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.

12 comments:

  1. It’s always educational to illustrate clinical correlation with actual Echo clips, as Dr. Smith has done here (serial clips in this case!). Although incidental to clinical management of this case (the Echo alone conveyed the need for prompt cardioversion) — there are several points of interest to highlight regarding this post-conversion 12-lead tracing: i) There is left anterior hemiblock (frontal plane axis clearly more negative than -30 degrees, as recognized by predominant negativity in lead II); ii) There is RAA ( = Right Atrial Abnormality) — recognized by the tall, peaked and pointed P wave in lead II; iii) There is LAA ( = Left Atrial Abnormality) — recognized by the deep negative component to the P wave in lead V1 (clearly more than 1 small box deep and wide); iv) LVH is diagnosed here by Cornell Criteria — which add the sum of the R wave in aVL + the S in V3 — which if ≥20mm for a female or ≥28mm for a male qualifies as voltage criteria. Note that there is ~6mm of overlap of that very deep S in lead V3 (overlaps with the rhythm strip below) — so that the S in V3 = 31mm + 9mm for the R in aVL, which demonstrates a marked increase in QRS voltage. The better known voltage criteria ( = Deepest S in V1,V2 + tallest R in V5,V6 ≥35mm — or — R in aVL ≥12mm) are not satisfied on this ECG — so awareness of Cornell criteria allows confident ECG diagnosis of LVH by voltage; v) Repolariation ST-T wave changes for LVH are interestingly best seen here in V2,V3 — which manifest the “mirror-image” of a typical strain pattern (ie, mentally “invert” the ST-T waves in V2,V3 — and you get a picture that is characteristic for the ST-T depression that we usually expect to see in lateral leads). The reason we see these repolarization changes here in V2,V3 is because of those tremendously deep S waves in V3; vi) There may or may not be anatomically “large” left and right atrial chambers. That’s because this ECG is taken soon after successful cardioversion of AFib — and increased atrial “pressure” sometimes produces transient ECG findings suggestive of atrial enlargement, that rapidly reverses after increased atrial pressure resolves; and vii) Although there are QS complexes in leads V1,V2 — the overall picture present on this 12-lead tracing does not suggest previous anteroseptal infarction. That’s because some r wave IS present by lead V3, AND because very deep posterior forces (produced by those LVH-induced huge S waves in V3) may oppose and reduce anterior forces, and in the extreme produce QS complexes in leads V1 and V2. Statistical odds of anteroseptal infarction are minimal as long as at least some r wave is present by lead V3 — and in the tracing here, you’ll note that substantial R wave develops by V4. THANKS again to Dr. Smith for presenting this case!

    ReplyDelete
    Replies
    1. There is also the Peguero - Lo Presti criteria, recently published. Tallest precordial S + S in V4 > 28 males, 23 females shows best sensitivity with excellent specificity. Here it is certainly positive. See https://www.ncbi.nlm.nih.gov/pubmed/28359515

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  2. Very interesting and informative case, sir. I just have 2 questions :
    1. Should the patient be administered anticoagulation ( such as intravenous unfractioned heparin or subcutenous LMWH ) before performing electrical cardioversion to prevent stroke?
    2. This is a case of paroxysmal atrial fibrillation. So, should we cardiovert with a lower energy ( 50J-100J , biphasic) instead of 200J like this case?
    Thank you sir!

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    Replies
    1. 1. Anticoagulation cannot be achieved before cardioversion. That takes up to 4 weeks! We need to cardiovert now. Anticoagulation should be started immediately afterward in case there is thrombus present or in case the patient reverts to atrial fib again
      2. Higher energy is more likely to be successful and if the patiens is adequately sedated, there is no disadvantage.

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  3. Hey. A question if i may. What will happen if you were to give the patient isoket?
    Isoket appears at pulmonary edema protocol and the only contraindications are inferior/posterior Ischemia and low BP.
    Will the isoket worsen the hemodynamic condition? And why?

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    Replies
    1. This would only be a decision to be made after cardioversion, if the BP is still too high. The major reason for the pulmonary edema is rhythm, secondarily blood pressure.

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  4. I think I'd have been tempted to give nitroglycerin to reduce afterload given that sky high BP on presentation. Can you comment on how that might have played out?

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    Replies
    1. The sky high BP is a result, not a cause. The patient has terrible cardiac output and poor filling. NTG will reduce filling and also reduce afterload. Could result in shock. Why do that when you can fix the problem?

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  5. I'm curious why the patient wasn't cardioverted in the field by EMS. Did he not meet cardioversion criteria prior to arriving to the ED?

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    Replies
    1. I'm not certain but probably because their hands were full.

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