ICU stories (common): Middle-aged pt w hx of COPD was brought to the ED by EMS after SOB x 2 days. No fever or chest pain. Very quickly after ED arrival, he was intubated. CXR showed hyperinflated, “COPD” lungs. Here depicted in two images:
Post-intubation ABGs showed:
BP dropped post-intubation to 55/40; propofol was started & then discontinued due to hypotension. iv fluids (2L Lactate Ringer's) were started & patient was brought to the ICU w SBP in upper 80s. Re-institution of propofol led again to hypotension. What would be the next step?
Patient came from the ED with these vent settings 👇 (RR was increased from 18 to 22 to ⬇️ the PCO2 of >100 in the first ABGs):
There was suspicion of auto-PEEP ---> presence of expiratory flow when every new breath was given. Next step was to check lung mechanics: Pplateau was 38 and PEEPtotal 25 (revealing an auto-PEEP close to 20…)
Next step?
We discontinued the patient from the ventilator for 15 sec and decreased RR to 14. Five minutes later, P plateau & auto-PEEP had decreased nicely 👇. Hemodynamics improved without fluids/pressors & despite the patient being back on propofol.
Next step to decrease auto-PEEP further?
IMHO, if you do the basic right things (⬇️ RR) and give patient time, things will continue to improve. No other change was made in the ventilator settings and, 30 min later, lung mechanics continued to improve:
Reminder: Extrinsic PEEP is set by the clinician on a ventilator while auto-PEEP is unintentional
Pepe and Marini used the term "auto-PEEP" back in 1982 👇
In the same paper, Pepe and Marini described the method of quantifying auto-PEEP by occlusion of the expiratory port
I love this paper not just because it's classic and brings physiology at the bedside, but also because it gives us a chance to glimpse at the ICU practices of the times... Please take a look at dopamine use, dopamine doses and tidal volume:
Excessive auto-PEEP can impede venous return and can also precipitate acute right ventricular failure. Volume expansion can help up to a point; the point where a dilated RV will i) be unable to eject its preload into the pulmonary circuit impair and ii) impair LV filling...
The auto-PEEP phenomenon still remains under-recognized. Sometimes, it is so dramatic that patients in PEA arrest spontaneously "recover" when they are disconnected from the ventilator circuit ("Lazarus
effect"). Especially in bad asthmatics or COPD patients that suffer PEA,
consideration should be given to simply discontinue ventilation transiently for 10-20 sec during CPR and observe the patient for return of circulation.
It would be interesting to learn what the highest autoPEEP you have seen is and if there is an easy way to determine if by going to zero “set PEEP” helps with air emptying
Pt 1 in the Pepe-Marini paper: "it was observed that systolic BP ⬆️ to 140 mmHg within 30 s of a brief IPPV interruption, whereas wedge decreased to 10-13 mmHg. Simultaneously, mean PAP & HR ⬇️. Whenever IPPV was reinstituted, HR, BP, wedge, PAP returned to their previous values
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ICU pictorials: A patient was admitted for "weakness". Unimpressive vitals / phys exam / labs. A few days later because of temp 101 F, a fever w/u was initiated. Due to "SOB", a CT chest angio was done:
👆Massive saddle PE extending in both sides w evidence of R heart strain
It seems that the textbook 👆 uses a sodium correction factor of < 1.0 mEq/L for every 100 mg/dL of Glu above 100 or applies the correction starting from a higher Glu level (probably 200 mg/dL?)
ICU stories (last night): A patient had been admitted w pneumonia / intubated / on norepi 0.12. At 01:00 am, the nurse notifies you that urine output is 5-10 cc/hr for the previous 3 hours. BP is 99/44, HR 90, CRT 3 sec. You take the US in patient's room to see what's happening.
What POCUS finding(s) is/are likely to explain the oligo-anuria in the shortest amount of time?
If you (and the patient) are lucky, you may find this:
ICU stories: Pt w "severe COPD" (ex-smoker; FEV1 30%) / chronic hypoxic-hypercapnic resp failure on 2-4 l/m O2 @ home / diastolic HF / HTN / HLD was brought to the ED due to "altered mental status" & "shortness of breath". S/he left the hospital 3-4 months ago after an episode
of "COPD exacerbation" (the 4th during the last 12 months). In the ED: sat in low 80s & after a brief non-rebreather mask trial, pt was placed on NIV. ABGs: PCO2>100 (above detection limit), pH 7.14, HCO3 undetectable. Pt suffered 2 grand mal seizures, & after receiving
lorazepam & 2l NS, s/he was intubated (roc+keta) & rushed to the ICU. Per ED: ECG w sinus tach & CXR "COPD lungs" & R basilar infiltrate. Labs: WBC 14K, creat 2.0 (baseline 1.4). You examine the pt quickly: sedated-?paralyzed/decr BS & wheezing bil/trace ext edema/skin not cold
ICU stories (a brief one): A 40+ yo pt w hx of bipolar disorder/asthma/GERD/HTN was brought to the ED by EMS after his wife found him lethargic ("altered mental status"). Apparently, he had spent the previous 2 days isolated in his forest cabin. Upon ED arrival, he was obtunded
& was given Narcan with no improvement. Vitals: 140/90, hr 80, rr 22, afebrile, sat 97% on room air. He could respond to simple questions. CT brain was negative. Lab work/up showed Hct of 59%, wbc 11k, PLT 400k and a chemistry panel showed:
A urine drug screen was sent 👇 while patient admitted that he had probably taken more Xanax (alprazolam) pills than he should. However, he denied that he wanted to hurt himself.