Vent management: Auto-PEEP and peak pressures, acid-base

Thanks for presenting a great case Kathy! This is a case of a middle age person with persistent asthma and a history of an extensive unprovoked DVT (sp IVC filter placement), who developed hypercarbic hypoxic respiratory failure requiring intubation secondary to an acute bacterial necrotizing pneumonia who presented to our ICU for hemoptysis s/p bronchial blocker placement. The patient was hypercarbic at presentation, which was thought 2/2 auto-PEEP. The hospital course was complicated by spontaneous pneumothorax thought multifactorial 2/2 underlying lung disease, the bronchial blocker, and necrotizing pneumonia.


Main points:

  1. ) We briefly discussed the differential of hemoptysis which includes categories such as oropharyngeal/ airways, parenchyma (infectious vs inflammatory vs malignancy), vasculature, drug/ toxins, and misc. See this great blog from Monday on the differential.
  2. ) In a patient with underlying obstructive lung disease, ventilated with a high RR, and persistent hypercarbia, consider auto-PEEP as the cause.
  3. ) A stepwise approach that Sharon Anderson teaches to evaluate a blood gas includes the components:
    1. ) acidosis or alkalosis? (pH >/< 7.4)
    2. ) respiratory or metabolic? (pH and PaCO2 deranged in same way = metabolic; opposite = respiratory)
    3. ) appropriate compensation or underlying second disorder? (various formulae and shortcuts)
    4. ) concurrent AGMA? Concurrent simultaneous non-gap and gap acidosis?
    5. ) does this result fit with the clinical picture?

Want to learn more?


  • Auto-PEEP occurs when expiratory time is not long enough to fully exhale, leading over time to more and more air trapping
  • This can lead to high intrathoracic pressures, hypotension and PEA arrest if not noticed
  • Patients with obstructive lung disease are more prone to auto PEEP
  • Ways to evaluate for auto PEEP include: visualization of incomplete return to baseline of the expiratory flow curve (above), “shark finning” on waveform capnography (EtCO2; 2/2 slower rate at exhaling CO2), and diagnostically & therapeutically disconnecting the ETT from the vent to observe for prolonged exhalation and wheezing.
  • Here's a great Life in the Fast Lane (awesome blog by some ICU/EM docs down under) entry on this topic

PIP and Pplat

  • In a patient with acute alarms for high peak pressures, consider whether this is an airways, compliance or PEEP problem
  • Recall:

    • PIP/ peak inspiratory pressure/ peak pressure ~ flow x resistance + alveolar pressure
    • Pplat/ plateau pressure ~ alveolar pressure ~ volume/ compliance + PEEP
  • PIP is displayed on the ventilator
  • Pplat can be measured via a button on the vent that initiates an inspiratory breath hold (aka flow = 0) to isolate alveolar pressure

  • In patients with only a high PIP and normal Pplat this is most likely an airways/ tubing problem and consider tube kinking, bronchospasm, mucus plugging, and compression

  • In patients with a high PIP and Pplat, consider acute problems with lung compliance/ PEEP including pneumothorax, right mainstem bronchus intubation, worsening effusion

The OHSU library has an e-subscription to the Marino ICU book as a good reference for these topics and more.