Conclusion: 38 Year Old Male – Chest Pain and Leg Paralysis.

Recap

In the post yesterday , the paramedic crew was evaluating a 38 y.o. male who had sudden, severe chest pain, as well as leg numbness and paralysis, and whose vital signs showed a mild bradycardia and pronounced hypertension.

screenshot696

The ECG obtained by EMS appears to be junctional, with an unclear contribution from the SA node. More concerning, however, is the ST segment elevation in V2-V5, with modest ST depression in aVF and perhaps in III. This would usually define an anterior wall acute coronary occlusion (i.e. STEMI). However, the depth of the S wave in V2 and V3, combined with the high R wave in V5 and V6, strongly suggest that left ventricular hypertrophy (LVH) is complicating interpretation of the ECG.

Clinical Course

At the time, the ED did not activate the cardiac catheterization lab based on paramedic interpretation of a STEMI. However, the emergency physician met the EMS crew as they were backing in, and immediately called for cath lab activation from the parking lot.

Given the “off-hours” presentation, the patient was evaluated in the ED while the cath lab team was assembling. The patient received multiple doses of morphine for the unremitting pain, and in fact was administered over 60 mg of morphine over the next hour, with no hypoxia or lethargy. The ED physician asked for a repeat ECG, assuming that it would demonstrate evolution of an ongoing and large MI. This ECG was obtained about 20 minutes after the EMS ECG:

AAortic_Dissection_ED_ECG

Although there were minor changes in R wave height, the ST morphology in the anterior leads had not changed significantly. In fact, the mild ST depression in the inferior leads seemed to have resolved.

Although acute coronary occlusions sometimes spontaneously reperfuse, the patient’s continuing pain did not suggest clinical resolution. A bedside echo demonstrated aortic root dilation, and a CT angiogram of the aorta was performed. This image from the scan is transverse, with the chest up, at the level of about the 3rd intercostal space:

screenshot702It shows a massively dilated aorta, with a clear dissection flap (shown between the 2 red arrows above). It extended from the aortic root down to the iliac bifurcation, looking pretty much exactly like the “Stanford A” in the figure below.

The cath lab team was cancelled, and the cardiothoracic surgeon immediately began planning for surgery.

The patient received maximal medical therapy before the OR was ready. In addition to the liberal use of opioids, labetalol was delivered in escalating amounts until the maximum dose was reached. As this was being given, a nitroprusside drip was being prepared, and was was started after the beta-blockers had been initiated. The goal in aortic dissection is to drop the SBP as low as possible, as fast as possible. In our patient’s case, a SBP of 140 was the lowest pressure obtained before he left for surgery.

Was the ECG “typical” for aortic dissection?

Yes and no.
Yes, since the ECG criteria for LVH suggested severe, chronic hypertension, which is a well-established risk factor for dissection.
No, since there are no such typical ECG signs to look for.  In a 2010 article (which is free, so go download it), Japanese researchers found that, on the one hand, most people with dissection have either chronic or acute ECG changes – only 27% are normal.

However, these chronic and acute ECG findings, as shown in the table, are all over the map. For example, the most common acute ECG change is ST depression, which is quite non-specific. The ECG will not be the key to diagnosing a dissection in  the field.

 When to suspect dissection

Of course, aortic dissection is far less common than ACS or STEMI, so most of the time the patient won’t have it. However, a few clinical elements can suggest it, as illustrated in this case, although I withheld a number of them in the presentation. Our patient had abrupt, severe pain that was actually described as “ripping.” Furthermore, he had a neurologic deficit (paralysis) as well as a pulse deficit (unable to doppler a pulse in his left foot).  A recent retrospective study validates our impression that this patient had high risk features for aortic dissection

Take-home Points

  • LVH can mimic STEMI, and sometimes fool the computer.
  • Obtain serial ECGs if the first is atypical or equivocal for ACS. Lack of dynamic evolution suggests an alternative diagnosis.
  • Aggressive efforts at treating hypertension should likely be delayed until after evaluation in the ED.
  • Aggressive pain control, however, is an essential component of prehospital treatment of suspected aortic dissection.

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