Ear Oximetry Research Articles

Sex-Specific Effects of Respiratory Muscle Endurance Training on Cycling Time Trial Performance in Normoxia and Hypoxia.

Objectives: We tested the hypotheses that respiratory muscle endurance training (RMET) improves endurance cycling performance differently in women and men and more so in hypoxia than in normoxia.Design: A prospective pre–post cross-over study with two testing conditions.Methods: Healthy and active women (seven, 24 ± 4 years, mean ± standard deviation [SD]) and men (seven, 27 ± 5 years) performed incremental cycling to determine maximum oxygen consumption (VO2peak) and power output (Wpeak) and on different days two 10-km cycling time trials (TTs) in normoxia and normobaric hypoxia (FiO2, 0.135, ~3,500 m equivalent), in a balanced randomized order. Next they performed supervised RMET in normoxia (4 weeks, 5 days/week, 30 min/day eucapnic hyperpnea at ~60% predicted maximum voluntary ventilation) followed by identical post-tests. During TTs, heart rate, ear oximetry reading, and Wpeak were recorded.Results: The VO2peak and Wpeak values were unchanged after RMET. The TT was improved by 7 ± 6% (p < 0.001) in normoxia and 16 ± 6% (p < 0.001) in hypoxia. The difference between normoxic and hypoxic TT was smaller after RMET as compared with that before RMET (14% vs. 21%, respectively, p < 0.001). All effects were greater in women (p < 0.001). The RMET did not change the heart rate or ear oximetry reading during TTs.Conclusion: We found a greater effect of RMET on cycling TT performance in women than in men, an effect more pronounced in hypoxia. These findings are congruent with the contention of a more pronounced performance-limiting role of the respiratory system during endurance exercise in hypoxia compared with normoxia and more so in women whose respiratory system is undersized compared with that of men.

Accuracy and precision of pulse oximeter at different sensor locations in patients with heart failure.

BackgroundDespite its wide use in clinical practice, few studies have assessed the role of pulse oximetry in patients with heart failure. We aimed to evaluate the accuracy and precision of the pulse oximeter in patients with heart failure and to determine this accuracy at three different sensor locations.MethodsComparison of pulse oximetry reading (SpO2) with arterial oxygen saturation (SaO2) was reported in 3 groups of patients with heart failure (HF); those with ejection fraction (EF) >40%, those with EF <40%, and those with acute HF (AHF) with ST and non-ST segment elevation acute myocardial infarction (STEMI and non-STEMI).ResultsA total of 235 patients and 90 control subjects were enrolled. There were significant differences in O2 saturation between control and patients’ groups when O2 saturation is measured at the finger and toe, but not the ear probes; p=0.029, p=0.049, and 0.051, respectively. In HF with EF>40% and AHF with O2 saturations >90%, finger oximetry is the most accurate and reliable, while in HF with EF<40% and in patients with AHF with O2 saturations <90%, ear oximetry is the most accurate.ConclusionPulse oximetry is a reliable tool in assessing oxygen saturation in patients with heart failure of different severity. In HF with EF>40% and in AHF with O2 saturations >90%, finger oximetry is the most accurate and reliable, while in HF with EF<40% and in patients with AHF with O2 saturations <90%, ear oximetry is the most accurate. Further studies are warranted.

Peripheral chemoresponsiveness during exercise in male athletes with exercise‐induced arterial hypoxaemia

What is the central question of this study? Do highly trained male endurance athletes who develop exercise-induced arterial hypoxaemia (EIAH) demonstrate reduced peripheral chemoresponsiveness during exercise? What is the main finding and its importance? Those with the lowest arterial saturation during exercise have a smaller ventilatory response to hypercapnia during exercise. There was no significant relationship between the hyperoxic ventilatory response and EIAH. The findings suggest that peripheral chemoresponsiveness to hypercapnia during exercise could play a role in the development of EIAH. The findings improve our understanding of the mechanisms that contribute to EIAH. Exercise-induced arterial hypoxaemia (EIAH) is characterized by a decrease in arterial oxygen tension and/or saturation during whole-body exercise, which may in part result from inadequate alveolar ventilation. However, the role of peripheral chemoresponsiveness in the development of EIAH is not well established. We hypothesized that those with the most severe EIAH would have an attenuated ventilatory response to hyperoxia and hypercapnia during exercise. To evaluate this, on separate days, we measured ventilatory sensitivity to hyperoxia and separately hypercapnia at rest and during three different exercise intensities (25, 50% of and ventilatory threshold (∼67% of )) in 12 males cyclists ( =66.6±4.7mlkg-1 min-1 ). Subjects were divided into two groups based on their end-exercise arterial oxygen saturation (ear oximetry, ): a normal oxyhaemoglobin saturation group (NOS, =93.4±0.4%,n=5) and a low oxyhaemoglobin saturation group (LOS, =89.9±0.9%, n=7). There was no difference in (66.4±2.9vs.66.8±6.0mlkg-1 min-1 , respectively, P=0.9), peak ventilation during maximal exercise (182±15vs.197±32lmin-1 , respectively, P=0.36) or ventilatory response to hyperoxia (P=0.98) at any exercise intensity between NOS and LOS groups. However, those in the LOS group had a significantly lower ventilatory response to hypercapnia (P=0.004, (η2 =0.18). There was also a significant relationship between the mean hypercapnic response and end-exercise (r=0.75, P=0.009) but not between the mean hyperoxic response and end-exercise (r=0.21, P=0.51). A blunted hypercapnic ventilatory response may contribute to EIAH in highly trained men due to a failure to increase ventilation sufficiently to offset exercise-induced gas exchange impairments.

Patent Foramen Ovale Screening by Ear Oximetry in Divers

The aim of this study was to test the hypothesis that ear oximetry immediately after the release of a sustained Valsalva maneuver accurately detects patent foramen ovale (PFO). One hundred sixty-five scuba divers underwent transesophageal echocardiography (TEE; reference method) for PFO assessment. Ear oximetry of the right earlobe was performed in a different room within a time frame of 2 hours before or after TEE. The subject and the oximetry operator were unaware of the results of TEE. Oxygen saturation (SO(2)) measurements were obtained at baseline and during the release phase of 4 Valsalva maneuvers within 10 minutes, and the average SO(2) change (SO(2) at baseline minus SO(2) at Valsalva release) was determined as the primary study end point. One hundred seventeen divers had no PFO, and 48 (29%) had PFO by TEE (mean age 39 ± 8 years). The average SO(2) change was 0.79 ± 1.13% (i.e., a slight absolute SO(2) decrease in response to the Valsalva maneuver) in the group without PFO and 1.67 ± 1.19% in the PFO group (p <0.0001). Using receiver-operating characteristic curve analysis, a PFO as defined by TEE could be detected at a threshold of a Valsalva-induced decrease in SO(2) of ≥0.825 percentage points in comparison to baseline (sensitivity 0.756, specificity 0.706, area under the receiver-operating characteristic curve 0.763, p <0.0001, negative predictive value 0.882). In conclusion, the entirely noninvasive method of ear oximetry in response to repetitive Valsalva maneuvers is accurate and useful as a screening method for the detection ofa PFO, as shown in this study of divers.

Fibrinolytic Activity and Platelet Function in Subjects with Obstructive Sleep Apnoea and a Patent Foramen Ovale: Is There an Option for Prevention of Ischaemic Stroke?

Obstructive sleep apnoea (OSA) carries an increased risk of ischaemic stroke, but the underlying mechanism is not clear. As right-to-left shunting can occur through a patent foramen ovale (PFO) during periods of apnoea, we investigated nocturnal changes in fibrinolytic activity and platelet function in subjects who had OSA with or without PFO and in controls. We determined plasminogen activator inhibitor 1 (PAI-1) activity and antigen and platelet activation parameters. The severity of OSA was verified by polygraphy and PFO was detected by ear oximetry. We found a higher PAI-1 activity and antigen and a lower ratio of 2,3-dinor-PGF1α to 2,3-dinor-TXB2 in the subjects with OSA than in the controls. Linear regression analysis showed the apnoea-hypopnoea index (β-coefficient, 0.499; P = 0.032) and PFO (β-coefficient, 0.594; P = 0.015) to be associated independently with PAI-1 activity in the morning, while the increment in PAI-1:Ag from evening to morning was significantly associated with the presence of PFO (rs = 0.563, P = 0.002). Both OSA and PFO reduce fibrinolytic activity during nocturnal sleep. We hypothesize that subjects having both OSA and PFO may develop a more severe prothrombotic state during sleep than those having either OSA or PFO alone.

Tissue and Arterial Oxygen Saturation During Exercise of Varying Intensity in Asthmatic Subjects

PURPOSE: Previous research suggests that respiratory and limb muscles compete for blood flow during heavy exercise in normal subjects (Harms et al., J Appl. Physiol. 82:1573–83, 1997). Our aim was to characterize the effects of exercise of varying intensity upon limb and respiratory muscle oxygen saturation during exercise in individuals with asthma, where inspiratory muscle work may be elevated as a consequence of hyperinflation. METHODS: Fourteen asthmatic subjects to undertake 3 separate exercise tests. Peak power (PP) output was determined during a continuous incremental ramp test on a cycle ergometer. On a separate occasion, graded submaximal exercise was undertaken at 20, 30, 40, and 50% of PP (3 min stages). The final test was at 70% of PP to the limit of tolerance (Tlim). Near-infrared spectroscopy (NIRS) recorded local tissue oxygenation continuously; the optodes were placed on the vastus lateralis (VL) of the subjects left leg, and at the 6th intercostals (IC). Mean NIRS values were determined for the last min of each stage in the submaximal test, for each min of the Tlim test during the 1st 5 min and at Tlim isoendpoint. Arterial O2 saturation (SaO2) was measured each minute by ear oximetry. RESULTS: During the submaximal test, there was no significant (p>0.05) decline in SaO2 or change in deoxy-hemoglobin (deoxy-Hb) in the VL or IC, but there was a significant increase (p<0.05) in total hemoglobin content (THC) and oxy-hemoglobin (HbO) at the end of the 50% PP stage in the VL. During the Tlim test there was a significant decrease (p<0.05) in SaO2 at all time points. There was a significant increase (p<0.05) in THC at the VL at the endpoint of the Tlim test, but no significant differences (P<0.05) were found for HbO. Deoxy-Hb was higher at min 3, 4, 5 and the isoend in the VL and the IC in the Tlim test. There was no significant change (p>0.05) in THC at the IC, but a significant decrease in HbO. CONCLUSION: These data confirm that during submaximal exercise there is an increase in blood flow to the active VL with no change in blood flow to the IC. During the high intensity exercise of the Tlim test, oxygen extraction increased in the VL and IC.

Lateral Decubitus Position Generates Discomfort and Worsens Lung Function in Chronic Heart Failure

Lateral decubitus position is poorly tolerated by heart failure patients. To evaluated pulmonary function and lung diffusion in heart failure patients in the following five body positions: sitting, prone, supine, and left and right decubitus. Heart failure unit of a university hospital. We studied 14 chronic heart failure patients in New York Heart Association class III and 14 healthy volunteers. After 15 min of a selected position, subjects were evaluated by a discomfort scale, ear oximetry, and pulmonary function, which included FEV1, FVC, vital capacity (VC), alveolar volume, and diffusing capacity of the lung for carbon monoxide (D(LCO)) with subcomponent membrane resistance (DM) and capillary volume. In healthy subjects, we observed a reduction of D(LCO) and capillary volume in both lateral decubiti. Some discomfort was documented in both lateral decubiti when selected positions were compared with the sitting position. In the sitting position, pulmonary function suggested slight restriction ([mean +/- SD] FVC, 89.8 +/- 22.3% predicted; FEV1, 84.7 +/- 16.9% predicted, VC, 88.6 +/- 21.5% predicted; and FEV1/VC, 74 +/- 7) with low D(LCO) (73 +/- 19% predicted). Compared with sitting, lung mechanics were unchanged in prone and supine positions; FEV1, FVC, and FEV1/VC were lower when patients were lying on their side, with unchanged alveolar volume and VC. D(LCO) was similar when comparing sitting, prone, and supine positions, and it was lower in lateral decubitus because of the lower capillary volume (vs sitting) and DM (vs prone and supine). Body position-related FVC and D(LCO) reduction were greatest in the largest hearts (deltaFVC and deltaD(LCO) vs left ventricle diastolic volume R = 0.524, p < 0.05 and R = 0.630, p < 0.02, respectively; deltaFVC and deltaD(LCO) vs cardiothoracic index R = 0.539, p < 0.05 and R = 0.685, p < 0.01, respectively). In heart failure, lateral decubitus airway obstruction and lung diffusion impairment become greater as heart dimensions increase.

The history of clinical oxygen monitoring

Oxygen is monitored by using its effect on blood hemoglobin color, its concentration in gas, its pressure in blood or tissue and using infrared light through the scalp and skull. The effect of oxygenation on hemoglobin color was discovered in 1860, used in a human hand in 1875, in a human ear in 1935, and made practical by Glen Millikan in 1942. Multiwavelength accurate ear oximetry was introduced by Shaw in 1964. Pulse oximetry was discovered by Takuo Aoyagi in 1972. Gas monitoring using oxygen's paramagnetism was invented by Linus Pauling in 1945. Continuous gas mass spectrometry became available about 1950. Polarography monitoring dissolved oxygen using an electrochemical cell to consume oxygen diffusing in proportion to pO 2 (dissolved oxygen pressure) through a semi-permeable membrane to a noble metal cathode was discovered by Leland Clark in 1954. Transcutaneous Clark electrodes were shown to approximate arterial pO 2 when mounted on skin heated to 43 °C by Dietrick Lübbers and associates in 1972. They are used in premature infants to control inspired oxygen to prevent eye damage. Lübbers also introduced optical glass fibers coated with substances in which fluorescence is quenched in response to liquid oxygen pressure for use in pump-oxygenators and indwelling arterial catheters.

Dietary salt alters pulmonary function during exercise in exercise-induced asthmatics

Epidemiological and experimental studies have suggested that dietary salt may play a role in airway responsiveness. We have previously shown that a low salt diet improves and a high salt diet exacerbates post-exercise pulmonary function in individuals with exercise-induced asthma. The aim of this study was to determine the influence of both elevated and restricted salt diets on pulmonary function during exercise in individuals with exercise-induced asthma. Nine men and six women participated in this double-blind, crossover study. The participants entered the study on their normal salt diet and were placed on either a low or high salt diet for 2 weeks. Each diet was randomized, with a 1 week washout period between diets before crossing over to the alternative diet for 2 weeks. The participants underwent treadmill testing at 85% of their age-predicted heart rate on the normal salt diet and at the end of each treatment period. Pulmonary function was assessed during exercise by arterial saturation (ear oximetry) and indirect calorimetry. Twenty-four hour urine collections confirmed compliance with the diets. Arterial saturation was reduced on the high and improved on the low salt diet at higher exercise intensities. Tidal volume and frequency selection during exercise varied with the diets, with a higher tidal volume and lower frequency on the high salt diet, but a lower tidal volume and higher frequency on the low salt diet. This suggested greater airway resistance during the high salt diet. In conclusion, the low salt diet improved and the high salt diet exacerbated pulmonary function during exercise in individuals with exercise-induced asthma. The mechanism of action remains unclear.

Exercise-induced hypoxaemia in highly trained cyclists at 40% peak oxygen uptake.

A group of 15 competitive male cyclists [mean peak oxygen uptake, VO2peak 68.5 (SEM 1.5 ml x kg(-1) x min(-1))] exercised on a cycle ergometer in a protocol which began at an intensity of 150 W and was increased by 25 W every 2 min until the subject was exhausted. Blood samples were taken from the radial artery at the end of each exercise intensity to determine the partial pressures of blood gases and oxyhaemoglobin saturation (SaO2), with all values corrected for rectal temperature. The SaO2 was also monitored continuously by ear oximetry. A significant decrease in the partial pressure of oxygen in arterial blood (PaO2) was seen at the first exercise intensity (150 W, about 40% VO2peak). A further significant decrease in PaO2 occurred at 200 W, whereafter it remained stable but still significantly below the values at rest, with the lowest value being measured at 350 W [87.0 (SEM 1.9) mmHg]. The partial pressure of carbon dioxide in arterial blood (PaCO2) was unchanged up to an exercise intensity of 250 W whereafter it exhibited a significant downward trend to reach its lowest value at an exercise intensity of 375 W [34.5 (SEM 0.5) mmHg]. During both the first (150 W) and final exercise intensities (VO2peak) PaO2 was correlated significantly with both partial pressure of oxygen in alveolar gas (P(A)O2, r = 0.81 and r = 0.70, respectively) and alveolar-arterial difference in oxygen partial pressure (P(A-a)O2, r = 0.63 and r = 0.86, respectively) but not with PaCO2. At VO2peak PaO2 was significantly correlated with the ventilatory equivalents for both oxygen uptake and carbon dioxide output (r = 0.58 and r = 0.53, respectively). When both P(A)O2 and P(A-a)O2 were combined in a multiple linear regression model, at least 95% of the variance in PaO2 could be explained at both 150 W and VO2peak. A significant downward trend in SaO2 was seen with increasing exercise intensity with the lowest value at 375 W [94.6 (SEM 0.3)%]. Oximetry estimates of SaO2 were significantly higher than blood measurements at all times throughout exercise and no significant decrease from rest was seen until 350 W. The significant correlations between PaO2 and P(A)O2 with the first exercise intensity and at VO2peak led to the conclusion that inadequate hyperventilation is a major contributor to exercise-induced hypoxaemia.

The effect of repeat exercise on pulmonary diffusing capacity and EIH in trained athletes.

The purpose of this study was to determine the effects of repeated heavy exercise on postexercise pulmonary diffusing capacity (DL) and the development of exercise induced arterial hypoxemia (EIH). 13 endurance-trained, male athletes (age = 27+/-3 yr, height = 179.6+/-5.0 cm, weight = 71.8+/-6.9 kg, VO2max = 67.0+/-3.6 mL x kg(-1) x min(-1) performed two consecutive, continuous exercise tests on a cycle ergometer to VO2max, separated by 60 min of recovery. Arterial oxygen saturation (%SaO2) was measured via ear oximetry, and resting DL was measured and partitioned by the single-breath method, before exercise and 60 min after each exercise bout. No significant differences resulted in VO2max, VE, peak heart rate (HR), or breathing frequency between exercise bouts (P > 0.05). There was a small but significant decrease (454-446 W; P < 0.05) in peak power output in the second test. %SaO2 decreased from resting values during both exercise tasks, but there was no difference between the minimum saturation achieved in test 1 (91.4) or test 2 (91.6; P > 0.05). After the initial exercise bout, significant decreases (P < 0.05) occurred in DL (11%), membrane diffusing capacity (DM) (11%) and pulmonary capillary volume (VC) (10%). Further decreases occurred in DL (6%; P < 0.05), DM (2%; P > 0.05), and VC (10%; P < 0.05) after the second exercise bout. These observations question the meaning of post exercise measurements of pulmonary diffusion capacity, and its components, relative to pulmonary gas exchange and pulmonary fluid accumulation during exercise. The fact that there was no further change in %SaO2 after the second test suggests that if any interstitial edema developed, it was of no clinical significance; alternatively, the changes in DL(CO) may be related more to redistribution of blood than the development of pulmonary edema.

LOW-SODIUM DIET IMPROVES EXERCISE PULMONARY FUNCTION IN EXERCISE-INDUCED ASTHMA

1069 Subjects with exercise-induced asthma (EIA) typically demonstrate marked reductions in pulmonary function post-exercise. Little data is available regarding pulmonary function during exercise in EIA. Additionally, there are no data regarding the potential role of dietary sodium on the severity of EIA. This study investigated the role of low- (LSD) and high-sodium (HSD) diets on pulmonary function and metabolism during exercise. Fifteen, clinically-diagnosed EIA subjects participated in a randomized, double-blind, crossover study. Subjects were studied on their normal sodium diet (NSD) and then randomized to LSD (≈1500 mg/d) or HSD(≈4000 mg/d) for 2 wks, followed by a 1-wk washout on NSD, then crossed over to the opposite diet for 2 wks. 24-hr urine collections documented sodium intake. EIA medication was withheld prior to the exercise test. Subjects performed a treadmill test to 90% of age-predicted heart rate, which was held for 5 min. Oxygen saturation (SaO2) was measured by ear oximetry; VO2 and VCO2 were measured by analysis of breath-by-breath expired gases. LSD improved (93%sat) and HSD worsened (78%sat) SaO2 during exercise. Tidal volume/frequency selection during LSD vs. HSD implied reduced airway resistance. In each case, the values on NSD were intermediate to those on LSD and HSD. All measured variables indicated that pulmonary gas exchange improved on LSD and worsened on HSD, and that airway resistance may have been less during LSD. Dietary sodium restriction improved pulmonary function while usual and elevated sodium intakes demonstrated progressive decrements in pulmonary function during exercise in subjects with EIA.

EXERCISE-INDUCED ARTERIAL DESATURATION IN ICE HOCKEY PLAYERS

1089 In order to determine the incidence of exercise-induced arterial hypoxemia(EIH) in elite ice hockey players, 13 members of a University hockey team (Wt= 87.5±2.3 kg; Ht = 180±1.8 cm, [horizontal bar over]x±SE) performed a progressive cycle test to fatigue. Percent arterial O2 saturation (% SaO2) as determined by ear oximetry (Ohmeda 3700) declined (P<0.05) from 96.5±0.26 at rest to 91.0±0.71 at fatigue. The incidence of EIH, defined as a reduction in% SaO2 greater than 4% below resting values was found in 62% of the players. The EIH group possessed a higher absolute ˙VO2max(+6.7%), a higher relative ˙VO2max (+11.1%) and a lower body weight(-4.9%) than the normal responders. At ˙VO2max, heart rate and ventilation were similar between groups. Resting hematocrit and height were also comparable. It is concluded that elite ice hockey players demonstrate a greater incidence of EIH than previously reported in elite athletes in other sports. Moreover, since the EIH occurred in the absence of a large˙VO2max per unit body weight as has been reported in cyclists and runners, other factors appear to be involved. One possibility is that diffusion limitations occur because of the large body size (muscle mass) and the large absolute ˙VO2max values that are observed. However, similar to other trained athletes demonstrating EIH, a high relative˙VO2max appears to be linked to EIH within the hockey group.

Sleep Deprivation Worsens Obstructive Sleep Apnea: Comparison Between Diurnal and Nocturnal Polysomnography

Daytime polysomnography (DPG) has been suggested for diagnosis of obstructive sleep apnea syndrome (OSAS), because it is less expensive than whole-night polysomnography investigation (NPG). To ensure sleep during day recordings, patients are often instructed to stay awake the night preceding DPG. This procedure has been validated against NPG, and also against apnea mattress recordings combined with ear oximetry (AMO). Twenty patients with OSAS symptoms were examined with NPG and simultaneous AMO and 2 to 3 weeks later with DPG 3 to 4 h in the morning after 1 nights sleep deprivation. Median apnea-hypopnea index (AHI) of DPG was 37 (95% confidence interval [CI], 19 to 44), significantly higher than median AHI of NPG (14; 95% CI, 12 to 27), whereas median nocturnal oxygen desaturation index (ODI) (11; 95% CI, 9 to 25) did not differ significantly from median AHI of NPG. Sensitivity values for DPG increased from 81 to 100% when the criteria AHI greater than 5, greater than 10, greater than 15, and greater than 20 were used, respectively. Specificity values also increased with the AHI used as cutoff point, from 50% (AHI>5) to 75% (AHI>20). In AMO, there were one false-negative case and four nonclassifiable borderline cases. If these types of simplified tests for OSAS are used for diagnosis, the risk of both false-negative and positive results (DPG) or nonclassifiable borderline cases (AMO) must be considered. Since there was a significant increase in AHI in DPG after sleep deprivation in comparison to conventional NPG, the former procedure should not be used for staging of the disease. These results also stress the importance of advice to OSAS patients concerning regular sleeping habits.

Validation of a Portable Sleep Apnea Monitoring Device

To assess the sensitivity and specificity of a portable sleep apnea monitoring device (PolyG; CNS Inc; Chantassen, Minn) using standard polysomnography (PSG) as a gold standard. The University of Alberta Hospitals Sleep Disorders Laboratory. One hundred and four consecutive patients referred for assessment of sleep complaints. Patients underwent simultaneous PSG and PolyG overnight recordings. The PSG included recordings of EEG, Chin electromyogram, electroculogram, ECG, oronasal airflow, thorax and abdomen respiratory movements, bilateral tibialis anterior electromyogram, and ear oximetry. The PolyG monitoring included oronasal airflow (thermistors), chest and abdomen pneumobelts, oximetry, ECG, and body position sensor. The raw data were screened and analyzed separately by two technicians without knowledge of results of the other system. The coefficient of correlation for apnea index (AI) was 0.94. The r value for apnea-hypopnea index (AHI) was 0.97. Using the criteria of AI more than 5 as diagnostic for sleep apnea syndrome, 23 out of the 104 patients had the disease based on PSG results. Twenty-six patients had AI more than 5 based on PolyG results. The sensitivity was 82.6% and the specificity was 91.4%. The positive predictive value was 73.1% and the negative predictive value was 94.9%. The overall accuracy was 89.4%. Using the criteria of AHI more than 15 as diagnostic for sleep apnea syndrome, 28 of the 104 patients had the disease based on the PSG results. Twenty-four patients had AHI more than 15 based on PolyG results. The sensitivity was 85.7% and the specificity was 94.7%. The positive predictive value was 85.7% and the negative predictive value was 94.7%. The overall accuracy was 92.3%. The PolyG monitoring device is useful in identifying patients without significant sleep apnea.

Detection and Correction of Hypoxemia Associated with Air Travel

Hypoxemia occurs during air travel because the pressure in aircraft cabins is not maintained equal to barometric pressure at sea level. Identification of patients who will develop significant arterial hypoxemia is most conveniently achieved by exposing these individuals to inspired oxygen tensions similar to those experienced during air travel. We utilized commercial Venturi devices with nitrogen as a source gas to lower inspired oxygen tensions (114 and 99 mm Hg) to simulate exposure to altitude (6,700 and 10,000 feet) that occurs with air travel. Oxygen was administered by nasal cannulas to correct the induced hypoxemia. Eleven normal subjects had baseline oxygen saturations of 97.3% as determined by ear oximetry. Exposure to reduced oxygen tensions for 20 min using 35 and 40% Venturi devices caused minimal O2 desaturation (94.8 and 93.8%, respectively). Mean baseline arterial oxygen saturation was 93.2% in 11 patients with chronic obstructive lung disease. Oxygen saturation fell to 89.5 and 87.5%, respectively, with exposure to the two levels of reduced oxygen tensions. Hypoxemia was corrected with administration of O2 by nasal cannulas at rates of 1.2 and 1.5 L/min, respectively. We conclude that individual patients can be evaluated conveniently for possible development of hypoxemia associated with air travel using available Venturi devices. This approach also permits determination of the oxygen therapy needed to correct hypoxemia.

Re-examination of the incidence of exercise-induced hypoxaemia in highly trained subjects.

The purpose of this study was to examine the occurrence of exercise-induced hypoxaemia (EIH) during maximal exercise in highly trained athletes. Eleven trained cyclists (mean(s.d.) age 23(3.5) years; mean(s.d.) VO2max 66.9(4.8) ml kg-1min-1) performed a continuous, multistage (270 kpm min-1) cycle ergometer test to exhaustion. Measurements of arterial oxygen-haemoglobin saturation (%HbO2) were obtained simultaneously at rest, every 2 min during exercise, and at maximum exercise capacity from arterial blood sampling (%SaO2) and ear oximetry (%SpO2). Exercise induced hypoxaemia (%HbO2 < or = 91%) was present in 64% of the athletes examined when EIH was determined using pulse oximetry, whereas none of the subjects exhibited EIH when %HbO2 was determined using arterial blood. At rest the values for %HbO2 were similar with mean(s.d.) %SaO2 being 97.3(0.6)% and mean(s.d.) %SpO2 being 96.5(1.6)%. During exercise, statistically significant differences were found for %HbO2 between arterial blood and ear oximetry at the 6-min, 8-min, and maximal exercise sampling times (repeated measures analysis of variance, P < 0.05). The results indicate that ear oximetry overestimates the incidence of EIH and underestimates the oxyhaemoglobin saturation in highly trained cyclists during exercise in comparison with those measurements made from arterial blood.

Effects of Meals on Respiratory Functions in Patients with Cystic Fibrosis

To determine the effect of meals on respiratory function in patients with chronic lung disease, we performed spirometry before and after a standard hospital lunch on 12 cystic fibrosis patients with varying severity of lung disease, as determined by Shwachman-Kulczcki (S-K) scores. The patients were monitored for oxygen saturation by ear oximetry before, during, and after the meal. The patient's ages ranged from 5 to 30 years (mean 16.8). The mean initial vital capacity was 58% of predicted, with a range of 22% to 89%. The mean initial oxygen saturation was 92%, with a range of 88% to 96%. Four patients had a decrease of 6% or more in their vital capacity. Four patients had a decrease of 3% or more in their oxygenation saturation. Three patients had decreases in both parameters. The mean initial vital capacity, oxygen saturation, and S-K score of the patients who experienced drops in vital capacity did not differ significantly from those of the other patients. However, the mean initial vital capacity of the patients who experienced drops in oxygen saturation was significantly lower than that of the other patients. Both groups had comparable mean oxygen saturation and S-K score. We conclude that some patients with chronic lung disease experience significant decreases in vital capacity and oxygen saturation during meals. A low vital capacity may predict the patients at risk for oxygen desaturation.

Reliability of Noninvasive Oximetry in Black Subjects during Exercise and Hypoxia

The effect of skin pigmentation on the reliability of noninvasive oximetry, especially during exercise and hypoxia, has not been thoroughly investigated. This is the first study, to our knowledge, that specifically addresses this question. Thirty-three young black men performed multistage, steady-state cycle ergometry, breathing gas mixtures simulating different altitudes: 33 breathed gas simulating sea level (PIO2 = 146 mm Hg), 11 breathed gas simulating 2,300 m (PIO2 = 110 mm Hg), and 22 breathed gas simulating 4,000 m (PIO2 = 85 mm Hg). Co-oximeter SaO2 determinations were performed in arterial blood samples obtained concurrently with ear oximetry that was measured using Hewlett-Packard 47201A (HP) and Blox IIA oximeters. The mean error or bias for the [HP - SaO2] and for [Biox IIA - SaO2] +/- 95% CI were: at simulated sea level (SaO2 greater than 96%): -0.4 +/- 0.3% and 2.1 +/- 0.3%; at simulated 2,300 m (range of SaO2 means, 89 to 94%): -0.8 +/- 0.5% and 3.5 +/- 0.9%; for simulated 4,000 m (range of SaO2 means, 75 to 84%): -4.8 +/- 1.6% and 9.8 +/- 1.8%, respectively. A better coefficient correlation was observed for all the pairs between SaO2 versus HP (r = 0.94, p less than 0.001, n = 279) than for the SaO2 versus Biox IIA (r = 0.80, p less than 0.001, n = 242). In conclusion, the HP oximeter appears to estimate SaO2 more accurately than the Biox IIA oximeter. The previously described overestimation for the Biox IIA ear oximeter and the underestimation for the HP ear oximeter at low SaO2 values in whites is exaggerated in blacks.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventricular function during supine bicycle exercise in univentricular connection with absent right atrioventricular connection

Fourteen patients with univentricular connection, absent right connection (tricuspid valve atresia) and normally related great arteries underwent rest, and supine bicycle exercise equilibrium radionuclide blood pool studies. Ejection fraction, heart rate, systemic blood pressure and oxygen saturation (ear oximetry) were measured. There were 6 male and 8 female patients. Mean age ± standard error of the mean was 14.5 ± 1.1 years (range 6.3 to 21.1). Eight patients (group 1) had systemic to pulmonary shunts placed as palliation 8.2 ± 2.2 years before study and 6 patients (group 11) had caval to pulmonary shunts placed 11.8 ± 1.6 years previously. Ejection fraction at rest was 54 ± 2% and an abnormal response to exercise (failure of ejection fraction to increase ⩾5% from rest to peak exercise) was found in 9 of 14 patients When analyzed separately, ejection fraction at rest in group 1 was higher than in group 11; however, this difference disappeared at peak exercise. There was a significant negative correlation between ejection fraction at peak exercise and the interval since palliative surgery, although it was not apparent at rest. These data suggest that ventricular function is compromised during exercise and that abnormal performance is influenced by long-standing volume overload: Importantly, this abnormal state is concealed at rest and the choice of palliative shunting procedure appears to have little effect on normalizing pump performance.