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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Mixed cardiogenic shock (CS) -herein classified as CS with at least 1 additional contributing cause of shock state- is common (& usually quite challenging to treat...)
20% of all shock patients admitted to contemporary cardiac ICUs have mixed CS
Besides this old-school approach
It's good to keep in mind the proposed "normal" hemodynamic compensation & criteria for mixed cardiac-vasodilatory shock:
Simplified approach to identifying mixed shock states in patients presenting with primary cardiogenic or vasodilatory shock in the cardiac ICU using invasive hemodynamic parameters:
40 yo male, previously healthy, referred to the ED post-CPR after documented ventricular fibrillation
(VF). Vitals & physical exam: OK. No family history of sudden death. No drugs.
Any concern from this 12-lead electrocardiogram (ECG)?
What do you think the most likely concern/explanation is?
ECG shows sinus rhythm with prominent J waves in leads II, III, and aVF and V4 through V6. The height of the J wave was > 0.2mV (> 0.3mV in leads II, III, and aVF). The slope of the ST segment was horizontal in lead II and down-sloping in leads III and aVF
ICU (Central Venous/Arterial) Line Secrets - Part 3:
Following from where I stopped last week & if you are not already bored by parts 1 & 2, there are some additional points that may be worth noting
Here the (probably) final part begins:
41. If you think that the patient will need dialysis or right heart catheterization in the next few hours, consider placing a dialysis catheter or an introducer sheath from the beginning
42. Classical teaching is that we should never lose sight of the back end of the wire when advancing it. But - trust me - this complication still happens even in the best hospitals. Before calling Vascular or Radiology, you may still have a chance to save the day: get an x-ray &
ICU (Central Venous/Arterial) Line Secrets - Part 2:
Following from where I stopped last week (that's why I keep same numbering) & without hoping to a provide tutorial about how to place lines, there are some additional points that I find worth mentioning
21. Femoral vein (FV) catheters have been demonized. A recently published study of 55,663 CVCs showed no difference of catheter-related bloodstream infection incidence rates between the three insertion sites (). IMHO,doi.org/10.1007/s00134…
placing a FV catheter is perfectly fine especially if you anticipate the patient to experience a fairly fast clinical recovery (examples: a patient in diabetic ketoacidosis or urosepsis)
50 yo ♂︎ with no significant medical history presented to the ED after acute onset of sharp chest pain. No family hx of heart disease, & no tobacco or illicit drug use. Episode lasted ~30 min before pt arrived to the ED. He was pain-free with normal vitals. ECG:
Physical exam: no acute distress, & normal heart-lung exam. Labs sent & were all normal: CK, 193; CK-MB, 3.0; troponin T, 0.03. Patient remained pain-free for the next hour
What would you do next?
ECG had showed biphasic T waves in V1 -> V5. Patient underwent emergent cath which revealed a 95% stenosis in the proximal LAD that was treated with a drug-eluting stent...