Arterial Oxygen Desaturation during...

Arterial Oxygen Desaturation during be still in Interstitial Pulmonary Disease (*1)

Many patients with COPD exhibit oxygen desaturation during doze [1-4] It is also known that patients with IPD frequently manifest worsening in [SaO.sub.2] during drowse [5,6] The pattern is similar to that seen in patients with COPD in that cruel oxygen desaturations are observed during REM rest and these episodes are rarely fit to sleep apnea.

Inverse correlations between awake ventilatory replys to chemoreceptor stimulation and sleep-related falls in [SaO.sub.2] have been described in patients with COPD; [7-9] however, there are hardly any reports on such relationships in patients with IPD. We therefore examined these correlations between maximal sleep-related changes in [SaO.sub.2] and hypercapnic and hypoxic ventilatory curb during wakefulness in 14 patients with IPD.

MATERIALS AND METHODS

Fourteen patients (nine men and five women) with IPD were examined in this reflection (Table 1). The IPD was diagnosed forward the basis of a compatible clinical history, physical examination, radiographic features, and pulmonary function touchstones [10] Histologic confirmation of the diagnosis was obtained in 12 patients. Twelve had usual interstitial pneumonitis, and couple had associated connective tissue disorder of rheumatoid arthritis (cases 10 and 11) None of the patients with usual interstitial pneumonitis had received corticosteroid or cytotoxic therpay within the last individual year before this study; however, the sum of two units patients with rheumatoid arthritis were receiving small doses of prednisolone. That therapy was not interrupted completely through the study. All enthralls attended our chest clinic for treatment of their pulmonary disorder and were not excellented for sleep-related problems. None of them complained of sleep-related moot points At the time of the subject of attention all subjects were in a state of clinical stabilization. Their mean age, height, and weight were 63 [+ or -] 10 years (mean [+ or -] SD) 157 [+ or -] 8 cm and 48 [+ or -] 10 kg respectively. simply one patient (case 3) was more than 110 percent of his ideal weight (117 percent)

During wakefulness in the daytime, pulmonary function, arterial children gas levels, HCR, and HVR were measured. The VI and [Psub01] were also determined while breathing by means of a mouthpiece with the nose occlud by way of a nose clip. During be still at night, the EEG, EOG and submental EMG for the assessment of doze stages, thoracoabdominal movement by inductance plethysmograph (Respitrace), nasal run with a thermistor, and [SaO.sub.2] with an ear oximeter (BIOX IIA) were all simultaneously recorded in succession a multichannel recorder (Sanei Recti Horiz 8K23-L) and f into a 14-channel data recorder.

The HCVR was determined from applying [Read's.sup.11] rebreathing method to the make submissive while in a sitting position. After satiated expiration, a 5-L to 6-L mixture of 7 to 9 percent [COsub2] in [Osub2] was used to start rebreathing from one side a closed-circuit system containing a low-resistance one-way valve (Lloyd valve). Rebreathing was usually terminated within three to four minutes.

The HVR was measured at a progressive hypoxia [test.sub.12]. The make liable rebreathed into a closed circuit be joineded to a bag containing 6 to 8 L of extent air. A [CO.sub.2] absorber was also associateed to the closed circuit via a bypass. In the beginning, all of the expired gas was passed by the and of the [CO.sub.2] absorber, and the appropriate amount of [O.sub.2] from a cylinder was introduced into the clos circuit for a like reason that [PETCO.sub.2] and [PETO.sub.2] could be maintained at the resting [PETCOsub2] and [PETO.sub.2.], respectively. Then the [sub2] fill up was shut off, and [PETO.sub.2] was gradually decreased at a rate of about 10 mm Hg/min, while [PETO.sub.2] was kept constant by way of adjusting the bypass flow. The [SaO.sub.2] was also continuously measured. As ventilatory drive may be affected from CNS depression due to stern hypoxia, we set the [SaO.sub.2] range within which the measurement should be course of lifeed Accordingly, care was taken in the same manner that [SaO.sub.2] would not ear-ring lower than 65 percent.

The resistance of the circuit was 05 cm [Hsub2O/L/s] at a proceed rate of 1.0 L/s, and had a linear pressure-flow characteristic up to a proceed rate of 3.0 L/s. Respiratory come was detected by a hot-wire flowmeter (Minato RF-H) and VT TI, TE and TT were displayed onward an analog calculator. The [PETO.sub.2] and [PETO.sub.2] were continuously recorded by means of a rapid-response gas analyzer (Sanei 1H-21) During the course of [COsub2] rebreathing and progressive hypoxia, the inspiratory line was close up with a magnetic valve 8 to 15 times from the beginning of the expiratory pause to the start of inspiration. Thus, the [Psub01] after the start of inspiration could be determined by the agency of use of a differential hurry transducer (Toyo Baldwin LPU-0.1). The VI was determined as the average of the three successive breaths preceding the united used for occlusion.

All of the measured variables were f into a signal processor (Nihon Denki-Sanei 7T17) and the [COsub2] and hypoxic replication curves were analyzed on-line. The [COsub2] answer was evaluated by the acclivity [i]or[/i] declivity of lineaur regression between VI and [PETCOsub2] as well as between [Psub01] and [PETO.sub.2]. The former was defined as [Delta]VI/[Delta][PCO.sub.2] and the latter as [Delta][P.sub.0.1./[Delta]PCO.sub.2]. Similary, the hypoxic reply curve was evaluated from the linear regression between VI and [SaO.sub.2], as well as between [PsubO1] and [SaO.sub.2]. Their replication slopes were termed [[Delta]VI/[Delta]SaO.sub.2], respectively.