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Dr. Kvale is associated wtih the Division of Pulmonary and Critical Care Medicine, Henry Ford Health System.
Correspondence to: Paul A. Kvale, MD, FCCP, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System, 2799 W. Grand Blvd, Detroit, MI 48202-2689; e-mail: pkvale{at}hfhs.org
Generally, hypoxemia is very common with diagnostic fiberoptic bronchoscopy. Hypoxemia occurs with insertion of the bronchoscope through the glottis into the trachea, and becomes worse when local anesthetics or saline solution are instilled into the lower airways. BAL is associated with greater levels of oxygen desaturation than when lavage is not done. This has led physicians routinely to monitor oxygen saturation during and after bronchoscopy, and to the nearly universal use of supplemental oxygen to prevent severe hypoxemia during bronchoscopy.1 2 A more parsimonious approach, providing supplemental oxygen only to those patients who actually do exhibit desaturation, was the subject of a recent report.3 At times, the fall in oxygen saturation can be sufficiently profound or sustained as to require aborting the procedure, or taking some measure to correct it in order to complete what is intended. While the hypoxemia is associated with cardiac arrhythmias in 11 to 40% of patients who undergo fiberoptic bronchoscopy, the cardiac rhythm disturbances are rarely important clinically.4 5
In the current issue of CHEST, Chhajed and colleagues (see page 1350) report a simple and novel approach (inserting a nasopharyngeal tube) for managing or preventing hypoxemia in lung transplant recipients as they underwent bronchoscopy as part of their posttransplant management. Most patients (88%) had relief of bronchoscopy-related hypoxemia with insertion of a nasopharyngeal tube.
Snoring with upper-airway obstruction and desaturation were the initial observations in this population of lung transplant recipients undergoing bronchoscopy. The authors then developed a stepwise approach for such patients. When snoring in association with saturation fell to 
90%, the jaw was supported and oxygen flow via nasal prongs was increased from 4 to 6 L/min. If desaturation persisted, a nasopharyngeal tube was inserted and the bronchoscope was withdrawn to the trachea. If desaturation still persisted, additional oxygen was administered with a 7F catheter passed nasally to a position just above the larynx or in the proximal trachea. By utilizing these maneuvers, only 5 of 714 procedures required termination with withdrawal of the bronchoscope, reversal of the sedating agents, and bag and mask ventilation of the patient.
The patients in this study received larger doses of sedating agents than most bronchoscopists find it necessary to administer. (For a 70-kg person, the preprocedure morphine dose was 2.5 to 5 mg, followed by an average IV dose of midazolam of 10.5 mg, along with 125 µg of fentanyl.) Like the authors, we have found that larger doses of conscious sedating medications may be needed in lung transplant recipients than other groups of patients undergoing bronchoscopy. While these sedating agents are central respiratory depressants, another mechanism is needed to account for more than transient hypoxemia after boluses of these drugs are administered carefully. For example, the degree of airflow obstruction as judged by FEV1 is a predictor of clinically significant bronchoscopy-related hypoxemia.3 6 Inserting a flexible bronchoscope into the airway by the transnasal route causes a 17% rise in the functional residual capacity of the lungs, altering gas exchange.7 Instillation of local anesthetic solutions or saline solution, and especially high-volume BAL, causes changes in ventilation/perfusion relationships. This leads to a right-to-left shunt-like phenomenon, with systemic arterial hypoxemia.
However, unmasking latent obstructive sleep apnea (OSA) is a far more attractive explanation for the hypoxemia that accompanies bronchoscopy with conscious sedation. Chhajed and colleagues provide convincing arguments to support this mechanism of hypoxemia with bronchoscopy. They noted what you and I have also observed: when we administer sedating agents as we begin diagnostic bronchoscopy, many patients begin to snore and exhibit signs of upper-airway obstruction. In the lung transplant recipient population that constitutes this report, the authors noted that body mass and central adiposity tends to increase after lung transplantation, presumably as a result of corticosteroids. Patients with an increased body mass index were significantly associated with insertion of a nasopharyngeal tube to treat their hypoxemia. And, the amount of sedation administered for procedures in the nasopharyngeal tube group was significantly less than for the procedures where the nasopharyngeal tube was not used. As the authors point out, this strongly suggests that the patients who desaturate during fiberoptic bronchoscopy do so because of upper-airway obstruction, rather than because of central respiratory depression. OSA was confirmed in 23 of 49 patients who underwent sleep studies, and 18 of 23 patients with OSA required insertion of a nasopharyngeal tube.
Even though conscious sedation causes many patients to snore and exhibit signs of upper-airway obstruction, not all of them have frank OSA. They may be at risk of OSA developing, and therefore are at greater risk for obstruction of their upper airways while undergoing diagnostic bronchoscopy with sedation. Upper-airway reflexes, as influenced by sedation and topical anesthesia, are discussed in detail by the authors and may be responsible for the observed desaturation and need for nasopharyngeal tube insertion.
Since I observe the same phenomenon of snoring and desaturation in many patients undergoing diagnostic fiberoptic bronchoscopy—not just lung transplant recipients—I intend to make the approach described by the authors a regular addition to my bronchoscopy practice.
References
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