Thread by @UAlberta_Sono

Sometimes you stumble across a case that challenges everyone-even those who with super skills...but even more--a case ripe for diagnostic bias. This is one of them (written consent obtained to share these images:forewarning-->no ECG gating). A thread. @UAlberta_ICU #POCUS

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A colleague was looking after a 30-ish yo female who was several wks postpartum. She had been SOB; an early comprehensive echo demonstrated an impaired LV function (EF ~30%). She was admitted to ICU and placed furosemide for CHF, requiring NIPPV. Transitioed to prongs PAD #1.

A couple days later, she became quite hypotensive, more SOB and was initiated on norepinephrine through a peripheral IV. This was unexpected and the attending asked for a focused cardiac exam for ?worsening depression of LVEF. She was in mild respiratory distress sitting up.

Parasternal views (sitting up!) demonstrated the severely depressed LV and a left pleural effusion, mild consolidation. Could this be the cause for the SOB and hypotension?

For a better appreciation of the myocardium--see here. Nonetheless, in comparison to the previous echo, the LV appeared similarly depressed.

Now the IVC was also readily obtainable. It was <1.2 cm and highly collapsible.

How does this change the above questions?

Based on a preliminary assessment, the attending wondered if this was just a pleural effusion and perhaps some hypovolemia from furosemide.

But that would be too simple. The exam continued along in an atypical sequence. A subcostal 4-chamber shown below. Now what do you think?

Wait! What's this? a pericardial effusion? Surely this & "separation" is just a sliver. Or is it? Well the IVC is flat surely "it must be dilated for tamponade"? See here: albertasono.ca/pericardial-sp…

But...the RV seems awfully collapsed (RA poorly seen).A conundrum is now roaring.

Well it just so happens that the apical view was also high quality. The RA and RV are clearly *very low volume. The right atrium is collapsing during late diastole. Shoot, could this really be tamponade? N.B. Color Doppler not shown but all valves intact.

Yes--this is a case of low-volume tamponade with a regional effusion. Cardiology was contacted and helped care for this patient--performed a pericardiocentesis. The patients hemodynamics improved greatly and came off inotropes/pressors and felt significantly better.

Some of you may be wondering-what is this? Well in this case, the effusion was localized over the RV. The pericardial pressures were likely low, **but the ventricular pressures were even lower--esp with diuresis and fluid depletion. Trans-myocardial pressures here favour collapse

"Low-volume tamponade" is uncommon but a concerning phenotype. These patients are far less likely to have clinical findings of jugular venous distension and pulses paradoxus. Exaggerated inflows are similar to traditional tamponade (not shown here).

Please see this excellent hemodynamic study for further details. ahajournals.org/doi/full/10.11…

We should say that there are many on #MedTwitter with far greater expertise in this domain than us, but we thought it important to share this case and the lessons learned.

1. With every rule, comes an exception. The IVC is no different. While this condition is uncommon, be weary of caveats. The IVC is *generally distended with traditional tamponade as there is an atrial-->caval gradient that leads to obstructed inflow and a dilated IVC.

2. "Point-of-care" should be rigorous, with multiple views acquired and a systematic assessment. Early on in this case, it would be easy to be misled. Pleural effusions, depressed LV, collapsed IVC--lots of potential solutions, all of which would lead to premature closure.

3. It takes time to make decisions. While #POCUS can occasionally offer bedside solutions, sometimes you have to sit-back and survey the land from a thousand feet. For us, this was one of those times.

4. "Consciously incompetent". This is an exceptional & difficult case. We engaged our cardio colleagues early as we new we were wading into unchartered territories. Managing this patients hemodynamics was challenging no question. First thing we did was turn off the lasix!

This was followed by small fluid boluses while we awaited transport to the lab for drainage. Normally, we would be more aggressive with IV fluids--but we worried this patients competing LV dysfunction may make fluid management difficult.

Anyways that is it for now. Hope this case was instructive. Come visit us at @UAlberta_Sono and AlbertaSono.ca