Ivor Popovich @InternSupp
NZ Intensivist. Physiology geek. Book author, “A Dim Prognosis.” https://t.co/PP58ZrN5SI Joined August 2018-
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@IM_Crit_ I think landmark SC and US guided are two completely different lines… really an axillary vein line most of the time with US
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@PulmCrit While your broader point is true, just be fast, co2 production is much higher in someone with metabolic acid production
@allisonoconn The most common cause is prior abx treatment
@IM_Crit_ Then I’m very glad to work where we control our own dialysis
@IM_Crit_ Can’t UF because of hypotension but giving beta blocker/CCB?
@volatilehead @AndromedaShock @icmteaching @khaycock2 Thanks. Just an assumption.
My new paper in Critical Care on the microcirculation. @icmteaching @khaycock2 link.springer.com/article/10.118…
@AndromedaShock @icmteaching @khaycock2 Thanks Glenn! Glad you enjoyed reading it.
@khaycock2 @icmteaching Thanks Korbin!
For now it’s just a model, but hopefully adds to our attempts to understand the confusing and paradoxical events in the microcirculation that are the true cause of sepsis mortality.
On the latter point; we know that sepsis impairs shear sensing through endothelial damage. If we could restore shear sensing pharmacologically we may be able to treat septic microvascular failure.
On the latter point; we know that sepsis impairs shear sensing through endothelial damage. If we could restore shear sensing pharmacologically we may be able to treat septic microvascular failure.
This is a theoretical model that needs further experimental validation. But it could explain how vasoconstrictors work, why spontaneously hyperdynamic patients seem to do better, and how microvascular failure could persist despite resuscitation
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