Reductions In SaO2 Research Articles

The Complications after General Anesthesia between Female and Male Genders in the First 24 Hours after Surgery

Background During surgery, the body responds to injury. These physiological responses lead to an imbalance in the physiologic activity of the body. Objective This study aimed to compare the incidence of complications after general anesthesia between males and females in the first 24 hours postoperatively. Methods This is a cross-sectional study. The study population included 150 patients who were candidates for surgery in the age range of 18-55. The sampling method was simple and sequential, and the selection of samples continued to reach 75 in both male and female groups. The collected data were analyzed by SPSS v.18 software and descriptive statistics, chi-square and Repeated Measure tests. Finally, P <0.05 was considered statistically significant. Results The incidence of some complications after general anesthesia was significantly higher in women than in men, including hypertension, tachycardia, tachypnea, restlessness, reduction of SaO2, hypotension, pain, vomiting, nausea, and drowsiness. Also, some complications were observed in women more than men, but they were not statistically significant, including voice violence, urinary retention, bradypnea, and shivering. Bradycardia was the only complication that was seen in men more than women but was not statistically significant. It was also observed that all complications after 24 hours significantly decreased in all patients. Conclusion It is suggested that in future studies, this type of study should be conducted with a larger sample size in different populations and compared with other types of anesthetics.

Oxygen Saturation During Dental Surgery with Local Anesthesia Alone and in Combination with Sedation in Medically Compromised Patients

Objective. The aim of this study was to determine which specific operative events are associated with change in SaO2 and blood pressure and heart rate in patients undergoing exodontia or minor oral surgery with local anaesthetic Medically compromised patients with Local anaesthesia alone or in combination with sedation. Methods. Arterial oxygen saturation (SaO2) with Heart rate and blood pressure was measured in 60 patients divided into two equal groups. Group I consisted of 30 patients receiving LA alone and undergoing simple extraction minor oral surgery, group II 30 patients receiving LA with oral midazolam and undergoing simple extraction or minor oral surgery. Results. There was a decrease in SaO2 from the baseline in 10% of group I patients, represented in 3 patients, 2 of them asthmatic and one anxious patient who the BP and HR raised slightly during LA admiration. There was a fall in SaO2 from the baseline in 53% of patients in group II, represented in 16 patients, the majority of them asthmatic and anxious patients, 6 patients with history of ischemic heart disease. The majority of these decreases in SaO2 or raining in BP or HR were associated with breath holding, in response to fear or emotional stress, during administration of LA due to vasoconstrictor effect or during elevation of teeth. The patients in group II showed a significantly (P<0. 001) greater maximum decrease in SaO2 from the baseline value compared to group I. The length of the operating time was longer in group II than that in group I, and the patients of group II were more anxious than the patients in group I. Conclusion. It was concluded that during simple extraction and minor oral surgery under LA alone or in combination with sedation procedures such as elevation of the tooth or administration of the LA may as a result of Breath holding cause reduction in SaO2 or raising in BP or HR. In fit patients this may be of little consequence, however patients with existing airway disease or Medically compromised patients may suffer significant falls in SaO2 or alter the Blood Pressure and Heart Rate. Therefor Monitoring of vital signs and oxygen saturation recommended during simple extraction dental surgery procedure and sedation as premedication for cardiac patients would be recommended.

Role of CT angiography in detecting acute pulmonary embolism associated with COVID-19 pneumonia

PurposeRecently coronavirus disease (COVID-19) caused a global pandemic, characterized by acute respiratory distress syndrome (ARDS). The aim of our study was to detect pulmonary embolism (PE) in patients with severe form of COVID-19 infection using pulmonary CT angiography, and its associations with clinical and laboratory parameters.MethodsFrom March to December 2020, we performed a prospective monocentric study collecting data from 374 consecutive patients with confirmed SARS-CoV-2 infection, using real-time reverse-transcriptase polymerase-chain-reaction (rRT-PCR) assay of nasopharyngeal swab specimens. We subsequently selected patients with at least two of the following inclusion criteria: (1) severe acute respiratory symptoms (such as dyspnea, persistent cough, fever > 37.5 °C, fatigue, etc.); (2) arterial oxygen saturation ≤ 93% at rest; (3) elevated D-dimer (≥ 500 ng/mL) and C-reactive protein levels (≥ 0.50 mg/dL); and (4) presence of comorbidities. A total of 63/374 (17%) patients met the inclusion criteria and underwent CT angiography during intravenous injection of iodinated contrast agent (Iomeprol 400 mgI/mL). Statistical analysis was performed using Wilcoxon rank-sum and Chi-square tests.ResultsAbout, 26/60 patients (40%) were found positive for PE at chest CT angiography. In these patients, D-dimer and CRP values were significantly higher, while a reduction in SaO2 < 93% was more common than in patients without PE (P < 0.001). Median time between illness onset and CT scan was significantly longer (15 days; P < 0.001) in patients with PE. These were more likely to be admitted to the Intensive Care Unit (19/26 vs. 11/34 patients; P < 0.001) and required mechanical ventilation more frequently than those without PE (15/26 patients vs. 9/34 patients; P < 0.001). Vascular enlargement was significantly more frequent in patients with PE than in those without (P = 0.041).ConclusionsOur results pointed out that patients affected by severe clinical features of COVID-19 associated with comorbidities and significant increase of D-dimer levels developed acute mono- or bi-lateral pulmonary embolism in 40% of cases. Therefore, the use of CT angiography rather than non-contrast CT should be considered in these patients, allowing a better evaluation, that can help the management and improve the outcomes.

Effects of Carbohydrate and Glutamine Supplementation on Oral Mucosa Immunity after Strenuous Exercise at High Altitude: A Double-Blind Randomized Trial.

This study analyzed the effects of carbohydrate and glutamine supplementation on salivary immunity after exercise at a simulated altitude of 4500 m. Fifteen volunteers performed exercise of 70% of VO2peak until exhaustion and were divided into three groups: hypoxia placebo, hypoxia 8% maltodextrin (200 mL/20 min), and hypoxia after six days glutamine (20 g/day) and 8% maltodextrin (200 mL/20 min). All procedures were randomized and double-blind. Saliva was collected at rest (basal), before exercise (pre-exercise), immediately after exercise (post-exercise), and two hours after exercise. Analysis of Variance (ANOVA) for repeated measures and Tukey post hoc test were performed. Statistical significance was set at p < 0.05. SaO2% reduced when comparing baseline vs. pre-exercise, post-exercise, and after recovery for all three groups. There was also a reduction of SaO2% in pre-exercise vs. post-exercise for the hypoxia group and an increase was observed in pre-exercise vs. recovery for both supplementation groups, and between post-exercise and for the three groups studied. There was an increase of salivary flow in post-exercise vs. recovery in Hypoxia + Carbohydrate group. Immunoglobulin A (IgA) decreased from baseline vs. post-exercise for Hypoxia + Glutamine group. Interleukin 10 (IL-10) increased from post-exercise vs. after recovery in Hypoxia + Carbohydrate group. Reduction of tumor necrosis factor alpha (TNF-α) was observed from baseline vs. post-exercise and after recovery for the Hypoxia + Carbohydrate group; a lower concentration was observed in pre-exercise vs. post-exercise and recovery. TNF-α had a reduction from baseline vs. post-exercise for both supplementation groups, and a lower secretion between baseline vs. recovery, and pre-exercise vs. post-exercise for Hypoxia + Carbohydrate group. Five hours of hypoxia and exercise did not change IgA. Carbohydrates, with greater efficiency than glutamine, induced anti-inflammatory responses.

Effects Of Normobaric Hypoxia And Exercise On Cold-induced Vasodilation, Body Temperature, And Oxygen Saturation

PURPOSE: The purpose of the current study was to investigate the effects of normobaric hypoxia on the thermoregulatory and the cold-induced vasodilation (CIVD) response before and following submaximal exercise. METHODS: Ten apparently healthy men (23±3 years) volunteered for two experimental trials during which they were exposed to differing O2 saturations (13% O2 and 21% O2) in an environmental chamber. Trials were counterbalanced and blinded from the participant. Following a 60-min acclimation the experimental trials consisted of two 15-min exposures to 5°C water of the non-dominant hand. The exposures were separated by a 30-min bout of submaximal exercise producing the equivalent of 400 watts (W) of metabolic heat. Mean body temperature (MBT), oxygen saturation (SaO2), and thermal sensation (TS) were collected during the final 5 min of each stage. CIVD was measured pre- and post-exercise during each of the cold water exposures on the nailbed of the middle finger on the non-dominant hand. RESULTS: ANOVA revealed a significant time (baseline, acclimation, CIVDpre, exercise, and CIVDpost) by condition (13% O2, 21% O2) interaction for SaO2 (F = 38.4, p < 0.001). Significant differences (p < 0.001) between conditions existed at all time-points with the exception of baseline (p = 1.0). A main effect of time was observed for amplitude temperature (F = 20.034, p < 0.001), which was significantly greater (p < 0.001) at CIVDpost compared to CIVDpre (CIVDpost: 1.13 °C; CIVDpre: 0.28 °C). No significant difference across time or condition exists for MBT or TS. In the 13% O2 condition, the reduction in SaO2 during exercise (81.5%) was positively associated (r = 0.656, p = 0.039) with amplitude temperature at CIVDpost (0.69 °C), which was significantly greater (p < 0.05) compared to CIVDpre (0.14 °C). CONCLUSION: It appears that during rest in normobaric hypoxia, a cold stress test has minimal effect on the CIVD response. During exercise, reduced CIVD amplitude is associated with reduced SaO2. It appears that a submaximal bout of cycling exercise is not the proper stimulus to acutely induce a CIVD response to the magnitude at which physiological changes ensue.

Rate of ascent and acute mountain sickness at high altitude.

To examine the effect of ascent rate on the induction of acute mountain sickness (AMS) in young adults during a climb to Jiaming Lake (3350 m) in Taiwan. Prospective, nonrandomized. Climb from 2370 to 3350 m. Young adults (aged 18 to 26 years) (N = 91) chose to participate in either the fast ascent (3 days; n = 43) or slow ascent (4 days; n = 48) group (1 and 2). Two criteria were used to define AMS. A Lake Louise score ≥3 and Lake Louise criteria [in the setting of a recent gain in altitude, the presence of headache and at least 1 of gastrointestinal discomfort (anorexia, nausea, or vomiting), fatigue or weakness, dizziness or lightheadedness, or difficulty sleeping]. Heart rate, blood oxygen saturation (SaO2), and symptoms of AMS were monitored each morning and evening. Baseline characteristics were similar between groups, except for significant differences in history of alcohol consumption (P = 0.009) and climbing experience above 3000 m (P < 0.001). The incidence of AMS was not associated with the rate of ascent. Acute mountain sickness was most prevalent in group 1 on day 2 in the evening and in group 2 on day 3 in the evening. In both groups, AMS correlated with the initial reduction in SaO2. Body mass index (BMI) >24 kg/m was identified as a significant risk factor for AMS. The development of AMS was closely associated with an initial reduction in SaO2. A BMI >24 kg/m also contributed to the occurrence of AMS. These findings indicate that factors other than ascent rate should be considered when trying to ameliorate the risk of AMS.

Effect of acute hypoxia on regional cerebral blood flow: effect of sympathetic nerve activity

We examined 1) whether global cerebral blood flow (CBF) would increase across a 6-h bout of normobaric poikilocapnic hypoxia and be mediated by a larger increase in blood flow in the vertebral artery (VA) than in the internal carotid artery (ICA); and 2) whether additional increases in global CBF would be evident following an α1-adrenergic blockade via further dilation of the ICA and VA. In 11 young normotensive individuals, ultrasound measures of ICA and VA flow were obtained in normoxia (baseline) and following 60, 210, and 330 min of hypoxia (FiO2 = 0.11). Ninety minutes prior to final assessment, participants received an α1-adrenoreceptor blocker (prazosin, 1 mg/20 kg body mass) or placebo. Compared with baseline, following 60, 220, and 330 min of hypoxia, global CBF [(ICAFlow + VAFlow) ∗ 2] increased by 160 ± 52 ml/min (+28%; P = 0.05), 134 ± 23 ml/min (+23%; P = 0.02), and 113 ± 51 (+19%; P = 0.27), respectively. Compared with baseline, ICAFlow increased by 23% following 60 min of hypoxia (P = 0.06), after which it progressively declined. The percentage increase in VA flow was consistently larger than ICA flow during hypoxia by ∼20% (P = 0.002). Compared with baseline, ICA and VA diameters increased during hypoxia by ∼9% and ∼12%, respectively (P ≤ 0.05), and were correlated with reductions in SaO2. Flow and diameters were unaltered following α1 blockade (P ≥ 0.10). In conclusion, elevations in global CBF during acute hypoxia are partly mediated via greater increases in VA flow compared with ICA flow; this regional difference was unaltered following α1 blockade, indicating that a heightened sympathetic nerve activity with hypoxia does not constrain further dilation of larger extracranial blood vessels.

Regional tissue oxygenation in association with duration of hypoxaemia and haemodynamic variability in preterm neonates

ObjectiveTo assess the effect of the duration of spontaneous hypoxic episodes and variations in haemodynamic parameters on cerebral and renal tissue oxygenation (rSo2C and rSo2R) in clinically stable preterm infants.DesignObservational...

Trained Women Demonstrate Greater Preservation Of Peak Exercise Capacity During Acute Hypoxia Than Trained Men

The lower hemoglobin concentration and consequent lower arterial oxygen content in women compared to men may result in gender differences in the physiological response to acute hypoxia. However, very few reports of direct gender comparisons in the physiological response to acute hypoxia are available to date and indirect comparisons between studies exclusively of men or women are largely equivocal. PURPOSE: To determine the effects of acute normobaric hypoxia on cardiovascular hemodynamics at rest and during maximal exercise in endurance trained men and women. METHODS: Peak exercise capacity (Wpeak) at sea level (SL) and normobaric hypoxia (NH, 12.8% FIO2, ∼3900 m) was determined for 20 male (26 ± 1 yr, 56.6 ± 1.2 ml/kg/min VO2peak, mean ± SE) and 15 female (25 ± 1 yr, 45.3 ± 1.2 ml/kg/min VO2peak) trained cyclists and triathletes at least 48 h apart. At rest and during exercise, heart rate (HR), stroke volume (SV), and cardiac output (Q) were measured continuously by noninvasive impedance cardiography while arterial oxygen saturation (SaO2) was measured by pulse oximetry. RESULTS: HR, SV, and Q at rest did not change from SL to NH in men or women and both genders demonstrated similar reductions in SaO2 at rest (96 ± 1 to 85 ± 1%, p < 0.05). Wpeak was significantly reduced from SL to NH in both men (325 ± 8 to 250 ± 6 W, p < 0.05) and women (245 ± 7 to 201 ± 6 W, p < 0.05), but the relative decrease in Wpeak from SL to NH was significantly greater in men than women (-22.7 ± 0.9 vs. -17.5 ± 1.5%, p < 0.05). Peak Q was similarly reduced in both genders from SL to NH (-9.5 ± 3.6%, p < 0.05), while peak SV did not change and peak HR was reduced in men more than women (-7.3 ± 0.7% vs. -4.9 ± 0.8%, p < 0.05). SaO2 at peak was similarly reduced in men (94 ± 1 to 71 ± 2%, p < 0.05) and women (94 ± 1 to 72 ± 2%, p < 0.05) from SL to NH. CONCLUSION: Endurance trained women appear to be more capable of preserving peak exercise capacity during acute NH than endurance trained men despite similar decrements in Q and SaO2. Supported by the World Anti-Doping Agency

Inspiratory muscle work in acute hypoxia influences locomotor muscle fatigue and exercise performance of healthy humans

Our aim was to isolate the independent effects of 1) inspiratory muscle work (W(b)) and 2) arterial hypoxemia during heavy-intensity exercise in acute hypoxia on locomotor muscle fatigue. Eight cyclists exercised to exhaustion in hypoxia [inspired O(2) fraction (Fi(O(2))) = 0.15, arterial hemoglobin saturation (Sa(O(2))) = 81 +/- 1%; 8.6 +/- 0.5 min, 273 +/- 6 W; Hypoxia-control (Ctrl)] and at the same work rate and duration in normoxia (Sa(O(2)) = 95 +/- 1%; Normoxia-Ctrl). These trials were repeated, but with a 35-80% reduction in W(b) achieved via proportional assist ventilation (PAV). Quadriceps twitch force was assessed via magnetic femoral nerve stimulation before and 2 min after exercise. The isolated effects of W(b) in hypoxia on quadriceps fatigue, independent of reductions in Sa(O(2)), were revealed by comparing Hypoxia-Ctrl and Hypoxia-PAV at equal levels of Sa(O(2)) (P = 0.10). Immediately after hypoxic exercise potentiated twitch force of the quadriceps (Q(tw,pot)) decreased by 30 +/- 3% below preexercise baseline, and this reduction was attenuated by about one-third after PAV exercise (21 +/- 4%; P = 0.0007). This effect of W(b) on quadriceps fatigue occurred at exercise work rates during which, in normoxia, reducing W(b) had no significant effect on fatigue. The isolated effects of reduced Sa(O(2)) on quadriceps fatigue, independent of changes in W(b), were revealed by comparing Hypoxia-PAV and Normoxia-PAV at equal levels of W(b). Q(tw,pot) decreased by 15 +/- 2% below preexercise baseline after Normoxia-PAV, and this reduction was exacerbated by about one-third after Hypoxia-PAV (-22 +/- 3%; P = 0.034). We conclude that both arterial hypoxemia and W(b) contribute significantly to the rate of development of locomotor muscle fatigue during exercise in acute hypoxia; this occurs at work rates during which, in normoxia, W(b) has no effect on peripheral fatigue.

EXERCISE-INDUCED HYPOXEMIA IS AMELIORATED BY NEDOCROMIL SODIUM AND DIPHENHYDRAMINE HCL

Diffusion limitation is a purported cause of exercise-induced hypoxemia (EIH)(Torre-Bueno et al, 1985). Specifically, diffusion limitation secondary to accumulation of extra vascular lung fluid has been reported and may contribute to the impairment of pulmonary function observed in humans in response to intense exercise (Hopkins et al, 1997). To test the hypothesis that EIH may occur secondary to pulmonary endothelial cell activation, eight highly-trained, college-age men (age, 21.1 ± 2.0; VO2max, 74.7 ± 3.5 ml/kg/min) were invited to participate in the study. Subjects completed a progressive, maximal exercise test to exhaustion, and then completed three, 5-min incremental exercise (IE) bouts at 70%, 80% and 90% VO2max. Prior to the laboratory visits, subjects received, in a quasi-random, single-blind fashion, either placebo (PL), nedocromil sodium (NS) or diphenhydramine HCl (DH). The DH treatment was the last treatment for all subjects. A repeated measures design was employed such that all subjects performed a VO2max test, as well as the subsequent IE bouts, under each treatment. Paired t-tests (one-tailed) revealed that there were no statistical differences (p. > 0.05) among any of the metabolic and ventilatory variables in each treatment, with the exception of arterial oxygen saturation (SaO2). With respect to SaO2, statistically significant comparisons (p. < 0.05; *) were observed between PL vs. NS and PL vs. DH in all treatments except at 70% VO2max. No statistical differences were observed between NS and DH in any condition. Figure 1 shows SaO2 at the end of the 5-min IE bouts and at VO2max. Results indicate that the reduction in SaO2 during intense exercise may be due to pulmonary endothelial cell activation, and, furthermore, is ameliorated secondary to the actions of NS, a mast cell stabilizer, and DH, an H2-receptor antagonist.Figure 1: Arterial oxygen saturation at the end of each 5-min IE bout and at VO2max

Blood gas changes during incremental and sprint exercise

We investigated and compared arterial blood gas and ventilatory changes during rapid acceleration sprint and during incremental treadmill exercise. Seven clinically normal racehorses completed standardised incremental exercise tests and rapid acceleration tests at speeds calculated to elicit 115% VO2max. Arterial oxygen tension decreased (P < 0.001) between 15 s (mean +/- s.d. 103.8 +/- 14.3 mmHg) and 30 s (85.0 +/- 7.7 mmHg) after the onset of rapid acceleration exercise, but did not change significantly during the remainder of the sprint. This was accompanied by an increase in PaCO2 of 5.9 mmHg (P < 0.05). Despite reductions in SaO2 during exercise, CaO2 did not change due to increases in haemoglobin concentration. Heart rate increased rapidly (P < 0.001) during the first 15 s of exercise and thereafter remained constant. The mean maximum speed during the incremental test (11.4 +/- 0.5 m/s) was not significantly different to the speed calculated to elicit 115% VO2max during the sprint test (12.2 +/- 0.8 m/s). The mean peak HR and Hb during the sprint test were significantly less than during the incremental test. However, there were no significant differences in the maximum or minimum values achieved for other variables. We conclude that rapid acceleration exercise is accompanied by rapid changes in blood gas variables, reaching steady state within 45 s. Blood gas responses during the simpler incremental test describe maximal changes during high-intensity sprint exercise.

Is epinephrine contraindicated during cardiopulmonary resuscitation?

Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear. Forty-four anesthetized swine received an infusion of six inert gases. Animals underwent ventricular fibrillation with CPR and intravenous administration of saline (control), epinephrine (15 microg/kg), or methoxamine (150 microg/kg). Cardiac output, aortic blood pressure, pH, and arterial oxygen saturation were recorded. Distributions of VA and Q were determined by the multiple inert gas elimination technique. Ventricular fibrillation and CPR caused significant decreases in cardiac output, aortic blood pressure, and arterial pH. With epinephrine (versus saline), diastolic blood pressure was significantly higher (23+/-7 versus 8+/-4 mm Hg), but the increase in shunt (from 7+/-4% to 29+/-17%) and the reduction in SaO2 (from 99.7% to 76.8%) were significantly larger. Also, the increase in dead space was greater and elimination of CO2 less. There were no differences between animals given methoxamine or saline, except for increased diastolic blood pressure. During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt approximately 300% more than saline or methoxamine and significantly reduced arterial oxygen saturation. We suspect that the beta-adrenergic receptor activity of epinephrine attenuated hypoxic pulmonary vasoconstriction. Methoxamine is as effective a pressor as epinephrine for CPR and devoid of beta-adrenergic activity. We recommend that such an agent be considered, instead of epinephrine, for CPR.

Modifications of Oxygen Saturation During Transesophageal Echocardiography.

The present study was designed: (1) to establish the effects of transesophageal echocardiography (TEE) on arterial oxygen saturation (SAO(2)%); (2) to verify the possible clinical consequences of this phenomenon; and (3) to study the possibility of predicting modifications of SAO(2)% by clinical or hemodynamic variables or by specific factors related to the TEE procedure. We prospectively studied 116 unselected patients, aged 61 +/- 12 years, who underwent diagnostic TEE for various clinical indications. Thirty-seven patients had mitral valve disease, 19 aortic valve disease, 14 combined mitroaortic disease, 8 congenital heart disease, and 38 other cardiovascular diseases. Eight patients were affected by chronic obstructive pulmonary disease. Ninety-seven patients were sedated by 4 +/- 2 mg of diazepam IV SAO(2)% (5-min average) (Ohmeda Biox 3700 pulse oxymeter finger probe), heart rate (HR), and blood pressure (BP) were considered during baseline transthoracic examination, after pharmacological sedation but before the introduction of the probe, and finally during TEE. Neither clinical complications nor major arrhythmias were observed. Baseline SAO(2)%, HR and BP were, respectively, 93.6 +/- 3.3%, 76 +/- 14 beats/min, and 129 +/- 20/75 +/- 10 mmHg. Pharmacological sedation did not modify SAO(2)%, HR, and BP (P > 0.1). During TEE a small but significant reduction in SAO(2)% by an average of 1.2 +/- 3.2% was observed (P < 0.005), as well as a small and significant increase in HR by an average of 3 +/- 10 beats/min (P < 0.01). BP did not change significantly (P > 0.1 for both systolic and diastolic). The changes of SAO(2)% and HR were not interrelated and were not related to the duration of the procedure and to any of the clinical and hemodynamic variables taken into consideration. TEE can induce a small but significant drop in SAO(2)% and a small increase in HR even without any clinical relevance. No clinical or hemodynamic variable or specific factors related to the TEE procedure were related to these changes.

Cluster headache: the ventilatory response to transient hypoxia with pure nitrogen.

To determine whether the carotid body plays a pathogenetic role in cluster headache, 20 cluster headache patients have been studied. Of these, 11 patients were in the interparoxysmal cluster phase, and 9 were in remission. Comparison was made with healthy subjects matched for sex, age, and smoking habits. Transient hypoxia was induced by inhalation of 1-8 breaths of 100% nitrogen (N2), until the arterial oxygen saturation (SaO2) decreased to around 80%. Changes in ventilation (tidal volume, inspiratory minute ventilation (VI), and end-tidal PCO2 (PETCO2)), were analyzed breath-by-breath. Under basal conditions, cluster headache patients had a slightly higher SaO2 and VI when compared to controls. PETCO2 was significantly lower (P < 0.05) during the cluster period as measured by Wilcoxon signed rank test for paired data, and during remission, according to the Student's paired t-test, in comparison with controls. After exposure to N2, no significant difference was found in the rate of reduction of SaO2 between any of the groups. A higher absolute increase in VI, but a relative (%) decrease in VI at moderate hypoxia were measured, the differences between patients and controls being on the border of the level of significance. Chemoreceptor sensitivity of the carotid body, expressed as the slope of a regression curve obtained by plotting the increase in VI against the reduction in SaO2, showed no statistical difference between the groups. The results do not support the hypothesis of a pathogenetic role for the carotid body in cluster headache.

Apnoea, bradycardia, and oxygen saturation in preterm infants.

To analyse the effects of apnoea and bradycardia on the oxygen saturation (SaO2) of preterm infants and to make recommendations for apnoea alarm limits, polygraphic recordings were made on 89 occasions of 27 preterm infants; 1029 apnoeic episodes were analysed. Reduction in SaO2 was positively correlated with duration of apnoea, but the scatter of results was such that reductions in SaO2 of up to 40% occurred with apnoeas of less than 10 seconds duration. The median initial SaO2 was significantly lower in those episodes that resulted in bradycardia (92% compared with 95%), and there was also a significantly greater reduction in median SaO2 (9% compared with 5%). This study illustrates the difficulty of setting alarm limits for the detection of apnoea. We suggest that rather than simply detecting apnoea it is more appropriate to monitor heart rate and SaO2 in infants with recurrent apnoea.

Cluster Headache: The Effect of Low Oxygen Saturation

The present study concerns the possible relationship between hypoxia and the generation of cluster headache attacks. Fifteen controls and 25 cluster headache patients were studied. The patients were allocated into two groups according to cluster headache stage, i.e. cluster or remission period. During the tests, all the subjects were asked to inhale 12% oxygen (88% N2) for 30 min, and the decreasing oxygen saturation (SaO2%) was monitored. Patients in the remission period showed nearly the same decrement of SaO2% as controls. At the end of the test, patients in the bout showed significantly less reduction of SaO2% than the controls. In 5 patients, the test was carried out both in and outside the cluster periods. The tendency to less decrement in oxygen saturation in the cluster phase was as marked with this comparison, but the difference between the groups was not significant, probably partly due to the low number of tests carried out. Only one patient got a typical attack. It seems that hypoxia of this magnitude per se is not the cause of attacks. The different pattern with respect to SaO2% following 12% O2 inhalation in cluster headache may be due to an abnormality in central regulation and/or chemoreceptor sensitivity.

Precordial Doppler Monitoring and Pulse Oximetry During Cesarean Delivery

Venous air embolism (VAE) is a potential but rare complication of cesarean delivery that can be associated with morbidity and death. Uterine sinuses are susceptible to the entrance of air during cesarean delivery. To define the incidence of VAE and its relation to arterial oxygen saturation (SaO2) and consequent electrocardiographic (ECG) changes, a prospective study was undertaken in which precordial Doppler monitoring was conducted during cesarean delivery. Concomitant, SaO2 and ECG were recorded in 78 patients. Fifty-one of 78 (65%) of the subjects had Doppler changes consistent with VAE. Of these, 37 patients (72%) showed a decreased SaO2, (average decline 5.2%). The remainder of the patients with Doppler changes showed no SaO2 change. Twenty of the patients with Doppler changes and decreased SaO2 complained of chest pain and dyspnea. Three of these patients exhibited ECG changes including ST segment depression. Although all ECG changes resolved spontaneously without sequelae, the potential clearly existed for life threatening embolic events. Thus, precordial Doppler monitoring of cesarean delivery patients demonstrated a surprisingly high incidence of Doppler changes consistent with VAE. Some episodes were associated with a significant reduction in SaO2 and rarely with ECG changes.

Changes in Oxygen Saturation During Inhalation Induction of Anaesthesia in Children

Changes in oxygen saturation (SaO2) were studied during induction of anaesthesia in 48 healthy children receiving halothane or isoflurane for outpatient dental extractions. Substantial reductions in SaO2 occurred in more than 50% of the children given isoflurane and were associated with the irritant effects of this agent on the airway. SaO2 was largely unaltered during the use of halothane. These findings indicate that the airway complications caused by isoflurane may be associated with decreases in SaO2.

CHANGES IN OXYGEN SATURATION DURING INHALATION INDUCTION OF ANAESTHESIA IN CHILDREN

Changes in oxygen saturation (SaO2) were studied during induction of anaesthesia in 48 healthy children receiving halothane or isoflurane for outpatient dental extractions. Substantial reductions in SaO2 occurred in more than 50% of the children given isoflurane and were associated with the irritant effects of this agent on the airway. SaO2 was largely unaltered during the use of halothane. These findings indicate that the airway complications caused by isoflurane may be associated with decreases in SaO2.