A 52-year-old male presented with cardiac arrest after suddenly collapsing at work. An AED was placed and recommended shocking. He received two shocks, CPR was initiated, and 911 was called. EMS arrived 5 minutes later. The initial rhythm was ventricular fibrillation. He received two more shocks, 3 doses of epinephrine, 1 dose of vasopressin, 300 mg of amiodarone, and after approximately 25 minutes had recovery of spontaneous rhythm. On arrival in the ED he was hemodynamically stable.
Physical Exam
BP 130/80 mmHg, HR 95 bpm, RR 20, intubated
Lungs: clear
Cardiac: regular rate and rhythm, normal S1S2, no murmurs
Abdomen: soft, non-tender, minimal bowel sounds
Extremities: no edema
Neuro: pupils were minimally reactive, no purposeful movement.
ECG NSR, QTc 550 msec, No Q waves, 0.5 mm ST depression in V5 and V6
Emergent coronary angiography was performed, which showed mild luminal irregularities without significant stenosis, with an LVEF of 40% and mild global hypokinesis.
Labs
BUN/Creatinine 15 mg/dl 0.8 mg/dL
Na 140 mmol/L
K 4.0 mmol/L
Hgb 15.9 g/dl wbc 11.3 10e9/L
Initial Cardiac Markers
CK 560 U/L
MB 15 ng/mL
TnI 0.25 ng/ml
Peak, 18 hours later
CK 1246 U/L
MB 37 ng/ml
TnI 1.2 ng/ml
He was treated with induced hypothermia and four days later was extubated with full neurologic recovery.
The most likely diagnosis is:
Show Answer
The correct answer is: C. Non-ACS related troponin elevation related to hypoperfusion cardiac contusion and/or multiple defibrillator shocks
The frequency of troponin evaluations after cardioversion is infrequent, particularly when limited to one or only two shocks.(1) Prolonged CPR could also be contributory, resulting in possible cardiac contusion. In addition, hypotension with patchy necrosis could potentially lead to troponin elevations.
Type 1 MI, traditional ACS related to plaque erosion or rupture, and Type 2 MI, related to supply/demand mismatch, both appear unlikely in the current patient, as coronary angiography showed no significant stenoses and no segmental wall motion abnormalities.
Hospital Course
Further evaluation included cardiac MRI with contrast which did not demonstrate any areas of MI. The final diagnosis was thought to be a malignant arrhythmia related to prolong QT.
Discussion
Although MI can usually be diagnosed within the first few hours of presentation using a combination of clinical variables, ECG and biomarkers, in some cases the diagnosis may not be evident for hours to days, until additional information is obtained. The current definition of MI includes a serial rise and fall of troponin in conjunction with evidence of myocardial ischemia. This includes at least one of the following: ischemic symptoms, ECG changes indicative of new ischemia or new pathological Q waves, or imaging evidence of new loss of viable myocardium or new regional wall motion abnormality.(2)
Sudden cardiac death, involving cardiac arrest, in which death occurring before samples can be obtained, is also considered an MI equivalent, if there are symptoms suggestive of myocardial ischemia, and accompanied by presumably new ST elevation or new LBBB, and/or evidence of fresh thrombus by coronary angiography and/or at autopsy. However, in many cases after cardiac arrest, coronary angiography will not be performed due to significant neurological damage. In addition, an accurate history is frequently unobtainable, the ECG is often non-diagnostic and, as this case illustrates, troponin elevations are frequently seen after cardiac arrest(3), and may be elevated for a variety of reasons other than acute MI. Although serial changes have been recommended to differentiate ACS from non-ACS causes(2), serial changes also occur frequently after cardiac arrest.(3)
The diagnosis post-cardiac arrest patients receive has important implications, as treatment and outcomes of patients with MI is included in numerous registries and organizations as quality measures. Given the high mortality of patients with cardiac arrest, there is concern that hospitals specializing in resuscitation will be inappropriately penalized.(4)
References
Alaiti MA, Maroo A, Edel TB. Troponin levels after cardiac electrophysiology procedures: review of the literature. Pacing Clin Electrophysiol. 2009;32:800-10.
Thygesen K, Alpert JS, White HD; Joint ESC/ACCF/AHA/WHF Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. J Am Coll Cardiol. 2007;50:2173-95.
Kontos MC, Kurz MC, Roberts CS, Ornato JP, Peberdy M, Dhindsa H, Reid R. Prevalence of troponin elevations in patients with cardiac arrest. Circulation. 2009;120:S1471.
Nichol G, Aufderheide TP, Eigel B, et al. Regional systems of care for out-of-hospital cardiac arrest: A policy statement from the American Heart Association. Circulation. 2010;121:709-29.
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