This is the discussion to 64 year old male CC: Indigestion.
If you recall, we had a stubborn gentleman complaining of indigestion with a significant cardiac history. Considering the symptoms kept our patient awake, are highly suggestive of a coronary event, and we have uncompensated hypotension, we should have a keen interest on any ECG findings.
The rhythm appears to be regular, sinus in origin, rate of ~70 bpm, without ectopy. There is a fixed PR-interval of 0.2 s and a 1:1 association of P-waves to QRS complexes. The QRS is wide at 0.18 s, likely due to a bundle branch block. Normal sinus rhythm with a bundle branch block.
Evaluating the QRS complex in V1, we see it is wide and V1-positive confirming our suspicion of a bundle branch block. However, given the changes in leads I and V6, it is not a classic Right Bundle Branch Block. Instead we have a non-specific intraventricular conduction defect, or IVCD. A right axis deviation is present.
Looking at the contiugous lead groups:
- Inferior: pathologic Q-waves present, isoelectric ST-segments, non-specific T-wave abnormalities
- Septal: baseline wander, minimal ST-depression in V1-V2 (potentially attributed to the baseline)
- Anterior: pathologic Q-wave in V4, isoelectric ST-segments, non-specific ST-T-wave abnormalities
- Lateral: pathologic Q-wave in V5-V6, isoelectric ST-segments, non-specific ST-T-wave abnormalities
- High-Lateral: unremarkable outside of underlying conduction defect
- aVR: unremarkable outside of underlying conduction defect
Pathologic Q-waves in the inferiolateral lead groups are consistent with our patient's history of multiple prior MI's, however, without a prior ECG it is tough to determine if these are not from a recent myocardial infarction.
The potential ST-depression in the septal leads may be reciprocal changes in the setting of a posterior MI. The patient's skin condition made acquisition difficult, but coupled with the patient's signs and symptoms it would be prudent to explore this possibility. Attempts could be made at the acquisition of a posterior view.
The interventricular conduction defect present may be an acute finding or it may be a baseline finding. Given the QRSd is around 0.18 s there is a non-trivial defect present. Without access to the patient's prior ECG's we are unable to determine its significance.
While examination of the 12-Lead ECG for this patient did not yield any acute findings, in conjunction with our patient assessment we have enough to form a differential diagnosis:
- Acute myocardial infarction
- Recent myocardial infarction
- Congestive heart failure
- Pulmonary embolism (albiet less likely due to symptoms)
However, any differential diagnosis for this patient is rendered moot by his stubborn desire to refuse transport!
The paramedics on this call rolled up their sleeves and got to work convincing this gentleman that his signs and symptoms were anything but normal. He begrudingly sat on the stretcher and consented to transport.
They placed him on O2 by nasal cannula, obtained IV access, administered a fluid bolus, and transmitted the 12-Lead ECG to a local STEMI receiving center. His blood pressure improved enough with fluid administration to allow nitroglycerin, which the patient said improved his discomfort.
Transmission of the patient's ECG was key in this case as the receiving facility determined acute changes were present.
The patient was taken directly to the cath lab where a 90% occlusion of the LAD, just proximal to a previous stent, was found. The lesion was ballooned and stented, and the patient was admitted to the CCU for recovery.
Some additional questions for discussion:
- Why was this patient's hypotension uncompensated?
- Are there any differentials we missed?
- Why was indigestion left off the list of differentials?