We developed a browser-based tool to predict ventilation impairments such as iPEEP buildup, hypoventilation, and desynchronization due to the tube resistance (also during bronchoscopy). Check it out: fabrylab.github.io/Bronchoscopy/

Prediction and Prevention of Ventilation Impairments During Bronchoscopy Bronchoscopy in mechanically ventilated patients is performed by passing a bronchoscope through the endotracheal tube (ETT), which substantially increases airflow resistance and may compromise ventila...

The flow limitation imposed by the endotracheal tube is a major cause of weaning failure, patient-ventilator desynchronization, and PSILI. During bronchoscopy, the tube resistance becomes prohibitive. Check out our paper medrxiv.org/cgi/content/...

Drop me a line if you are interested in this new technology. Also, if you a manufacturer of ventilators, I would love to test one of your ventilators in my lab, if you are willing to loan me one for one or two weeks.

Commercial ventilators often (perhaps all of them?) suffer from sluggish demand-flow delivery and cannot exploit the full potential of ATC. I have therefore developed a new ventilator featuring a fast and precise demand flow controller to deliver proper ATC.

Unfortunately, current pressure support modes cannot deal with weak patients with rapid shallow breathing, or with large inspiratory efforts. The solution to this problem is proper Automatic Tube Compensation (ATC), if needed in combination with proportional assist ventilation (PAV).

Empowering patients to breathe spontaneously as early as possible, and only support the work of breathing the patient cannot produce on their own, is the best way to reduce the pressure load on the lungs, and to avoid VILI.

YouTube video by lpmtvideo Comparison ATC-mode Dräger V600 vs self-made ATC ventilator

How does a commercial ventilator (Dräger V600) in ATC mode compare to my 3D printed ATC ventilator? Poorly, I would say, but judge for yourself. I am convinced that weaning can be greatly improved and shortened with real ATC. youtu.be/Y4To7-krE14

Yesterday, with the retirement symposium of my academic mentor Jeff Fredberg, the era of respiratory physiology research at the Harvard School of Public Health that began with Jim Whittenberger in 1948 came to an end.

.. and just in case you are wondering what whale research has to do with respiratory physiology - have you ever seen a whale blow? We develop thermal imaging systems that pick up the thermal signature of whale blows to study whale ecology. doi.org/10.1175/JTEC...

The #FREEPAULWATSON petition On July 21 2024, Captain Paul Watson was arrested by Danish police upon arrival in Nuuk, Greenland, onboard the M/Y John Paul DeJoria. We need your help to #FREEPAULWATSON.

Few of you know that my lab is also active in whale research. That's why I’m urging you to sign the petition to free anti-whaling activist Paul Watson. Denmark may extradite him to Japan, where he faces a 15-year prison sentence. www.paulwatsonfoundation.org/freepaulwats...

Not sure I understand the question. Perhaps this: A pressure support of 15 mbar is adequate for "normal" patients, but not for those with higher resp. drive (Vmin > 10 L/min). doi.org/10.1007/s001...

I visited a cardiac ICU almost every day for 5 years and never saw a case of VILI. Of course, you don't want to overinflate the healthy lungs of cardiac patients, but that's mainly for hemodynamic reasons.

A Python script for the numerical power minimization can be downloaded from github.com/fabrylab/MP_...

How to minimize mechanical power during controlled mechanical ventilation - Intensive Care Medicine Experimental High intrapulmonary pressures, large tidal volumes, and elevated respiratory rates during controlled mechanical ventilation can lead to barotrauma, volutrauma, and atelectrauma. Mechanical power—defin...

"How to minimize mechanical power during controlled mechanical ventilation" is now published in Int Care Med Exp (doi.org/10.1186/s406...). Main insight: the elastic power is ALWAYS minimized at a VT of twice the anatomic dead space, or ~4.4 ml/kg of body weight.

Paw is irrelevant as Ptrach will still remain at PEEP at all times. The patient can freely breathe as if extubated, and is free to choose a small or large tidal volume, like you and me.

Yes, during a vigorous inspiratory effort, Paw can rise to >35 mbar above PEEP, but that does not cause VILI, rather, it prevents Ptrach and Palv to become negative and hence prevents PSILI.

You mean you are afraid that Paw drops below PEEP during expiration? Don't be. Ptrach will still remain at around PEEP. And also consider that proper ATC, unlike CPAP or PSV, prevents Ptrach to become negative during inspiration.

Could not agree more.

YouTube video by lpmtvideo Dräger Evita V600 in CPAP and ATC mode

Today, I tested the Dräger Evita V600 ventilator in CPAP and ATC mode with a lung simulator. CPAP worked well, but in ATC mode, the V600 compensates only ~25% of the total tube resistance, and that is possibly not enough to make a difference for patients. youtu.be/AcRkQqnk-gg

I imported my Twitter posts using Porto (Chrome extension) to add some content. Sorry for cluttering up your timeline. I also have to say that Porto did not work so well, it ignored most of my tweets, for no reason.

I used to be on Twitter (@ATC_Ventilator) and now join Bluesky; my aim is to discuss topics around the mode Automatic Tube Compensation, weaning, lung physiology and mechanical ventilation with intensivists.

New on medRxiv! “How to minimize mechanical power during mechanical ventilation”
For any given V'min, a tidal volume of twice the anatomic dead space (~4.4 ml/kg in adults) always minimizes elastic mechanical power (the energy needed for lung expansion).

medrxiv.org/content/10.110…

The inflamed lung is full of immune cells, but how do they get there? We found that immune cells can generate large traction forces - comparable to fibroblasts - that help them migrate through narrow pores. Read more in Nature Physics:

rdcu.be/dU9Nj

Minimization of Mechanical Power happens at high tidal volumes beyond what is lung-protective. But why? One reason is the resistive work, which decreases at larger tidal volumes. This resistive power is dominated by the resistance of the endotracheal tube.

For a given alveolar minute ventilation, which combination of frequency and volume minimizes mechanical power according to the @Gattinon equation? This depends on lung parameters but may result in dangerously high tidal volumes. DO NOT try to minimize the mechanical power.

Excessive strain (e.g. due to a large tidal volume) causes tissue damage due to overdistension, but most of the damage occurs already in the first cycle. Subsequent cycles add smaller and smaller increments.@thomasanderson
@gattinon

bio.physik.fau.de/publications/M…

This is how the elastic work of breathing (WOB) is depicted in a Campbell diagram, which was misrepresented in a recent @ERSpublications on ventilatory muscle recruitment during exercise in patients with COPD and interstitial lung disease:

bit.ly/3HVrsuh

Great Blue Journal viewpoint on "Mechanical Power and Ventilator-induced Lung Injury: What Does Physics Have to Say?.. physical first principles dictate that purely elastic work delivered during inspiration has no impact on tissue damage."

doi.org/10.1164/rccm.2…

Lumping together PEEP, peak pressure, volume, and what have you into a half-baked formula for mechanical power obfuscates the real issues: stiff lungs, high pressure, regional lung tissue overdistension, and atelectrauma.

Lung tissue is a weakly frequency-dependent power-law material. This means that the mechanical power dissipated by lung tissue increases only weakly with frequency, and that all(!) simplified equations to estimate the mechanical power during mech. ventilation are deeply flawed.