Whether it makes sense or not, there is no increased WOB with an ETT in place. This has been shown in many studies. When the previous poster was intubated, I would venture to say that anxiety / inadequate vent management contributed to the perceived WOB, not the tube. If you intubate people and measure their WOB before and after with no added support, it is always lower with the ETT in. Check out the reference for a more detailed explanation. I routinely have even tiny babies intubated and completely off the vent or on CPAP, and they are totally comfortable. This says nothing about what an appropriate weaning strategy is - weaning ps after prolonged intubation is obviously useful. My point is that the ETT should not be a consideration in that strategy. ANd yes, I have been intubated, and no the ETT is not an obstruction.

to say an et tube does not increase WOB is kinda blind. yes, an et tube can provide smoother flow because of its structure as opposed to the design of the natural airway, but resistance caused by the et tube will definitely increase wob on a pt. you are inserting an artifical airway which is much smaller than the patient is used to breathing through, and resistance causes wob to increase... its simple physics, give someone a more narrow airway to breathe through, and they will have to work harder to move the same amount of air...

to simplify, get in a swimming pool, go underwater, and attempt to breath through a 7.0 et tube, one end in your mouth, one above the water... now, you may be able to ventilate yourself just fine, but its an obvious given that you will have to work harder to move the same amount of air that you would above the water(and dont give me anything about the pressure of the water, im not talking 20ft under water)

Bwillis,
I do not want to get into all of the books and other research that says your statements are not correct becasue I believe that you have probably already heard many of these in your battle of this topic, so I ask you these things. Could your patients that showed increase WOB after being extubated have shown this do to laryngeal swelling following extubation and the act of being intubated itself? Could the increase in WOB after extubation also be partly do to the fact that you had your bicore line obstructing airflow in the extubated patient that was not being expressed on the intubated patient becasue of the air going up and down the ETT? Were your patients more sedated with the tube inplace, this might have effected WOB numbers becasue their inspiratory flows might have been less than after you extubated them and reduced sedation?

As far as doing a flowby before extubation, what about the inability to add peep to a flowby and recreate the effect of the glotis closing? Are you not causing derecruitment of the AW's by using flowby and not giving back the patients natural FRC? Which would also effect WOB after you extubated them, had they had a decrease in pulmonary compliance. I do not think that flow-by is the most benificial form of a SBT (Spontaneous breathing trial), we should always try to at least give the patient PEEP to prevent derecruitment.

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Other interesting reads on this subject

Crit Care Med. 2000 May;28(5):1341-6. Links
Prediction of post-extubation work of breathing.Mehta S, Nelson DL, Klinger JR, Buczko GB, Levy MM.
Division of Pulmonary and Critical Care Medicine, Rhode Island Hospital/Brown University, Providence, USA.

OBJECTIVE: To evaluate which mode of preextubation ventilatory support most closely approximates the work of breathing performed by spontaneously breathing patients after extubation. DESIGN: Prospective observational design. SETTING: Medical, surgical, and coronary intensive care units in a university hospital. PATIENTS: A total of 22 intubated subjects were recruited when weaned and ready for extubation. INTERVENTIONS: Subjects were ventilated with continuous positive airway pressure at 5 cm H2O, spontaneous ventilation through an endotracheal tube (T piece), and pressure support ventilation at 5 cm H2O in randomized order for 15 mins each. At the end of each interval, we measured pulmonary mechanics including work of breathing reported as work per liter of ventilation, respiratory rate, tidal volume, negative change in esophageal pressure, pressure time product, and the airway occlusion pressure 100 msec after the onset of inspiratory flow, by using a microprocessor-based monitor. Subsequently, subjects were extubated, and measurements of pulmonary mechanics were repeated 15 and 60 mins after extubation. MEASUREMENTS AND MAIN RESULTS: There were no statistical differences between work per liter of ventilation measured during continuous positive airway pressure, T piece, or pressure support ventilation (1.17+/-0.67 joule/L, 1.11+/-0.57 joule/L, and 0.97+/-0.57 joule/L, respectively). However, work per liter of ventilation during all three preextubation modes was significantly lower than work measured 15 and 60 mins after extubation (p < .05). Tidal volume during pressure support ventilation and continuous positive airway pressure (0.46+/-0.11 L and 0.44+/-0.11 L, respectively) were significantly greater than tidal volume during both T-piece breathing and spontaneous breathing 15 mins after extubation (p < .05). Negative change in esophageal pressure, the airway occlusion pressure 100 msec after the onset of inspiratory flow, and pressure time product were significantly higher after extubation than during any of the three preextubation modes (p < .05). CONCLUSIONS: Work per liter of ventilation, negative change in esophageal pressure, the airway occlusion pressure 100 msec after the onset of inspiratory flow, and pressure time product all significantly increase postextubation. Tidal volume during continuous positive airway pressure or pressure support ventilation overestimates postextubation tidal volume.



The one thing with the Studys and what we were originally discussing is the patient population we are talking about. These studys were done on healthy individuals not the ones that we are putting up on APRV/Bivent

Other interesting reads are some of the Doctors own references that discuss the fact that their is resistance associated with the ETT, so in that case there is WOB associated with that Raw. So even if you go with the fact that the Raw is no different in a intubated or nonintubated patient you still have a WOB element that can be relieved with some type of support when using APRV. We all know about the oxygen cost of WOB, so in these patients that have a need for APRV why not reduce any oxygen consumption aspects that we can to help them out.


Other aspects to some of Dr. Willis references one of the studys that went along with his (prediction of post extubation work of breathing, critical care med) had 20% of the patients that were extubated had to be reintubated within 24hours of extubation. could their respiratory struggles skewed the extubation numbers up making them look worse than the intubation numbers? What other factors were their in their need to be reintubated? Could the fact that they had to go through a T-piece trial and have derecruitment occur, could this have casued their respiratory failure?

Many, Many questions at Hand here. But back to my original point. Different Patient population!

Our bench study was to look at the fact that some say PS will increase the pulmonary pressures higher than the set Phigh in APRV. We found this to be untrue untill your reached pressure around 8-10 cmH2O.


I am not sold on Dr. Willis argument, but I do think it is interesting. However in the patient population that we were originally discussing I do not know if it relevant.

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Jamie,
The only problem with your analogy is the fact that you are taking into account the RAW of the ETT and the RAW of the natural AW with you snorkel example. This deffinetly would increase your WOB. Doctor Willis is stating that the WOB of a extubated and intubated patient are the same if not actually lower in the intubated patient.


There is some not much from what I have found that agrre with him, but I have also found some that disagree with him.

The 840 Ventilator does offer Tube Compensation with all Spontaneous breath types. It is not considered a mode and is available in Bilevel/APRV. I use it in my ICU when in Bilevel or APRV.

Just like to point out that the Engstrom carestation also has TC. The compensation is applied to the inspiratory phase of all pressure-controlled, CPAP, and pressure-supported breaths. I'm a rep of course stationed in the Middle East and use your forum extensively to keep myself updated. I often refer your site to clinicians and therapist in the region who are looking for info on the latest in respiratory care.
Technology is moving much faster then it use to so when stating what manufacturer does or does not do try not to make sweeping statements. Drager, Siemens and PB are not the only kids on the block.

Susan B,
I believe I had corrected that statement on a later post, but yes I had mispoke. We had a old software version (very old), it is now updated to include everything that PB offers in the adult world including PAV.