Complete Journal Club Article
Sharifi M et al.. "Pulseless electrical activity in pulmonary embolism treated with thrombolysis (from the “PEAPETT” study)". American Journal of Emergency Medicine. 2016. 34(10):1963-1967.
PubMed Full text

Clinical Question

  • Does low dose tissue plasminogen activator (tPA) improve survival in patients with pulseless electrical activity and cardiopulmonary arrest due to confirmed pulmonary embolism?


  • Rapid administration of 50mg of tPA is safe and effective in achieving ROSC in patients with PEA due to massive pulmonary embolism leading to increased survival and reduction of pulmonary artery pressures

Major Points

  • Approximately 8%-13% of unexplained cardiac arrests are due to a massive pulmonary embolism (PE)[1]. Current ACLS and AHA guidelines suggest that thrombolytics should be considered in cardiac arrests that are thought to be secondary to a PE. This study was created to understand better the usage of tPA, efficacy, and safety in cardiopulmonary arrest in confirmed PE. This study was a single-center study of 23 patients on whom the group was consulted. All patients received 50mg tPA IV push during active CPR within 6.5 ± 2.1 minutes from initiation of cardiopulmonary resuscitation. All patients received heparin afterwards. ROSC was achieved in 22/23 patients following 2 to 15 minutes after tPA administration. At two year follow up, 20 patients (87%) were still alive and reported a return to baseline functional capacity without any restrictions. No major or minor bleeding reported.

Study Design

  • Single-center study, unblinded
  • N=23 patients with confirmed pulmonary embolism, cardiac arrest with PEA
  • Study investigators were consulted on 23 patients
  • This cohort was then retrospectively identified via the medical record and followed prospectively on clinical and echocardiographic outcomes *Surviving patients were followed up 3 weeks after discharge and every 6 months after until 22 ± 3 months


  • All recruited from a single US center

Patient Demographics

  • Men 39% (n=9)
  • Age 72 ± 5
  • PE risks: unprovoked PE: 70%, smoker: 43%, cancer history/active: 35%, estrogen or testosterone therapy: 26%, prothrombotic: 26%, concomitant DVT: 65%, previous VTE: 30%
  • 100% had D-dimer elevation, troponin elevation, BNP elevation, RV enlargement, and RV hypokinesia

Inclusion Criteria

  • Cardiopulmonary arrest with PEA secondary to massive pulmonary embolism

Exclusion Criteria

  • None


  • All 23 patients received 50mg of tPA while CPR was ongoing. tPA was given in 1 minute via IV push followed by administration of 10mL of saline
  • All patients received chest compressions and epinephrine. Atropine was given to 19 patients
  • Asystole developed in 9 patients after PEA. No patient developed ventricular tachycardia or ventricular fibrillation
  • Subsequently, between 2000-5000 of heparin was given as bolus and patient started on a maintenance drip at 10U/kg/hour. Dose was not weight adjusted and just given to deliver low-heparin bolus. aPTT was kept between 60-100 seconds
  • Heparin was discontinued between 24-30 hours after tPA
  • Within 1 hour of heparin discontinuation, apixaban or rivaroxaban was started orally at maintenance dose
  • Surviving patients were screened for DVT at the second office visit
  • All patients were screened for DVT or PE if there was enough suspicion throughout follow up time


Primary Outcome

  • ROSC and hemodynamic stability (palpable pulse + systolic BP >100 mm Hg) was achieved 2-15 minutes after tPA in all but 1 patient who died of irreversible shock 10 hours after admission.
  • Time from CPR to tPA administration was 6.5 ± 2.1 minutes
  • All surviving patients (n=20) reported a return to before event functional capacity without any restrictions that could be attributed to PE

Secondary Outcomes

  • No major or minor bleeding found on patients with administered tPA during hospitalization or at 22 ± 3 months of follow-up
  • No recurrent VTE in hospital or at follow-up, all surviving patients were on indefinite anticoagulation

Criticisms & Further Discussion

  • Unblinded study and only performed at a single center
  • No control groups
  • 16 of 23 patients had PE diagnosed before tPA administration, only 3 were diagnosed via thrombus seen in right ventricle on POCUS during cardiac arrest
  • Study states patients were administered tPA within 6.5 ± 2.1 minutes from initiation of CPR. This is pretty fast. The authors state 17 patients developed cardiopulmonary arrest in the ED, 2 in the ICU, 1 on the floor, and 3 in the radiology department. Unclear what the utility would be of administering tPA in patients with out of hospital arrest with prolonged downtime
  • Conflicting literature of tPA use in undifferentiated PEA

See Also


  • Not reported


  1. Hess EP, Campbell RL, White RD. Epidemiology, trends, and outcome of out-of hospital cardiac arrest of non-cardiac origin. Resuscitation 2007;72:200–6