Elder Male with Syncope
Updated: May 15
David Didlake
@DidlakeDW
EMS personnel responded to the residence of an 81 y/o Male with syncope. His spouse had called 911 after she heard a loud “thud” in the adjacent room. He was found altered, hypotensive, and with a large hematoma to the left periorbital region. No 12 Lead ECG was captured, but telemetry did reveal the following:
The spouse offers a pertinent medical history to include HTN and HLD, and furthermore states that he hasn’t previously complained of any chest discomfort, or shortness of breath. He awoke earlier that morning in his usual state of health.
His confusion progressively dissipated enroute to the hospital. At the time of ED arrival he was alert, oriented, and verbalizing only a headache with a normalized BP. The fall was not a mechanical etiology. He denied any specific prodrome of gross palpitations, however did endorse feeling quite dizzy just before the event. There was no chest pain.
The ED activated trauma services, and a 12 Lead ECG was captured.
V1 and V2 are probably placed too high on the chest given close morphological similarity to aVR. Otherwise, there is diffusely populated ST-depression with corresponding ST-elevation in aVR. This was deemed “non-specific” by the ED physicians.
Many of the changes seen are reminiscent of LVH with “strain,” and downstream Echo may very well corroborate such a suspicion, but since the ECG isn’t the best tool for definitively establishing the presence of LVH, we must favor a subendocardial ischemia pattern, instead.
More detailed reviews of subendocardial ischemia, as well as acute ECG patterns that breach the typical presentation, can be found here:
Imaging revealed no acute head, or spinal, injuries. The CXR demonstrated no pulmonary edema. There was equally no anemia, sepsis, or hypoxia—only transient hypotension in the field. The Trop I returned 0.051 ng/mL, and cardiology was requested.
NOTE: As this case began to gain momentum no other Troponin’s were acquired. Thus, a conventional peak was never formally established.
Given no clinical prelude of anginal (or equivalent) descriptors, prior to the acute event, risk stratification of the ECG and Troponin was pursued via Echo and nuclear Myocardial Perfusion Imaging (MPI).
Both data set unfolded almost simultaneously.
The Echo showed LVEF 35, indeterminate diastole, trace AI, mild MR, and a small apical thrombus. Of interest, the LV chamber was normal size with normal wall thickness. Thus, the ED admission ECG changes cannot be blamed on LVH.
A secondary ECG was captured just prior to nuclear MPI.
The ST/T changes are not quite so dramatic. However, at the moment of regadenoson (aka, Lexiscan) administration, the patient verbalized intense chest discomfort with following ECG.
There is a dramatically more intensified subendocardial ischemia pattern. What’s interesting about this ECG is that the max ST-depression appears confined to V3/V4. And rather than ST-depression in all inferior leads, Lead III is inappropriately baseline. So, one can reasonably consider this an “Aslanger equivalent” until proven otherwise.
Nuclear MPI dictation
Conclusions:
1. Strongly positive stress ECG Lexiscan administration.
2. The MPI images are grossly abnormal. There is increased LV cavity dimensions with an increase in transient ischemic dilation, suggesting Left Main, or 3-vessel coronary artery disease. There is a partially reversible perfusion defect encompassing the anterior septum and apex, consistent with a prior infarction with acutely superimposed ischemia in the proximal LAD distribution.
3. Abnormal gated wall motion of the LV with an ejection fraction of 18%.
He was taken to the Cath Lab.
RCA
Left Main / LAD / LCX
Cath dictation
1. Moderate sedation.
2. Coronary angiography reveals significant and severe CAD involving all three epicardial vessels. The LM has an irregular 30% distal stenosis, followed by an 80% ostial LAD stenosis, and total occlusion of the LAD proximally with TIMI grade 1 flow in the distal vessel. A large Diagonal artery has subtotal occlusion proximally. The LCX demonstrates an ostial 80% stenosis prior to the bifurcation of a large OM artery.
3. The RCA is large, dominant vessel. It shows a long 80-90% stenosis in the proximal through distal vessel.
4. Left Ventricular End-Diastolic pressure is 16 mmHg
He was referred to cardiothoracic surgery for possible bypass, but it was deemed most appropriate to first medically treat the LVEF, anticoagulate the apical thrombus, and outfit a LifeVest.
Follow-up is pending.
Learning Points
A fantastic triage tool for syncope is the ECG, which can screen for any arrhythmic / structural contribution, such as Delta wave, QT prolongation, AV block, Hypertrophic Cardiomyopathy, Epsilon wave, or Brugada.
Subendocardial ischemia ECG pattern is typically STE aVR with/without STE V1, and global STD that is maximal in Leads II / V5. The underlying etiology is either Type 1 or Type II ischemia, although sometimes there’s overlap of both.
Type I ischemia. Sudden narrowing of a coronary artery due to ACS (plaque rupture with thrombosis and/or downstream showering of platelet-fibrin aggregates).
Type II ischemia. An increase in myocardial oxygen demand due to tachycardia, elevated ventricular afterload (BP or Aortic stenosis), increased wall stretch, or a decrease in oxygen supply due to hypotension, anemia, hypoxia, sepsis, or a combination of all of the above.
Access the links provided for a detailed review of varying ECG patterns when ACS breaches the typical subendocardial ischemia pattern.
LV dysfunction is often pro-arrhythmic, and poor contractility can also lead to thrombus formation within the chamber. This latter part has been implicated in embolic CVA.
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