Wednesday, December 22, 2010

Cardiac Arrest, hypotension, tachycardia

A 65 yo woman had felt ill for 36 hours, had seen her MD but without undergoing a cardiac evaluation. She collapsed and 911 was called; she was found pulseless. After epinephrine, atropine, and defibrillation x 2, there was a return of pulses. Exact rhythm during arrest is uncertain. The patient presented with a bp of 90/60 and heart rate of 140. Here is the initial ECG:
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There is sinus tach with PACs. The axis is vertical and down, and is suggestive of left posterior fascicular block (small r in aVL followed by deep S-wave). There is ST depression in II, III, and aVF that is concerning for reciprocal depression from high lateral STEMI in aVL, where there is some ST elevation. There is also ST depression in precordial leads, greatest in V3 and V4, concerning for posterior STEMI. However, with widespread ST depression, this could also be due to diffuse subendocardial ischemia.
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Arguing for posterior STEMI are two things: 1) precordial ST depression is not pronounced in V5 and V6; 2) T waves are inverted away from the ST segment deviation in aVL (down) and in II, III, aVF (up) and in V3 and V4. This is all highly suggestive of posterolateral STEMI that is either subacute or reperfused, but not very acute (in the acute phase, T-waves are upright with the ST elevation).
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Everything is complicated by the arrest and hypotension: Is the ischemia caused by the instability, or the instability caused by the ischemia? What was the inciting factor?
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The diagnosis is in doubt.
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Thus, a bedside echo was performed by the emergency physician and is shown 30 seconds into this video:

65 yo F witnessed arrest from hqmeded.com on Vimeo.
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For those who haven't watched the video, it shows pericardial clot, consistent with myocardial rupture. The patient was taken to the OR by cardiovascular surgery and found to have a necrotic lateral wall with a ventricular leak. The patient died is spite of resuscitative efforts.
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Myocardial rupture is not uncommon. It is found on 1% to 3.5% of autopsies of patients who died of MI. It is associated with transmural MI; since most STEMI are aborted with reperfusion therapy, it is not as common as it once was. It is more common in women, and in patients who have a first MI and have a good EF, as it requires a pump force from the healthy myocardium to produce high pressure which ruptures the infarcted myocardium. The "rupture" is not an explosion, rather a small tract through the myocardium which leaks blood into the pericardium, and kills by tamponade.
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Myocardial rupture is usually preceded by postinfarction regional pericarditis (PIRP). PIRP is indicated on the ECG by 2 findings: 1) persistenly positive (upright) T-waves at 48 hours, or 2) premature reversal of inverted T-waves to positive deflection by 48 to 72 hours after STEMI. In contrast to re-occlusion of the infarct-related artery, this reversal should be gradual. There should be QS-waves indicative of completed transmural MI.
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Patients who present with chest pain or cardiac arrest and have an ECG diagnostic of STEMI could have myocardial rupture. Obviously, administration of heparin and/or lytics is hazardous. These patients may survive. In a report of 6 cases at our institution (Hennepin County Medical Center), 2 survived with cardiac surgery. 5 of 6 presented with chest pain and an ECG indicating reperfusion therapy, but were detected by bedside ultrasound.
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Plummer D et al. Emergency Department Two-Dimensional Echocardiography in the Diagnosis of Nontraumatic Cardiac Rupture. Annals of EM 23(6):1333-1342; June 1994.
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For more information, see chapter 28 of Smith's "The ECG in Acute MI."

2 comments:

  1. Fascinating case! Thank you! However, allow me to argue against this ECG suggesting a posterior MI. The hallmark of an acute posterior infarct is ST depression in V1-V2 (the equivalent of ST elevation in other leads). Also, there are no tall R waves in V1-V2 to along with that. This patient's event was likely that time she started feeling unwell which was 36 hrs ago. I would expect a tall R wave in those leads, the equivalent of a Q wave elsewhere.
    This patient, no doubt, has ST elevation in the lateral leads. The changes in the inferior leads could very well be reciprocal. However, the ECG is very suggestive of diffuse sub-endocardial ischemia from hypotension, the cardiac arrest and the catecholamines she was resuscitated with. ST elevation in aVR is classical for this phenomenon and we see it clearly in this patient.

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  2. Thank you for your input, Hatim. You may very well be correct.

    I should clarify that I also do not find the ECG diagnostic of posterior STEMI, but there are features that argue for it. There appears to be a posterior fascicular block, and this will eliminate the Q-wave of a lateral MI and may also eliminate the increased precordial R-wave of posterior STEMI. Subendocardial ischemia usually, not always, extends to V5 and V6. STE in aVR seldom has any independent value, in spite of the many articles featuring it: it is really the same as ST depression in the lead (-) aVR, which is at 30 degrees, between I and II. The best measure is ST axis, which in this case is -90, or straight up, corresponding to an isoelectric ST in I, and negative in (-)aVR, II, aVF, III. I agree with you that an ST axis straight up is usually subendocardial ischemia (or STEMI at the base of the heart). And subendocardial ischemia is likely with high demand (hypotension and tachycardia). So the ECG is inconclusive. We know from the surgical findings that it was a lateral transmural completed infarct, but know little else about the coronary anatomy.

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