Sunday, December 13, 2015

Briefly without pulse, has pulmonary edema and LBBB with 10 mm of ST Elevation

A middle-aged male was found down.  EMS was able to get the patient to climb onto the ambulance by himself, then during transport he became less responsive.  They briefly could not find pulses, and gave a short period of CPR with ROSC, but he did not require a shock. They gave Narcan without improvement.  An oral airway was placed and BVM oxygenation provided.  The patient arrived unable to provide any further history.

BP was 180/100, HR 130, Oxygen saturations 84%.

He was intubated.  A bedside ultrasound showed poor global function and B-lines of pulmonary edema.

Here was the first ECG:
There is sinus tach and left bundle branch block (LBBB).
There is massive ST Elevation in V2 and V3
The ST segment in V3, as I measure it, is 10 mm, with a 38 mm S-wave.
The ratio is 10/38, which is greater than 0.25, consistent with LAD occlusion.
This meets the modified Sgarbossa criteria, which have been derived and validated.
Should we diagnose anterior STEMI?
Should we activate the cath lab?
Here is the chest x-ray, in case you don't believe in B-lines:
Profound Pulmonary Edema

Remember:

In both of the studies of the Modified Sgarbossa criteria, we excluded patients with extremely elevated BP, pulmonary edema, extreme tachycardia, or hyperkalemia.

That is because these patients need supportive care and then, subsequently, a decision on the cath lab.

This patient would have been excluded from the studies.

The blood gas returned with severe acidemia, with both metabolic and respiratory acidosis:
pH 6.8, pCO2 = 86, HCO3 = 14
Lactate was greater than 15.
K was normal.

The patient was stabilized with supportive care.  The respiratory acidosis improved with good ventilation.  The lactate had time to metabolize.  The patient was well oxygenated.  The elevated BP resolved with propofol.

By the time of the second ECG, the pulse was about 100, O2 sats 95%, BP 144/80.

100 minutes after first:
Supportive Care has resolved all the pathologic ST elevation.

The Peak troponin I overnight was 2.382 ng/mL, consistent with NonSTEMI.

An ECG was recorded the next AM:
Remains without obvious ischemia.  It does not even show reperfusion T-waves.


Case continued

The next AM more data revealed a history of coronary disease with stent placement in the circumflex 3 years prior.  Since then, he has had progressively worsening dyspnea on exertion, and orthopnea.

Echo the following AM showed EF 35%, asynchronous interventricular septal motion (due to LBBB), inferior wall motion abnormality, LV enlargement, and LVH.

It was unclear exactly what had caused acute decompensation.  Hypotheses included brief dysrhythmia or ACS leading to shock and pulmonary edema.  

Given the coronary history and findings on TTE (inferior wall motion abnormality), ACS was high on the differential, and so he went for cath later that day.

Cath result:  total occlusion of a small right posterior descending artery (RPDA) which filled by left to right and right to right collaterals.  No intervention was done because the artery was too small and the territory it supplied had good collateral circulation.

The patient was later able to relate that he was having some SOB and trying to contact his doctor when he decompensated.

The explanation of his deterioration:

He has baseline poor LV function with increasing heart failure symptoms, then had an acute occlusion of a very small RPDA which affected his LV function just enough to tip him over the edge into acute pulmonary edema.

He was managed medically and did well.  He was scheduled for cardiac resynchronization therapy (a biventricular pacemaker which improves cardiac output in patients who have LBBB with a QRS greater than 130 ms).

Learning Point:

Respiratory failure with hypoxia, hypertension, tachycardia, and acidosis can lead to profound ECG changes, in both LBBB and in normal conduction.  Before making the reperfusion decision, stabilize the patient.

Although in this case he did have a coronary occlusion, it was small and neither needed PCI, nor could be intervened upon.

It was not the LAD, so these ECG findings had nothing to do with the very small coronary occlusion.












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