5.6 ACLS Algorithms & Emergency Medications in the EP Lab
Key Takeaways
- High-quality CPR means 100-120 compressions per minute at 2-2.4 inches depth with full recoil, minimal interruptions, and rhythm checks every 2 minutes.
- Only ventricular fibrillation and pulseless ventricular tachycardia are shockable; asystole and pulseless electrical activity are treated with CPR and epinephrine.
- Epinephrine 1 mg IV every 3-5 minutes is used in every arrest rhythm; amiodarone 300 mg then 150 mg or lidocaine is added for refractory shockable rhythms.
- Synchronized cardioversion times the shock to the R wave to avoid the vulnerable period; unsynchronized defibrillation is used for VF and pulseless polymorphic VT.
- Intravenous magnesium sulfate is the specific treatment for torsades de pointes even when the serum magnesium level is normal.
5.6 ACLS Algorithms & Emergency Medications in the EP Lab
The EP lab is the one place in the hospital where ventricular fibrillation is induced on purpose. CCI names Advanced Cardiac Life Support (ACLS), Basic Life Support (BLS), and emergency procedures and equipment in its published knowledge list, and task D8 requires assisting with management of procedural complications including emergency pacing.
1. High-Quality CPR
| Element | Standard |
|---|---|
| Rate | 100-120 compressions per minute |
| Depth (adult) | 2 to 2.4 inches (5-6 cm) |
| Recoil | Full chest recoil between compressions |
| Interruptions | Less than 10 seconds, including for rhythm checks |
| Compression fraction | Target > 60% of arrest time spent compressing |
| Ventilation, no advanced airway | 30:2 compression-to-ventilation |
| Ventilation, advanced airway | 1 breath every 6 seconds (10/min) with continuous compressions |
| Compressor rotation | Every 2 minutes with the rhythm check |
| EtCO₂ | < 10 mmHg suggests inadequate compressions; an abrupt rise toward normal suggests return of spontaneous circulation |
In the EP lab three modifications apply. Compressions must not dislodge intracardiac catheters, so catheters are withdrawn to a safe position or removed if the arrest is prolonged. The fluoroscopy C-arm is swung clear immediately so it does not obstruct compressions or defibrillation. And because the patient is draped and often sedated, the team leader must explicitly assign airway, compressions, defibrillator, medications, and documentation rather than assume the usual code-team roles exist.
2. The Cardiac Arrest Algorithm
Unresponsive, no pulse
|
Start CPR, attach monitor
|
------------------------------
| |
SHOCKABLE NON-SHOCKABLE
VF / pulseless VT Asystole / PEA
| |
DEFIBRILLATE CPR 2 min
CPR 2 min Epinephrine 1 mg ASAP,
Epinephrine 1 mg then q3-5 min
q3-5 min Treat reversible causes
Amiodarone 300 mg |
(or lidocaine) Rhythm check q2 min
Treat reversible causes
Shockable rhythms are ventricular fibrillation and pulseless ventricular tachycardia only. Asystole and pulseless electrical activity are never shocked; treatment is compressions, epinephrine, and reversal of the underlying cause.
Reversible causes — the Hs and Ts, with their EP-lab-specific flavors:
| Hs | Ts |
|---|---|
| Hypovolemia (occult retroperitoneal bleed) | Tension pneumothorax (subclavian puncture) |
| Hypoxia (over-sedation) | Tamponade, cardiac (perforation — the most likely cause in this lab) |
| Hydrogen ion (acidosis) | Toxins (local anesthetic, antiarrhythmic proarrhythmia) |
| Hypo-/hyperkalemia | Thrombosis, pulmonary |
| Hypothermia | Thrombosis, coronary (air embolism into the RCA) |
In an EP lab arrest the first two considerations are almost always tamponade and hypoxia from sedation, and the fastest diagnostic tool for the first is the intracardiac echo catheter already in the right atrium.
3. Defibrillation Versus Synchronized Cardioversion
| Defibrillation (unsynchronized) | Synchronized cardioversion | |
|---|---|---|
| Timing | Immediate, any point in the cycle | Synchronized to the R wave |
| Indication | VF, pulseless VT, polymorphic VT with a pulse that is too disorganized to synchronize | Unstable SVT, atrial fibrillation, atrial flutter, monomorphic VT with a pulse |
| Why | No organized R wave to track | Avoids delivering energy in the vulnerable period of the T wave, which would induce VF |
| Biphasic energy | 120-200 J (device-specific), escalating | AF 120-200 J; flutter and SVT 50-100 J; monomorphic VT 100 J |
The most important trap: attempting to synchronize on a disorganized polymorphic rhythm causes the defibrillator to fail to discharge because it cannot find an R wave. If the patient is pulseless or the rhythm is polymorphic and unstable, switch to unsynchronized defibrillation.
Pad placement is anterolateral by default, or anteroposterior when the anterior chest is occupied by a sterile field, an implanted device, or when atrial defibrillation is anticipated. Pads are placed at least 8 cm from an implanted generator, and the device is fully interrogated after any external shock.
4. The Emergency Drug Set
| Drug | Dose | Indication | Mechanism |
|---|---|---|---|
| Epinephrine | 1 mg IV/IO q3-5 min (arrest); 2-10 mcg/min infusion (bradycardia/hypotension) | All arrest rhythms | α₁ vasoconstriction raises coronary perfusion pressure; β₁ inotropy/chronotropy |
| Amiodarone | 300 mg IV push, then 150 mg for refractory VF/pVT; 150 mg over 10 min for stable VT | Refractory shockable rhythms | Multi-channel: K⁺, Na⁺, Ca²⁺, beta blockade |
| Lidocaine | 1-1.5 mg/kg, then 0.5-0.75 mg/kg | Alternative to amiodarone | Class IB Na⁺ channel blocker, ischemic tissue selective |
| Magnesium sulfate | 1-2 g IV over 5-20 min | Torsades de pointes | Stabilizes membrane, suppresses early afterdepolarizations |
| Atropine | 1 mg IV q3-5 min, max 3 mg | Symptomatic bradycardia | Antimuscarinic — blocks vagal tone at the SA and AV node |
| Dopamine | 5-20 mcg/kg/min | Bradycardia/hypotension | Dose-dependent dopaminergic, β, then α effect |
| Adenosine | 6 mg rapid push, then 12 mg | Regular narrow-complex SVT | Transient AV nodal block via A₁ receptor and IKACh |
| Calcium chloride/gluconate | 1 g IV | Hyperkalemia, calcium blocker overdose | Membrane stabilization |
| Sodium bicarbonate | 1 mEq/kg | Hyperkalemia, sodium channel blocker toxicity, prolonged arrest with acidosis | Alkalinization, sodium loading |
| Naloxone | 0.04-0.4 mg titrated | Opioid-induced respiratory arrest | µ-receptor antagonist |
| Protamine | 1 mg per 100 units active heparin | Heparin reversal in tamponade | Binds and neutralizes heparin |
Atropine's critical limitation is tested constantly: it acts at the AV node, so it is ineffective — and can be harmful — in infranodal (Mobitz II or complete heart block with a wide escape), where accelerating the sinus rate simply increases the number of blocked impulses and can worsen the ventricular rate. Those patients need transcutaneous pacing or an isoproterenol/epinephrine infusion while a temporary transvenous wire is placed.
Atropine is also ineffective in a transplanted (denervated) heart, which has no vagal innervation to block.
5. Bradycardia and Tachycardia in the Lab
Symptomatic bradycardia (hypotension, altered mental status, shock, ischemic chest pain, acute heart failure):
- Atropine 1 mg IV, repeat every 3-5 minutes to a maximum of 3 mg.
- If ineffective: transcutaneous pacing, and/or dopamine 5-20 mcg/kg/min or epinephrine 2-10 mcg/min.
- Prepare for transvenous pacing — which in the EP lab means a catheter is often already in the right ventricle and can be connected to the stimulator for immediate emergency pacing.
That last point is a genuine EP lab advantage and a testable one: emergency pacing through an existing RV diagnostic catheter is faster than either transcutaneous or new transvenous access, provided output is set well above threshold and the connection is verified.
Tachycardia with a pulse: the first question is always stable or unstable. Instability — hypotension, altered mental status, shock, ischemic chest pain, acute heart failure — mandates immediate synchronized cardioversion regardless of the rhythm's name. Stable patients are managed by rhythm:
| Rhythm | First-line |
|---|---|
| Regular narrow-complex | Vagal maneuvers, then adenosine 6 mg then 12 mg |
| Irregular narrow-complex (AF) | Rate control with a beta blocker or non-dihydropyridine calcium blocker |
| Pre-excited AF (irregular, wide, very fast) | Procainamide or ibutilide; cardiovert if unstable. Never adenosine, verapamil, diltiazem, digoxin, or beta blockers |
| Regular wide-complex, presumed VT | Amiodarone, procainamide, or sotalol; cardiovert if unstable |
| Torsades de pointes | Magnesium sulfate, correct potassium, remove offending drug, overdrive pace if recurrent |
6. Emergency Equipment Readiness
Task A1 requires preparing the procedure room, and readiness is checked before every case:
- Defibrillator with pacing capability, tested, charged, with pads applied to the patient before draping.
- Airway cart: bag-valve-mask, oral and nasal airways, laryngoscope or video device, endotracheal tubes, suction that is on and verified.
- Code cart with unexpired drugs, sealed and checked on the current shift.
- Pericardiocentesis tray immediately available — in an EP lab it is not "in the hallway", it is in the room.
- Protamine drawn up or immediately accessible for any left-sided case.
- Temporary pacing generator with fresh batteries and a temporary pacing wire.
- Chest tube tray for subclavian access cases.
The single most consequential preparation step is applying defibrillation pads before draping. Once a patient is draped for a device implant, exposing the chest to place pads costs minutes that a VF arrest does not allow.
During programmed ventricular stimulation, the patient degenerates into a disorganized polymorphic rhythm and loses the arterial waveform. A team member charges the defibrillator and presses the sync button, but the device will not discharge. What is the problem and the correct action?
A patient in the EP lab develops complete heart block with a wide-complex escape rhythm at 28 beats per minute, a blood pressure of 72/40 mmHg, and confusion. A diagnostic quadripolar catheter is already positioned at the right ventricular apex. What is the most appropriate immediate intervention?
A patient on dofetilide develops recurrent polymorphic ventricular tachycardia with a long QT interval and a serum magnesium of 2.0 mg/dL. What is the correct first-line pharmacologic therapy?