Transnasal humidified rapid-insufflation ventilatory exchange is an airway technique that consists of high-flow warmed humidified nasal oxygen therapy at a rate of up to 70 L/min using OptiFlow system (Fisher and Paykel Healthcare Limited, Auckland, New Zealand) (Figure). It extends apnea time, maintains oxygen saturation, is more effective in carbon dioxide clearance compared to apneic oxygenation,1 and improves respiratory status in patients with acute heart failure, acute respiratory failure, and sleep apnea.2 Although the underlying mechanisms are not fully elucidated, contributing factors include apneic diffusion oxygenation, washout of the nasopharyngeal dead space, provision of continuous positive airway pressure (Paw), decreasing shunt, and a reduction in work of breathing.1,3
Cystic fibrosis is a chronic multisystem disease involving primarily pulmonary and gastrointestinal systems. As medical management of cystic fibrosis has improved over time, more patients are surviving into adulthood and experiencing worsening respiratory complications with its progression.4
We report a case of the use of transnasal humidified rapid-insufflation ventilatory exchange during deep sedation for a dental procedure on a lung transplant candidate with severe cystic fibrosis. The patient gave written consent for this case publication.
DESCRIPTION OF THE CASE
A 29-year-old, 47-kg woman with body mass index 18 and with severe cystic fibrosis was scheduled for extraction of 9 carious teeth as a precondition for lung transplantation. She presented with chronic shortness of breath and productive cough, requiring home oxygen at 1–2 L/min during sleep. Recent pulmonary function tests showed forced expiratory volume in 1 s (FEV1) of 0.95 (28% of predicted). Despite frequent hospitalizations due to respiratory infections, she did not require mechanical ventilation. Medical history included liver cirrhosis, severe anxiety, depression, exocrine pancreatic insufficiency, and distal intestinal obstructive syndrome. Anesthetic history included only minor procedures. Her medications included quetiapine, nitrazepam, nabilone, vitamin K, and inhalers. The only positive finding on physical examination was bilateral mild basal wheezes.
Due to extreme anxiety, the patient was adamant to be intubated under general anesthesia and refused to have the procedure under conscious sedation and local anesthesia. However, we advocated the procedure to be performed under deep sedation with transnasal humidified rapid-insufflation ventilatory exchange support for spontaneous ventilation and oxygenation because of increased risk of prolonged intubation and complications associated with mechanical ventilation. In the operating room, routine anesthesia and bispectral index (BIS, Aspect Medical Systems, Inc, Natick, MA) monitors showed blood pressure 140/80 mm Hg, heart failure 98, oxygen saturation measured by pulse oximetry 98%, and BIS 98. Transnasal humidified rapid-insufflation ventilatory exchange was started at 40 L/min and gradually increased to 60 L/min just before the start of the surgical procedure. Sedation was initiated with propofol infusion at 25 µg·kg−1·minute−1 increasing to 70 µg·kg−1·minute−1 and IV boluses of 20–30 mg (total 550 mg), followed with boluses of 0.5 mg midazolam (total 3 mg), 25 µg fentanyl (total 100 µg), and 10–20 mg ketamine (75 mg) until the patient was not responsive to painful stimuli. After infiltration of the oral nerves with lidocaine and bupivacaine, a throat pack was placed in the posterior oropharynx, and suction was used continuously. Total procedural time was 110 minutes. The hemodynamic parameters were stable with BIS 70–75 and oxygen saturation was above 98%. Ventilation and airway patency were assessed by inspection and with intermittent hand placement on the abdomen below the diaphragm.
After completion of the surgical procedure, the patient regained consciousness 5 minutes after propofol infusion was stopped. The patient was discharged the following morning without any complications. Follow-up by phone 8 days after surgery showed no respiratory compromise.
Pulmonary complications are responsible for >90% of morbidity and mortality in patients with cystic fibrosis. Pulmonary function tests most frequently reveal a pattern of obstructive airway disease due to progressive loss of airway cartilaginous support, and thus patients are more reliant on muscle tone to maintain airway patency.5 As cystic fibrosis progresses, ventilation-perfusion mismatch leads to hypoxemia and, ultimately, hypercarbia. Patients with advanced cystic fibrosis may require home oxygen therapy during exertion or at night to help ameliorate the effects of both.4,5 Our patient fulfilled the advanced criteria because she required home oxygen and was referred for lung transplantation secondary to progressive pulmonary function impairment as evidenced by FEV1 <30% predicted.6
Cystic fibrosis patients with severely reduced FEV1 should have their limited pulmonary function and reserve protected as much as possible, with goals to produce minimal ventilatory depression and have airway reflexes fully recovered at the end of the procedure. Humidifying and warming gases lessen the production of secretions.4 Therefore, maintenance of upper airway patency is very important for patient safety during sedation. Nasal high-flow system was reported to have beneficial effects in patients with obstructive sleep apnea syndrome, chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, and acute respiratory failure, etc.7 Other studies already have shown that transnasal humidified rapid-insufflation ventilatory exchange is an adjunct that helps maintain oxygenation when patients are sedated.7,8 Knowing all these considerations and the extreme anxiety of the patient, we decided that the safest option would be deep sedation using transnasal humidified rapid-insufflation ventilatory exchange as an adjunct.
The primary method of increasing the apneic window is through preoxygenation, which denitrogenizes the lungs and creates an alveolar oxygen reservoir. The clinical application of this phenomenon is apneic oxygenation, which can maintain oxygen saturation but cannot cause carbon dioxide removal. The rate of increase in end-tidal carbon dioxide (ETco2) was 1.13 mm Hg/min1 on patients under transnasal humidified rapid-insufflation ventilatory exchange, compared with 3.75 mm Hg/min on apneic oxygenation. These findings support the idea that some amount of carbon dioxide is flushed out of the airway.9–11 Transnasal humidified rapid-insufflation ventilatory exchange provides low-level Paw that keeps the upper airway open. The degree of pressure generated increases with gas flow rate and is greater with closed mouth compared to open. In healthy volunteers, at flow rates ranging from 0 to 60 L/min, the expiratory pharyngeal pressure varied from 0.8 to 7.4 cm H2O during mouth-closed breathing and from 0.3 to 2.7 cm H2O during mouth-open breathing.12 We assumed in our case that the generated pressure was between mouth-closed and mouth-open breathing. A previous study using transnasal humidified rapid-insufflation ventilatory exchange in patients undergoing dental procedures and deep IV sedation showed no interventions were needed for upper airway obstruction when a 50 L/min flow was used.7
The use of transnasal humidified rapid-insufflation ventilatory exchange in this patient with severe cystic fibrosis was effective because of 3 possible mechanisms: (1) warming and humidifying the oxygen to produce less secretions, (2) maintaining low level of Paw to keep the airway patent, and (3) eliminating carbon dioxide by washout of the nasopharyngeal dead space to maintain carbon dioxide at an acceptable level. These underlying mechanisms allow for conditions in our patient to maintain oxygenation >98% with a patent airway throughout the duration of deep sedation, avoid intubation, awake rapidly without mental confusion, and prevent postoperative pulmonary complications.
During our case, we did not monitor ETco2 due to continuous work in the mouth which could affect the accurate ETco2 measurement. Analysis of carbon dioxide in apneic patients using transnasal humidified rapid-insufflation ventilatory exchange showed increases of approximately 1.8 mm Hg/min with arterial gas samples and 0.9 mm Hg/min with capnography. This implies that capnography is not a reliable monitor for this situation.13 Considering that minimal muscle activity of the diaphragm can eliminate carbon dioxide during apnea and minimal recovery of neuromuscular transmission resulting in spontaneous ventilation enhanced carbon dioxide clearance,13 it is likely that the carbon dioxide rise would be low in our patient. In fact, a recent study demonstrated that the combination of intravenous anesthesia and transnasal humidified rapid-insufflation ventilatory exchange in patients under spontaneous ventilation for elective microlaryngoscopy generated a mean carbon dioxide increase of 0.26 mm Hg/min in arterial gas samples.14 These were supported by our observation of a fast awakening with no signs of mental confusion.
In conclusion, this case report shows that transnasal humidified rapid-insufflation ventilatory exchange can become an important noninvasive airway adjunct for airway management and oxygenation of patients with severe respiratory compromise undergoing deep sedation.
Name: Kong E. You-Ten, MD, PhD, FRCPC.
Contribution: This author helped care for the patient and edit the manuscript.
Name: Fabricio B. Zasso, MD.
Contribution: This author helped care for the patient and edit the manuscript.
This manuscript was handled by: Mark C. Phillips, MD.
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