Capnography and Severe COPD

Abstract

To The Editor: The influences of chronic obstructive pulmonary disease (COPD) on end-tidal CO2 concentration (ETco2) monitoring are well known and consist primarily of the appearance of a significant gradient Paco2/ETco2 secondary to the increase of the alveolar dead space, and the appearance of an ascending capnogram, of which the slope is proportional to the degree of expiratory airway obstruction (1). The extreme stressing of these phenomena can lead to surprising clinical presentations, one of which is described below. A 51-yr-old female patient was scheduled for bilateral thoracoscopic lung reduction for severe postnicotinic bronchoemphysema. Preoperatively, forced vital capacity and FEV1 were 58% and 16%, of normal values, respectively, and Pao2 and Paco2 in air were 59 and 46 mm Hg, respectively. Ventilation and perfusion ratios were respectively 33% and 34% for the left lung and 67% and 66% for the right lung. Anesthesia consisted of a combined thoracic epidural analgesia and general anesthesia that included propofol, sufentanil, and cisatracurium. The trachea was easily intubated with a 37-ch left double-lumen endotracheal tube, of which the right positioning was checked by fibroscopy. Ventilation was controlled with a Fio2 of 0.5, with a maximal peak pressure limit set to 30 cm H2O, at a frequency of 12 breaths/min. Ten minutes after initiation of the mechanical ventilation, ETco2 was 31 mm Hg for a Paco2 value of 47 mm Hg. The operation was performed in dorsal decubitus. The left pulmonary reduction was uneventfully achieved in 68 min during one-lung ventilation. The right thoracoscopy was then started after the exclusion of the right lung. The total absence of a reading on the capnogram was noticed concomitant to the development of increased insufflation pressure and a decrease of tidal volume (120 mL). The permeability of both the endotracheal tube and the left bronchial tree were then checked again by fibroscopy. Surprisingly, the Sao2 remained normal. The reventilation of the right lung systematically allowed the reappearance of breathed out CO2 as well as a slight increase of the tidal volume, whereas the left one-lung ventilation was always associated with a “flatline” capnogram. The examination of the patient did not reveal the cause of this problem. The thoracic drain of the left side had a moderate air leak, but this could not explain the clinical picture by itself. It was then noticed that a several-seconds period of apnea resulted in a very slow appearance of CO2 coming from the left lung. Obviously, the degree of expiratory obstruction of the left lung airway were such that the extent of the ascending inclination of the ETco2 did not allow the appearance of CO2 while breathing out before occurrence of the next ventilatory cycle (Fig. 1). The reason for this was probably a result of the severity of the broncoemphysematic pathology on the left side, increased by the fact that this lung had been previously nonventilated during 68 min, which most certainly caused a slight interstitial edema, worsening the degree of stenosis of the small airways. Last, the presence of the bronchopleural air leak could explain the persistence of moderate alveolar ventilation although no ETco2 has been measured. Obviously, our patient was hypoventilated (maximum Paco2 value of 70.7 mm Hg) because of the important increase of the insufflation pressures of the left side and the subsequent decreasing of its tidal volume, but its oxygenation remained satisfactory. Finally, the right pulmonary reduction was completed in 50 min. The return to two-lung ventilation allowed the reappearance of ETco2, and the trachea could finally be extubated just after the procedure.Figure 1: ETco2 (upper curve) and airway pressure (lower curve) trends showing absence of capnogram during mechanical ventilation (small arrows) and progressive appearance of ETco2 during a period of apnea (large arrow) resulting from severe expiratory airway obstruction.In conclusion, the absence of capnographic reading in patients showing severe COPD is not an absolute indicator of no ventilation. Serge M. Broka, MD Sihem Boujlel, MD