Severe Obstructive Physiology on the Ventilator: Peak Pressure, ASV, and pH Targets
Severe obstructive physiology on the ventilator is an area I’d like to better understand, especially COPD/asthma patients with high airway resistance, prolonged time constants, dynamic hyperinflation, and auto-PEEP.
A lot of great ventilator discussion focuses on ARDS, PEEP, oxygenation, and synchrony, but I’d love to hear more expert thoughts on the obstructive side.
Specifically, how do you approach high peak pressures in these patients? In volume-targeted modes, especially on transport ventilators like the Hamilton T1, there are times where the pressure limit may need to be raised to deliver an appropriate tidal volume when resistance is very high. My understanding is that the key is not peak pressure alone, but whether plateau pressure/driving pressure, delivered tidal volume, expiratory flow return, auto-PEEP, and hemodynamics suggest unsafe alveolar distension or worsening dynamic hyperinflation.
I’m also curious about ASV in obstructive patients. I realize many clinicians consider ASV controversial or often avoid it in COPD/asthma, often because of concern that the mode may generate larger tidal volumes or make choices that do not fit severe obstructive physiology. For those who use Hamilton ventilators, does anyone use ASV in selected obstructive patients? If so, what patient characteristics, settings, limits, and monitoring parameters make you comfortable continuing it? Have you found it successful, or do you generally avoid it because the physiology makes it too risky or unreliable?
For those managing these patients in the ICU, ED, or transport environment:
How high of a peak pressure or pressure limit are you comfortable with in severe obstruction?
What variables guide your decision to accept higher peak pressures versus reduce minute ventilation further?
How do you approach this when plateau pressure measurement is limited or unavailable?
Do you generally target pH correction rather than PaCO₂ normalization, and what lab values guide that decision?
Keith, if you’re reading this and the topic is of interest, I think this could also make for a great podcast discussion.
Thank you all for the discussion. This has been very helpful.
One related question I’ve been thinking through is the rate of correction. In transport, we typically trend VBGs when available, especially pH and pCO₂, and we usually emphasize slow correction rather than trying to normalize CO₂ quickly.
For those managing these patients frequently, do you intentionally avoid rapid PaCO₂ correction in acute-on-chronic obstructive patients, even when airway pressures and auto-PEEP are not the limiting issue? I’m thinking specifically about the risk of overcorrecting a chronically compensated patient into post-hypercapnic alkalosis, versus the need to correct dangerous acidemia.
I realize there may not be a specific “optimal rate,” but I’d be interested in how others think about the practical target: correcting the pH enough to improve physiology without chasing a normal PaCO₂.