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
• • •
Missing some Tweet in this thread? You can try to
force a refresh
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
The phenomenon of "hemodynamic incoherence" is observed when microcirculatory dysfunction persists despite the restoration of macro-circulatory indices
In this case, MAP was 88 mmHg & cardiac index was 2.8 l/min/m2 on a small dose of norepinephrine
Despite the apparent normalization of systemic & regional blood flow, sublingual video-microscopy revealed persistent tissue hypoperfusion:
The latest generation of handheld vital microscopes,
uses incident dark field (IDF) illumination & has advanced the field w higher-resolution optics & autofocusing capabilities (3-fold increase in the field of view), allowing more comprehensive microcirculatory assessments
ICU Snapshots - Ventilator waveforms (from a patient I just saw):
Patient on "volume control" (or: VC-CMVs). Please notice the significant change in the pressure waveforms while the flow waveforms remain "mostly" unchanged
What happened?
What happened between breath (A) and breath (D)?
In breath (A), there is severe work shifting (what we called "flow starvation" or "flow asynchrony" or "air hunger") with the pressure falling below the set PEEP level & the pressure waveform being deformed due to the presence of Pmus (patient's effort)
Did you ever admit to the ICU a patient with COPD exacerbation who came from the ED on NIV? Or who went home on NIV? If you are a pulmonologist, you will not learn anything from this post but the rest of us
from different specialties (I am Internal Medicine) should remember that NIV settings are not just inspiratory/expiratory pressure (IPAP/EPAP) and FiO2
We have to admit that not every COPD patient will do well with “10 over 5” *. So what else should we pay attention to?
Trigger: beginning of inspiratory support and switch from EPAP to IPAP
Rise time: the time to get from EPAP to IPAP (aka pressurization time)
Inspiratory time: duration of inspiratory support
Cycle: end of inspiratory support and return from IPAP to EPAP
ICU Physiology Secrets - Return to Basics Edition:
If you are placing Swan-Ganz (SG) catheters or you like reading/interpreting their waveforms, this is for you:
You walk in a patient’s room exactly when your fellow intensivist tries to “wedge” a newly placed SG catheter:
At which point - approximately – do you think that the pulmonary capillary pressure (Pcap) should be measured?
1. Please assume that the recording is taken during an expiratory hold while on mechanical ventilation 2. Please feel free to choose any point other than these choices
Why do we care about pulmonary capillary pressure? Because it is a primary determinant of fluid flux across the pulmonary capillary wall (normal: 8-10 mmHg). It is determined by the mean pulmonary artery pressure, pulmonary vascular resistance, and total blood flow