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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Elderly patient with multiple medical problems (HFpEF / A fib / HTN / PE / obesity etc) was admitted w CHF exacerbation. Improved w diuresis but developed left upper extremity edema; diagnosed with extensive DVT for which Interventional Radiology (IR) was consulted
IR found severe L subclavian stenosis at the intersection of the clavicle & 2nd rib & upstream LUE extensive DVT. Performed successful image-guided LUE DVT mechanical thrombectomy & stenotic site angioplasty with near complete resolution of clot burden & improvement of stenosis
Towards the last hour of the procedure, patient developed hypotension that did not improve with fluid boluses. Had received fentanyl & midazolam & and this was thought to play a role. Transferred to the ICU and
Assessment of the efficacy (stroke volume) and tolerance (left ventricular filling pressures) of blood volume expansion using Doppler echocardiography:
The 1st fluid challenge resulted in a large ⬆️ in LV stroke volume (38 to 65 mL), whereas the 2nd was unsuccessful (65 to 69 mL). The mitral Doppler profile progressed from “abnormal relaxation” to “restriction to filling” consistent with a gradual ⬆️ in left cardiac pressures
From:
Philippe Vignon and Michel Slama in:
"Hemodynamic Monitoring Using Echocardiography in the Critically Ill"; DOI 10.1007/978-3-540-87956-5
There is not such a thing as a “normal” cardiac output (CO). A CO of 3.5 l/min may be adequate for a 90 years’ old, 100 pounds sedated patient but inadequate for a 40 years’ old, 250 pounds patient with septic ARDS. Ideally,
any CO value should be accompanied by an assessment of the adequacy of perfusion (clinical: mental status, urine output etc or laboratory: central venous O2 saturation, lactate etc)
Many times, we don’t time/energy/means to measure CO, and we employ workarounds to convince ourselves that CO is adequate even when we don’t know what its actual value is. One of them is ScvO2, the O2 saturation in a venous blood sample drawn from a catheter in the SVC;
This is a recently published, information-dense document. It may be a bit technical for the average POCUS user but if you manage patients who harbor a right heart, consider reading it:
It is a 40+ pages' document, so I will just highlight some of the most useful points:
Approach to acquisition of the RA- & RV-focused views:
To obtain the RV-focused apical 4Ch view, place the transducer @ the apex, & rotate until the maximal RV chamber dimension is obtained. Often, the transducer must be positioned more laterally & tilted upward toward the RV
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"