The Effects of Fiberoptic Bronchoscopy With Ad Without Atropine Prernedication on Pulmonary Function in Humans

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1 The Effects of Fiberoptic Bronchoscopy With Ad Without Atropine Prernedication on Pulmonary Function in Humans A. Neuhaus, M.D., D. Markowitz, M.D., H. H. Rotman, M.D., and John G. Weg, M.D. ABSTRACT Pulmonary function studies, including arterial blood gas analysis, were performed in 21 patients undergoing fiberoptic bronchoscopy. Eight received premedication with atropine and 13 did not. In the atropine-treated group there was no significant deterioration in pulmonary function immediately after bronchoscopy compared with baseline. Compared with the values obtained after topical lidocaine anesthesia, however, there was a decrease in peak expiratory flow rate (PEFR) (20 f 20%), forced expiratory volume in one second (FEV,.o) (11 f 12%), forced expiratory flow between 25 and 75% of vital capacity (FEF,-,,) (22 f l6%), and forced expiratory flow at 75% of exhaled vital capacity (FEF,,) (28 f 38%) and an increase in residual volume (RV) (16 f 19%). In the no-atropine group, postbronchoscopy values showed a decrease in PEFR (13 f 19%), forced vital capacity (FVC)(13 f 19%), FEV,., (14 f l6%), and oxygen partial pressure (Pao,) (11* 9%) and an increase in RV (19 f 31%) and alveolar-arterial oxygen pressure gradient (AAaPq) (91 f 129%) compared with baseline values. In this group also, topical lidocaine anesthesia resulted in a decrease in FVC compared with baseline. We conclude that the deleterious effect of bronchoscopy on pulmonary function is counterbalanced by the beneficial effect of atropine and that atropine is therefore a useful premedication for fiberoptic bronchoscopy. Fiberoptic bronchoscopy is widely employed to diagnose and treat a variety of pulmonary disorders. Its safety has been well established, and only a few relative contraindications exist [5,18, From the Pulmonary Division, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor, MI. Supported in part by National Heart and Lung Institute Pulmonary Academic Award No Accepted for publication Sept 23, Address reprint requests to Dr. Rotman, Pulmonary Division, University Hospital, Ann Arbor MI In one recent report 1191, the procedure produced reversible increased airway obstruction in patients with underlying chronic obstructive pulmonary disease, but not in normal controls who underwent the same procedure. This increase in airway obstruction was attributable to the procedure itself since topical lidocaine anesthesia (TLA) alone had no deleterious effects. In addition, a decrease in arterial oxygen tension (Pao,) has been observed with fiberoptic bronchoscopy as well as with TLA [l, 191. This decrease in PaOz has been attributed to ventilatiodperfusion inequality, but its relationship to any observed changes in pulmonary mechanics has not been studied. Atropine has been employed for many years as a premedication for bronchoscopy and fiberoptic bronchoscopy [14, 171 to prevent vagally mediated bradycardia and to decrease bronchial secretions. Because atropine is also known to block the vagally mediated bronchoconstriction that results from irritation of the airway, and to have a potent bronchodilator effect, its use in bronchoscopy has important practical implications completely apart from its cardiac effects [ZO]. The purpose of this study was to measure the influence of fiberoptic bronchoscopy on pulmonary mechanics and to determine whether premedication with atropine altered these effects. In addition, the effects of fiberoptic bronchoscopy on arterial blood gases were measured, and an attempt was made to correlate any alterations with changes in pulmonary mechanics. Methods Clinically stable patients who were to undergo fiberoptic bronchoscopy and who were physically and mentally able to perform pulmonary function tests were selected, and informed con by A. Neuhaus

2 394 The Annals of Thoracic Surgery Vol 25 No 5 May 1978 sent was obtained. Twenty-one patients were randomly allocated to one of two groups, one to receive atropine intramuscularly and the other, no premedication, The dose of atropine administered, 1.2 mg, inhibits secretions in the respiratory tract 1111, increases heart rate [ll], and induces bronchodilation All patients had baseline spirometry and flow-volume loops using the Systems Research Laboratory (SRL) Model MlOOB Automated Pulmonary Function Laboratory. In addition, plethysmography was performed using an Ohio 3000 plethysmograph 163. The following measurements were made: forced vital capacity (FVC), forced expiratory volume in one second (FEV,.,), peak expiratory flow rate (PEFR), forced expiratory flow between 25 and 75% of vital capacity (FEFz5-75), forced expiratory flow at 75% of exhaled vital capacity (FEF,,), residual volume (RV), and specific airway resistance (SRaw). Thirteen of the 21 patients had an indwelling arterial cannula inserted prior to the study, and arterial blood Pa%, carbon dioxide partial pressure, and ph were measured with the Radiometer Model 27 ph meter and appropriate electrodes, and the alveolar-arterial oxygen pressure gradient (daapoz) was calculated. These measurements were obtained at baseline, 15 minutes after the administration of atropine, immediately after fiberoptic bronchoscopy, and 4 and 24 hours later. The usual time period between administration of atropine and fiberoptic bronchoscopy was 45 minutes. The paired Student t test was used to evaluate differences following each interventionlidocaine, atropine, and fiberoptic bronchos- COPY. For comparison with normal controls, published values for PaOz [21], AAaPoz [15], SRaw 1101, RV 141, PEFR [8], FEF75 [31, FVC [9, 131, FEV,., [9,131, and FEF,,-,, [161 were employed. Material A total of 21 patients were in the study: 14 men and 7 women. The mean age for the group was 52 years (range, 18 to 72 years). The atropine-treated group had 8 patients, 5 of whom were smokers. Only 2 smokers had a history consistent with chronic bronchitis characterized by cough and sputum production. Of these 8 patients, 3 had either normal pulmonary function or only mild airway obstruction (FEV,.,/FVC > 70%). The other 5 had moderate or severe obstruction (FEV,.,/FVC < 70%). The group not receiving atropine had 13 patients, of whom 10 were smokers. Of the smokers, 5 had a history consistent with chronic bronchitis. Four of the 13 patients were normal or had only mild airway obstruction, and the rest had moderate to severe obstruction. There was no statistical difference between the two groups in baseline pulmonary function tests. Results Atropine-treated Group Intramuscular atropine caused a statistically significant improvement in the following measurements: FEFZ,-,, (24 f 33%; p < 0.05); FEF,, (36 f 39%; p < 0.025); and SRaw (-15 f 20%; p < 0.05) (Table 1). The figures represent mean percent change from baseline f one standard deviation. TLA had no deleterious effects on pulmonary function tests. When the postbronchoscopy values were compared with baseline, there were no significant differences in any of the measurements. However, when the effects of fiberoptic bronchoscopy were assessed by comparing values after this procedure with those after TLA, fiberoptic bronchoscopy had caused a significant deterioration in the following: PEFR (20 k 20%; p < 0.025); FEV,.o (11 f 12%; p < 0.01); FEFZ5-,, (22 f 16%;~ < 0.005); FEF75 (28 f 38%;~ < 0.05); and RV (16 f 19%; p < 0.05). At 4 and 24 hours after fiberoptic bronchoscopy, the values were not significantly different from baseline. Blood gas data showed that baseline P%, was 76 f 5 mm Hg, and there was no change after atropine was administered. No-Atropine Group After TLA there was an 8 f 9% decrease from baseline in FVC (p < 0.05), but no other measurements were significantly changed. Compared with baseline, the postbronchoscopy values showed a decrease in the following measurements: PEFR (13 f 19%;~ < 0.005); FVC (13 f 19%; p < 0.001); FEV,., ( %; p <

3 395 Neuhaus et al: Effects of Fiberoptic Bronchoscopy on Pulmonary Function Table 1. Pulmonary Function Values: Comparison with Normal and Percent Change from Baseline in the Group Receiving Atropine Mean Percent Change from Baseline f SD Mean Percent Determination Baseline f SD Predicted f SD After Atropine After TLA After FB PEFR (Llsec) 412 f f f f f 25.7 Fvc f f f f 19.7 FEVI.0 (L) 2.68 f & f & f 26.4 FEF25-75 (Llsec) 132 f f f f f 41.8 FEF,, (Llsec) 52 f f f f f 53.8 RV (L) 2.45 f f f f f 31.3 SRaw (sec cm HzO) 10.2 f f f f f 27.8 Pao* (mm Hg) 76 f 5 91 f f f f 13.0 AAaPo2 (mm Hg) 22 f f f f f 14.7 TLA = topical lidocaine anesthesia; PEFR = peak expiratory flow rate; FVC = forced vital capacity; FEV,,, = forced expiratory volume in one second; FEF2,_,, = forced expiratory flow between 25 and 75% of vital capacity; FEF,, = forced expiratory flow at 75% of exhaled vital capacity; RV = residual volume; SRaw = specific airway resistance; Pao, = oxygen pressure; h apq = alveolar-arterial oxygen tension gradient. Table 2. Pulmonary Function Values: Comparison with Normal and Percent Change from Baseline in the Group Not Receiving Atropine Mean Percent Change from Baseline f SD Mean Percent Determination Baseline f SD IJredicted f SD After TLA After FB PEFR (Llsec) 295 f f f f 19.0 Fvc (L) 3.19 f f f f 18.6 FEVI." (L) 1.97 f f f f 16.5 FEF,,-,, (Llsec) 84 k f f f 24.8 FEF,, (L/sec) 39 k f f k 27.7 RV (L) 2.70 k f f f 31.2 SRaw (sec cm HzO) 21.4 k k f f 54.2 Paop (mm Hg) 78 f f f f 9.3 AAaPo, (mm Hg) 19 k k f f Abbreviations same as for Table ); and Pa- (11 f 9%; p < 0.05). There was an increase in RV (19 k 31%; p < 0.025) and in hapo, (91 f 129%; p < 0.025) (Table 2). At 4 and 24 hours after TLA, all values had returned to baseline levels. Comment The bronchodilator effects of atropine have been known for some time, but the fear of drying up bronchial secretions delayed its clinical application. However, recent studies [12, 231 indicate both the effectiveness and safety of atropine as a bronchodilator in a group of patients with chronic bronchitis and in asthmatic children. The use of atropine as premedication for fiberoptic bronchoscopy is commonly advocated to reduce bronchial secretions and to prevent bradycardia, but proof of its effectiveness is not advanced in the same reports [2, 71. The present study demonstrates the bronchodilator effect of atropine. The drug improved all indicators studied, with the FEF25-75, FEF,,, and SRaw values achieving statistical significance.

4 396 The Annals of Thoracic Surgery Vol 25 No 5 May r w 2 v) 12k $ 8 L $ 4 i-121 l, o No Atropine 9 *Statistically significant LL -16 change from baseline BASE POST POST POST 4HOURS 24HOURS ATROPINE LlDOCAlNE BRONMS- COPY Fig I. Mean percent change in forced vital capacity from baseline with time. Although no formal attempt was made to quantify the amount of bronchial secretions, the physicians performing the bronchoscopies were unable to detect any differences in the bronchial secretions between the two groups. However, the patients not receiving atropine had copious mouth secretions, which required frequent suctioning. These mouth secretions were managed without difficulty, and the procedure was carried out in all instances in the usual manner. One previous report [19] indicated that TLA had no effect on pulmonary mechanics. Except Fig2. Mean percent change in peak expiratoryflow rate from baseline with time. for a decrease in FVC, it produced no adverse effect in our study. Fiberoptic bronchoscopy deleteriously affects pulmonary function, and this was seen in both groups of patients. The beneficial effects of atropine on pulmonary function were approximately equal in magnitude to the deleterious effects of fiberoptic bronchoscopy, and thus the net effect of premedication with atropine followed by fiberoptic bronchoscopy resulted in no overall significant alteration from baseline. These changes were observed only through pulmonary function testing. No patient suffered any major adverse effects, but most patients had a mild cough and complained of soreness in the nasopharynx. It is believed that fiberoptic bronchoscopy causes deterioration in pulmonary mechanics

5 397 Neuhaus et al: Effects of Fiberoptic Bronchoscopy on Pulmonary Function I6 - W z m. i% 8- H LL 4: g 0- Q - I 0-4- I - - Z a :. w a W LL 0 Atropine o No Atropine * Statistically significant change from baseline 1 I BASE POST POST POST 4HOURS 24HOURS ATROPINE LlDOCAlNE BRONCHOS- COPY it Fig 3. Mean percent change in forced expiratory volume in one second from baseline with time. through direct activation of cough and irritative reflexes in the airway and perhaps through the development of mucosal edema. These changes are short-lived since at 4 and 24 hours after the procedure, all patients were essentially back to baseline levels. Figures 1, 2, 3, and 4 illustrate the longitudinal changes observed for the two groups in the measurements of FVC, PEFR, FEV,.,, and RV. Atropine improved these measurements, and, with the exception of a fall in FVC, no further effects were noted after TLA. Although fiberop- Fig 4. Mean percent change in residual volume from baseline with time. w g 20[ 16 0 Atropine o No Atropine * Statistically significant > -12 change from baseline a BASE POST POST POST 4 HOURS 24HOURS ATROPINE LlDOCAlNE BRONCHOS- COPY tic bronchoscopy deleteriously affected pulmonary function in both groups, atropine counterbalanced its negative effects, so that the net change from baseline was not significant. Several reports [l, 2,71, which include the use of atropine in doses lower than those used in this study, indicate that transient hypoxemia is common after fiberoptic bronchoscopy. Our study confirms this finding in the group not receiving atropine. However, the values for ho, and AAaPo, in the patients receiving atropine were not significantly different from baseline levels. This suggests a further protective effect of atropine. Using the coefficient of concordance, we were unable to demonstrate any statistical correlation between changes in Pa% and the changes in pulmonary mechanics in this group of 21 patients. Based on these data, we conclude that atropine has a useful role as a premedication for fiberoptic bronchoscopy, and we currently use it routinely on our bronchoscopy service. Its efficacy would be most marked in patients with reactive airway or in those with severely compromised pulmonary function in whom any further deterioration might be poorly tolerated. References 1. Albertini RE, Harrell JH, Kurihara N, et al: Arterial hypoxemia induced by fiberoptic bronchoscopy. JAMA 230:1666, Albertini RE, Harrell JH, Moser KM: Management of arterial hypoxemia induced by fiberoptic bronchoscopy. Chest 67:134, 1975

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