IV push
  • Idarucizumab (Praxbind) for dabigatran — 5 g IV
  • Andexanet alfa for apixaban and rivaroxaban — bolus + infusion per protocol
  • 4-factor PCC (Kcentra) — alternative for factor Xa inhibitor reversal, also for warfarin (with FFP and vitamin K)
  • Vitamin K 10 mg IV slowly for warfarin (works over hours, not minutes)
  • Flumazenil for benzodiazepine reversal — 0.2 mg IV, repeat — use cautiously, can precipitate seizures
  • Naloxone for opioid reversal — 0.04–0.4 mg IV titrated

After the event

Every code in the lab requires:

  • Documentation — times, rhythms, drugs given, defibrillations, lines placed, response
  • Family communication — early, honest, with the attending leading
  • Disposition decision — ICU vs floor vs lab observation
  • Cardiothoracic surgery awareness if mechanical complication suspected or confirmed
  • Debrief within 24–48 hours — what worked, what slowed the response, what to do differently
  • M&M presentation for events involving complications, deaths, or near-misses

The pattern of recognition and response in the lab is built one event at a time. Even uncomplicated codes — that resolved quickly, that the team handled well — deserve the same structured review.

Last reviewed by Dr. Colombowala on May 24, 2026.

Clinical-reference content, not medical advice. This page is written for EP staff and does not create a doctor-patient relationship. It does not replace institutional policy, current device manuals, or attending direction during a case. See the full disclaimer.

© 2026 Ilyas K. Colombowala, MD. All rights reserved. Reproduction, redistribution, or republication of this content in any form without written permission is prohibited.

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