This post is from a suggested group
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…
1. Peak airway pressure alone is only telling me about circuit pressure and resistance...it’s not my primary concern in severe obstructive physiology. I’m more focused on what’s happening at the alveolar level: plateau pressure (when available), driving pressure, evidence of dynamic hyperinflation, and overall patient tolerance/hemodynamics.
2. In these patients, time constants are critical. With high resistance and prolonged exhalation, I prioritize maximizing expiratory time to reduce air trapping and auto-PEEP. This often means significantly lowering the respiratory rate, I’ve gone as low as 5–6 breaths/min to allow for complete exhalation.In pressure modes, I ensure expiratory flow returns to baseline (zero); if not, that’s a red flag for breath stacking. I also allow end-inspiratory flow to reach zero and assess pressure at that point to better understand true alveolar pressure in the setting of high resistance.
3. I’m not a frequent ASV user in this population, not due to lack of understanding. Just not preferred with this patient population.
4.I lean into permissive hypercapnia, targeting pH rather than normalizing PaCO₂. If the patient is stable, I’m generally comfortable with elevated CO₂ as long as pH remains acceptable. When plateau isn’t available (e.g., transport), I rely on flow-time waveforms, EtCO₂ vs PaCO₂ trends, and clinical signs including hypotension of hyperinflation to guide management.
https://www.journalmechanicalventilation.com/wp-content/uploads/2021/06/Adaptive-Support-Ventilation-ASV.-Beneficial-or-not.pdf Summary of Literature