Country cardiograms case 4: Acute posterior myocardial infarction
Can J Rural Med vol 2 (2):87
© 1997 Society of Rural Physicians of Canada
Findings
The electrocardiogram (ECG) presented on p. 76 showed marked ST depression anteriorly, along with nonspecific ST depression and T-wave inversion laterally. These changes could be due to anterior ischemia or acute posterior myocardial infarction (MI).
A 15-lead ECG was obtained by moving the V4 lead from the left precordium to the same position on the right anterior chest (V4R), the V5 lead to just below the tip of the scapula on the left back (V8), and the V6 lead to a point halfway between V8 and the spine (V9), as shown in Fig. 1.
Figure 2 shows the QRS complexes in V8 and V9. There was a 1-mm ST segment elevation in both leads, which is direct evidence of acute posterior MI. The ST depression seen anteriorly (V1 to V4) was therefore reciprocal ST depression, given that these leads face the opposite side of the heart from the current of injury that caused ST elevation in the two posterior leads (Fig. 1).
Discussion
Acute MI must be diagnosed immediately by rural physicians, because the goal is to start thrombolysis within 30 to 60 minutes from the time the patient enters the hospital.[1] Acute posterior and far right MI are difficult to diagnose from a 12-lead ECG, because the 12 leads do not face those areas of the heart.
A 15-lead ECG is indicated when a standard 12-lead ECG fails to give good evidence for acute MI in cases in which posterior or right ventricular MI is suspected, and when the extent of damage in the right ventricle must be determined in cases of inferior MI. ST elevation in lead V4R would be evidence for right ventricular infarction and in leads V8 and V9 for posterior MI. The presence of the anterior reciprocal ST depression significantly improves the positive predictive value of the ECG for acute MI.
There have been no randomized trials showing any benefit of thrombolysis in acute posterior MI. In this case, the ECGs were sent immediately by fax to a cardiologist, who agreed with the diagnosis and recommended immediate thrombolysis during a telephone consultation. He documented his support in a note faxed back to the rural physician. The patient was given tissue plasminogen activator without incident. The creatine kinase level peaked at 500 U/L, and the patient has done well since.
The patient was transferred subsequently to an urban hospital for further care. Rural hospitals differ in their ability to care for acute MI patients after thrombolysis.[2,3] This particular rural hospital usually transfers such patients, because the on-call physician does not stay in the hospital and the nursing staff are not able to recognize and treat critical complications of acute MI rapidly enough, given the staffing pattern they have to use. The main complication that cannot be managed satisfactorily is hemodynamically unstable ventricular fibrillation or tachycardia. No research has been done in rural hospitals to determine which patients might suffer sudden severe complications after thrombolysis.
References
- Heart and Stroke Foundation of Canada, Canadian Cardiovascular Society and Canadian Association of Emergency Physicians, for the Emergency Cardiac Care Coalition. Recommendations for ensuring early thrombolytic therapy for acture myocardial infarction. Can Med Assoc J 1996;154(4):483-7.
- Hindle H, Norheim J, Renger R. Rural Alberta thrombolysis study. Survey of practice patterns for managing acute myocardial infarction. Can Fam Physician 1995;
41:1180-7.
- Marshall SA, Godwin NM, Miller RT. Availability of thrombolytic therapy in rural Newfoundland and Labrador. Can Med Assoc J 1995;152(2):177-81.
