Chapter 01: The equation of motion of the respiratory system. I will try to keep the next tutorials a little less math-heavy, but since it is so fundamental, I could not help myself. (there is a wee little experiment at the end, as a reward)
I will be producing a series of short video tutorials on clinically important concepts of respiratory mechanics that I feel are not universally known, but are absolutely essential. More to come.
Episode 2: The origin of patient-ventilator asynchrony. Don't blame the ventilator for everything. All of us breathe somewhat asynchronously, and it gets worse with higher breathing frequency, higher resistance, and – surprise – also with higher (=better) compliance.
Work of Breathing (WOB) is an elusive concept. I have translated WOB for normal, quiet breathing into the equivalent of a weight on your chest that you have to lift (by 1 cm) with every breath. During a T-piece trial, an 8 mm ETT packs an extra 2.4 kg on your chest.
Episode 3: How do you know if your patient is ready for extubation? In this video, I demonstrate the pros (are there any?) and cons of a T-piece trial versus a CPAP trial (without or with added pressure support).
The dogma that small tidal volumes are lung protective may be wrong for spontaneously breathing ARDS patients with high respiratory drive. Limiting the tidal volume (= flow starvation) leads to negative pressure, which contributes to "patient-induced lung injury".
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:
I tried to compile Chatburn’s taxonomy of ventilatory modes in a simple diagram. I find this taxonomy somewhat unintuitive (e.g. PC-CSVr is the mode ATC) and ambiguous (PAV is also PC-CSVr). And don’t get me started on “optimal” or “intelligent”. But I have no better idea.
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.
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.
The term “patient self-inflicted lung injury” is an insult to patients. The injury is inflicted by ventilators delivering insufficient support, causing negative alveolar pressure during strong inspiratory efforts. This is preventable with proper tube compensation.
The resistance of the endotracheal tube is inversely proportional to its radius (or diameter) raised to the fourth (4th !!!) power. This is known as Poiseuille’s law. A 10 % smaller diameter increases the resistance by more than 50%.
What kills lung cells: excessive strain (volume) or stress (pressure)? It’s strain! For the same stress, stiffer cells deform less and survive much better. Bottom line: Avoid volume-controlled ventilation, use pressure-controlled modes instead!
This paper explains how to predict the hemodynamic response to different ventilatory modes, and why Automatic Tube Compensation is good not only for the lungs but also for the heart.
I need your input: I am building a ventilator that can provide near perfect Proportional Assist Ventilation (PAV) and Automatic Tube Compensation (ATC). In addition, I also want the ventilator to provide the essential modes. What are the essential modes? And why? (1/4)
"The endotracheal tube mimics the work of breathing after extubation" according to a 25-year-old study by Straus et al, Am J Res Crit Care Med 1998 (). Do you agree? Let's look at the evidence. A 🧵
Interesting study. Patients with moderate to severe ARDS required less sedatives under a pressure-controlled mode with spontaneous breathing, compared to a volume-controlled mode without spontaneous breathing. Strangely, the PC patients could not be weaned earlier.
Pressure control + spontaneous ventilation vs volume assist-control ventilation in
#ARDS
, 🇫🇷 RCT
🔎PC-SV vs ACV, similar Vt/PEEP
PC mode set to encourage spontaneous ventilation ⬇️ need for sedation/adjunctive therapies for hypoxemia but not ⬇️ mortality
🔓
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
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.
Respirator and anaesthesia ventilator at the German Antarctic Research Station (Neumayer III, Queen Maud Land). Well equipped for emergencies. We have two doctors (surgeons) with us, just in case.
The first paper to report patient-ventilator dyssynchrony during pressure support ventilation (Fabry et al. Chest 1995 ) also showed that Automatic Tube Compensation (with or without Proportional Assist) can prevent dyssynchrony 100% of the time.
Proportional Assist Ventilation (PAV) and Automatic Tube Compensation (ATC) are not for the faint-hearted, quite literally. Low cardiac output causes transport delays between the lungs and the chemoreceptors, which can lead to periodic (Cheyne-Stokes) breathing.
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.
Critical Care Scenarios host Brandon Oto has taken my ramblings and distilled them into a coherent podcast about Automatic Tube Compensation. Also check out the podcast summary website.
We discuss the principles and application of automatic tube compensation (ATC) on modern ventilators, with its creator Ben Fabry.
#criticalcare
#medtwitter
This is a photo of the second Automatic Tube Compensation (ATC) prototype. It was used in numerous clinical trials on ATC from 1995 - 2003. How well did this machine perform? A 🧵
This remarkable historical video was produced in 1985 by Josef X. Brunner. He was later the director of Hamilton Medical. The quality of lung function research in the ICU back in 1985 (led by Gunther Wolff, my PhD mentor) is still unsurpassed. Full video:
@DrSateeshPCCM
A patient with any remaining form of respiratory drive should be put on pressure controlled ventilation, not on volume control. This will not prevent all desynchronization problems, but at least some.
If dyssynchrony and ventilator- (and endotracheal tube-) induced additional work-of-breathing could be eliminated ...
by how much do you think ARDS mortality would decrease?
Retweet if you want to know what other RTs and intensivists think.
Please, please, please, everyone, always post your papers on open access preprint servers like medRxiv or bioRxiv before publishing them in journals with paywalls.
You will get more reads, more citations, and your publicly funded research will not be wasted.
Disappointing that the new ESICM guidelines on ARDS dodge the issue of early pressure support for intubated spontaneously breathing patients, which could help decrease peak pressure and barotrauma and spead-up weaning.
It is neither intuitive nor physio-logical why minimizing mechanical power based on the simplified equation below, should be lung protective. That higher VT is bad makes sense, but the power dissipated by the airway resistance (Raw) should not (and does not) damage lung tissue.
In non–zero-flow conditions, the intratracheal pressure
is different to the pressure measured at the ventilator. An important concept understand for
#PedsICU
. Just published...
Proximal and Tracheal Airway Pressures During Pressure Controlled Ventilation
@JmNunezSilveira
The consequences of the dyssynchrony we are seeing here are are: 1) The ventilator works against the patient's muscle effort, thereby increasing the pressure load. 2) The expiration is incomplete (the patient tries to inhale), which causes auto PEEP.
Dräger introduced ATC in its then brand-new Evita 4 in 1995. Dräger's ATC was not quite as crisp and stable, especially during expiration (pink = deviations from constant tracheal pressure). But it was still ok-ish. Are today's top ventilators better? Please let me know.
I am back in Antarctica doing penguin research. Avian flu has not arrived here yet, but elsewhere in Antarctica, and we are very concerned. Emperor penguins are such magnificent animals and they are already severely threatened by global warming.
I changed my profile picture to reduce the number of fake followers (who follow 5000+ accounts but have <9 followers and zero posts). Instead of a middle-aged man, new photo shows Mabel, our puppy in training. She will become a guide dog for the blind if everything works out.
Thanks to all who participated. To my knowledge, there is no conclusive study that says who is right or wrong. My own guess is around 10% reduction in mortality - that's huge.
The flow resistance of an endotracheal tube alone is already breathtaking. But that's not the only problem. The swivel and flexible connectors and, God forbid, a filter/humidifier can double the load. And the difference between a 7mm and an 8mm tube is just insane.
Due to popular demand, we now present our data on the resistance of 7mm and 8mm tubes plus various add-ons together with a Methods and Discussion section. Measured data points in blue, power-law fit in orange. How much pressure support do You give during a weaning trial?
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."
@ArielG_RRT
That's the question. You can have a pressure trigger (insp. valve closed, zero flow) or a flow trigger (pressure is controlled to be constant (PEEP)) but not both. Something is fishy.
Conclusion: The endotracheal tube adds significant work of breathing that is tolerable only in patients who breathe quietly. A generalization of the statement "The endotracheal tube mimics the work of breathing after extubation" is not supported by evidence.
This study shows that high Mechanical Power (MP) of ventilation is a less accurate predictor of outcome (death) than high PEEP, RR, peak pressure, and low (!) tidal volume, each of them considered in isolation. One is tempted to conclude that MP is not a very useful concept.
@OfVentilation
Just provide the raw value of auto PEEP or the difference above PEEP. A good physician will know what to do, as the definition or interpretation of severity depends on many other things.
I sometimes hear "I don't understand how automatic tube compensation (ATC) works". It's imple: ATC works like CPAP (or a T-piece), but instead of keeping airway pressure (yellow line) constant as in CPAP (left), the tracheal pressure (magenta line) is kept constant (right).
Next, look at the flow and pressure data. The inspiratory flow is small both before and after extubation, so the resistive WOB is relatively small (compared to the elastic work), but the peak flow is 50% higher after extubation. Why? Because the extra tube resistance is gone!
The ETT, however, is part of the ventilator. Resistive power consumption by the ETT (or the airways) does not damage the patient’s lungs. There is no plausible physiological reason to include the resistive power in a scheme for optimizing the ventilator settings.
@Avishek15828581
The patient's breathing effort and the resulting flow/volume pattern are heavily modulated by the endotracheal tube resistance, the demand flow control behavior of the ventilator, and of course the pressure support. I say we don't really know much about spont. breathing in pts.
The other reason is the build-up of intrinsic PEEP at low VT and high rr. However, this build-up of iPEEP can be compensated by reducing the external PEEP – hence, there is no practical need to select a combination of low rr and excessive VT.
When applied to intubated patients, the term "airway pressure" is a terrible misnomer. Humans are not born with a narrow plastic tube in their airways and don't feel or care about the pressure at the ventilator-end of that tube. Only the tracheal pressure matters.
@OfVentilation
I strongly side with the pro-spontaneous breathing crowd, even for ARDS patients. But we don't need opinions and gut feelings - we need facts. We need well-planned, meticulously conducted clinical trials.
@respcare
Zero pressure support and zero PEEP? I can't help but point out that all three ventilators deliver pressure well above zero most of the time, with fluctuations of 3-5 cm. This "unpredictable nature", as the authors call it, is unacceptable.
@OfVentilation
To reduce peak pressure and dyssynchrony without further lowering tidal volume, I would try to decrease PS and trigger threshold, increase rise time and exp. flow trigger. Or better switch to ATC+PAV. Lower PEEP depending on SaO2.
@TimBalthazar
@gattinon
MP increases with higher V'min, elastance and (small ) airway resistance, all of which are patient-specific parameters known to contribute to poorer outcomes. So yes, MP can be a helpful concept, although it is still better to know the individual components.
However, the MP
@gattinon
@yourICM
@Dr_Cit
Great read! I have a small clarification: to detect a 6% reduction in mortality (from 40% to 37.6%), you actually need to enroll about 2200 patients in each group, i.e. 4400 in total! That study would take not 10 but 20 years to complete.
Love this article by Gattinoni, Citerio and Slutsky, who advocate common sense. "Despite the statistical results ..... physiology indicates that the safest ventilatory strategy is the one which minimises its harmful components"
"Back to the future: ARDS guidelines, evidence, and opinions."
Luciano Gattinoni, Giuseppe Citerio and Arthur S. Slutsky
....for those who may be interested
@yourICM
@Dr_Cit
@DocMusician
You could actually ventilate a patient using only 1 mode: PC-IMV (you just need to lower the mandatory RR when the patient starts breathing spontaneously)
Here is my suggestion for the lowest possible mechanical power:
1) Select a VT of twice the anatomical dead space.
2) Compute the rr for the desired alveolar V’min
3) Select the smallest PEEP that maintains open lungs
4) Reduce the PEEP by the amount of iPEEP build-up
Interesting preliminary results from 78 participants so far. 35% think that ARDS mortality could be reduced by more than 10% by avoiding dyssynchrony and added WOB. That would be detectable already in relatively small clinical trials. Vote @ .
If dyssynchrony and ventilator- (and endotracheal tube-) induced additional work-of-breathing could be eliminated ...
by how much do you think ARDS mortality would decrease?
Retweet if you want to know what other RTs and intensivists think.
(And just to be clear, my wife and I are not dog trainers; we are only responsible for the first year of basic training and socialization before a professional trainer takes over).
For these two reasons, only the elastic mechanical power should be considered. Elastic power is minimized for a tidal volume that is exactly twice the anatomical dead space, regardless of anything else (E, R and alveolar minute ventilation).
If you are a resp. therapist or IC doctor and you haven't yet tried it, you should breathe through a 7 mm endotracheal tube. Do some exercise for good measure to match the Vminute of a patient with pneumonia. Keep it up for 10 min. How does it feel?