Today on the podcast, I interview Martin Tobin on 3 papers he has recently written on COVID pulmonary physiology.
* Praise for Dr. Tobin
* Bio Page
Caution about Early Intubation in COVID-19
From 2 studies, 1 on sheep breathing with a human-equivalent Vt of 502 ml
2nd study was observational with a questionable connection to Vt--it was confounded by a number of other factors
Absence of Obtundation
L vs. H Subtypes
Physio Diversion - Looking for the Patient that needs more Inspiratory Flow
* Tobin Vent Review in NEJM
Basing Respiratory Management of COVID-19 on Physiological Principles
Tachypnea in Isolation is Not an Indication for Intubation
Not indicative of increased WOB
Avoiding Intubation with NIPPV
Correlation of saturation with a host of other evils, but it is possible that the saturation is merely a marker--similar to pH. Vicious cycle of shunt, low SvO2, encephalopathy, decreased resp. drive. COVID has been different, with decreased saturation without the horrible lung injury that normally accompanies it. We are also used to patient discomfort from the disease causing the hypoxemia. Retained good compliance. We have not seen the isolated hypoxemia of COVID in many situations before.
The Baffling Case of Silent Hypoxemia
Happy Hypoxemia vs. Silent Hypoxemia
Dr. Tobin defines silent hypoxemia as PaO2 39 mmHg (as a PaCO2 39 mmHg 
Definition of Hypoxemia
Do we need to factor in FiO2? Dr. Tobin and I say no!
I define by pulse ox or (PaO2), doesn't matter how much O2. e.g. "He is still hypoxemic despite being placed on NRB."
When does Hypoxemia Become Dangerous?
Pulse Ox Inaccuracy
OxyHemoglobin Dissociation Curve Shifts
Fever shifts to the right, Decreased CO2 shifts left
Mechanism of Silent Hypoxemia
ACE2 is expressed in the carotid body and may be partially to blame
COVID breaks our Heuristics
Heuristic representation of how bad their lung disease actually is. Projecting expected course...
COVID first disease that unlinks it
Now on to the Podcast...