Transpulmonary Pressure (Ptp)-Guided Ventilation: A Case. #FOAMed, #FOAMcc

So in my last post I quickly reviewed the basics of Ptp-guided ventilation. So here is a case. We had a woman in her 60’s admitted with bilateral pneumonia, intubated and ventilated. She is morbidly obese and diabetic. Despite antibiotics and usual care, she was getting progressively worse, and was labelled “ARDS.”  POCUS showed she was not in terrible venous congestion, and she had been digressed to a relatively normal IVC. Slowly her ventilator settings crept up to a PEEP of 14 and FiO2 of 100%. As the plateau pressures were approaching 35, we were getting a little antsy, so decided to put in the esophageal balloon and get a better grip as to what was going on.

Here are her original readings:

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So here we can see that her Pes in expiration is around 23. With a PEEP at 15, that gives us a Pep (exp) of -8. That likely represents a fair bit of atelectasis/derecruitment. Here are some measurements:

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Her dynamic compliance is 21, and static 24. Not too great. Her PV loops are interesting, certainly not showing any over distension (the penguin beak look), and, as Jon Emile Kenny (@heart_lung) cleverly explains about the Pop tracing:

“On this patient, the stress index appears to be low, which is somewhat consistent with your Ptp tracing. there is a terminal fall in the Ptp [wave looks like an upside down U] which suggests terminal airway recruitment; that is, during the terminal portion of the breath, the Ptp is falling with equivalent volume delivered [again only works with square-wave/constant flow]. in other words, if [at the end of the breath] less Ptp is needed to accommodate equivalent flow/volume, there is terminal increase in compliance/decrease in elastance – or lung units are recruitedSo these numbers suggest that there is extrinsic compression of the lung, due to chest wall weight and abdominal pressure. This makes the airway pressure (Paw) not representative of alveolar stretch, and hence not a good guide of ventilation. The PEEP, despite being fairly high, is below the level needed to prevent atelectasis.”

Indeed Jon, that appears to be the case.

So we started to raise the PEEP, trying to get the Ptp (exp) closer to zero:

 

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So we can see that our Ptp (exp) is approaching zero, and the PV loops suggest there is still no over distension. In fact, the compliance, as Jon had predicted, improves slightly. The plateau pressures are up into the mid 40’s which, without a balloon, would be pretty concerning. But the Ptp (insp) is less worrisome, in the mid 20’s, about at the limit we’d like.

At this point, still seeing that increasing compliance, we continue raising the PEEP to 23, and actually see the plateau pressures start to drop, consistent with having recruited lung. Now the Ptp (insp) is 23, and the compliances have increased.

 

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We thus leave things as is, and by the next morning, we are down to 30% FiO2. Here are the before and after CXRs:

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So a fair bit of her “ARDS” was actually atelectasis related to obesity and increased intra-abdominal pressure, and that what seems like exceedingly high PEEP is actually just enough to prevent atelectasis.

 

Love to hear from others who use the technology, or just interested!

cheers

 

Philippe

 

N=1 Principle in ARDS and esophageal pressure directed mechanical ventilation. #FOAMed, #FOAMcc

So i recently came across a review on esophageal pressure-guided ventilation in ARDS, which is in fact a technology I’ve had in my shop since 2008, but rarely use.

The truth is that I haven’t seen much “ARDS” in the last years, and I believe quite strongly that this reflects simply our hospital’s increased awareness of the nocive effects of over-zealous fluid resuscitation. Although in the ICU we still admit patients who, in our opinion, have received a bit more fluid than they should have, we have become more aggressive with diuresis “despite” the presence of shock, and usually see “ARDS” resolve. This is a direct consequence of actually “looking” at our patients’ volume status using ultrasound (for more see, well…most other posts on this blog!).

However, what seems like genuine ARDS does come around once in a while, and we recently had severe respiratory failure develop in a morbidly obese patient, and all of a sudden, in the presence of an FiO2 of 100%, a PEEP of 14, intra-abdominal pressures between 20 and 25, and on Flo-Lan, it seemed it might be a good idea to tailor ventilation.

Current Practice:

The most common practice currently is the ARDSnet type low volume (5-7ml/kg) lung protective ventilation, using a PEEP/FiO2 scale and aiming for plateau pressures (Pplat) below 30. Generally speaking a good idea, but one has to understand that this is, once again, a one-size-fits-all (except for the per kg) approach, which isn’t ideal if you try to follow  the N=1 Principle.

Why is this?  Because, due to physical characteristics (obesity, chest wall stiffness, etc,) and pathology (increased abdominal pressure, etc), the airway pressure reflects the respiratory system pressure (Prs) rather than the transpulmonary pressure (Ptp), which is the variable most related to volutrauma (which has eclipsed barotrauma as the mechanism for most ventilator-induced lung injury (VILI).  Ptp essentially relates to overdistension, which is what results in pneumothoraces. In terms of parenchymal micro-injury, it seems to be most related to atelectrauma, in essence the opening and closing of alveoli, with the resultant shear forces disrupting surfactant and cell surface. This type of injury relates best to finding optimal PEEP to both recruit and prevent de recruitment – in effect minimizing the amount of lung tissue collapsing and reopening.

 

Esophageal pressure (Pes)-guided Practice:

So Pes is used as a measure of pleural pleural pressure, and:

Ptp = Paw – Pes

That equation is the central tenet to this, and basically, you have to reset your goals to:

a. Ptp (exp) around zero – optimal PEEP – (meaning no over distension and no de-recruitment)

b. Ptp (insp) below 25 – though this is not really individualized as a hard data point, but has been shown to be a reasonable cutoff for volutrauma.

 

How do you do this?

By slipping in a special oro/naso-gastric tube with a balloon connected to the ventilator, one is able to simultaneously measure airway pressure (as is standardly done) and esophageal pressure. This is what it looks like:

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Here we can see that this patient has a PEEP of 20 (top), a Pes of about the same, and thus a Ptp (bottom) near zero.

We’ll discuss this case hopefully tomorrow, but just to show the mechanics/technique of it.

 

Bottom Line:

So this involves tossing out the ARDSnet charts and trying to individualize and optimize Ptp (insp and exp) instead of plateau pressures and PEEP.  How may it be useful clinically? Well, you may be able to detect unsuspected states of de-recruitment/ateletasis due to excessive chest wall or abdominal pressure, and allow you to increase PEEP “safely.”

When should I use this?

I’m not sure what everyone else is doing, but we are in the process of setting up a protocol where esophageal balloons will be inserted for any patient whose ventilator settings are approaching or exceeding FiO2 70%/PEEP 15, indicative of sufficiently severe respiratory failure warranting this additional level of fine-tuning.

I tend to use it when ventilating two groups: those with (a) elevated intraabdominal pressure, and (b) the obese patients, as they often have elevated Pes (usually due to diaphragmatic displacement. Interestingly, the correlation between obesity and Pes is not very good, so one should not “blindly” feel they can crank up the PEEP to 25 and ignore plateau pressures, as some obese patients have normal Pes (likely due to compliant abdominal walls.

Would love to hear what others do.

 

Here are the relevant articles/references:

talmor-nejm-2008

ajrccm-2014-review

 

Cheers!

 

Philippe

 

Musings with Jon-Emile and Philippe 4: A Podcast on Pointers, Pearls and Opinions on Tough Ventilation Cases. #FOAMcc, #FOAMed

Hi, so in this little discussion, we go over some points about ventilating ARDS, obese patients, looking for optimal PEEP and other obscure physiological point that we are somehow interested in…

 

Love to hear comments and questions!

 

 

cheers

 

 

Philippe

Pleural effusion in the sick patient (Part 1of 3): Don’t miss it!!! #FOAMed, #FOAMcc

This, in my opinion, is an under-recognized problem when bedside ultrasound is NOT a routine part of examination of critically ill patients. I’m happy to say that as many of my colleagues have been picking up probes, it is somewhat less of an issue now, whereas a couple of years ago I’d often put in 4 or 5 pigtail catheters on day 1 of taking over the ICU.

The first and foremost reason for this is that the portable supine ICU CXR sucks at picking up the small to moderate to, yes, even the large pleural effusion.  Largely owing to the fact that many of our patients have some lung parenchymal abnormalities and to the recumbent position that causes a layering of the effusion, it is often difficult to properly assess the size of a pleural effusion.  Radiologists will usually report the presence of a probable effusion, but quantification is difficult, and physicians not performing routing bedside sonography will often realize the presence of a submassive effusion only on CT scan – after all it isn’t like you can turn and rotate your patient to percuss the shifting dullness, can you?  Not very practical.

So the following can often be seen:

pleural effusion

this is fairly large, or you might see:

pleural effusion and pneumonia

So the obvious and critical question is: when is it necessary to drain?

There are two elements to this question:

a) for diagnostic purposes: unless the diagnosis is clear (eg CHF, post-resuscitation “michelin man” patient, etc) a new effusion should be tapped.  Panapneumonic effusions, in particular, warrant ruling out empyema unless there is a compelling reason not to.  For diagnostic purposes a 22g needle usually does the trick unless you have frank pus – which generally shows up differently on ultrasound.

b) for therapeutic purposes: effusions are space occupying lesions which compress the lung and result in a variable degree of respiratory compromise, depending on chest wall and diaphragmatic compliance, as well as effusion volume.  The clinical effect is highly variable due to the above as well as the degree of parenchymal lung disease and the degree of PEEP.  In the ICU or ED, a simple way to think about it is that if your patient is in respiratory failure and has a large effusion, chances are that draining it will improve things.  It gets a little more controversial and complicated if you have a patient who is mildly dyspneic with a moderate sized effusion.

Here are a few clinical scenarios I like:

Mr. A is a 65 year old man with CHF, intubated, with large bilateral effusions. He has been aggressively diuresed to the point of his IVC being less than 5mm in diameter.  He has not been able to wean in the last 48 h.

Yes, I definitely drain this fellow. Been there and done that time and time again.  The pleural effusions are essentially the last to resolve (being the most “distal” to the circulation – vs the alveolar tissue itself) and hence can lag and cost a few more days or more of ventilation).

Mr. B is a 47 year old man with pneumonia, breathing spontaneously with a moderate (maybe 500ml) effusion. It appears free flowing and clear, he is afebrile with an improving white count, and mildly dyspneic.

Nah, I skip on this one.  If fever and WBC recur, I do a diagnostic tap to r/o empyema.

Mrs. C is intubated on PEEP 18 FiO2 85% for ARDS due to pancreatitis. She has some degree of intraabdominal hypertension (IAP 18) and has bilateral moderate pleural effusions, maybe 400-500ml.

Yup. She can physiologically benefit from decreased intra-thoracic pressure, both from the ventilatory and the intra-abdominal pressure standpoint (Remember the diaphragm is not a rigid structure so that IAP and ITP are very similar in most cases).

So is there any evidence for this?  Some. And that’s for part 2, coming within the next days. Part three will explain and show my procedure of choice for drainage.

Thanks!

love to hear what other guys’ practices are!   Apparently only about 15% of ICU guys “routinely” drain effusions.

Philippe

COMMENTS

Hi Philippe,
I am very happy to read your post tonight, bacause I am part of that 15% and luckily most of my colleagues are in the same group. I agree in particular when you say that pleural effusions are the last to resolve, being the most “distal” to the circulation. I often find patients, at a certain point during their ICU stay, be not only like a “michelin man” but also (and at the same time!) hypovolemic. I call this situation, when I try to explain it to residents, “empty in full” (maybe in english it doesn’t sound as good as in italian): we are trying with diuretics and some fluid restriction to manage those extravascular fluids that prevent weaning from mechanical ventilation, but often we get the only effect of causing renal failure rather than eliminating pleural effusions. In this case the only way is to drain.
Another important point is that bedside chest x-ray is absolutely useless when you have to discriminate between pleural effusion and parenchimal consolidation, both of them often coexisting in ICU patients.
In our routine we use 14-gauge single lumen CVCs, inserted with Seldinger technique and ultrasound assisted procedure, effective in 95% of the effusions and less invasive than a pleurocath (that we use most of the times for pneumothorax) or a real chest tube, which I keep for blood or traumatic pneumothorax.
Greetings from Italy,
Marco

 

Glad to hear it Marco!  I started with CVCs as well before we were able to find inexpensive pigtails – email me for info if you want I don’t want to “brand” these things!  They are actually really good because I found CVCs would often occlude. Patient comfort with either is so much more than chest tubes. 

Great point about the “michelin man” who is very “wet” but intravascularly dry, which we see commonly post acute phase of critical illness, especially when physicians are so keen to use crystalloids.

thanks for reading!

 

Philippe

Blood transfusion and serum S1P levels in Sepsis: a leaky proposition? (Protecting the Glycocalyx Part1) #FOAMed, #FOAMcc

So in my ongoing quest to reframe my resuscitation step-by-step, I’ve been following up on a number of leads regarding the glycocalyx, as previously stated, and John’s reference to this article in a previous comment I feel is highly relevant. So this is it:

Synergistic Effect of Anemia and Red Blood Cells Transfusion on Inflammation and Lung Injury,  Anping Dong, Manjula Sunkara, Manikandan Panchatcharam, Abdel Salous, Samy Selim, Andrew J.Morris, and Susan S. Smyth

Advances in Hematology, Volume 2012, Article ID 924042, 8 pages

http://www.hindawi.com/journals/ah/2012/924042/

S1P (sphingosine-1-phosphate) is a regulator of endothelial permeability and immune function.  Uh-oh, why had I not heard of it? Hmmm…I don’t think it was in Guyton’s or in Harrison’s…and there hasn’t been an RCT about it… Ok, that about explains it.

So here are some factoids about S1P:

–       serum levels correlate with HCT as RBCs serve as an S1P reservoir.

–       anemic patients’ S1P levels are NOT fully replenished by transfusion, especially the older the transfused blood is.

–       In fact, older RBCs may actually remove plasma S1P.

The study:

They basically took mice, and in the first group, bled them (by 20ml/kg) and looked at inflammatory markers, lung permeability and also S1P levels. That’s basically the control group, and they noted that hemorrhage significantly increased inflammatory markers (interesting in and of itself) . They then transfused these mice using wither fresh, S1P-loaded RBCs, or 14-day old RBCs, and, lo and behold, the fresh blood resulted in less inflammation, increased S1P, but most importantly, markedly decreased lung permeability. So clearly, S1P attenuates transfusion associated lung permeability.

In the next group, they injected the mice with LPS following hemorrhage, and found a synergistic effect of blood loss and LPS on inflammation and lung permeability, as could be imagined. Following the LPS, they were transfused with one of four strategies: fresh blood, old blood, fresh blood + S1P or old blood + S1P.  Well, lung permeability still increased in all groups, but least in the fresh blood + S1P, and the old blood + S1P a close second.

Note, interestingly enough, that saline alone (the “control”) also increased lung permeability, highlighting yet again that NS (and probably any crystalloid) is not innocuous…

So here we’re looking at the finer effects of transfusion, and why, against “common-sense” correcting a patient’s hemoglobin level does not seem to help in all situations.  We have understood the aging issue and loss of deformability, but it is time to take a finer look.  We are familiar – at least in concept – with transfusion-associated lung injury or TRALI, but the mechanism remains unclear.

Summary and Take-Home message:

S1P infusions in sepsis?  Maybe someday…

Yes, this is an animal study, and the results cannot be extrapolated directly to humans, but it is food for thought, as John had mentioned.  Certainly at least this should tell us to keep and ear/eye out for human work with S1P, but personally, it will make me even more comfortable in not transfusing my septic patients with hb’s in the low 70’s and maybe even high 60’s (try repeating the cbc, more often than not comes back a couple points higher and you can avoid transfusion), and for those who are a little more aggressive with transfusion, maybe this should make them think twice…

I’ll add what I can dig up on human S1P studies soon.

cheers!

Philippe