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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The pulmonary artery occlusion pressure (PAoP) may not adequately reflect the left ventricular end-diastolic pressure (LVEDP) & the LVEDP may bear little relationship to the left ventricular end-diastolic volume (LVEDV)
A graphic display is preferred to allow measurement of pressures at end-expiration when the effects of superimposed respiratory variations on intrathoracic pressures are minimized
This is the weekly refresher on basic hemodynamic monitoring:
Hemodynamic variables determining perfusion pressure and oxygen delivery:
Dynamic response of the arterial pressure measurement system:
Cyclic changes in arterial pressure during mechanical
ventilation and calculation of the dynamic cardiac preload variables pulse pressure variation (PPV) and stroke volume variation (SVV):
1. The definition of insanity* is to give bolus iv 40 mg of Lasix (furosemide) without seeing any effect and then starting Lasix drip at 10 mg/hr hoping for a brisk diuretic response... 🤷♂️
#foamed #foamcc #meded #medtwitter #medstudent
Along the same lines:
2. Switching the ineffective Lasix drip to Bumex (bumetanide) drip at 1 mg/hr and keep hoping to see this:
There is more:
3. Checking serial labs (BUN / creat / electrolytes) because the patient is on continuous infusion of a diuretic...
What do you think the mean blood pressure is just before terminal cardiovascular collapse (TCC)? 20? 30? 40?
TCC defined as the abrupt (< 5min) & exponential decrease in heart rate (>50% compared to preceding values) followed by cardiac arrest
Good to know, right?
...
Patients w congestive heart failure (39 ± 13 versus 34 ± 10 mmHg; P = 0.04), L main stem stenosis (39 ± 11 versus 34 ± 11 mmHg; P = 0.03) or acute R heart failure (39 ± 13 versus 34 ± 10 mmHg; P = 0.03) had HIGHER arterial blood pressures than patients without these risk factors
While walking around the ICU at the beginning of your night shift, you notice that the respiratory therapist increased the FiO2 from 90 to 100% in a mechanically ventilated patient. Bedside monitor shows O2 sat 90%. You decide to read a bit more about the patient:
This is a 50 yo pt with hx of atrial fibrillation / diastolic HF / HTN / COPD / morbid obesity (190 kg; BMI 55) who presented 3 days earlier with dyspnea & atrial fibrillation with rapid ventricular response
He was treated for heart failure w iv diuresis & for atrial fib w amiodarone drip. He was intubated due to worsening of his respiratory status. His arterial blood gases before & after intubation 👇: (please notice initial pCO2 > 120 & incalculable HCO3; this is > 65 in our lab)
80 yo pt w HTN/HLD/CKD (creat ~ 3.0 mg/dl) underwent off-pump CABG (LIMA>LAD). Came to ICU intubated.
Surgeon's sign-out: "easy case"
Anesthesiologist's sign-out: "good LV/RV, mild-moderate MR, needed pressors"
What don't u like from what u see on the monitor?
When pt was first seen in the ICU, he was on norepi 1.0 mcg/kg/min. Intra-operatively had also received ~500 mcg of phenylephrine boluses, 7 boluses of epi (10 mcg each) & 15 u of vasopressin (in 1-2 u boluses). No Swan-Ganz in place. Did I mention he was on FiO2 100% w PaO2 65?
POCUS: fairly normal LV/RV systolic function & bilateral B-lines. Turns out that pt had already received close to 3 liters crystalloids % 1 liter albumin 5%
(Sorry, I have an archaic US device these days & cannot save US clips easily)