Probability of PEA Arrest Being Caused by ACS
Acute coronary syndrome accounts for approximately 12.5% of pulseless electrical activity cardiac arrests, making it a significant but minority cause that must be systematically evaluated alongside other reversible etiologies. 1
Epidemiologic Data on PEA Etiologies
The most comprehensive analysis of PEA causes comes from a Swiss retrospective study of 144 out-of-hospital cardiac arrest patients with PEA as the first recorded rhythm 1:
- Hypoxia: 23.6% (most common cause) 1
- Acute coronary syndrome: 12.5% 1
- Trauma: 12.5% 1
- Unknown etiology: 17.4% 1
- Pulmonary embolism, hypovolemia, intoxication, and electrolyte abnormalities: <10% each 1
- Nonischemic cardiac disorders: 8.3% 1
- Intracranial hemorrhage: 6.9% 1
Mechanistic Considerations for ACS-Related PEA
When acute coronary occlusion does cause PEA, the underlying mechanism is typically acute pump failure rather than primary electrical instability, particularly in patients with preexisting severe left ventricular dysfunction. 2
Key Pathophysiologic Insights:
- In patients with severe baseline LV dysfunction (EF ~15%), acute coronary occlusion produces PEA within 1.7 ± 1.1 minutes due to immediate pump failure 2
- In patients with normal baseline LV function, acute coronary occlusion more commonly produces ventricular fibrillation after 23.5 ± 9.0 minutes 2
- This explains why PEA-SCA survivors have high prevalence of heart failure (49% in one cohort), suggesting preexisting myocardial dysfunction as a substrate 3
Clinical Implications for Diagnosis
Among PEA-SCA survivors who undergo comprehensive evaluation, 30% are found to have acute myocardial infarction as the precipitating event, but triggers remain undetermined in 65% despite thorough investigation. 3
Diagnostic Approach:
- Obtain a 12-lead ECG immediately post-ROSC to assess for STEMI 4
- If STEMI is present, activate the catheterization lab immediately (Class I recommendation) 4
- For hemodynamically and electrically stable non-STEMI patients, defer immediate catheterization for risk stratification (Class 3: No Benefit) 4
- Bedside cardiac ultrasound should be performed during resuscitation to identify reversible causes and differentiate true PEA from pseudo-PEA 5
Risk Stratification Context
The probability that PEA is caused by ACS increases substantially in patients with traditional coronary risk factors:
- Elevated LDL cholesterol, hypertension, diabetes, current smoking, and family history of premature CAD all increase likelihood of underlying coronary disease 6
- Age >70 years is the strongest independent prognostic risk factor 6
- Chronic kidney disease (eGFR 15-59) and polyvascular disease are high-risk enhancers 6
Important Caveat:
Even in patients with known severe coronary disease and baseline LV dysfunction who develop PEA, the immediate precipitant may not be acute coronary occlusion—other reversible causes must still be systematically evaluated. 5
Prognostic Implications
PEA-SCA survivors have heterogeneous long-term outcomes, with 45% mortality over 4.2 years of follow-up, though young survivors (<40 years) have excellent prognosis. 3
- Survival to hospital discharge for PEA is approximately 11%, compared with 36% for shockable rhythms 5
- The 48-hour survival rate in one cohort was 29% 1
Systematic Evaluation During Resuscitation
During each 2-minute CPR cycle, providers must systematically recall the "H's and T's" to identify reversible causes, recognizing that ACS represents only one of multiple potential etiologies. 5
The Complete Differential:
- Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/hyperkalemia, Hypothermia 5
- Toxins, Tamponade, Tension pneumothorax, Thrombosis (coronary or pulmonary), Trauma 5
- Additionally consider: Nonischemic cardiac disorders (8.3%) and intracranial hemorrhage (6.9%), which equal or exceed some classical "4H&4T" causes 1