Prolonged Cardiac Arrest and Vasopressin

Abstract

A 29 year old man presented to the emergency with a sudden onset of shortness of breath and syncope. Electrocardiogram showed a right bundle branch block, ST elevation in leads V1-V4 ( Figure 1A). A transthoracic echocardiography showed an embolus in transit at the inferior vena cava and right atrial junction. He had two episodes of Pulse Less Electrical Activity (PEA), lasting 2 and 62 minutes. ACLS protocol [1], was followed and LUCAS device was used to provide chest compressions. Multiple epinephrine [2], and atropine boluses were administered in addition to tissue plasminogen activator. With no signs of circulation and resuscitation chart review, a single dose of vasopressin (40 IU) intravenously was administered by anesthesia team [3,4]. A return of spontaneous circulation (ROSC) was observed. Later patient underwent a sternotomy and pulmonary embolectomy on cardiopulmonary bypass in the operating room. Transesophageal echocardiography also showed an echogenic material in the RVOT ( Figure 1C) in addition to dilated right ventricle ( Figure 1D Patient was transferred to the ICU and hypothermia protocol was used. He was extubated on day three and a neurological exam revealed bilateral lower extremity motor deficit. An MRI of the spine showed an abnormal increased T2, STIR signal in the central gray matter of the spinal cord from T9 to T12 vertebral level (Figure 2A and 2B). STIR (short TI inversion recovery) is a global and homogenous method to null the signal from fat, to distinguish the two tissue components. Increased STIR signal reflects a prolonged ischemic episode. After three months of rehabilitation, patient was seen walking with a cane