Saturday, August 22, 2015

Sudden Severe SOB and ST Segment Elevation: What is the Diagnosis and Treatment?

A middle aged man with history of MI presented by EMS for the sudden onset of difficulty breathing. 

Prehospital, he was in respiratory distress and tachypneic, and was tachycardic to 130.  SpO­­­­­­­­2 was 85% on high flow oxygen.  Prehospital ECG (not available) was read as  ***ACUTE MI***  and the cath lab was activated by EMS.  

He was agitated upon arrival.  Lung exam revealed good air movement but no rales or wheezes (clear).  [Think: what does this mean?]  Heart rate was 140 bpm.  Extremities were cool. His left leg was mildly swollen compared to the right.  He was in severe shock.

The patient was intubated immediately upon arrival.  The end-tidal CO2 was low (~18 mm Hg).

The physician requested tPA to be prepared due to concern that this represented a massive PE.  It was withheld pending confirmation of the diagnosis and partially due to the uncertainty about whether he could go to the cath lab for STEMI if he received tPA. 

An ECG was recorded while a bedside ultrasound was also done:
There is sinus tachycardia.  There is inferior ST elevation with reciprocal ST depression in aVL and  in lead I, very suggestive of STEMI.  There is RV conduction delay (R'-wave in V1) with ST elevation in V1-V3 that is not suggestive of STEMI.  
Another possibility to consider is inferior and RV MI (STE in V1), with acute severe right sided failure.

Thus, the initial EKG was concerning for STEMI.

The bedside cardiac ultrasound was revealing: 

There is LV hypertrophy and a low volume LV with adequate systolic function.  The RV is hypokinetic and dilated (high volume RV).

The providers were concerned that the generous RV in the setting of respiratory distress, hypoxia, tachycardia, and unilateral leg swelling was very concerning for PE, but they felt that it did not fully explain the EKG findings.

Here is a view of the inferior vena cava:

It is dilated.  This is very suggestive of high right sided pressures.  But that by itself does not help in the diagnosis, because shock from both LV STEMI and PE would increase right sided pressures.

There was a discussion about whether this represented PE or STEMI. Treatment options were considered including TPA or cath lab activation. A second EKG was recorded:

Comment: What is going on?

Salient facts: The patient had sudden SOB with severe hypoxia and shock, but with clear lungs.  Ultrasound further confirmed this with absence of B-lines (not recorded).

Furthermore, a low end tidal CO2, though also associated with cardiac arrest, is common in patients with massive pulmonary embolism.  Because the lungs are ventilated but not perfused, the CO2 cannot be excreted through the airways and the etCO2 is low.

One might be tempted to attribute right sided failure to inferior MI with right ventricular MI and RV failure, but RV failure from RV MI does not cause hypoxia.

Acute STEMI only causes hypoxia if it results in pulmonary edema.  This patient had clear lungs.  When patients have severe pulmonary edema, the gas exchange is poor, and areas of the lung that are ventilated are OVER-perfused (causing pulmonary edema) and the end tidal CO2 (and arterial and venous pCO2) are high because the alveoli are filled with fluid.

A chest X-ray, taken 5 minutes after the ECG was recorded, confirmed clear lungs:
There is no pulmonary edema

Acute hypoxia with clear lungs and clear chest X-ray is pulmonary embolism until proven otherwise!

But another ECG showed even larger STEMI:
Sinus tach with PACs.  Now there is additional ST elevation in lateral leads, also diagnostic of STEMI.

STEMI on an ECG only tells you there is transmural ischemia.  The STE does not tell you the etiology.

In other words, the ECG may diagnose ischemia; it does not diagnose ACS.  

Rather, in less than 5% of STEMI cases, the ischemic ST elevation is caused by severe demand ischemia such as that caused by massive pulmonary embolism. 

The ECG findings were more pronounced now with ST elevation in II, III, aVF, and V4-V6. The cath lab activation was confirmed.

The patient became bradycardic and hypotensive.  tPA was given.

Another echo was done:

There is now worsening function of both ventricles.

There was no response to norepinephrine infusion nor to external pacing. He soon became pulseless and compressions were started. The resuscitation was continued for a prolonged period but the patient remained in PEA and never achieved ROSC. No autopsy was performed.

Learning Points:
1. Hypoxia with clear lungs is pulmonary embolism until proven otherwise (see other etiologies below)
2. STEMI only causes hypoxia by causing pulmonary edema
3. Massive Pulmonary Embolism can result in a STEMI ECG, identical to ACS STEMI.  (I have seen this numerous times but this is the first time I've posted one)
4. Low end tidal CO2 is typical of massive PE.  High end tidal CO2 is typical of severe pulmonary edema.
5. Shock from STEMI has unmistakably poor LV function and on bedside echo
6. RV failure from RV MI does not cause hypoxia.
7. Perhaps most important: if the differential is STEMI vs. massive PE, just give the tPA, front loaded (100 mg).  There is no contraindication to angiography and PCI for a patient who has received thrombolytics and remains in shock.  In fact, it is the therapy that is recommended therapy for patients who are in shock and need to be transferred to a PCI capable institution.

(Certainly if you know without doubt that STEMI is the diagnosis, then do not give tPA if you are at a PCI capable institution and rapid PCI can be done.)

Hypoxia with clear chest X-ray
1. Pulmonary Embolism.
2. Asthma
3. Hypoventilation (high pCO2)
4. Sepsis (pulmonary vasodilation and shunting)
5. Anatomic right to left shunt (VSD etc.)
6. Vasodilators such as nitroprusside (cause pulmonary vasodilation and shunting)

2013 STEMI Guidelines.  JACC 61(4):p. e97

5.3. Transfer to a PCI-Capable Hospital After Fibrinolytic Therapy

5.3.1. Transfer of Patients With STEMI to a PCI-Capable Hospital for Coronary Angiography After Fibrinolytic Therapy: Recommendations.  

1. Immediate transfer to a PCI-capable hospital for coronary angiography is recommended for suitable patients with STEMI who develop cardiogenic shock or acute severe HF, irrespective of the time delay from MI onset (354). (Level of Evidence: B)

Also in this section:

Angiography and PCI may be done also for:

2.  Patients with STEMI who receive thrombolytics at an outside hosptial and do not have reperfusion (as determined by EKG) should go immediately for PCI.

3.  Patients who have successful reperfusion with thrombolytics should wait 2-3 hours for their PCI.


  1. Why STE in V1 not suggestive of STEMI(First EKG) , a ST/T wave in this lead has same direction of last deflection of QRS complex? I consider second possibility RV infarction .
    Any explanation for STE in V1-V3 NOT suggesting STEMI?
    Thanks with regards

    1. There is ischemic ST elevation, you are correct. But it is not STEMI because it is not due to ACS. Due to severe supply demand ischemia (type 2 MI)

  2. Thank you for the presenting these great cases. In the second ECG isn't there QRS alternans? Maybe a little on the first ECG as well? No pericardial effusion is visible on the ECG though...
    I also wanted to comment that Chagas' disease also leads to hypoxia and clear lungs as it usually affects the right ventricle much more than the left ventricle.

    1. How does Chagas cause hypoxia? (We do not see it in north america)

    2. So... it doesn't – I didn't revise what I wrote.

      In chagasic patients that heave heart disease and dysfunction, it does cause biventricular dysfunction, and the right side is usually more affected. So the there is a predominance of right-sided symptoms such as jugular vein distension, hepatomegaly, ascitis, lower limb edema. Patients usually complain of weakness instead of dyspnea. Atypical chest pain is not uncommon and this is correlated microcirculatory damage and not coronary stenosis. Besides heart failure, these patients are prone to arrhythmias, bundle blocks and pauses. A typical ECG finding is RBBB + LAFB, but this is not sensitive or specific. There is an indeterminate phase (clinically silent phase) before overt heart symptoms develop that can last as long as 30 to 40 years.

  3. Steve...

    It's a shame there was no autopsy. This would have been an excellent M&M conference. Did anyone ever comment in the physical exam part of the chart whether there was distended neck veins or cannon a waves? Also, since the diagnosis of RV myocardial infarction was apparently entertained, was a right-sided ECG (or at least a V4R) obtained? One thing I noticed on his ECG was that the tachycardia was really pushing his P waves into ventricular systole, so that also could have been a contributing factor to the systemic hypotension.

    I'm not sure I would immediately rule out a right ventricular MI. Patients with RV MIs can certainly get hypoxemic. Many people have patent or potentially patent foramen ovales which can open up as the right atrium becomes more and more distended allowing a significant right-to-left shunt. How this would affect hypoxia as opposed to hypoxemia, I'm not sure. Also, for such a massive PE I really don't see much in the way of the classic changes of acute cor pulmonale which should certainly be present on the ECG of such a patient with a massive PE. He does show right ventricular delay but that could occur with a right ventricular infarction as well. The ST elevations in V4-6 show up later. The left ventricle was hypertrophied which makes it even more susceptible to ischemia itself and this may have be more a secondary manifestation of the state of shock which appears to have been worsening. The failure to respond to pacing could have been due to the pacing wire in contact with infarcted RV.

    Overall, I think you are probably right that this is a massive PE and I totally agree that administration of a front-loaded thrombolytic possibly could have helped (but I really think only "possibly"). All in all, a right-sided ECG may have shed more light on the diagnosis. I'm surprised an autopsy wasn't done. Here in Texas where I live, anyone who presents to a hospital with an acute illness and dies in-house within 24 hrs automatically gets an autopsy (or at least, they used to).

  4. If I had a strong enough suspicion of PE, which there probably is here, I would have put this person on VA-ECMO as a bridge to surgical embolectomy. Lots of cases of full recovery from PE even after cardiac arrest. Something to think about if that's a possibility at your facility.

  5. Jerry,
    Right to left shunting would cause both hypoxia and hypoxemia, but if signiificant enough to do so, it would lead to adequate LV filling, in contrast to what was seen on echo.
    What would have made the diagnosis even more clear would be an ultrasound of that swollen leg, if it showed thrombus.

    1. Thanks Steve! Did you or any of the other posters get the impression that the right lung appears more lucent than the left?

    2. Jerry,
      Very good observation!

  6. Sometimes ago was a similar case on Facebook. European Guidelines regarding PE: 3 types: a) cardiogen shoc, b) with right ventricular dysfunction and/ or positive troponin and c) patient with low risk. Positive troponin could appear by: demand ischemia, dilation of pulmonary artery that compresses RCA or a thrombus that has passed through a foramen ovale and then occludded the RCA. Personal history, Geneva or Wells score, D dimers, infrainguinal veins Doppler, cardiac echography and chest angioCT will establish the diagnosis. Some specialists say that chest angioCT can be adapted in a way that makes possible cardiac imaging. Sure, it is difficult because the heart rate is too high for cardiac CT.

  7. Seems to me there is excessive echos in the IVC hard to say from the one view if these emboli in transit. The ivc lumen is usually clear


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