Management of PEA Arrest with Reversible Causes
Immediate Management Priorities
High-quality CPR with minimal interruptions remains the cornerstone of PEA management, combined with immediate systematic evaluation for reversible causes using the "H's and T's" framework and bedside ultrasound. 1, 2
Core Resuscitation Protocol
- Begin immediate high-quality CPR with chest compressions at 100-120/minute and depth of at least 2 inches, minimizing interruptions to maintain coronary perfusion pressure 3, 1
- Administer epinephrine 1 mg IV/IO every 3-5 minutes as the primary vasopressor throughout resuscitation 3, 1
- Establish vascular access (IV or IO if IV not readily available) for medication administration 3, 1
- Secure advanced airway as hypoxia is a leading cause of PEA, making airway management theoretically more critical than in VF/VT arrests 2
Systematic Evaluation for Reversible Causes
Perform bedside cardiac ultrasound immediately during rhythm checks (≤10 seconds interruption) to identify reversible causes and differentiate true PEA from pseudo-PEA with cardiac wall motion 1, 2, 4
The "H's and T's" must be systematically recalled during each 2-minute CPR cycle 1, 2:
Hypovolemia:
- Administer IV/IO crystalloid boluses empirically if suspected 2
- Ultrasound shows collapsed IVC and small, hyperdynamic ventricles 4, 5
- Blood transfusion for severe hemorrhage 2
Hypoxia:
- Ensure adequate oxygenation and ventilation with advanced airway 2
- Lung ultrasound can identify pneumothorax or pulmonary pathology 4
Hydrogen ion (Acidosis):
- Identify and correct metabolic abnormalities 2
Hypo/Hyperkalemia:
- Treat electrolyte abnormalities immediately, particularly hyperkalemia which directly causes cardiac arrest 2
Hypothermia:
- Rewarm if core temperature <35°C 2
Tension Pneumothorax:
- Perform immediate needle decompression at 2nd intercostal space, mid-clavicular line if clinically suspected—do not delay for imaging 2
- Ultrasound shows absent lung sliding and absent B-lines 4
Tamponade (Cardiac):
- Ultrasound has 100% sensitivity for detecting pericardial effusion with tamponade physiology 2
- Perform pericardiocentesis guided by echocardiography 2
Thrombosis (Pulmonary Embolism):
- Consider thrombolysis, surgical embolectomy, or mechanical embolectomy as reasonable emergency treatment for suspected massive PE 3, 1
- Early systemic thrombolysis is associated with improved outcomes compared to use after conventional ACLS failure 1
- Ultrasound shows RV dilation, RV dysfunction, and potentially visible thrombus (100% sensitivity, 97% specificity when performed by experienced personnel) 2, 6
Thrombosis (Coronary - Acute MI):
- Ultrasound can identify regional wall motion abnormalities (86% sensitivity, 94% specificity) 2
- Consider emergent cardiac catheterization if ROSC achieved 1
Toxins:
- Higher epinephrine doses may be indicated for β-blocker or calcium channel blocker overdose 1
- Sodium bicarbonate for sodium channel blocker toxicity (see below) 3
Trauma:
Specific Pharmacologic Considerations
Sodium Bicarbonate
Routine use of sodium bicarbonate is NOT recommended for PEA cardiac arrest 3
However, sodium bicarbonate has specific indications:
- Sodium channel blocker toxicity (cocaine, tricyclic antidepressants, local anesthetics): Administer sodium bicarbonate as standard advanced life support with addition for life-threatening dysrhythmias 3
- Severe metabolic acidosis with known cause: In cardiac arrest, rapid IV dose of 44.6-100 mEq (one to two 50 mL vials) may be given initially and continued at 44.6-50 mEq every 5-10 minutes as indicated by arterial pH and blood gas monitoring 7
- Hyperkalemia-induced arrest: May be beneficial as part of hyperkalemia treatment protocol 2
Critical caveat: Bicarbonate solutions are hypertonic and may produce undesirable rise in plasma sodium concentration; however, in cardiac arrest, the risks from acidosis may exceed those of hypernatremia 7
Calcium
Routine administration of calcium for treatment of cardiac arrest is NOT recommended 3
Calcium has specific indications in PEA:
- Hyperkalemia-induced arrest: Calcium chloride or calcium gluconate to stabilize cardiac membrane 2
- Calcium channel blocker toxicity: High-dose calcium administration as part of toxicologic management 3
- Hypocalcemia-induced arrest: Documented severe hypocalcemia 2
Magnesium
Routine magnesium administration is NOT recommended for PEA arrest 3
Magnesium has limited specific indications:
- Documented hypomagnesemia contributing to arrest 2
- Torsades de pointes (though this typically presents as VF/pulseless VT, not PEA) 3
Medications NOT Recommended
- Atropine: Available evidence suggests routine use during PEA is unlikely to have therapeutic benefit 3
- Transcutaneous or epicardial pacing: NOT effective as routine treatment in PEA cardiac arrest, regardless of timing or location 8
Advanced Interventions
Consider venoarterial ECMO (VA-ECMO) early for refractory PEA with suspected reversible cause, as implementation takes time and can be lifesaving for cardiogenic shock or dysrhythmias unresponsive to other measures 3
Critical Pitfalls to Avoid
- Do not delay CPR while searching for causes—continue high-quality compressions with minimal interruptions while systematically evaluating 2
- Do not prolong ultrasound examinations beyond 10 seconds during rhythm checks, as any pause reduces coronary perfusion pressure 2
- Do not rely on physical examination alone—pulse assessment is unreliable and findings are frequently misinterpreted during cardiac arrest 1
- Do not prematurely terminate resuscitation—prolonged efforts are more likely successful in PEA than asystole, particularly in young patients with healthy cardiovascular systems 1
- Do not assume fixed, dilated pupils indicate irreversible brain injury—this is an expected pharmacologic effect of epinephrine administration during CPR 1
Post-ROSC Care
If ROSC is achieved: