Cleveland Clinic’s Critical Care Transport (CCT) service has the ability to function as a mobile version of Cleveland Clinic’s intensive care units. Skilled CCT team members work with our referring healthcare providers to deliver Cleveland Clinic ICU care to the bedside, and continue this care during the transport process to Cleveland Clinic for definitive therapy. Our critical care transport system is about having the means and resources to bring Cleveland Clinic’s expertise to the patient’s bedside anywhere in the world and at anytime – reflecting the ideal of “no patient too sick, and no patient too far.”
A 59-year-old man was at home with his wife vacuuming when he suddenly collapsed suffering a cardiac arrest. His wife called EMS and immediately initiated CPR. When paramedics arrived, he was defibrillated and intubated.
Upon arrival at Medina Hospital (a Cleveland Clinic community hospital), the patient was actively seizing. He was given lorazepam (Ativan®) and stabilization measures were undertaken by the emergency department physician. The physician at Medina subsequently initiated transfer to Cleveland Clinic’s main campus. However, while being transferred to the helicopter, the patient again suffered cardiac arrest, requiring defibrillation.
Upon arriving at Cleveland Clinic, the patient was taken directly to the cardiac catheterization laboratory. Coronary angiogram revealed one-vessel obstructive coronary atherosclerosis, which was treated with insertion of a bare metal stent to the right coronary artery.
The patient was then moved to the coronary intensive care unit, where the hospital’s cooling protocol was initiated. Neurology was consulted and the patient was placed on phenytoin. An EEG was recommended, demonstrating findings consistent with encephalopathy without epileptiform activity.
Post intervention, the patient developed complete right bundle branch block and T wave changes. His peak CPK level was 777, with a CK-MB of 16.1 and CK-MB% of 2.1. Transthoracic echocardiogram revealed mild left ventricular hypertrophy, an ejection fraction of 50-55%, and some distal apical hypokinesis.
The patient’s neurological status began to improve while in the coronary ICU. He had no subsequent chest pain, SOB or arrhythmias. Electrophysiology was consulted and maximization of beta blocker was recommended, with no ICD needed. The patient was subsequently transferred to the stepdown intensive care unit.
Outcome and Follow-up
By the end of a week, the patient had nearly complete recovery of neurological function. Serial EEGs revealed improvement of encephalopathy. A head CT was negative for acute intracranial abnormalities. Phenytoin was stopped as seizures were felt to be due to lidocaine administration. Ejection fraction was normal on follow-up echocardiogram. He was started on lisinopril and atorvastatin. The patient was discharged five days following his heart catheterization, with a plan for routine post-MI care.
At one-month follow-up the patient has been doing well. He has continued with routine care and has been walking twice daily for about a mile. He experienced one brief episode of chest pain since, and underwent EKG, troponin and CK-MB testing all of which were unremarkable. The chest pain never recurred. He was found to be slightly orthostatic and had his enalapril decreased to 2.5 mg from 5 mg.