1) thank you for the correction on all viral PNAs being bilateral, vs. bacterial being lobar. Is that due to the smaller size of the virions affecting how they are transported through the body?
2) The alveoli being filled, is from an MD-sponsored YouTube presentation early in the epidemic: they found a higher survival rate on severe cases, when the patient was prone, and with the head lower than the feet. Somewhere along the way (maybe not that same video) was a clinician saying they saw improved results from pounding / massaging on the back of the lungs to keep things loosened up.
3) Any proposed mechanism for follow-on cardiac injury? I've seen but didn't bookmark a medical journal article in the last 36 hours detailing this as a delayed result of Sars2-2019 (or whatever they're calling it *this* afternoon) infection.
4) All gold standard studies in critical care point that a restrictive transfusion practice has a higher survivability at 30 days and one year.
Can't be talking about this virus then, there haven't been any patients around for a year yet.
Therefore, in that particular instance, you're the one talking through your hat based on approximate data. Not anecdotal, but of the kind "why are you looking for your wallet over here if you lost it down the street?" / "Well, there's a streetlight over here" sense.
Your points are well taken...In the order presented...
1. I can’t explain why viral PNA looks bilateral and bacterial PNA is lobar. That is an exquisite question that we are just not sophisticated enough to answer. My guess is that bacterial PNA infects a lobe but can’t make it across the fissures so you see lobar consolidation. I suspect (but my opinion only) is that viral replication creates a different and more diffuse release of cytokines that are not limited to a specific lobe.
2. I saw the same Youtube, but it just makes no sense. I am sure there is necrotic debris in the alveoli of ARDS, however, it is so deep in the lung circuity that if you stood on your head for a year it wouldn’t drain. Secondly, the ideas of proning has to do with physiological oxygenation called the West Zones (the sentinel work in respiratory physiology). Briefly, West Zone I is dead space, It is where there is ventilation but not a lot of blood flow. In the supine human standing up, the gravitation effect on liquid (blood) creates a gradient that the apices of the long have less blood flow than the bases. So — dead space mismatch. West Zone 2 is optimal, it is where ventilation and perfusion are matched. It is the site of most efficient oxygen an CO2 exchange. West Zone 3 are where hydrostatic pressures (liquid weighs more than gas) exec alveolar ventilation. So there is Shunt (blood flowing past collapsed gas spaces). So, proning someone tends to create more West Zone 2 because there is less hydrostatic forces across the entire lung (biophysics suggest that in the spin position there is more dorsal lung surface area than ventral). So, putting the thorax below neutral axis would actually expand west zone 3 and increase shunt physiology — it just doesn’t make sense from a bedside perspective
3. I think the myocardial injury is demand ischemia from tissue level hypoperfusion. There is always an increase in Troponin I when there is a patient with shock and ARDS. Positive pressure ventilation is inotropic in nature so without a long discussion of Starling curve, there is improved contractility, BUT it beat the hell out of preload, (impedance to venous inflow). Mechanical vent support is a beast to balance fluid resuscitation and pressure forces to maintain optimal cardiac output and reduce tissue level hypoperfusion....add to this the idea that we should run ARDS patients dry to facilitate oxygenation. Its like walking a tight rope across Niagara Falls in an ice storm
4. When I refer to restrictive transfusion practices, blood transfusion is an ORGAN transplant, and stimulates a SIRS response. All comers studied, including ARDS patients have better survivability at 30 days and one year. The studies are impressive enough that it is a standard of care. Truthfully the survive sepsis work tells the story best on this. We should really perhaps draw VBG and only transfuse when there is saturation <65% st the SVC or 60% at the PA if there is a swan Ganz catheter present.
At the end of the day —
1. I will not transfuse CoVID patients liberally because what I do know is that it will promote SIRS which is what we are trying to avoid
2. I will keep looking though the labs and literature to refine my knowledge of the ferritin and hub deficiencies, but I agree with MOM MD that if this were a primary Hgb problem, we would see a different clinical picture (and then hyperbaric may work).
3. Its the daily dilemma to treat critically ill patients because the above is balancing just one of the eight systems that we worry about...