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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IKYK that: i) blood pressure (BP) is the driving force for organ perfusion, but ii) hypotension does not always lead to hypoperfusion
One of my favorite reviews (PMID: 34392972) tries to reconcile the paradox and expand on the topic:
Fact:
Although an abundance of cohort studies have suggested an association between hypotension & unfavorable outcomes, several RCTs have failed to demonstrate consistently improved outcomes from maintaining a higher BP
Back to basics:
Arterial blood pressure is the result of multiple hemodynamic parameters:
When you prepare for the "average" intubation (no cardiac arrest, no active emesis), how do you pre-oxygenate the patient?
In PREOXI, a multicenter, randomized trial conducted in 24 🇺🇸 EDs and ICUs and published in 2024 (PMID: 38869091), 1,301 critically ill adults were randomly assigned to receive preoxygenation with either noninvasive ventilation (NIV) or an oxygen mask (O2M)
Hypoxemia (defined by O2 sat < 85% during the interval between induction of anesthesia & 2 minutes after tracheal intubation) occurred in 9.1% in the NIV group & in 18.5% in the O2M group (difference, −9.4%; 95% confidence interval [CI], −13.2 to −5.6; P<0.001)
For the average RSI - rapid sequence intubation (no cardiac arrest, no active emesis), do you provide bag-mask ventilation between induction and laryngoscopy (I & L)?
RSI flow(s):
In PreVent, a multicenter, randomized trial conducted in 7 academic 🇺🇸 ICUs and published in 2019, 401 critically ill adults were randomly assigned to receive either ventilation with a bag-mask device (BMV) or no ventilation (NoV) between I & L
In a multicenter study of 283 acute heart failure patients, changes in renal filtration markers (cystatin C or creatinine) with aggressive diuresis were not associated with changes in markers of renal tubular injury (NAG, NGAL, or KIM-1)
In this aggressively diuresed population (560 mg iv furosemide -> urine output of 8425 mL over 72h), both worsening renal function & increases in tubular injury biomarkers were not associated with adverse outcomes; rather, there was a trend towards improved outcomes
The data suggested that the small-moderate ⬇️in GFR that commonly occur during aggressive diuresis, colloquially referred to as "bumps in creatinine", may not primarily be a manifestation of renal tubular injury; rather, they represent clinically benign changes in filtration
Ten things that -for no good reason- we don't do in the ICU:
OK, in general a "less is more" approach is reasonable & there is a "rationale" behind many of the following but the truth is that they don't make sense if scrutinized
Here it begins:
1. Holding tube feeds or
any type of nutrition, because the glucose is "high"...
I see it often when I do morning rounds; the tube feeds were held at 2:00 am (and never restarted) because glucose was 400. Obviously, the right approach is to adjust the insulin regimen and keep feeding the patient.
2. Not starting or stopping TPN because the patient is bacteremic/septic...
Does this mean that if a patient cannot be fed enterally and remains bacteremic for 5-7 days (not uncommon scenario in S. aureus bacteremia), she cannot have any caloric intake for a week? 🤷♂️
77 yo patient admitted to the ICU from a nursing home w hyperglycemic-hyperosmotic state & acute kidney injury. On day 6, he spikes a temp 38.3. BP 96/59, HR 110/min. UA suggestive of urinary tract infection. The next day, urine culture grows Enterobacter cloacae
A day later, the blood culture grows Gram (-) rods (eventually proven to be the same bug). The susceptibility profile is:
You discuss with the team about treatment options: