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We evaluated the accuracy of a new device for continuous noninvasive measurement of cutaneous Pco 2 . The Hewlett-Packard capnometer (model 47210/HA) works by means of an infrared transducer applied to the forearm over an area of skin that has been stripped of the stratum corneum. Capnometer transcutaneous carbon dioxide pressure (CPco 2 ) was compared with arterial carbon dioxide pressure (PaCO 2 ) during 60 simultaneously obtained measurements in 13 hemodynamically stable patients. Each patient was studied for 1½ to 5 hours, and a wide range of PaCO 2 values (21 to 82 mm Hg) was represented. The data show a clinically significant relationship whereby PaCO 2 = CPco 2 – 4.13, with a SE of ± 2.19 mm Hg. Clinical usefulness of noninvasive cutaneous CO 2 monitoring can be foreseen in patients whose ventilatory support is being tapered, in those with respiratory depression caused by various neuromuscular disorders, and in patients with chronic obstructive pulmonary disease and acute respiratory failure. Our results indicate that continuous transcutaneous CPco 2 measurements are safe and accurate and strongly suggest that they can be of clinical usefulness in a select group of hemodynamically stable patients.

Chronic low flow oxygen is useful therapy for patients with chronic obstructive lung disease who are crippled by hypoxemia despite optimal programs of usual respiratory care. Patients should be considered for chronic oxygen therapy who have (a) a resting Pao2 less than 55 mm Hg while breathing room air; or (b) profound tissue hypoxemia measured by mixed venous Pao2 and suggested by symptoms such as cor pulmonale and congestive heart failure; or (c) pulmonary hypertension or polycythemia even though daytime Pao2 is greater than 55 mm Hg. Arterial blood must be obtained to demonstrate hypoxemia and assess the benefits of oxygen therapy. Patients on chronic oxygen must remain under close medical supervision. There are no absolute contraindications to chronic oxygen therapy, other than refusal of the patient to quit smoking. Complications of therapy appear to be negligible. The exciting suggestion of improved prognosis in patients with chronic obstructive lung disease on oxygen therapy and the possibility of delaying the long-term sequelae of chronic respiratory failure bear careful watching in the future.

Using standard sleep techniques, we performed a placebo-controlled and randomized study to assess the effect of alcohol ingestion (2 ml/kg of body weight) on breathing and oxygen saturation during sleep. Twenty asymptomatic men volunteered for the two-night study: 11 were given a placebo on night 1, and alcohol on night 2 (group A); nine were given alcohol on night 1 and a placebo on night 2 (group B). We compared the incidence of sleep events (apnea, hypopnea and arterial oxygen disaturation) during the nights the subjects received alcohol and during the nights they received the placebo. Alcohol was associated with significant increases in the occurrence of the following: the number of sleep events (207 to 383,p less than 0.01), the events of arterial oxygen disaturation (118 to 226, p less than 0.01) and the number of apneic events (20 to 110, p less than 0.01). Alcohol had no significant effects on the number of times hypopnea occurred. Values obtained during sleep on the control night after alcohol ingestion also showed that the episodes of arterial oxygen desaturation remained statistically increased over control values before the ingestion of any alcohol (p = 0.01). These results show that in asymptomatic men alcohol ingestion increases the incidence of arterial oxygen desaturation and disordered breathing during sleep and that the increase in arterial oxygen desaturation persists for an additional night, even when no alcohol is consumed.

Twelve patients with hypoxemia associated with severe chronic obstructive pulmonary disease were treated with continuous portable oxygen therapy and have been followed up for a mean period of 25.2 months at sea level. Pulmonary function testing has revealed no further significant deterioration at long-term follow-up (17 months). After oxygen therapy was initiated, arterial carbon dioxide tension increased slightly, but decreased to pretreatment levels when patients were allowed to breathe room air. The electrocardiogram, which was unchanged at one month, has shown some reversal of cor pulmonale in five patients. Six patients have died, yielding a 56 percent survival rate at two-and-one-half years by the life table analysis. Five patients were autopsied, with possible oxygen toxicity being present in only one. The quality of life in our patients was improved and was especially represented by a reduction in hospital admissions for respiratory illness. We believe that continuous oxygen therapy is beneficial and worthwhile economically in certain patients.

Men who snore heavily have an increased incidence of hypertension, angina, stroke, and neuropsychologic dysfunction, which may be due to nocturnal oxygen desaturation. Nocturnal oxygen therapy might be beneficial to such individuals by improving oxygenation and relieving tissue hypoxia. Twenty-eight asymptomatic heavy snoring men were recruited for polysomnographic monitoring during sleep. During the first half-night, air was breathed through a nasal cannula, and during the latter half-night, 2 L/min oxygen was administered. Breathing air, 20 subjects demonstrated sleep apneas, hypopneas and nocturnal oxygen desaturation. Eighteen subjects had more than ten apneas plus hypopneas per hour. Thirteen subjects reached low oxygen saturation below 80 percent and eight below 70 percent. Only 13 of the 20 subjects showed improvement with oxygen therapy. Apneas alone were not decreased in frequency and were lengthened with oxygen therapy. Episodes of oxygen desaturation were improved by oxygen therapy and consequently, rates of hypopnea were decreased. Severe sleep apnea, hypopnea and oxygen desaturation are common in asymptomatic male snorers, and oxygen therapy is not always beneficial.

Oxygen was administered at sea level to 12 severely debilitated hypoxemic patients with chronic obstructive pulmonary disease. Arterial hypoxemia was relieved for one month by the constant administration of two liters per minute of oxygen by nasal cannula. Despite no change in measured pulmonary function, marked improvement was seen in exercise tolerance, neuropsychologic functioning, and in the ability to carry out the activities of daily living. In four patients, right-sided cardiac catheterization revealed pulmonary hypertension which did not improve when hypoxemia was relieved. Investigation of compensatory mechanisms in hypoxemia revealed decreases after oxygen therapy in hematocrit, hemoglobin, red cell 2,3-diphosphoglycerate (2,3-DPG) and speed of oxygen release from hemoglobin. The reversal of these compensatory mechanisms did not prevent the marked clinical improvement. Chronic oxygen therapy for suitably hypoxemic patients therefore appears to produce similar benefit at sea level as it has previously been reported to produce at altitude.

We assessed the effect of 30 mg of oral flurazepam on sleep-disordered breathing and nocturnal oxygen desaturation by performing a double-blind, placebo-controlled, randomized study. Asymptomatic subjects, 17 men and three women (mean age 49 years, mean weight 79 kg), were monitored for two consecutive nights. Flurazepam was given to 10 subjects on night 1 and to 10 subjects on night 2. Placebo was ingested on the other nights. Polysomnographic determinations included chest wall movement by impedance pneumography, nasal and oral airflow by thermistor probes, and continuous oxygen saturation by ear oximetry. Flurazepam was associated with significant increases in the number of sleep events (p = 0.01), episodes of apnea (p less than 0.01), and total duration of apnea (p less than 0.01). The number of episodes of hypopnea of desaturation did not significantly increase, although the degree of desaturation increased after flurazepam ingestion (p = 0.04). Total sleep time significantly increased (p = 0.04), but could not account for the increased number of events. Sleep stage distribution was minimally altered by ingestion of flurazepam.

The effects of oral medroxyprogesterone acetate (MPA) (20 mg three times daily) were assessed on sleep-disordered breathing and on arterial blood gas levels in awake patients with chronic obstructive pulmonary disease (COPD). Seventeen men and two women (mean baseline PaO2, 65 mm Hg; PaCO2, 41 mm Hg; and FEV1/FVC ratio, 48 percent) participated in a double-blind, placebo-controlled, randomized study. After an initial night of polysomnography and daytime arterial blood gas analysis, the patients were randomized to receive either MPA or an identical placebo for one month; the studies were then repeated. The alternate compound was given for an additional month, and the studies were performed a third time. MPA in awake patients was associated with an increased mean PaO2 value, reduced FaCO2, and increased pH. Although there was no significant change in the number of episodes of sleep apnea, hypopnea, desaturation, or the minimal saturation, MPA marginally decreased the number of minutes of total sleep time when oxygen saturation was less than 90 percent (p = .06). In conclusion, MPA improves oxygenation and CO2 elimination and increases the pH in awake patients with COPD, but during sleep, does not significantly affect disordered breathing and only marginally improves desaturation.

A simple, practical method is described for estimating unilateral lung function. Overall lung function is multiplied by right-left fractional perfusion estimated from a quantitative technetium ferric hydroxide macroaggregate lung scan. The calculated function attributed to the lung to be resected is then subtracted from the overall pulmonary function. The data from 13 patients indicate that the following postpneumonectomy functions can be predicted: forced vital capacity, forced expiratory one second volume, maximum voluntary ventilation, functional residual capacity, total lung capacity and diffusing capacity. The precedures described are available in most hospitals and represent a practical alternative to classic bronchospirometry, xenon radiospirometry and unilateral pulmonary artery balloon occlusion in the estimation of split lung function.

We evaluated 33 high-risk patients before pneumonectomy, all of whom had a forced expiratory volume in one second (FEV1) of less than 2.0 L before surgery. A quantitative perfusion lung scan was used to assess the right-left distribution of blood flow. A predicted postoperative FEV1 was calculated from the information on the lung scan and the preoperative FEV1. If this calculated value exceeded 800 ml, the patient was physiologically cleared for surgery up to and including a pneumonectomy. Surgery was otherwise believed to be contraindicated in the absence of studies using balloon occlusion. Perioperative mortality (less than or equal to 30 days after surgery) was found to be 15 percent (5/33). In surgery of this magnitude, we find this to be an acceptable percentage of mortality and have continued to use these simple physiologic criteria to determine whether a patient can tolerate pneumonectomy.

A case is presented of pathologically proved unilateral pulmonary edema due to uremia and blood transfusion. The lung that was spared had been denervated by a thoracic sympathectomy eight years earlier. That this denervation may have been responsible for the unilaterality of the pulmonary edema is suggested by experimental evidence supporting a neurogenic etiology of noncardiac pulmonary edema. The literature is briefly reviewed, and implications for therapy are discussed.

Oxygen desaturation occurs during sleep in many patients with chronic obstructive lung disease (COLD) and is often caused by sleep-disordered breathing (SDB). Nocturnal oxygen therapy should improve nighttime hypoxemia, but might also worsen SDB. Using standard polysomnographic techniques, we evaluated the frequency and duration of oxygen desaturation and SDB during sleep in 11 patients with stable COLD. During half of the night the patients breathed air through a nasal cannula and during the other half of the night they breathed oxygen at 2 liters per minute. Five patients had arterial lines inserted for determination of arterial blood gas levels during periods of SDB or desaturation. The ten men and one woman slept 70 minutes (52 percent of time in bed) while on air and 111 minutes (80 percent of time in bed) while on oxygen (p < 0.001). Oxygen therapy reduced the number of episodes of desaturation per hour and the time spent in desaturation. However, there was no difference between air and oxygen in episodes of SDB per hour, the duration of episodes of SDB, baseline sleeping PaCO2 or PaCO2 during episodes of desaturation or SDB. Therefore, in most patients with stable COLD, administration of oxygen at 2 liters per minute improves oxygenation, prolongs sleep, but does not adversely affect SDB.

Eighty to 100 per cent oxygen, breathed by lambs one or two weeks of age, is lethal after two to four days. Artificial ventilation did not aggravate or significantly ameliorate the pulmonary response. Lambs ventilated with air on respirators for comparable periods had no significant pulmonary damage. The cause of death of the oxygen-treated lambs was the pulmonary injury, characterized by edema. Studies of the excised lungs showed that the lesion was spotty, that the normal-appearing portions of the lung were normally distensible, and no significant alterations in pulmonary surfactant occurred. Several methods of assessment of the mechanical derangements are presented.

Four patients with diffuse pulmonary sarcoidosis were treated with alternate-day corticosteroid therapy. Prompt resolution of physiologic, radiologic and symptomatic evidence of disease occurred without significant side-effects of therapy. While corticosteroid therapy may not alter the longterm prognosis in sarcoidosis, prompt complete remission can be induced safely with an alternate day regimen. Such therapy is advised for acute, symptomatic pulmonary involvement.

The utility of the apnea index (number of apneic events per hour of sleep) in diagnosing sleep apnea syndrome is reviewed. Data from currently extant reports indicate that many otherwise normal, aging subjects may be classified as having sleep apnea syndrome based on the current diagnostic threshold of five apneic episodes per hour. A χ2 analysis suggests a relationship between age and level of sleep apnea. Several other reports indicate that use of a threshold of five apneic episodes per hour does not reliably predict increased health risk or somnolence in aging subjects. Adjustment of the apnea index, based on studies of aging normal subjects and of aging patients with sleep apnea syndrome is necessary to ensure reliable results in clinical and research applications.

Described are two patients whose initial symptom was acute respiratory failure requiring mechanical ventilation. Initially, the cause of the respiratory failure in each patient was obscure, but diaphragmatic paralysis was subsequently demonstrated fluoroscopically in each case. Further neurologic evaluation then supported the diagnosis of amyotrophic lateral sclerosis. Postmortem examination corroborated this diagnosis.

Ingestion of 2 ml/kg of 100 proof vodka before bedtime did not cause sleep-disordered breathing or nocturnal oxygen desaturation in 20 premenopausal women. These findings are opposite to the results of earlier studies of men, in which ingestion of the same amount of alcohol significantly increased these findings. Protection of young women from sleep-disordered breathing or oxygen desaturation may be related to the respiratory stimulant effects of circulating progesterone.

Seven patients with chronic obstructive lung disease (COLD) were monitored during their overnight sleep to determine the occurrence of disordered breathing and oxygen desaturation. Nasal and oral airflows were sensed by thermistor probes, chest wall movement by impedance pneumography and arterial oxygen saturation by ear oximetry. These variables were correlated with electroencephalographic and electrooculographic tracings. The subjects had a mean base line oxygen saturation of 89.2 per cent and slept an average of 218 minutes. Six of these seven subjects had one to 30 episodes of oxygen desaturation (decrease more than 4 per cent), 4 seconds to 30 minutes in duration, with declines in saturation as great as 36 per cent. In two subjects, saturation dropped to less than 50 per cent. Breathing was disordered in five of the seven subjects and included apnea and hypopnea. Subjects experienced from nine to 37 episodes of disordered breathing. Disordered breathing caused 42 per cent of the episodes of desaturation, all of which were less than 1 minute in duration. The mean maximum decline in saturation was 7.6 per cent. All episodes of desaturation lasting longer than 5 minutes occurred in rapid eye movement (REM) sleep and were not caused by disordered breathing. The mean maximal decrease in saturation was 22 per cent. This study reveals that disordered breathing is common in subjects with COLD and often causes desaturation but that it cannot explain all episodes of sleep desaturation.

Excerpt Syndromes associated with hypersomnia and sleep apnea are well established (1). Breathing may cease during light sleep and rapid-eye-movement sleep because of upper airway obstruction, cent...

The effects were assessed of ingestion of 1 ml/kg of 100 proof vodka on sleep-disordered breathing, nocturnal oxygen desaturation, and ventricular ectopy in patients with chronic obstructive pulmonary disease (COPD). Ethanol ingestion (mean blood alcohol concentration of 40 mg/dl) was associated with a significant increase in the number of premature ventricular contractions (PVCs) per night and the number of PVCs per hour of sleep-period time, but was not associated with other ventricular dysrhythmias. Ethanol also increased the number of episodes of apnea, total duration of apnea, and the number of episodes of apnea per hour of total sleep time, but there was no significant change in hypopnea or oxygen desaturation. Ethanol decreased total sleep time but did not significantly alter sleep stage distribution. This study demonstrates that moderate ethanol consumption increased ventricular ectopy and sleep apnea in patients with COPD.

Theophylline was administered as an aerosol to nine patients with known bronchospastic disease. No significant improvement in the forced expiratory volume in one second was observed after administration of aerosolized theophylline, although improvement did occur following administration of aerosolized isoproterenol. The theoretic mechanisms of bronchodilator aerosols are discussed, as well as the possible reasons for not obtaining a response with administration of theophylline.

Twenty-one postmenopausal women were monitored for sleep-disordered breathing and nocturnal oxygen desaturation to evaluate the contribution of progestational hormones to the occurrence of these sleep events. For approximately one month 11 subjects received 30 mg of medroxyprogesterone (MPG) daily, and 10 received placebo tablets in a randomized, double-blind controlled study. Respiration, saturation and electroencephalography were monitored during one night of sleep before and one night after therapy. Contrasted with the low incidence of disordered breathing and desaturation in premenopausal women, 71 percent of the postmenopausal women had such events. In the placebo-treated group, all measured variables of sleep and breathing were identical on the two nights, which suggested that the findings of a single night of sleep monitoring may be representative of other nights of sleep. Although several subjects appeared to show improvement with MPG, only the maximum duration of apnea was significantly reduced the second night (p less than 0.03).21 postmenopausal women were monitored for sleep-disordered breathing and nocturnal oxygen desaturation to evaluate the contribution of progestational hormones to the occurrence of these sleep events. For approximately one month, 11 subjects received 30 mg of medroxyprogesterone (MPG) daily, and 10 received placebo tablets in a randomized, double-blind controlled study. Respiration, saturation and electroencephalography were monitored during one night of sleep before and one night after therapy. Contrasted with the low incidence of disordered breathing and desaturation in premenopausal women, 71% of the postmenopausal women had such events. In the placebo-treated group, all measured variables of sleep and breathing were identical on the 2 nights, suggesting that the findings of a single night of sleep monitoring may be representative of other nights of sleep. Although several subjects appeared to show improvement with MPG, only the maximum duration of apnea was significantly reduced the 2nd night (p0.03). The study supports the observation that disordered breathing and desaturation are similarly frequent in postmenopausal women and in men.

Certain patients with chronic obstructive pulmonary disease may be classified as blue bloaters or pink puffers. Recent studies suggest that physiologic changes during sleep contribute to the clinical expression of these syndromes. To investigate this, we monitored four blue bloaters and six pink puffers during one night's sleep to determine the incidence of sleep disordered breathing (SDB) and of arterial oxygen desaturation. There were no significant differences between the two groups for sleep period time, awake oxygen saturation, or the number of episodes of SDB. Blue bloaters had lower baseline oxygen saturations, more episodes of arterial oxygen desaturation, and larger falls in oxygen saturation and spent more time at low levels of oxygen saturation while asleep. We propose that the degree and the duration of sleep hypoxemia of blue bloaters but not of pink puffers may contribute to early pulmonary hypertension and cor pulmonale.

Fourteen morbidly obese subjects, referred to our Institution for bypass surgery for obesity, were studied with regard to pulmonary function and respiratory patterns during sleep. The seven female patients experienced no episodes of desaturation or disordered breathing during sleep. Six of the seven male patients experienced desaturation or disordered breathing. The one who did not had hypogonadism, suggesting that testosterone may have a role in the regulation of breathing during sleep. The two patients with the most frequent episodes of apnea and lowest oxygen saturation had a clinical picture consistent with the pickwickian syndrome. This supports the relationship previously noted between the degree of hypoxia and the presence of hypersomnolence.

Eighteen asymptomatic postmenopausal women volunteered to ingest 2 ml of 100-proof vodka per kg of body weight in orange juice on one night and a placebo on another. Overnight sleep monitoring was performed immediately thereafter. Alcohol ingestion caused reduction in total sleep time from 329 to 281 minutes and a decrease in rapid eye movement sleep. There was no difference from placebo in the number of episodes of apnea or hypopnea, or in the frequency, length, or severity of oxygen desaturation. In contrast to the effects of alcohol ingestion in men, the effects on breathing and oxygenation are minimal during the sleep of women if this amount of alcohol is ingested.

Twenty patients with mild to severe chronic obstructive pulmonary disease received ultrasonic nebulization to assess the danger of short-term changes in blood gas levels during this therapy. The status of arterial oxygenation was monitored during 20 minutes of therapy and for 20 minutes following therapy. In nine patients with periodic studies of arterial blood, the mean change in arterial oxygen pressure from base line was a decrease of 0.8 mm Hg at ten minutes into therapy, 2.8 mm Hg at the conclusion of therapy, and 2.9 mm Hg 20 minutes after therapy. In all 20 patients, ear oximetric studies showed only a small mean change at ten minutes into therapy, at the end of therapy, and at 20 minutes after therapy. Changes in the status of arterial oxygenation during and after therapy with ultrasonic nebulization in a group of patients with chronic obstructive pulmonary disease are generally small and of no statistical and limited clinical significance; however, alarming falls in arterial oxygenation can occur and cannot be predicted by base-line testing of pulmonary function or studies of arterial blood. It would be prudent to monitor patients with chronic obstructive pulmonary disease during therapy with ultrasonic nebulization or to withhold therapy altogether.

Oxygen desaturation occurs during sleep in some patients with COPD. To investigate the effects of these hypoxemic episodes on the pulmonary vasculature, we studied four patients with our routine polysomnographic techniques and simultaneously recorded pulmonary artery pressure. In all four subjects, nocturnal episodes of desaturation were accompanied by elevations in the pulmonary artery pressure. Low flow oxygen abolished the drops in arterial oxygen saturation (but not the breathing abnormalities) and no elevations in the PA pressure were observed. We postulate that in some COPD patients these initially transient events may lead to sustained pulmonary hypertension and cor pulmonale. Nocturnal oxygen therapy may be indicated in more patients than previously suspected and may prevent the development of cor pulmonale.

Breathing and oxygenation were monitored in 78 asymptomatic volunteers on two successive nights of sleep. Four groups of subjects were recruited: (1) 20 young men, (2) 20 young women, (3) 20 men older than 40 years, and (4) 18 postmenopausal women. In random order, subjects ingested either 2 ml/kg (body weight) of 100-proof vodka in orange juice or a similar amount of water in orange juice before bedtime. Alcohol ingestion shortened sleep in the older men and in the postmenopausal women. No effect of alcohol ingestion on breathing or oxygenation during sleep was seen in any group of women. In men, alcohol ingestion increased the numbers of desaturation episodes and caused more severe oxygen desaturation during sleep. The effect of alcohol ingestion on breathing and oxygenation during the sleep of asymptomatic volunteers appears to be limited to men.

A new cannula with a system of intermittent nasal flow was evaluated and compared with a standard constant-flow nasal cannula in 15 patients with chronic obstructive pulmonary disease. The intermittent-demand cannula released oxygen only when a negative pressure was detected in the nose (negative mode) or when a a positive pressure ceased to be detected in the nose (positive mode). At rates of flow varying from 0.63 to 5.60 L/min, the continuous-flow mode used 9 percent more oxygen than the negative mode and 31 percent more oxygen than the positive mode to achieve comparable improvement in arterial oxygen tension. The system using the intermittent-demand cannula was sensitive and reliable in over 150 hours of testing.

We monitored arterial oxygen saturation (SaO2) in 10 patients with severe chronic obstructive lung disease during 24 h of breathing room air followed by 24 h of breathing two litres of oxygen per minute. Three subjects without chronic obstructive lung disease were monitored while breathing room air. Greatest declines in SaO2 occurred during sleep, with intermittent decreases as great as 44% saturation (range, 12% to 44% saturation. Baseline SaO2 was significantly higher while patients breathed low-flow oxygen (94% versus 86% saturated), and declines in SaO2 during sleep were less noteworthy (1% to 27% saturation). Subjects without chronic obstructive lung disease showed declines in SaO2 of much lesser magnitude (3% to 11% saturation) with sleep. These declines were not primarily due to alveolar hypoventilation. Our data indicate that there are patients with chronic airways obstruction who suffer profound intermittent desaturation at night that can readily be relieved with low-flow oxygen administration.

A patient with chronic interstitial pneumonia was treated with steroids with excellent results. Electron microscopic examination of a lung biopsy taken before treatment showed the functional defect to be associated with a gross increase in the width of the anatomic barrier to gaseous diffusion into the blood. A peculiar sudanophilic and oleophilic inclusion was identified in the cytoplasm of his alveolar macrophages, and it is postulated that this material, which is of obscure origin, was the primary lung irritant.

Continuous ambulatory oxygen therapy was administered at 2 liters per minute by nasal cannula to a study group of ten hypoxemic patients with chronic obstructive pulmonary disease (COPD). Prior to therapy, a battery of neuropsychologic and psychologic tests was administered. These were repeated after hypoxemia had been relieved for four weeks. The results were compared to similar testing performed in a less severely hypoxemic comparison group of 12 patients with an equal degree of COPD. The comparison group was tested before and after four weeks, with no change in therapy. The hypoxemic treatment group initially scored significantly lower than the comparison group in five neuropsychologic tests. With oxygen therapy, significant improvement occurred in eight of ten neurophychologic test results and in four psychologic test results. No improvement was noted in the comparison group. After oxygen therapy, the previously noted differences between the treatment and comparison groups were no longer evident. These data suggest that hypoxemia is associated with depression in neuropsychologic and psychologic functioning which can be improved with relief of hypoxemia.

A 60-year-old white man with chronic bronchitis was noted to develop acute respiratory failure and metabolic acidosis four days after being started on methazolamide (Neptazane) for an ophthalmologic problem. The patient was intubated with ventilator support and improved after his metabolic acidosis resolved. Caution is emphasized in the use of carbonic anhydrase inhibitors in patients with obstructive airway disease.