Monday, March 21, 2016

What, besides large anterior STEMI, is so ominous about this ECG?

This late middle-aged male had sudden onset of chest pressure.  Here is the prehospital ECG:
The rhythm is a bit hard to discern.  It appears to be sinus with PACs.
It is obviously an anterior (and lateral) STEMI.
What other ominous finding is present?

The cath lab was activated prehospital, and on arrival, the patient was in shock, with hypotension and an StO2 of 55% (this is a tissue oxygen saturation; normal is 75%.  55% represents shock no matter what the blood pressure).  He denied SOB but immediate bedside ultrasound showed B-lines of pulmonary edema.  Oxygen saturations were 94% on nasal cannula.  BP was approximately 90 systolic.

Here is the ED ECG:
Now there is atrial fibrillation with moderately rapid ventricular rate (126)
There is huge ST elevation in V2-V4 and I and aVL, diagnostic of proximal LAD occlusion
Here is the ominous finding: 

Right Bundle Branch Block (RBBB) + LAFB (left anterior fascicular block).

I have seen a dozen cases of STEMI with RBBB and LAFB.  All were close to death.  This article by Widimsky illustrates the danger of this finding:

See these cases:

Chest Pain and Right Bundle Branch Block

1. Aspirin 325 mg
2. Ticagrelor 180 mg
3. Atorvastatin 80 mg (small studies support this)
4. Heparin bolus
5. Fluid challenge
6. Because cardiogenic shock is likely to get worse, even after reperfusion (because myocardial stunning lasts many days), we intubated the patient.
7. Vecuronium paralysis
8. Ketamine sedation (to avoid affecting hemodynamics)
9. K replacement.
10.  Should have cardioverted, but did not

By this time, the cath team was ready.

A proximal LAD thrombotic occlusion was opened.  Here is the post-reperfusion ECG:
Sinus rhythm at a rate of 117.
Uncertain if conversion was spontaneous, or done electrically in the cath lab
RBBB and LAFB persist (not a good sign).
ST elevation is greatly improved (a good sign), though still very elevated (not a good sign).
There is terminal T-wave inversion, an early sign of reperfusion.

A balloon pump was placed.

Here is the ECG the next day:
Q-waves and poor R-wave progression.  RBBB and LAFB are gone.  (A good sign).

Highest troponin I was extremely high at 230 ng/mL at 10 hours after arrival.

Echo showed anterolateral wall motion abnormality and EF of 35%.

In spite of maximal supportive therapy, balloon pump, and persistently open arteries, the patient succumbed to cardiogenic shock 5 days later.

Learning Points:

1. Cardiogenic shock due to STEMI has very high mortality even if the artery is opened.  The mortality is approximately 50%, and, surprisingly, use of a balloon pump appears to not change that terrible prognosis. (1)
2. RBBB and LAFB are signs of very severe ischemia
3. Although I know of no supporting literature, I almost always intubate STEMI patients with shock and pulmonary edema.  Work of breathing may require 50% of cardiac output.  Positive pressure ventilation and paralysis takes away all that work and all that excessive requirment for cardiac output.

1)  Thiele H et al.  Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial.  Lancet.   Volume 382, Issue 9905, 16–22 November 2013, Pages 1638–1645.


  1. Insightful case by Dr. Stephen Smith. Although the diagnosis is obvious (large anterior acute STEMI from proximal LAD occlusion) — the teaching points center around picking out ECG indicators of severity. As emphasized by Dr. Smith, these include new AFib as the rhythm (with loss of “atrial kick” and the fairly rapid rate contributing to reduced cardiac output and the patient’s cardiogenic shock) — new bifascicular block (RBBB/LAHB) — plus profound ST elevation in anterior and high lateral leads — with equally profound reciprocal ST depression in inferior and lateral chest leads. I’ll simply add 2 additional features conveying “ominous outcome” unless (albeit even if) prompt revascularization is undertaken: i) that large Q waves have already formed (in V1,V2,V3) with loss of R wave amplitude in lateral chest leads in this patient is obvious extensive ongoing stemi; and ii) the “Tombstone” ST segment appearance with “lambda” wave-like downsloping in leads aVL, V2,V3 — which some investigators feel portends imminent VFib in many of these patients. That said, rather than this “lambda-like” ST-T wave shape being predictive of imminent VFib — I’ve always felt the combination of OTHER findings specified above are more than enough to predict likely VFib secondary to cardiogenic shock in many of these gravely ill patients even when prompt treatment is undertaken. THANKS to Dr. Smith for posting this wonderfully illustrative tracing of these high-risk ECG findings.

  2. I am taking a bird's eye view of the first ECG and the morphology of the STE in V2,3 aVL I are strikingly reminiscent of Lambda STE, a harbinger of Electrical storms. In addition there is the reverse Lambda in II, III, aVF. Recently, a Cardiologist sent me 2 ECGs, the first look very much like a D1 Occlusion but it metamorphosed into Lambda STE and Reverse Lambda...angiogram showed LMS occlusion, he went into VF and died. I sent the ECGs to Prof Ken Grauer and he thinks that the Lambda STE and reverse Lambda were present. Subsequently, another Cardiologist sent me an ECG with Lambda and reverse Lambda...I wonder if you agree this might be the case here?

  3. Ken,
    All great comments as usual. I hadn't heard of lambda STE, but just read the paper and it is very interesting:
    (Aizawa, Yoshifusa et al. Characteristics of electrocardiographic repolarization in acute myocardial infarction complicated by ventricular fibrillation Journal of electrocardiology , 2012, Vol.45(3), p.252-259)
    1. The lambda STE apparently was not described with bundle branch block, but in normal conduction, and it is not clear if it applies to BBB. In this case, the lambda is only present in V2 and V3, which have large R' waves. aVL has a "type II" which has some upward slope from the J-point
    2. The STE in aVL is not lambda-type
    3. Lambda predicted ventricular fibrillation, not cardiogenic shock. However, it is well known that the more myocardium at risk, the higher the risk of BOTH VF and shock.
    4. In the study, the mean ST elevation was 7mm in patients who had VF vs. 3.5 mm in those who did not. So I don't think that lambda adds as much additional prognostic information as the authors claim, though clearly there is something to it.

    1. Thanks for your insights Steve after researching the lambda wave finding. I think we both view assessment of this finding similarly.

  4. My first thought was the patient was very unlucky since despite all efforts.
    Let me add also two more electrocardiographic signs of poor prognosis. The first one is atrial fibrillation which seems to imply a poor prognosis in the context of STEMI.
    The other one is terminal QRS distortion: I have some difficulties in interpreting the anterior leads because of the presence of RBBB but I see terminal QRS distorsion in aVL and perhaps in I. Isn’it?

    1. Mario,
      Good observations.
      By Birnbaum's definition, there is TQRSD: J-point more than 50% of the height of the ST segment. But there is an S-wave; it is followed by the large R wave of RBBB.

  5. Hi Prof Smith, Lambda STE and Reverse Lambda (Reciprocal), if I am not mistaken was described in Brugada and it was a foreshadow of VF. A very graphic ECG with Lambda STE and Reverse Lambda in a patient is to be found Brugada Syndrome Variant Or Atypical Brugada Syndrome
    I have seen lambda in one patient with Tombstone STEMI and he had a very bad time but survived, 2 other cases (With Lambda and reverse Lambda)I am acquainted with died, one of VF...


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