writing some discussion questions for a short resident teaching session this afternoon on ABG & VBG analysis. answers & explanation to follow later this evening... ABGs are presented as pH/pCO2/pO2/bicarb (1/6)
A woman with history of heart failure, COPD, and recent international plane travel presents with dyspnea to the ED. ABG shows 7.52/29/65/23. What does this test reveal about her diagnosis? (2/6)
A man with COPD presents with initial ABG 7.25/70/55/30. His mentation is fine, but he has substantial work of breathing with RR 35. After two hours of BiPAP he is feeling & looking better with RR 27/min. Repeat ABG shows 7.23/74/130/30. What is best management? (3/6)
A man presents with history of productive cough, fever, and dyspnea. His PMH is notable for severe OSA/OHS and chronic use of high-dose hydromorphone for back pain. Currently he is sleepy but easily arousible. ABG shows 7.2/105/65/40. What does this test mean? (4/6)
A COPD patient is about to leave ICU when she gets a bit sleepy. ABG shows 7.04/120/53/31 with a good pulse oximetry waveform showing saturation of 98% on 4 liters. Which of the following is most accurate? (5/6)
my answers w/ discussion & links for further reading. bottom line: ABGs aren’t nearly as helpful as commonly believed & we should get fewer of them. and when we actually *do* need blood gas analysis, VBG is generally fine (6/6) #zentensivistemcrit.org/squirt/abg/
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how to place a consult: you MUST understand the five stages of consultant grief.
once you can understand this painful and natural process, requesting consults will make a LOT more sense
buckle up, it can be a little rough…
🧵 1/6…
stage 1: denial
- You dont need a consult.
- You called the wrong service.
- 18 years old? consult pediatrics
- I’m not actually on call now
- Everything’s fine, just walk it off…
stage 2: anger
- you should have consulted us earlier/later
- you should have checked this test before calling us
- you’re a terrible doctor/student/human being
this is much better than MINDS (which contained ~90% hypoactive), but probably still not ideal.
(at this point, does anyone actually think that haloperidol helps with hypoactive delirium ??)
other than dilution of the patient population by patients with hypoactive delirium (who are unlikely to benefit & might conceivably be harmed by over-sedation), the methodology seems pretty solid.
I think it's time for a difficult discussion, folks.
Let's talk about CSF lactate 🫣
CSF lactate has been shown to be *superior* to traditional CSF studies in sorting out viral vs. bacterial meningitis in several studies & meta-analyses...
a subset of patients with viral meningitis will initially have a *neutrophilic* pleocytosis.
this can lead to unnecessary admissions & antibiotics
some patients are subjected to repeat LPs 😩
a low CSF lactate could avoid all of this, allowing patients to go home from the ED
CSF lactate measurement is recommended in guidelines from the United Kingdom, Europe, and France.
(it's not recommended in the ID society of America guidelines, but they're from *2004* and require revisions)