Author: Brandon O

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We discuss the principles and application of automatic tube compensation (ATC) on modern ventilators, with its creator Ben Fabry. Dr. Fabry is a professor and chair of biophysics at University of Erlangen-Nuremberg, originally trained as an electrical engineer, who originally developed ATC as part of his PhD program.

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Takeaway lessons

1. ATC, originally called “electronic extubation,” is meant to normalize or eliminate the resistance to flow created by the endotracheal tube. Since this resistance is always present, yet is dynamic and varies by flow (and tube size), it creates a continuous confounding variable, making the displayed pressure on the ventilator a measurement not of tracheal pressure, but of another, largely meaningless pressure (the pressure outside the patient).
2. ATC works by increasing airway pressure during spontaneous inspiration to eliminate the pressure gradient created by the tube at the current flow, and reducing it during expiration to reverse the effect.
3. While ATC can be used in any mode, it is mostly meant for pressure support or other spontaneous modes. It has no real role in volume control. In pressure control, it has little meaningful impact during inspiration, although it will reduce the airway pressure below the set PEEP during expiration, which may help facilitate expiration.
4. The original ATC test ventilator could drop pressure below atmospheric pressure during expiration, but this feature is not possible on modern ventilators, so the lowest possible pressure during ATC is zero (probably not quite even, that due to expiratory valve resistance). Some modern vents will not drop pressure during expiration at all.
5. In principal, actual tracheal pressure could be measured by a separate monitoring lumen. In practice, this is dangerous, as the lumen could be occluded by mucus, so the resistance constant is instead applied mathematically. The modifiers were derived empirically by testing a variety of tubes at different flow rates.
6. ATC will generally ask for the tube size. Length has some effect but a fairly trivial one, as resistance is mostly influenced by turbulence, which is mainly a product of diameter. Resistance is not a constant, but increases with (roughly) the square of the flow of gas.
7. A swivel connector on the ETT outlet adds about 1 cm H2O of resistance. An HME adds about 3 cm H2O.
8. Changes in gas composition at different FiO2 changes resistance trivially, although a mix like Heliox would change it significantly, and would make the internal calculations incorrect.
9. No fixed single pressure support value can accurately match tube resistance, due to its dynamic nature during and between breaths, even if you were willing to set the sort of pressure needed—which might be 50+ cm H2O in a strongly breathing patient.
10. The main downside of ATC is that modern ventilators don’t do it very well—they can only vary flow so quickly, so when there are brisk changes in pressure, they fail to match it. They usually can match only about 50% of tube resistance, with the worst at the start of a breath as they lag behind the initial drop in pressure. (You can appreciate this by seeing the airway pressure drop below the set PEEP.) Response is even less in some of the current generation of vents with radial blowers and slower valves
11. Quality check your ATC by watching the tracheal pressure—the vent will display this as a second pressure tracing. It should remain positive above the set PEEP for the whole breath. (The airway pressure should also remain positive, but the tracheal pressure will be a more sensitive marker.) If it becomes negative or drops to the PEEP at any point during inspiration, it implies a failure to fully support the patient. This problem can occur during vigorous spontaneous breathing in any mode, since it’s driven mostly by slow ventilator response; it is just compounded by ATC, because not only does flow have to vary to meet a set pressure, but the set pressure is varying during the breath too. The best way to solve this problem is probably better machines, with faster valves, and maybe situating them closer to the patient (shorter circuits) to speed up responsiveness.
12. When ATC fails to fully support, you can try adding PSV with a very fast rise time, but this is a bludgeon; the best mode is probably flow-proportional assist ventilation with ATC. PAV allows controlling not just tracheal pressure to a constant value, but alveolar pressure; it will further boost the pressure to try and maintain constant alveolar pressure during inspiration. Increase proportional assist until the tracheal pressure no longer drops below the PEEP. (You could achieve a similar effect by “lying” to your ATC and setting a smaller tube size, which will also increase the initial amount of support; but this is less precise and maybe less safe.) PAV plus ATC may be the ideal mode for patients spontaneously breathing without severe lung disease.
13. PAV could be used, by the way, in a patient with bronchospasm (or similar increase in airway resistance from physiologic factors), as it allows you to compensate for any amount of airway resistance you wish. However, it will only do this during inspiration, and will not drop pressure below the PEEP during expiration (i.e. to reduce autoPEEP and aid exhalation). This probably wouldn’t help them exhale anyway, since the resistance is in the lungs, not in the vent.
14. PSV in a weaker patient tends to mask some of their true spontaneous breathing patterns. ATC may unmask these, showing some odd patterns, such as very shallow or rapid breaths. This is not dyssynchrony; it is the true physiologic pattern that was merely being hidden in a less supportive mode. It is also not tiring, at least if the ATC is working correctly and you’re offering adequate support, because they are not experiencing resistance to breathing.
15. If present, a Cheyne Stokes pattern of breathing may also become amplified by the “signal boosting” properties of ATC, rather than being damped by inadequate support. If this results in phenomena like very long apneic pauses, it may (perhaps) be a problem.

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Our collaboration with Sarah Lorenzini of the Rapid Response RN podcast, discussing a case and general principles for diagnosing and managing obstructive shock. Check out the other episodes on shock in the Nurses’ Podcrawl 2024!

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We discuss the role of point-of-care ultrasound in evaluating the patient with kidney injury and assessing volume status, with Abhilash Koratala (@nephroP), nephrologist, Director of Clinical Imaging for Nephrology at the Medical College of Wisconsin, and champion of nephrology-focused ultrasound.

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Takeaway lessons

1. A quick kidney and bladder ultrasound to rule out urinary obstruction is appropriate for most significant AKIs, maybe even if it was done previously (as obstruction can develop at any time).
2. Ultrasound of the lungs and IVC help establish the presence of elevated filling pressures; if present, the VEXUS scan can be performed to establish the presence of venous congestion that might be contributing to kidney injury.
3. Pulmonary edema as evidenced by B-lines establishes that the patient is not fluid tolerant, and suggests that further volume loading may be harmful. It increases the chance that AKI is due to congestive nephropathy as well, although each can also occur in isolation (and of course AKI can be a cause, leading to volume retention and then pulmonary edema).
4. Abhilash does an 8-zone lung exam (2 anterior and 2 lateral zones on each side), which is plenty for cardiogenic pulmonary edema. He does not really count B-lines; if he sees B-lines in more than one dependent zone, he takes it as evidence the patient could be decongested.
5. IVC is a reasonable method of estimating RAP; it is not reliable to gauge fluid responsiveness or other questions. The internal jugular vein is a good fallback if the IVC is untenable or seems unreliable, such as if bandages limit access, or the presence of cirrhosis (which alters local vasculature in unpredictable ways). Look for the highest point of distention and measure roughly from the sternal angle, adding it to the right atrial depth to approximate the CVP (usually ~5 cm although this is not very reliable).
6. A non-plethoric IVC and absence of B-lines suggests a fluid tolerant patient. He uses the ACE guidelines of IVC >2.1 and <50% collapse with deep inspiration (sniff) to equate RAP ~15 mmHg.
7. In the presence of elevated RAP, VEXUS helps determine whether that change is likely to be affecting organ perfusion by altering flow characteristics. Higher VEXUS scores are well-associated with risk of AKI.
8. High RAP with a low VEXUS suggests that congestive nephropathy is not actively worsening renal function, whereas a higher VEXUS suggests the opposite. Serial VEXUS scans help track the progress of decongestion to dial in a patient to an optimal fluid balance.
9. VEXUS is a right-sided heart parameter, so the state of the left heart’s filling may differ somewhat (e.g. as evidenced by lung markers like pulmonary edema—so track your B-lines too!). It is probably more precise and reliable than other markers like peripheral edema.
10. Right and left heart filling should generally be well-linked. Venous congestion and elevated RAP usually indicate a well-filled LA as well, unless the lungs are acting as a significant resistor. If major PH is present, consider introducing measures like pulmonary vasodilators instead of further fluid loading; overdistending the RV will not help the LV.
11. Although portal vein pulsatility can usually move towards normal after optimal decongestion, hepatic vein waveforms may remain abnormal in some patients with TR, PH, etc. Flow chanegs in intrarenal vessels often lag behind other vessels, as renal edema takes time to resolve.
12. Hepatic vein waveform may be permanently blunted in cirrhotics, confounding it somewhat. Distinguishing the systolic and diastolic waves can also be hard to identify without ECG synching; ECG is highly recommended when available.
13. Portal vein is also probably unreliable in cirrhosis, due to portal hypertension and AVMs; it may be permanently pulsatile in some (although loss of pulsatility is still associated with decongestion). Since many cirrhotics have recurrent hospitalizations, you can compare against prior scans.
14. Intrarenal vessels are technically difficult, especially when patients cannot perform a breath hold; critically ill patients have a failure rate here >20%. It is easier in stable patients. However, CKD patients may have abnormal waveforms at baseline.
15. Overall, there should not be any disease state that falsely confounds ALL of the VEXUS vessels; while states like mechanical ventilation can increase flow changes and point to congestion, this is real congestion, not an artifact.
16. Invasive monitoring like a CVP or PA catheter replaces some of the function of the VEXUS scan, but VEXUS helps determine the degree of organ impact at the numbers reported by these devices. High filling pressures generally are associated with congestion and low pressures are associated with its absence, but VEXUS is often helpful in the gray area. Non-invasive measurements of filling using echo, such as RVSP or E/A and E/E’ may have a supplemental role as well; the latter may help distinguish cardiogenic from non-cardiogenic pulmonary edema, but do not tell much of a story about systemic congestion.
17. Femoral vein doppler could be a supplement to VEXUS, mainly when you cannot get or cannot trust one of the other vessels. It is farther from the heart, so may be less sensitive to changes in RAP. A normal femoral vein (continuous or mildly pulsatile) should probably not rule out venous congestion, but an abnormal femoral vein is very suggestive of it. This can sometimes be noted on routine DVT scans.
18. Abhilash runs a cardiorenal clinic where he finds outpatient VEXUS very useful to establish and monitor volume status. It is more difficult to use in a dialysis clinic due to lack of privacy and high patient volumes; quick lung ultrasound (8 or even 4 zone) might be more useful here.

References

Episode 4 with Philippe Rola on the VEXUS scan

NephroPOCUS

POCUS in AKI: Transcending boundaries: Unleashing the potential of multi-organ point-of-care ultrasound in acute kidney injury. Batool A, Chaudhry S, Koratala A. World J Nephrol 2023; 12(4): 93-103 [PMID: 37766842 DOI: 10.5527/wjn.v12.i4.93]

VEXUS for nephrologists: Koratala A, Reisinger N. Venous Excess Doppler Ultrasound for the Nephrologist: Pearls and Pitfalls. Kidney Med. 2022 May 19;4(7):100482. doi: 10.1016/j.xkme.2022.100482. PMID: 35707749; PMCID: PMC9190062.