Country cardiograms case 6:
Biventricular acute myocardial infarction
Jim Thompson, MD, CCFP(EM), FCFP
Sundre, Alta.
Clinical Associate Professor, Department of Family Medicine, University of Calgary, Calgary, Alta.
Can J Rural Med vol 2 (4):200
This paper has been peer reviewed.
© 1997 Society of Rural Physicians of Canada
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Findings
The ECG shows ST elevations both inferiorly (leads II, III and aVF) and anterolaterally (V1V6), with reciprocal ST depression high laterally (I and aVL).
It is unusual to find ST elevation in more than 1 coronary artery distribution during acute myocardial infarction. The differential diagnosis of this ECG might include dissection of the thoracic aorta, pulmonary embolism, myocarditis and pericarditis. The clinical picture was otherwise very typical of acute myocardial infarction, however, so thrombolysis was appropriate.
Discussion
This patient was later confirmed to have had a large myocardial infarction. In spite of prompt thrombolysis the creatinine kinase peaked at 3600, and he suffered damage to the ventricular myocardium.
Figure 1 shows the record of an angiogram taken soon after the acute infarction. This figure explains why 2 coronary artery distributions were so profoundly affected. He probably had a long-standing occlusion of the left anterior descending artery (LAD). The myocardial distribution of the LAD was supplied by collateral circulation from the right coronary artery (RCA), but a proximal stenosis had developed in the RCA as well. The infarction was caused by acute total occlusion of the proximal RCA, affecting large areas of both the left and right myocardium.
A 15-lead ECG for this patient might have shown significant ST elevation in lead aVR, since the infarct occurred in the proximal RCA.1 The significance of this finding in terms of management would be to avoid the use of sublingual nitroglycerine because it can cause profound hypotension in patients with proximal RCA infarction.
The patient suffered ventricular fibrillation, was successfully defibrillated and then treated with a thrombolytic in the rural hospital. Intravenous thrombolysis reduces mortality by about 25% in patients with acute myocardial infarction.2 This patient probably survived not only because he was defibrillated but also because he was given thrombolysis so promptly in the rural hospital.
He was stabilized with intravenous lidocaine, intravenous dopamine and oxygen, then transported to an urban hospital by helicopter for further management. Both the right and left coronary artery lesions were treated successfully with stents placed during angioplasty. He was discharged home 2 weeks later in good condition and continues to improve.
References
- Selker HP, Zalenski RJ, Antman EM, Aufderheide TP, Bernard SA, Bonow RO, et al. An evaluation of technologies for identifying acute cardiac ischemia in the emergency department: executive summary on a National Heart Attack Alert Program Working Group Report. Ann Emerg Med 1997;29(1):1-87.
- Ornato JP. Minimizing delays to thrombolytic therapy in patients with acute myocardial infarction. In: Gibler WB, Aufderheide TP, editors. Emergency cardiac care. St. Louis: Mosby; 1994. p. 28-37.
