STEMI with cardiac arrest
The case:
A 54-year-old woman with hypertension, hyperlipidemia, and an active 20-pack year smoking history presented to the Emergency Department with about 4 hours of substernal crushing chest pain radiating to the right arm. She reported associated dyspnea and nausea. Home medications included metoprolol 25 mg twice daily and gemfibrozil 600 mg twice daily. She was not taking any antiplatelet or anticoagulant drugs.
Her vital signs on arrival: HT 80, BP 160/101, RR 14, SpO2 100% on room air, T 97.5 F
Her skin is pale and clammy.
Her EKG on arrival:
Code STEMI was activated due to ST elevations in aVR and V1 with widespread ST depressions, concerning for diffuse ischemia.
She received a full dose aspirin, clopidogrel, sublingual nitroglycerin x 3, and an IV fluid bolus initially. Our hospital does not have interventional cardiology, so our next steps involved contacting the closest receiving hospital (about 2 hours away by ground) and administering fibrinolytic therapy.
The receiving cath lab and flight EMS crews were activated. The helicopter was about 45 minutes out. The patient received a 30 mg bolus of tenecteplase, and within 5 minutes she arrested due to ventricular fibrillation (VF).
CPR ensued. She was intubated and received multiple rounds of defibrillation and epinephrine. In a departure from current ACLS guidelines, we also gave her a bolus of lidocaine (40 milligrams), and with the next round of CPR she regained her pulse. Total code duration was about 30 minutes.
Her vital signs post-ROSC: HR 81 (sinus), BP 132/86, SpO2 100% on FiO2 100%.
She then received heparin bolus and drip, lidocaine drip, and was successfully transferred.
The brush up:
Lead aVR is somewhat of a sleeper. It's easy to overlook, but in the setting of an acute coronary syndrome it (and possibly its relationship to the ST segment in V1) can indicate an occlusion in the left main coronary (LMCA) or the proximal left anterior descending (LAD) arteries. It can also occur in triple vessel disease. The bottom line is it's a harbinger of severe pathology; the greater the degree of ST elevation, the more likely the patient is to require coronary artery bypass grafting (CABG), and the higher the mortality.
There was some discussion about whether the VF could have been a reperfusion injury leading to arrhythmia. While ventricular arrhythmias occur commonly during acute myocardial infarction (AMI), ventricular tachycardia and fibrillation that occur after fibrinolytic therapy are more likely due to ongoing ischemia rather than reperfusion. The most common reperfusion-associated arrhythmia is an accelerated idioventricular rhythm (AIVR).
Would giving lidocaine prior to fibrinolysis have minimized or even prevented VF? Probably not, but the data on this topic is sparse (animal models have of infarction have not shown reduction in reperfusion-induced VF arrhythmia with lidocaine infusion).
The conclusion:
The patient was transferred to the closest receiving facility where cardiac catheterization was performed. She was found to have a near complete left anterior descending (LAD) artery occlusion as well as total occlusions of the right coronary and circumflex arteries. Percutaneous coronary intervention (PCI) was aborted due to the diffuse nature of the patient's coronary artery disease. She suffered a second brief VF arrest and ROSC was achieved. After she was stabilized in the ICU, she was taken to the operating room for CABG. She had a 2-vessel bypass to the LAD and obtuse marginal arteries. The right side had adequate collateral circulation.
She was discharged on hospital day #20 with no neurologic deficits. She remains on supplemental oxygen by nasal cannula and has since quit smoking. Really!!
References:
1. Goldberger AL and Prutkin JM. Electrocardiogram in the diagnosis of myocardial ischemia and infarction. In: UpToDate, Saperia GM (Ed), UpToDate, Waltham, MA, 2016.
2. Yamaji H et al. Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segment elevation in lead V(1). J Am Coll Cardiol 2001 Nov 1;38(5):1348-54.