So I was glad to see some great answers on twitter about this case, so let me fill you guys in on the management and the details.
So my diagnosis was of a (likely viral) myocarditis as a subacute process over the last weeks, with a superimposed pneumonia causing the acute deterioration and presentation to ED. I didn’t think that his elevated lactate represented shock, but rather a reflection of adrenergic activation and reduced hepatic clearance due to congestive hepatitis. He also had congestive renal failure. Of course, the LV had a 4 x 2 cm apical thrombus, which is likely secondary to the dilated cardiomyopathy.
So the management was diuretics, antibiotics, and anticoagulation, which resulted in a gradual improvement of the respiratory status and renal/hepatic dysfunction. He had a coronary angiogram the day following admission which showed two 50% stenoses deemed to be innocent bystanders.
I think the learning point in this case is that, without POCUS, this could easily have been treated as severe sepsis with multiple organ failure (potentially rationalizing away the BP of 140 as a “relatively low” BP due to untreated hypertension), and as such, may have received fluids… Especially south of the border where they are mandated to give 30 cc/kg to anything deemed “septic.” This would have been the polar opposite of the necessary treatment.
The scarier thought is that he may have then progressed to “ARDS,” been intubated and then the debate between keeping him dry and giving fluids for the kidneys may have ensued. Though a formal echo likely would have been done, it may not have happened in the first 24-48 hours… If MSOF progressed and he succumbed, the rational may have been that he was “so sick,” and died despite “best care…”
The reality is that he is not yet out of the woods today, with an EF of 15% and afib, but he is off O2 and sitting up in a chair. Fingers crossed he falls in the group of those with myocarditis who improve…
Love to hear anyone’s thoughts!