This issue includes 4 hours of ACEP/AMA category 1 CME credit.
Authors: Bakhtiar Ali, MD and A. Maziar Zafari, MD, PhD, FACC, FAHA Peer Reviewers: Bentley J. Bobrow, MD, FACEP and Barbara K. Richardson, MD, FACEP
Publication Date: September 1, 2008
Excerpt from the issue… A 47-year-old man presents with nonspecific chest discomfort intermittently over the past 3 days. Episodes are not related to exertion and last 10 to 30 minutes. He has a history of hypertension and smokes 1 pack per day. In the ED, he is pain free and has an ECG with evidence of left ventricular hypertrophy and j-point elevation. You doubt that he has an acute cardiac syndrome but decide to err on the conservative side and admit him to your observation unit. The patient looks well, his first troponin is negative, and the monitor continues to show a normal sinus rhythm. Two hours later you go to check on the patient and find him disconnected from his monitor, unresponsive, and with no pulse (no wonder there was so much beeping coming from the obs unit). The nurse has been on break for the past 30 minutes, and due to “sick calls” there was no cross coverage. You call for help which doesn’t immediately come, and you must decide what is more important — beginning chest compressions, securing the airway, getting intravenous access, or getting the defibrillator. You decide on chest compressions but are not inclined to begin mouth to mouth — you wonder if that is negligence. When the crash cart finally arrives, you note the new biphasic defibrillator and wonder what voltage to start at and if you should “stack” shocks the way you used to. The nurse asks if you want to stop CPR to establish intravenous access and what drugs you want. You begin to realize there is more that you’re unsure of than you would like to admit.
Conclustion of the above case study... Cardiopulmonary resuscitation was immediately initiated. As the downtime was not known, the patient received 2 minutes of CPR, with a chest compression and ventilation ratio of 30:2. While CPR was ongoing, a biphasic AED was attached, which showed coarse VF. Peripheral venous access was established without interruption of CPR. After 2 minutes of CPR (approximately 5 cycles of compression and ventilation), the patient received his first shock. A pulse was detected after 2 minutes of CPR after the first shock, and the AED showed sinus rhythm. The patient regained consciousness with establishment of spontaneous circulation. The patient’s ECG immediately after resuscitation showed ST-segment elevation in V1 to V3 with reciprocal changes in inferior leads, consistent with anterior myocardial injury. He was immediately taken to the cardiac catheterization laboratory and received percutaneous coronary intervention to the left anterior descending epicardial coronary artery. Subsequent blood chemistry revealed elevated cardiac enzymes. Since he was not comatose, he was not deemed to be a candidate for induced hypothermia. His blood glucose was closely monitored and kept between 80 and 110 mg/dL by an insulin infusion. He had 1 episode of elevated temperature of 38ºC after the procedure, which was promptly treated. The patient’s electrolytes were closely monitored and any deficiency was corrected. He was discharged home neurologically intact.
About this issue: This issue of Emergency Medicine Practice highlights significant changes in the 2005 AHA guidelines, examines the evidence that prompted the changes, and explores future therapies that may impact outcomes from SCD.
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