Abstract 12166: Vasopressor Induced Generalized Coronary Vasospasm Presenting as Inferior ST Elevation in Post Cardiopulmonary Resuscitation.

Introduction: Post cardiopulmonary resuscitation (CPR) ST elevation is usually a sign of an urgent need for cardiac catheterization (CC), especially in the setting of shockable rhythm cardiac arrest. Post CPR ST elevation can be attributed to pericarditis, early repolarization or acute myocardial infarction. CC is mandated in this situation to rule out acute coronary syndrome. Hypothesis: We report a case of post CPR inferior ST elevation that is likely to be related to escalation of vasopressors which lead to generalized coronary vasospasm. There are few cases that report epinephrine-induced ST-elevation myocardial infarction during anaphylactic shock or septoplasty. To our knowledge, this is the first case report of a typical inferior ST elevation in post CPR that was due to vasospasm secondary to vasopressor escalation. Case: A 47 years old male with a history of malignant hypertension and end stage renal disease who presented to the hospital with cardiac arrest (pulseless electrical activity (PEA) and VT/VF). Initial electrocardiogram (EKG) post return of spontaneous circulation did not show acute ischemic changes but on a later repeat, it showed ST elevations in the inferior leads with ST depression in AVR consistent with possible inferior myocardial infarction. The patient was taken emergently to coronary angiogram which demonstrated severe diffuse vasospasm in all three coronary arteries that were completely reversed with intracoronary vasodilator injection. No definite obstructive coronary artery disease was found. The decision was to de-escalate vasopressors doses and follow up EKG demonstrated resolved EKG ischemic changes. Conclusions: Post CPR ST elevation EKG changes can be attributed to vasopressor induced coronary vasospasm without underlying obstructive coronary artery disease. Vasopressor's dose should be adjusted in this setting to avoid inducing myocardial infarction secondary to severe and prolonged coronary vasospasm. [ABSTRACT FROM AUTHOR]