The stability of individual patterns of autonomic responses to motion sickness stimulation.

As part of a program to develop a treatment for motion sickness based on self-regulation of autonomic nervous system (ANS) activity, this study examined the stability of an individual's pattern of ANS responses to motion sickness stimulation on repeated occasions. Motion sickness symptoms were induced in 58 people during 2 rotating chair tests. Physiological responses measured were heart rate, finger pulse volume, respiration rate, and skin conductance. Using standard scores, we examined stability of responses of specific magnitudes across both tests. Correlational analyses, analysis of variance, and a components of variance analysis all revealed marked, but quite stable, individual differences in ANS responses to both mild and severe motion sickness. These findings confirm our prior observation that people are sufficiently unique in their ANS responses to motion sickness provocation to make it necessary to individually tailor self-regulation training. Further, these data support our contention that individual ANS patterns are sufficiently consistent from test to test so as to serve as an objective indicator of individual motion sickness malaise levels.

Effect of aging on estimates of hypercapnic ventilatory response during sleep.

By recording only inspired PCO2 (PICO2) in a hood and transcutaneous PCO2 (PsCO2) the Hazinski method was used to estimate nonintrusively the slope (Sr) per Torr PsCO2 of the fractional ventilatory response to approximately 18 and 30 Torr PICO2 in 17 healthy elderly subjects (10 women) and 17 younger controls (9 women) during wakefulness, slow-wave sleep (SWS), and rapid-eye-movement (REM) sleep. Eight of the older subjects had sleep disturbance indexes (RDI) greater than 5. Sr fell with SWS from 0.90 +/- 0.34 to 0.60 +/- 0.29 (P less than 0.006) in the younger group (n = 16) but in the older subjects was 0.60 +/- 0.27 awake and 0.58 +/- 0.34 (NS) asleep (n = 15). The changes from awake to REM in subsets of 9 younger and 10 older subjects who successfully completed REM tests were from 0.95 +/- 0.32 to 0.70 +/- 0.38 (P less than 0.03) and 0.53 +/- 0.31 to 0.57 +/- 0.25 (NS), respectively. We conclude that the increased incidence of respiratory disturbance during sleep in these older subjects cannot be attributed to greater sleep-induced reduction of CO2 sensitivity.

Errors in 14 pulse oximeters during profound hypoxia.

The accuracy of pulse oximeters from fourteen manufacturers was tested during profound brief hypoxic plateaus in 125 subject sets using 50 normal adult volunteers, of whom 29 were studied two to nine times. A data set usually consisted of 10 subjects, and 13 sets were collected between August 1987 and July 1988. In the first 6 sets, six 30-second hypoxic plateaus were obtained per subject at 55 +/- 6% oxyhemoglobin (O2Hb) (range, 40 to 70%). In the last 7 sets, three hypoxic plateaus were obtained at each of four levels, approximately 86, 74, 62, and 50% O2Hb, for the purpose of linear regression analysis. Inspired oxygen was adjusted manually breath by breath in response to arterial oxygen saturation computed on-line from end-tidal oxygen and carbon dioxide tensions. End-plateau arterial blood O2Hb was analyzed by a Radiometer OSM-3 oximeter, and plateau pulse oximeter saturation (SpO2) was read by cursor from a computer record of the analog output. Three to 13 instruments were tested simultaneously by using 1 to 3 duplicate instruments from each of one to seven manufacturers. Variations introduced by manufacturers were tested on subsequent sets in several instruments. An index of error, "ambiguity" (alpha) of oxygen saturation, was defined as the absolute sum of bias and precision (mean and SD of SpO2 - O2Hb) at O2Hb = 55.8 +/- 4.5%, preserving the sign when bias was significant at P less than 0.05. Ambiguity values for finger probes (unless specified) with latest data were: Physio-Control, 3.9 (ear, 3.3); Puritan-Bennett, -4.4; Criticare, 5.8 (forehead, 4.7); Kontron, 5.9 (infant probe) and 6.1 (ear, 5.8; forehead, 7.1); Biochem, -6.0; Datex 6.4 (ear, 6.9; forehead, 6.8); Critikon, 8.4; SiMed, 8.6; Marquest, 9.0; Novametrix, 10.2; Invivo, -12.2 (ear, -14.3); Nellcor, -15.1; Ohmeda, -21.2; and Radiometer, -21.2 (ear, -9.6). Linear regression slopes of 36 instruments from twelve manufacturers generally deviated from 1 in proportion to alpha. The data showed substantial differences in bias and precision between pulse oximeters at low saturations, the most common problems being underestimation of saturation and failing precision.

Validation of a maskless CO2-response test for sleep and infant studies.

The Hazinski method is an indirect, noninvasive, and maskless CO2-response test useful in infants or during sleep. It measures the classic CO2-response slope (i.e., delta VI/delta PCO2) divided by resting ventilation Sr = (VI''--VI')/(VI'.delta PCO2) between low (')- and high ('')-inspired CO2 as the fractional increase of alveolar ventilation per Torr rise of PCO2. In steady states when CO2 excretion (VCO2') = VCO2'', Hazinski CO2-response slope (Sr) may be computed from the alveolar exchange equation as Sr = (PACO2'--PICO2')/(PACO2'--PICO2'') where PICO2 is inspired PCO2. To avoid use of a mask or mouthpiece, the subject breathes from a hood in which CO2 is mixed with inspired air and a transcutaneous CO2 electrode is used to estimate alveolar PCO2 (PACO2). To test the validity of this method, we compared the slopes measured simultaneously by the Hazinski and standard steady-state methods using a pneumotachograph, mask, and end-tidal, arterial, and four transcutaneous PCO2 samples in 15-min steady-state challenges at PICO2 23.5 +/- 4.5 and 37 +/- 4.1 Torr. Sr was computed using PACO2 and arterial PCO2 (PaCO2) as well as with the four skin PCO2 (PSCO2) values. After correction for apparatus dead space, the standard method was normalized to resting VI = 1, and its CO2 slope was designated directly measured normalized CO2 slope (Sx), permitting error to be calculated as Sr/Sx.(ABSTRACT TRUNCATED AT 250 WORDS)

Accuracy of response of six pulse oximeters to profound hypoxia.

Oxygen saturation, SpO2%, was recorded during rapidly induced 42.5 +/- 7.2-s plateaus of profound hypoxia at 40-70% saturation by 1 or 2 pulse oximeters from each of six manufacturers (NE = Nellcor N100, OH = Ohmeda 3700, NO = Novametrix 500 versions 2.2 and 3.3 (revised instrumentation), CR = Criticare CSI 501 + version .27 and version .28 in 501 & 502 (revised instrumentation), PC = PhysioControl Lifestat 1600, and MQ = Marquest/Minolta PulseOx 7). Usually, one probe of each pair was mounted on the ear, the other on a finger. Semi-recumbent, healthy, normotensive, non-smoking caucasian or asian volunteers (age range 18-64 yr) performed the test six to seven times each. After insertion of a radial artery catheter, subjects hyperventilated 3% CO2, 0-5% O2, balance N2. Saturation ScO2, computed on-line from mass spectrometer end-tidal PO2 and PCO2, was used to manually adjust FIO2 breath by breath to obtain a rapid fall to a hypoxic plateau lasting 30-45s, followed by rapid resaturation. Arterial HbO2% (Radiometer OSM-3) sampled near the end of the plateau averaged 55.5 +/- 7.5%. ScO2% (from the mass spectrometer) and SaO2% (from pH and PO2, by Corning 178) differed from HbO2% by + 0.2 +/- 3.6% and 0.4 +/- 2.8%, respectively. The mean and SD errors of pulse oximeters (vs. HbO2%) were: (table; see text) The plateaus were always long enough to permit instruments to demonstrate a plateau with ear probes, but finger probes sometimes failed to provide plateaus in subjects with peripheral vasoconstriction. Nonetheless, SpO2 read significantly too low with finger probes at 55% mean SaO2.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of aging on sleep-related changes in respiratory variables.

Several respiratory variables were examined in 11 healthy elderly (greater than 60 years) and 12 younger (30-39 years) control subjects during all-night sleep runs, with a view to determining the effect of the aging process on breathing during sleep. O2 saturation, end-tidal PCO2, and transcutaneous PCO2 were monitored, together with standard sleep staging measures. Estimates of tidal volume (Vt) and ventilation (Ve) were obtained using a Respitrace inductive plethysmography system, from which respiratory rate (fb) was also measured. Older subjects had more sleep apnea/hypopnea than younger subjects, an incidence of 55 versus 8%, respectively. More of their arousals were associated with respiratory disturbance than those of the younger subjects, and they had more brief, but not longer, arousals. Mean O2 saturation was lower in older subjects during wakefulness but did not decrease more in older subjects than in control subjects during sleep. Mean end-tidal/transcutaneous PCO2 did not differ between groups during wakefulness or sleep. Vt and Ve estimates did not decrease during slow wave sleep in older subjects as they did in the younger subjects. It was concluded that aging by itself does not significantly alter average sleep-related changes in O2 saturation or PCO2, although the increased incidence of respiratory disturbance does produce transient swings in these variables. The lack of a decrease in ventilation estimates during sleep in spite of the usual changes in O2 saturation and PCO2 in the older group indicates a possible decrease in effective gas exchange.

Biofeedback of alveolar carbon dioxide tension and levels of arousal.

This is a preliminary study designed to investigate the potential usefulness of alveolar (lung) CO2 feedback training in promoting sleep onset in primary insomniacs. The present study was undertaken to determine if normal subjects could, without obvious manipulation of breathing, bring alveolar (lung) CO2 tension under voluntary control using biofeedback techniques and, if so, whether this control would be accompanied by shifts in level of wakefulness. Subjects participated in five baseline and five training sessions in which EEG, alveolar CO2 tension, and thoracic/abdominal respiratory movement were monitored. The feedback consisted of a pitch-modulated tone plus visual scores. We found that CO2 tension in awake portions of "up" trials was significantly higher than for awake portions of "down" trials (p less than .01), indicating that learning had occurred. In the initial trials, when subjects raised CO2 tension they became drowsy and often fell asleep, and when they lowered CO2 tension they aroused themselves. However, when subjects were awakened immediately upon falling asleep, there developed a decoupling of EEG and CO2 changes. The presence of such a decoupling phenomenon makes it unclear whether CO2 feedback will be useful in promoting sleep onset in primary insomniacs.

The nature of respiratory changes associated with sleep onset.

This study provides a systematic examination of factors that may contribute to respiratory changes associated with sleep onset. The electroencephalogram, alveolar CO2 tension, patterns of abdominal and thoracic respiratory movements, and respiratory rate were measured in three sessions each on 12 normal subjects as they fell asleep, and also on 5 of them as they lay awake. Nonintrusive respiration measurement devices were used. Resting awake CO2 tension was found to increase significantly across sessions. In addition, CO2 tension was significantly higher during stages 1 and 2 of sleep than during wakefulness on days 2 and 3. There was also a shift from relatively greater abdominal expansion toward relatively greater thoracic expansion with sleep onset. None of these changes occurred when subjects remained awake during a session. We conclude that changes in respiration with sleep onset cannot be accounted for solely by changes due to habituation, merely lying quietly, or the effects of the measuring devices. Rather, they appear to be caused by a central interaction between centers controlling the level of wakefulness and those controlling respiration.