Sunday, April 20, 2014

Sudden Cardiogenic Shock

An elderly woman presented with rather sudden altered mental status, hypoxia, and hypotension.  She had no significant past medical history except for cognitive decline.  She was cool and mottled with thready pulses.  BP was 54/32.  No murmurs were heard.  Tissue perfusion monitor recorded 33% (very low) [see this explanation of StO2 by our new chief and prolific researcher, Jim Miner]

She was immediately intubated by blind nasotracheal technique (very fast, no complications).

Immediate ultrasound showed good sliding signs and B-lines (a sign of pulmonary edema) only on the right.

Here was her initial cardiac ultrasound, parasternal short axis:
This shows decreased LV function, but only moderate, not clearly bad enough to account for severe shock.  There seems to be an anterior wall motion abnormality.  What else is there?  Look at the density moving in the LV.  See below for further interpretation.

Here is a parasternal long axis view:

Again, there is moderately decreased LV function.  The base of the heart appears to be contracting well.  What else do you see?  (It is pointed out in the still picture with arrow below)


This is a flopping papillary muscle.  The first ultrasound (short axis) also shows this flopping.

Here is the inferior vena cava (IVC):

The echogenicity of the blood in the IVC is a sign of profound stasis.  You can see the blood moving not forward, but both forward and backward.  Thus, there are very high right sided pressures.

So there is right sided failure.
What is the etiology?  The most common etiology of acutely elevated right sided pressures is left sided failure.  Of course pulmonary embolism is a relatively common cause as well.  Right sided MI can give high right sided pressures with low pulmonary artery pressures.

B-lines suggest pulmonary edema and suggest left sided failure, not right side only failure.

How about the ECG? (this is an ECG blog, after all!):
This shows acute on old, or subacute (more likely) inferior MI.  There are Q-waves, minimal ST elevation with reciprocal ST depression in aVL.  There is also evidence of diffuse subenocardial ischemia with ST depression in V4-V6.
 A right-sided ECG was recorded:
No evidence of RV MI

A chest X-ray was done:
This shows a very significant finding which I had never known about before: right side pulmonary edema, which correlates with the right sided B-lines on pulmonary ultrasound.  The radiology boards use this image for one particular diagnosis.

Initial troponin I was 13 ng/mL.  K was 7.0. HyperK was treated but with no clinical improvement of the patient.  Lactate was 17 mEq/L.  She was started on Norepinephrine and the tissue perfusion (StO2 monitor) rose to 58%.  (significantly better, but still below the goal of 75%).  BP was 89/72.


Let's put this all together:
1. Sudden decompensation into shock
2. Pulmonary Edema on the right
3. LV function not so bad that she should necessarily be in cardiogenic shock
4. Subacute inferior MI, probably was a STEMI at onset
5. Very high right sided pressures


What is it?

Echo: this shows a loose papillary muscle
CXR: right upper lobe pulmonary edema is highly suggestive of severe mitral regurgitation.  It just so happens that when there is severe mitral regurg, the jet is directed exactly at the pulmonary veins that drain the right upper lobe!  Thus, it causes worse pulmonary edema in the right upper lobe than elsewhere.  The radiologist noted this finding.
ECG: Papillary muscle rupture is most commonly associated with posterior MI, which is very closely associated with inferior MI.

Outcome:

A formal echo was immediately done and confirmed papillary muscle rupture with severe mitral regurgitation.

Here is the report:
--Partial rupture of the posterolateral papillary muscle with chordae to the anterior mitral valve leaflet with resultant partial flail and eccentric moderately severe mitral regurgitation.
--Decreased LV systolic performance severe.  Estimated left ventricular ejection fraction is 27%.  The LV function may be worse because of the pressors.
--Regional wall motion abnormality-inferoposterior, akinetic.
--Regional wall motion abnormality-distal septum, apex and anterolateral, akinetic.

Getting this diagnosis right is critical not just to surgical therapy, but to medical as well: severe mitral regurgitation is treated with afterload reduction such as nitroprusside, to promote forward flow of blood.  This is just the opposite of using pressors!

The patient's wishes were to not have aggressive intervention and she was made comfort cares only.


Comment:

This is an incredibly hard diagnosis to make without doppler ultrasound.  One MUST keep it in mind in any kind of shock.  Even shock in trauma can be due to valvular disruption.  When I question providers about etiologies of cardiogenic shock, they almost NEVER mention valvular disorders.

Always keep valvular disorders in mind with cardiogenic shock!


9 comments:

  1. Ditto per Vince = GREAT case! Nice to see the Echos as well as the ECG with excellent explanation - :)

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  2. Thank you Dr. Smith. It was a very nice case which emphasize again to interpret everything with each other. I tried always to do a brief bedside echo in such situatioin that physical exam cannot help me too much and found 2 of these ruptures. I would say in an emergent situation you can never auscultate the heart properly, so echo is the decision. Excellent radiology point, I did NOT know that. We have never forget to look for mechanical complication of acute/subacute MI.

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  3. Please, has your hospital a protocol for MI treatment? We use all toghether ecg, trop test and echocardiography in the emergency room, performed by the cardiology resident. After initial evaluation are informed cath lab, UTIC and/ or cardiovascular surgery. What about counterpulsation ballon in this case?

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    1. IABP might be useful. This patient wanted no more intervention.

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  4. Excellent case, dr Smith!
    Since this is a ECG blog, as you've pointed out, I got a question about the ECG :)
    The first ECG shows reciprocal depression in both aVL and I, as well as a subtle ST elevation in lead V1. Some would argue (i.e. dr K Wang) that this is diagnostic of a right ventricular involvement, yet the right-sided leads showed no evidence of RVMI. What's your opinion on this?

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    1. In this regard, Dr. Wang is wrong. We just studied this, and ST depression in lead I in inferior MI has no relation to RV MI. We are presenting this at SAEM in May.

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  5. Had a similar 59 yr case that had CABG x 4 and MVR but didnt end up surviving. We are going to pick up more of these as we do echos in ED's by EP's. We had a similar white sided infiltrates reported by radiologist as infection. Could have been easily mistaken for Sepsis from pneumonia. We work in semi-urban ED with no cardiology or cardiothoracic support in house which makes it harder. Cardiology registrar who I rung said, "Are you sure, it's usually a post-mortem diagnosis". He was probably not wrong in the days when we weren't doing echoes in ED. The direction of the Mitral jet though depends on which papillary muscle is ruptured.....[say hello to Bill]

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  6. I am a medical resident on cardiology and I also wrote a few words about cardiogenic shock.

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