Abstract 218: Interaction Between Lung Disease and Anti-Psychotic Drugs in Pulseless Electrical Activity

Abstract

Introduction: There has been a paradigm shift in manifestation of sudden cardiac arrest (SCA), with decreasing rates of ventricular fibrillation/tachycardia (VF/VT) and an increase in the proportion of pulseless electrical activity (PEA). To elucidate mechanisms, we further evaluated the relationship between PEA and pulmonary disease, which has consistently been reported in epidemiologic and clinical evaluations of this condition. Methods: Cases with PEA and VF/VT (age ≥ 18 years) were enrolled from a large ongoing population-based study of out-of-hospital SCA in the Northwestern US (pop approx. 1 million). The presenting arrhythmia was determined from review of first responder resuscitation reports. Detailed clinical history was obtained from medical records prior to SCA. Pearson’s x 2 test and independent samples t -test were used for univariate comparisons. Logistic regression was used to evaluate significant factors associated with PEA vs. VF/VT. Results: Compared to VF/VT (n= 609), PEA cases (n= 346) were older, more likely to be female, were less likely to be witnessed, to arrest in public and have bystander CPR (p≤ 0.005). Survival to hospital discharge was lower in PEA than VF/VT (5% vs. 27%, p< 0.0001). History of COPD or asthma was more common in PEA (38% vs. 24%, p< 0.0001). Antipsychotic use was also more frequent in PEA group (13% vs. 4%, p< 0.0001). In a logistic regression model adjusting for demographic and arrest circumstances, there was significant interaction between COPD/asthma and antipsychotics (p= 0.04). Compared to subjects with no history of COPD/asthma and no antipsychotic use, subjects with COPD/asthma only had an increased odds of PEA [OR 1.8 (95% CI 1.3-2.5), while odds for subjects with only use of antipsychotics was 4.8 (95% CI 2.2-10.6). Subjects with both COPD/asthma and antipsychotics were also more likely to present with PEA [OR 2.6 (95% CI 1.2-5.7)]. Conclusion: Susceptibility to PEA involves a significant interplay between pulmonary disease and use of antipsychotic drugs. These findings have potential implications for the ongoing mechanistic investigation of PEA, especially development of animal models.