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July21

Posted by:John Ellis
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I just read a fascinating review article in Anesthesiology about mechanical ventilation and barotrauma. In the past decade, we’ve learned about protective lung ventilation strategies in ARDS patients. But it turns out that our usual 10ml/kg Vt in healthy people may be causing barotrauma as well!

Some quotes from the paper:

…general anesthesia promotes reduction in lung volume, which is a key determinant of atelectasis formation. Atelectasis occurs in the most dependent parts of the lungs of 90% or more of anesthetized patients from the first minutes of anesthesia induction, whether intravenous or inhalational agents are used.

,,,physical forces generated during mechanical ventilation may also initiate and propagate a systemic release of inflammatory mediators and thus contributing to systemic organ dysfunction (fig. 1).19 The mechanisms underlying the biotrauma hypothesis of ventilator-induced lung injury include mechanical ventilation–induced cell necrosis and decompartmentalization (i.e., stress failure of epithelial and endothelial barriers), mechanotransduction pathways (i.e., the conversion of a mechanical stimulus into biochemical information), and direct effects on the vasculature.

The effects of pulmonary barotrauma may become systemic:

In an experimental model of ARDS, Imai el al.20 have shown that 8h of an injurious mechanical ventilation, consisting of a combination of high VT and low PEEP, can lead to epithelial cell apoptosis in the kidney and the small intestine…

In abdominal surgery (certainly a high risk group for postop pulm complications, the recommended ventilation strategy reduced morbidity:

The Intraoperative PROtective VEntilation (IMPROVE) trial was a prospective, randomized, controlled study in which a multifaceted strategy composed of low VT ventilation, moderate levels of PEEP, and repeated RMs aimed at keep-ing the lung open was compared with nonprotective ventilation in 400 intermediate- to high-risk patients undergoing major abdominal surgery.28 Consistent with previous findings in similar abdominal procedures, we found an overall postoperative respiratory failure rate of 12%. Compared with nonprotective ventilation, prophylactic lung-protective ventilation was associated with improved postoperative clinical outcomes, as suggested by a 69% reduction in the patients requiring intubation or noninvasive ventilation for postoperative respiratory failure (relative risk, 0.29; 95% CI, 0.14 to 0.61; P = 0.001). Of note, the clinical beneficial effects of the lung-protective ventilation strategy persisted for 7 days after surgery.

So, how do you set your vent?

The authors recommend:

  • Lower tidal volumes (see below).
  • Not adjusted for weight, but rather “predicted body weight,” which is based on gender and height.
  • Routine use of PEEP
  • Routine use of recruitment maneuvers
  • FiO2 30-50% to avoid oxygen toxicity

This may be one reason why a randomized trial has shown lower pulm complication rates with LMA (ProSeal) vs ETT in lap gastric banding patients! Yes, we know the vast majority of you would NEVER do an outpatient lap gastric banding with an LMA. The aforementioned study was done in Italy; folks are more aggressive in using LMAs in Europe. The authors attributed the results to perhaps the lower need for NMB with the LMA. Also, PIP (peak inspiratory pressure) was lower, and leak fraction higher (not surprisingly) in the LMA group.




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