Critical Care Medicine • Volume 46 • Number 1 (Supplement) www.ccmjournal.org Learning Objectives: Multiple factors have reduced the usage of thrombolytics for coronary heart disease (CHD), including percutaneous coronary interventions… Click to show full abstract
Critical Care Medicine • Volume 46 • Number 1 (Supplement) www.ccmjournal.org Learning Objectives: Multiple factors have reduced the usage of thrombolytics for coronary heart disease (CHD), including percutaneous coronary interventions (PCI) and superiority of transfer for PCI rather than initial thrombolytics (1). Existing literature supports the usage of tissue plasminogen activator (TPA) during cardiac arrest due to suspected pulmonary embolism (PE), though conflicting results exist regarding the usage of TPA during cardiac arrest due to suspected CHD (2–5). While TPA during cardiac arrest related to suspected CHD is not FDA-approved, our objective is to describe a case in which this was performed. Methods: This is the case of a 47-year-old male who presented as a witnessed ventricular fibrillation (VFib) cardiac arrest who went without bystander CPR for 5 mins and arrived to our tertiary care center in refractory VFib arrest having received standard resuscitative care via emergency medical services. ROSC was obtained for 15 minutes during which an EKG revealed ST elevations and catheterization (cath) lab was activated. Quickly,the patient re-arrested with pulseless electrical activity (PEA) rhythm. We administered 50mg of TPA for suspected CHD due to the VFib and concerning electrocardiogram (ECG). ROSC was achieved again approximately 15 minutes after the second dose of 50mg of TPA. In total there was 100mg of TPA utilized and the total downtime was 68 minutes. The patient underwent therapeutic hypothermia. Computerized tomography imaging was negative for PE. He began to awaken on hospital day (HD) #4 and was extubated on HD #9. At this time he had Modified Ranking Scale (mRS) of 2. Delayed Cardiac cath was performed and was negative for any CHD. Cardiac imaging demonstrated basal septal myocarditis and prior to discharge patient underwent automated defibrillator placement. Patient is now at a mRS of 1 and is returning to work four months after his cardiac arrest. Results: Since this TPA recipient became a neurologically intact survivor despite no CHD on cardiac cath, we hypothesize that this TPA usage lysed the microvascular thrombi improving myocardial perfusion (6). This case demonstrates need to strongly consider TPA in patients during undifferentiated refractory and initially shockable cardiac arrest.
               
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