Authors Richard H. Zou, MD 1, Ian J. Barbash, MD, MS1 1 Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, PA
Case
A 49-year-old heavy smoker with a history of emphysema on home oxygen
presented with acute-onset fever and productive cough. She was found to
have an SpO2 of 64% on 8 L/min oxygen and immediately placed on bilevel
positive airway pressure with inspiratory pressure of 15 cmH2O and
expiratory pressure of 5 cmH2O. Follow-up arterial blood gas
demonstrated pH 7.28, pCO2 80 mmHg, pO2 127 mmHg, and HCO3 36 mEq/L. She
was started on systemic corticosteroids and scheduled bronchodilator
therapy. Infectious workup revealed a viral swab positive for human
respiratory syncytial virus A. Despite conservative measures, she
developed progressive hypercapnic respiratory failure requiring
intubation and mechanical ventilation. Her ventilator waveforms
immediately following intubation are shown below.
Image 1
Question
Which of the following is the patient most at risk for developing?
A. Non-cardiogenic pulmonary edema B. Barotrauma C. Repeated alveolar collapse and expansion D. Dynamic hyperinflation E. Oxygen toxicity
Answer
D. Dynamic hyperinflation
Discussion
The patient had a prolonged expiratory time, as demonstrated by her
flow-time waveform, volume-time waveform, and continuous waveform
capnography on mechanical ventilation. When the set respiratory rate was
increased from 5 breaths/minute to 6 breaths/minute, she demonstrated
dynamic hyperinflation with hemodynamic instability.
Dynamic hyperinflation, also known as auto-positive end expiratory
pressure (auto-PEEP) or intrinsic PEEP, occurs when a breath is
initiated prior to the complete exhalation of the previous breath,
leading to a gradual increase in end-expiratory lung volume. This
feature is most commonly observed in patients with underlying
obstructive lung disease, including emphysema and asthma, or high
respiratory rate. If left untreated, dynamic hyperinflation leads to
increased intrathoracic pressure, decreased venous return, hypotension,
and, ultimately, cardiac arrest [1].
Dynamic hyperinflation can be assessed using several methods. First, a manual end expiratory pause reveals the total PEEP (a)
and, therefore, calculation of auto-PEEP (total PEEP minus the set PEEP
on the ventilator); the dotted line in the figure below illustrates the
change in pressure-time waveform during end expiratory pause in the
setting of auto-PEEP. Second, visual estimation of unequal areas under
the curve of the inspiratory and expiratory portions of the flow-time
waveform (b) indicates that the inspired volume may be
higher than the expired volume; this may also be visualized on the
ventilator display. Third, persistent end expiratory flow on the
flow-time waveform (c) signifies continued expiration
at the initiation of the subsequent breath. Fourth, ineffective
triggering suggests an inability to initiate a breath due to significant
auto-PEEP and can be seen by deflections in waveforms that do not
trigger breaths [2]; this was not observed in the figure below as the
patient received peri-intubation neuromuscular blockade. Other markers
that raise clinical suspicion for severe obstruction include prolonged
expiratory phase on the volume-time waveform (d) and shallow expiratory phase slope on continuous waveform capnography (e) [3].
Image 2
Treatment focuses primarily on management of the patient’s underlying
obstructive lung disease. Ventilator maneuvers include decreasing the
set inspiratory time, respiratory rate, and/or inspired tidal volume;
permissive hypercapnia may be necessary. Systemic corticosteroids and
scheduled bronchodilators are the mainstay of medical therapy [4].
Helium-oxygen mixture may improve laminar flow and decrease turbulent
flow, thereby reducing resistance and the time required for exhalation
[5]. Paralysis with neuromuscular blockade may decrease dynamic
hyperinflation that results from ventilator dyssynchrony in patients
exceeding the set rate on the ventilator. In cases of hemodynamic
instability, prompt disconnection of the endotracheal tube and manual
chest decompression may be necessary. Ultimately, a high index of
suspicion and prompt recognition and treatment will allow clinicians to
avoid patient harm associated with dynamic hyperinflation during
mechanical ventilation.
Non-cardiogenic pulmonary edema (answer A) is
associated with acute hypoxia and respiratory decompensation from
increased capillary permeability and pressure gradient changes not
attributable to primary cardiac disease. Barotrauma (answer B)
occurs when the lungs are exposed to excessively high pressures and
crosses the upper infection point of the pressure-volume curve, with
resultant alveolar overdistension and rupture. Repeated alveolar
collapse and expansion (answer C) occurs when there is
expiratory alveolar collapse and crosses the lower infection point of
the lung pressure-volume curve, with resultant shear stress and alveolar
damage. Oxygen toxicity (answer E) is due to excessively high oxygen levels and is associated with oxidative stress and free radical formation.
References
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