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Last Update: 02/17/2025 02:35 AM

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Commit #284670

SS_TS 1.5 Discuss the pathophysiology of chronic obstructive pulmonary disease and the strategies available for artificial ventilation to minimise gas trapping

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Commit #284670

Pathophysiology

COPD is a chronic and progressive inflammatory condition affecting central and peripheral airways, lung parenchyma, and pulmonary vasculature. This leads to poorly reversible narrowing of the airways, remodelling of airway smooth muscle, increased numbers of goblet cells and mucus-secreting glands, and pulmonary vasculature changes resulting in pulmonary hypertension.

COPD is characterized by expiratory airflow limitation because of a combination of small airway inflammation (obstructive bronchiolitis) and parenchymal destruction (emphysema).

Effects on Mechanics of ventilation :

Increased airway resistance : increased expiratory airflow resistance and loss of radial traction that maintains alveolar opening, leading to narrowing and collapse especially in expiration. Intrathoracic pressure during expiration may be positive instead of a passive process. Mucus and secretions can further narrow airways
Dynamic hyperinflation : Increases WOB as breathing at higher FRC,
- can also lead to cardiac dysfunction -> worsening hypoxaemia

Strategies
When considering ways to reduce the harmful effects of air trapping, there are three approaches to consider:

Allowing more time for exhalation.

Reducing the respiratory rate or the I:E ratio (typically to 1:3–1:5) allows more time for exhalation thus reducing the likelihood of breath stacking.

Leads to reduced minute volume -> hypercapnia, hypoxia, or acidosis,

may elevate pulmonary vascular resistance and worsen haemodynamic instability.

May be preferable to increase the inspiratory flow rate and tolerate higher peak pressures, which risks pulmonary barotrauma.

Application of PEEP.

external PEEP in ventilated patients with COPD theoretical benefits by keeping small airways open during late exhalation, so potentially reducing PEEPi.
It has been suggested that if the values of applied PEEP are kept below PEEPi there should be no significant increase in alveolar pressure and so no worsening of the cardiovascular effects while hopefully attenuating PEEPi.

Clinical studies addressing this topic are inconclusive, partly because measurement of PEEPi is difficult, but also because patient responses to extrinsic PEEP have been found to be unpredictable, particularly in terms of improving gas exchange.

Treatment of bronchospasm.

Bronchospasm commonly occurs at induction of anaesthesia or during airway instrumentation.
It should be treated promptly either by inhaled bronchodilators or by deepening anaesthesia with propofol or increased concentrations of inhalation anaesthetics.

One of my ICU SMOs (In Whangarei) suggested you may need to disconnect from the circuit and apply external pressure to the chest to empty the lungs. I cannot find real papers or evidence on this.

Patients with COPD compromise may need to be made between oxygenation, normocapnia, and cardiovascular stability. Some derangement may need to be accepted to facilitate anaesthetic and surgery.

Initial ventilator settings and the mode used is usually dependent on operator and local practices. In general low tidal

volumes of 6 to 10 ml/Kg, FiO2 of 1.0, no added PEEP, respiratory of 10 to 14/minute and an inspiratory flow of 80 to 100L/minute with square wave form are considered ideal.

In general, adapting the following measures can reduce auto-PEEP:

Provide the longest expiratory phase that is possible.
Reduce patient ventilatory demand and minute ventilation.
Reduce airflow resistance by bronchodilators and steroids.

https://academic.oup.com/bjaed/article/14/1/1/336087 - 2014 article on COPD

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2699957/ - Ventilator settings