Friday, July 7, 2017

Acute Respiratory Distress and Pulmonary Edema

A 60-something called 911 for respiratory distress of acute onset.  Medics found him hypoxic with wet sounding lungs.  He was put on CPAP with improvement.  BP was 250/140 by manual measurement.

He was brought to the ED.  There was vomitus in his CPAP mask, and he began vomiting again.

He was intubated before he could even be placed on a cardiac monitor.

A bedside echo was performed.


There is an irregularly irregular rhythm with rapid response.
The myocardium is very thick (concentric ventricular hypertrophy)
There is very little ventricular filling, and thus very little cardiac output.
There is good LV function

There were many B lines and a very filled inferior vena cava.


Obviously, even without an ECG or monitor, this is atrial fibrillation with rapid ventricular response.

What do we do?

1.  Immediately cardiovert?  This will restore the important atrial contribution to ventricular filling, and we can see that ventricular filling is a big issue.  This will only work reliably in paroxysmal atrial fib.  Chronic atrial fib is unlikely to convert.  Furthermore, if it is chronic, then there is a stroke risk.
2. Slow the rate with an AV nodal blocker?  Diltiazem?  Esmolol?   This will not restore the atrial contribution, but will slow the ventricular rate and allow for more filling.
3. Give diuretics? This will worsen ventricular filling.

Figuring out whether this is chronic or paroxysmal is important.

The big question is: What initiated the critical situation?

1.  The patient has concentric LVH and suddenly developed atrial fibrillation.
Pulmonary Edema developed due to high left sided pressures due to poor forward flow due to:
          a) No atrial contribution to ventricular filling, and
          b) A rate too rapid for ventricular filling, this patient who has a stiff and noncompliant ventricle suddenly has a precipitous drop in cardiac output and develops pulmonary edema.

Catecholamine surge leads to peripheral vasoconstriction and very elevated BP (in spite of poor cardiac output), further diminishing cardiac output.

2.  Alternatively, there is chronic atrial fibrillation and something else caused the rapid response:
a. Patient became septic, dehydrated, had GI Bleed, etc.  However, this would lead to shock but not pulmonary edema.  And the inferior vena cava would show evidence of volume depletion.

3. The patient has chronic atrial fib and now has fluid overload.  But in such a case, the ventricular cavity would be dilated and filling well.

4. The patient has a sudden change in ventricular function (e.g., ischemia, ACS).  This is not supported by this echo which shows good LV function.

5. Valvular dysfunction: the only valvular dysfunction that is associated with a small ventricle is mitral stenosis.  This is a possibility and would be associated with atrial fibrillation and pulmonary edema.  However, it is relatively rare in the U.S. and it is also more likely to be a chronic problem.

Aortic insufficiency, Aortic stenosis, and Mitral insufficiency are all associated with a well-filling ventricle.


The typical patient who has chronic atrial fibrillation and has a rapid ventricular response is ill with second pathology that overlays the atrial fib, and cardioversion will not work and will not correct the situation.  Most of these patients have sepsis, hypoxia, resp failure, GI bleed, dehydration.  They are older and have become ill more slowly.  Their ventricles are usually dilated, not small and with concentric LVH.  This represents about 80-90% of ED patients with atrial fib and RVR who are ill.

But a younger patient with sudden symptoms, a tiny ventricle, and severe pulmonary edema is likely to have paroxysmal atrial fib and to benefit from cardioversion.

The risk of stroke is much lower as well.

Case progression

The patient was cardioverted after etomidate sedation with 200 J of biphasic synchronized cardioversion.

Here is the post cardioversion ultrasound:



Cardiac output is far better.  Filling is far better.

His clinical condition rapidly improved.

Here is the post conversion ECG:
Sinus rhythm.  LVH with typical ST-T (repolarization) abnormalities.




His blood pressure came down to 134/92, 158/97 without any ED medications.

This turned out to be his first episode of atrial fibrillation.  So, as expected, it was paroxysmal and was the initiating factor to his pulmonary edema.

Cardioversion was the exact right thing to do.

The patient did well.

Learning Points.

1. Even without the past history, one can make a very good assessment as to the chronicity of atrial fibrillation in critically ill patients.

2. Cardioversion can restore the atrial contribution to ventricular filling.

3. A slower rate can improve cardiac output.

4. Patients with LVH have very stiff ventricles that require particularly high filling pressures.

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