asked 2 years ago
Could you please explain the mechanism of action of CPAP on bronchoconstriction? I recently had a patient who stated they had both COPD and asthma. They were taking fluticasone and salbutamol and she met the conditions for CPAP, however, she had audible wheezing. Upon auscultation, it seemed that wheezing was coming from the upper airways. While this seemed it was a COPD exacerbation, we had concerns on how the CPAP would effect the obvious bronchoconstriction. Ultimately, we gave this patient salbutamol and dex, and they significantly improved by the time we arrived at the ED. However, I would like to know where the line is when it comes to these patients with respiratory comorbidities? And what cautions should we have with CPAP?
1 Answers
answered 2 years ago
Good question. Non-invasive positive pressure ventilation such as CPAP in the prehospital setting or BIPAP in the emergency room work to reduce the work of breathing by stenting open airways to improve exhalation. CPAP delivers continuous positive airway pressure to the upper airways and is designed to prevent airway collapse. It is very effective for those who are experiencing COPD exacerbations or acute congestive heart failure.
Patients with reactive airway disease such as COPD have upper airway narrowing secondary to inflammation resulting in obstruction to exhalation. So it takes them a long time to exhale. A fast respiratory rate shortens the time available for exhalation, leading to breath stacking and ultimately hyperinflation, which increases the obstruction to exhalation and compounds the patient's respiratory distress resulting in a vicious cycle.
Our treatment for COPD patients are designed to lessen the resistance to air entry and expulsion and we can do this with bronchodilators and CPAP. CPAP, for lack of better words, splints the airways and prevents their collapse during exhalation thereby allowing the lungs to empty. In situations where bronchodilators are not effective, CPAP is the next step. In fact CPAP should be started in conjunction with bronchodilators for any moderate to severe reactive airway COPD patient. Although exact pathophysiology of asthma is different than that of COPD, the respiratory compromise of this obstructive disease is similar. There is significant air trapping and excessive use of respiratory muscles to exhale against smaller airways. The air trapping and intrinsic PEEP makes inhalation difficult and taxes the respiratory muscles. NIPPV offers several mechanisms that may benefit an asthma exacerbation, such as offloading the work of inspiratory muscles, a direct bronchodilatory effect, allowing improved flow of bronchodilatory agents in the bronchial tree, and improving ventilation/perfusion matching. However medicine is like a snowflake in that no two diseases, no matter how similar, are alike with respect to treatment. The data supporting NIPPV in asthma are lacking. The existing limited data do not show the mortality benefit seen with NIPPV in the treatment of COPD. Improvements in respiratory rate and airflow have been noted. Some studies point toward an overall decrease in intubation rates and shorter ICU stays. For this reason we reserve pre-hospital CPAP for COPD and CHF patients. Asthmatic patients should be treated with aggressive bronchodilation and transported to the ED where the decision to start BiPap may be entertained. Thank you!
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