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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You can call me lazy but if a patient is admitted to the ICU with pneumonia (& this CXR), is diaphoretic, breathing 50/min, has HR 150/min & O2 Sat 88% on "FiO2 100%", I don't calculate the ROX index or the HACOR score. I just intubate...
The ROX (Respiratory rate-OXygenation) index was introduced in 2016 as a prediction tool to identify the need for IMV in pneumonia patients w AHRF treated wHFNC. It's calculated as [(SpO2/FiO2)/Respiratory Rate] & is typically assessed at 2, 6, & 12 hours after HFNC initiation
The HACOR (Heart rate, Acidosis, Consciousness, Oxygenation, & Respiratory rate) score is a tool for predicting NIV failure in pts with AHRF. It demonstrates good predictive power for NIV failure, w higher scores (>5) having a strong diagnostic accuracy in predicting NIV failure
Dexmedetomidine (D) (Precedex in 🇺🇸) is one of my favorite ICU drugs. It is a highly selective α-2 adrenoreceptor agonist, w sedative/analgesic/ anxiolytic properties & minimal resp depression. Its main side effects are hypotension & bradycardia
Herein I chose 10 less known D's effects/associations with:
1. Hypertension (the opposite from what you would expect): likely due to initial stimulation of peripheral a-1 or a-2b receptors. It is usually transient, mild, & does not require treatment. However, I have seen severe
D withdrawal after abrupt stop of prolonged infusion presenting w severe hypertension (plus tachycardia / diaphoresis / agitation). It went unrecognized for a while & was attributed to "prolonged alcohol withdrawal"
We divide patients with circulatory shock into 3 primary hemodynamic phenotypes, namely hypovolemic, vasodilatory/distributive, & cardiogenic (including obstructive)
But we all witness/manage "mixed" shock, an entity lacking a uniform, evidence-based definition
By analogy to the cardiorenal syndromes, Jentzer et al categorize mixed shock into 3 principal groups, each defined by the sequence & nature of the insult (ie, primary vs secondary hemodynamic process): cardiogenic-vasodilatory, vasodilatory-cardiogenic, & primary mixed shock:
The conceptual model of mixed shock etiology & pathogenesis describes "two-hit" & "single insult" scenarios:
We are all familiar w the concept of "protective ventilation": aiming for normal blood gases entails significant risk
What if we apply the same idea in hemodynamics & try to limit the damage associated w excessive vasoconstriction?
The CLEAR approach is not intended to be a series of
sequential steps but rather key elements that should be addressed simultaneously, depending on the clinical context and patient’s needs
In this recently published article, the authors propose a classification of different cardiovascular phenotypes potentially observed in septic shock into 3 profiles of LV-centric dysfunction, promptly recognizable by critical care echocardiography (CCE):
The figure speaks for itself, but we have to highlight a few points made throughout the paper...
1. Cardiovascular profiles are dynamic; patients may move from one to another according to fluid administration, correction of LV afterload & evolution of the disease. Therefore, CCE has to be repeated to personalize therapy