16.1 Restrictive and Obstructive Airway Disease
Key Takeaways
- COPD and asthma are obstructive: long expiratory time, permissive hypercapnia, and no stacking; auto-PEEP is leftover alveolar pressure that drops blood pressure.
- ILD, obesity, kyphoscoliosis, abdominal hypertension, and ARDS-like lungs are restrictive: smaller tidal volume, a higher rate if needed, and a plateau watch.
- Alert COPD often starts on BiPAP; intubate if the patient is tiring, sleepy, or silent-chested, and use ketamine as the usual bronchospasm induction.
- A post-intubation status-asthmaticus crash is tension physiology from trapped gas until you disconnect and empty the chest.
- Cabin hypoxia hits both pictures; raise FiO2 or request a lower cabin rather than speeding an obstructive rate or overfilling a restrictive lung.
Restrictive and obstructive airway disease are opposite mechanical problems that share a hypoxic cabin. Domain 4.C of the August 2026 Board of Certification for Emergency Nursing (BCEN) Certified Flight Registered Nurse (CFRN) outline lists restrictive airway disease and obstructive airway disease as separate jobs. Teach chronic obstructive pulmonary disease (COPD) and asthma as obstructive: high resistance, long expiration, and air trapping. Teach interstitial lung disease (ILD), obesity, kyphoscoliosis, abdominal hypertension, and acute respiratory distress syndrome (ARDS)-like low compliance as restrictive: a stiff lung or chest wall that will not take a large breath. Some third-party outlines swap those examples. Follow physiology, not the swapped list.
Obstructive disease: give time to get out
Obstructive lungs empty slowly. If you do not give them time, they stack.
Auto-PEEP, I:E, and permissive hypercapnia
Auto-positive end-expiratory pressure (auto-PEEP), also called intrinsic PEEP, is leftover alveolar pressure at the start of the next breath. It is the flight signature of stacked COPD and status asthma: a flow waveform that never returns to zero, falling blood pressure, and a quiet chest. Treat auto-PEEP as a time problem, not extra minute ventilation.
Lengthen expiratory time. Typical adult teaching is a slow rate (often 8–12 breaths/min), a modest tidal volume (Vt) of about 6–8 mL/kg ideal body weight (IBW), low positive end-expiratory pressure (PEEP), and an inspiratory-to-expiratory (I:E) ratio of 1:3 to 1:5 or longer. Those numbers are clinical teaching, not BCEN numbers. Allow permissive hypercapnia if potential of hydrogen (pH) is still compatible with life: a high partial pressure of carbon dioxide (PaCO2) is safer than stacking. Peak inspiratory pressure is high from resistance; plateau pressure (inspiratory hold) tells you whether alveoli are also over-stretched. A rising plateau plus falling pressure is stacking or a missed pneumothorax.
NIV versus the tube, ketamine, and stacking
Alert COPD exacerbation often starts on noninvasive ventilation (NIV)—usually bilevel positive airway pressure (BiPAP) with enough expiratory pressure to offset auto-PEEP and enough inspiratory pressure to unload the accessory muscles (Chapter 7). Intubate if the patient is tiring, becoming sleepy, showing a silent chest, or failing the mask. Ketamine is the usual induction for bronchospasm because it bronchodilates and leaves some drive. After the tube, do not celebrate a high minute ventilation. If blood pressure collapses, disconnect the circuit, compress the chest to empty trapped gas, then resume a slow rate. That crash is tension physiology from air trapping, not a mystery bleed.
Status asthmaticus is asthma that is not breaking with continuous nebulized beta-agonists, ipratropium, steroids, and magnesium. The silent chest after intubation is a trap, not a cure. Treat hypotension as stacked gas until proven otherwise. If disconnecting does not restore pressure, decompress a possible pneumothorax.
| Problem | What the lungs are doing | First ventilator move | What kills in the aircraft |
|---|---|---|---|
| COPD / asthma (obstructive) | High resistance, slow empty | Long expiratory time, permissive hypercapnia, avoid stacking | Auto-PEEP hypotension; a textbook rate |
| Status asthmaticus crash | Gas trapped like a tension pneumothorax | Disconnect, empty the chest, then slow ventilation | Pushing 16–20 breaths/min to normalize carbon dioxide |
| ILD / ARDS-like / obesity / chest wall (restrictive) | Low compliance, small usable volume | Smaller Vt, higher rate, watch plateau | Over-distention; ignoring plateau for a pretty end-tidal carbon dioxide |
Restrictive disease: small volumes, honest plateaus
Restrictive lungs and chests refuse volume. Forcing a large breath raises plateau and drops venous return.
Smaller Vt, higher rate, plateau watch
Compliance is volume change per pressure change. ILD, ARDS-like lungs, a gravid or hypertensive abdomen, severe obesity, and a rigid kyphoscoliotic chest all drop compliance. Teach about 6 mL/kg IBW as the usual adult starting Vt for an ARDS-like lung, then raise rate to hold pH, not to chase a normal end-tidal carbon dioxide (ETCO2). Watch plateau pressure—pause at end-inspiration. Many programs treat a plateau above about 30 cm H2O as a reason to cut volume further. Driving pressure (plateau minus PEEP) is the modern over-distention check. Those targets are clinical teaching.
Obesity and abdominal hypertension need a ramp or sitting position if the cabin and spine allow, and they need the abdomen treated (section 16.3), not just a higher peak. High PEEP may recruit an ARDS-like lung; it will not open a belly that is already at 25 mm Hg. Dose Vt on IBW, not actual weight.
Cabin hypoxia, Boyle, and what you cannot hear
Dalton's law drops the inspired oxygen partial pressure as cabin altitude rises. Both pictures desaturate. Request a lower cabin or raise fraction of inspired oxygen (FiO2) rather than adding rate to an obstructive patient or adding volume to a restrictive one. Boyle's law expands trapped gas: bullae, a missed pneumothorax, and a tight abdomen all get worse on climb. You will not hear the wheeze over the rotor. Watch the flow waveform, the plateau, the saturation, and the blood pressure.
- Treat COPD and asthma as obstructive: long expiration, permissive hypercapnia, no stacking.
- Treat ILD, obesity, chest-wall restriction, abdominal hypertension, and ARDS-like lungs as restrictive: smaller Vt, higher rate, plateau watch.
- Ketamine is the usual bronchospasm induction; NIV is a trial, not a delay to a failing airway.
- A post-intubation asthma crash is tension physiology from air trapping until you disconnect and empty the chest.
- Cabin hypoxia hits both; fix FiO2 and cabin altitude, not the wrong ventilator knob.
A recently intubated COPD patient becomes hypotensive when the transport ventilator is set at 18 breaths/min. The expiratory flow waveform never returns to baseline. What is the correct first move?
An obese patient with interstitial lung disease and an ARDS-like chest radiograph is being packaged for flight. Which ventilator strategy matches restrictive physiology?
After climb, both a stacked asthmatic and a patient with stiff interstitial lung disease desaturate. Which cabin rule applies to both pictures?