EMS is dispatched to a 62 year old male with a chief complaint of chest discomfort.
On arrival, the patient is found sitting at the dinner table. He appears acutely ill.
- Onset: Fairly sudden after sitting down for dinner 20-30 minutes ago
- Provoke: Nothing makes the pain feel better or worse
- Quality: Dull pressure/ache
- Radiation: The pain does not radiate
- Severity: 8/10 “feels like a 747 is sitting on his chest”
- Time: Feels slightly better since the onset
The patient’s skin is cool, pale, diaphoretic
Vital signs are assessed.
- RR: 20
- HR: 62
- NIBP: 84/48
- SpO2: 99% on room air
Breath sounds are clear bilaterally.
The cardiac monitor is attached.
A 12 lead ECG isÂ obtained.
The paramedic trouble-shoots the loose electrode.
The data quality looks good to me, but the computer disagrees.
Three’s a charm.
The paramedic in charge of the call elected to perform an additional 12 lead ECG using modified leads V4R and V5R.
Here is the result.
Consider this image from an editorial in the New England Journal of Medicine by HJ Wellens.
We can say that leads V4R and V5R are negative (there is no ST-segment elevation) but the T-waves are flat so it would seem to be a tieÂ between distal RCA and LCX according to this diagram.
Keep in mind that the patient’s initial blood pressure is only 84/48 so he shouldn’tÂ receive nitroglycerin whether leads V4R and V5R are positive for right ventricular infarction or not.
Consider Eskola et al. How to Use ECG for Decision Support in the Catheterization Laboratory – Cases With Inferior ST Elevation Myocardial Infarction. Journal of Electrocardiography Vol 37 No. 4 October 2004.
In this case both the amount of ST-segment elevation and the amplitude of the T-waves are equal in leads II and III. Again, no help in distinguishing between RCA and LCX occlusion.
Consider Sgarbossa et al., Electrocardiographic diagnosis of acute myocardial infarction: Current concepts for the clinician. Am Heart JÂ 2001;141:507-17:
â€œThe typical electrocardiographic pattern of inferior infarction consists of ST-segment elevation in leads II, III, and aVF. The occlusion is in the RCA in 80% to 90% of cases and is in the LCX in the remaining patients. Higher ST elevation in lead III than in lead II strongly suggests compromise of the RCA.
A bedside differential diagnosis between culprit arteries can also be attempted by examining additional electrocardiographic leads. Because the only lead that faces the superior part of the left ventricle and directly opposes the inferior wall is aVL, ST depression in lead aVL is almost always determined by RCA occlusion (sensitivity, 94%; specificity, 71%), without indicating concomitant involvement of the posterior wall or the right ventricle. Injury in leads II, III, and aVF without ST depression in aVL indicates proximal LCX occlusion.
Several studies in the 1980s concluded that ST elevation in leads V5 through V6 during inferior injury signaled LCX occlusion. However, because most inferior infarctions are caused by RCA occlusion, the positive predictive value of this sign is poor. The arteries that supply the posterolateral region of the left ventricle are the obtuse marginal branch of the LCX, the posterolateral, and the LAD branches. Thus ST changes in leads V5 and V6 indicate rather posterolateral ischemia triggered by either RCA or LCX occlusion. When this ST elevation is significant (>2 mm), it is probably a sign of â€œmega-artery-relatedâ€ (either the RCA or LCX) infarction with a large ischemic burden.â€
It appears as though the mere fact that there is ST-segment elevation in leads V5 and V6 (in addition to leads II, III, and aVF) does not settle the matter.
The patient was sent emergently to the cardiac cath lab.
The circumflex (LCX) was found to be 100% occluded.
After the lesion was crossed with a wire.
The right coronary artery (RCA) was small and non-dominant.
Sometimes it’s virtually impossible to predict the culprit artery based solely on the 12-lead ECG.