Feb 21, 2014 - Abstract. Objective: To compare oxygen saturation index (rSO2) obtained simultaneously in two different brachial muscles. Design: Prospective and observational study. Setting: Intensive care unit. Patients: Critically ill patients with
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Arterial oxygenation in patients was measured with an ear oximeter to assess factors that were associated with hypoxaemia at the induction of anaesthesia. Twenty patients breathed air during the induction of anaesthesia with thiopentone and following
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Oxygen saturation during daily activities in chronic obstructive pulmonary disease. N. Soguel Schenkel, L. Burdet, B. de Muralt, J.W. Fitting. ERS Journals Ltd 1996. ABSTRACT: Patients with chronic obstructive pulmonary disease (COPD) fre- quently de
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Where hypoxemia is defined as decreased partial pressure of oxygen in blood and low oxygen availabili- ty to the body or an individual tissue or organ. 3 Work done. The block diagram of pulse oximeter is shown in figure 2. It consists of seven stages
May 7, 2015 - The American Academy of Sleep Medicine (AASM) Manual specifies details for the recording and scoring of sleep and associated events in a sleep center . It is used to score the breathing events. Overnight polysomnography (PSG), is the
Near-infrared spectroscopy measures of haemoglobin oxygen saturation are often used as an indicator of sufficient oxygen delivery to assess injury susceptibility and tissue damage. They have also often been used as a surrogate measure of oxygen metab
Further, the model was externally inspected. By statistical significance test, the results of determina- tion were compared with those of standard methods with no significant difference. The method has been applied to simultaneously determine of Chem
Oxygensaturation and diffusion hypoxiain children following nitrous oxide sedation TamaraDunn-Russell,DMDStevenM. Adair, DDS,MSDeirdre R. Sams,DDS,MS Carl M. Russell, DMD,MS,PhDJamesT. Barenie, DDS,MS Abstract Oxygensaturation of arterial blood (SaO2) was assessed in children after discontinuing N20/O2 sedation for dental procedures. Twopost-treatment methodswere used: breathing 100%02for 5 min after the procedure, and breathing roomair for 5 min. Participants were 24 healthy children ages 41 to 113 months.Eachchild wastreated twice anda crossover design was used. The meanlength of proceduresthat were followed by 02 was 28.8 (+ 10.9 SD) rain;for those followed by roomair, 28.3 (+ 12.4 SD) min. SaO 2 was monitoredcontinuously by pulse oximetry and recorded at predeterminedintervals before, during, and after N20/02administration. Whenparticipants received post-treatment 02, the meanSaO 2 at I min after N20 cessation (99.91 + O. 63 SD)and 5 min after cessation (99.94 + O. 17 SD)wasstatistically significantly higher than the pretreatmentvalue of 99.28 (+ 0.63 SD). Whenparticipants received post-treatment roomair, the meanSaO 21 min after N20cessation (99.44 + 0.8) was also statistically significantly higher than the pretreatmentmean(99.08 + 0.96). After 2 min, however,the meanSaO 2 decreasedand was statistically indistinguishable from the pretreatment level after 5 min (99.13 + 0.9 SD). Fluctuations in SaO2,thoughstatistically significant, were less than 1%.Allowingchildren to breathe roomair immediatelyafter cessation of N20/O 2 inhalation did not reduce SaO 2 2belowclinically acceptable levels. This study further documentsthe safety of N20/O sedation, and gives the clinician additional informationconcerningthe safe and effective administrationof inhalation sedation. (Pediatr Dent 15:88-92, 1993) Introduction Nitrous oxide (N~O)has long been a valuable analgesic in both adult and pediatric dental practice. In pediatric practice, N20/O 2 is especially effective whencaring for mildly to moderately anxious children. Numerousreports have confirmed its ease of administration, wide margin of safety, analgesic and anxiolytic effects, and rapid 1-5 reversibility. The adverse side effects of N20/O 2 analgesia, which appear to be minor, include intra-administration dreams and postadministration headache, nausea, vomiting, and possibly diffusion hypoxia,s,6 Side effects were not commonin work reported by Hogue et al. s Although Houck and Ripa7 reported vomiting with N20 use in 8%of children studied, they concluded that someof these children had a tendency to vomit regardless of exposure to According to Langa,8 the most undesirable side effect of N20 / O2 administration was nausea and vomiting, but the incidence of these conditions was less than 1%. Diffusion hypoxia, frequently discussed as a possible untoward respiratory consequence of N20/O2 use, reportedly accounts for most occurrences of headache, nausea, and lethargy after N20/O2 sedation as employed in dentistry. 9 Hypoxia theoretically occurs when N20 administration is discontinued and the absorbed N20 diffuses out of the blood and into the alveolar spaces. Because N2 is less soluble in blood than the N20that replaced it, the uptake of N2 into the blood occurs more slowly than the excretion of N20. This dilutes alveolar oxygen and potentially lowers the oxygensaturation of arterial blood (SaOa).3 88 Pediatric Dentistry: March/April, 1993 - Volume16, Number 2
The greatest excret/on of N20occurs in the first 3- 5 rain following cessation of administration. 9 In standard clinical practice, 100%O2 is administered during this period, ostensibly to prevent diffusion hypoxia. Fink10 first reported the principle of diffusion hypoxia in 1955after an in-vitro experimentand a clinical study in which SaO2 dropped an average of 8% in eight healthy gynecologic patients whoreceived anesthesia and recovered in room air. Anesthesia included endotracheal intubation for administration of 75%N20 in 02 and intravenous administration of 2.5% thiopental. Fanning and Colgen11 concurred with Fink after demonstrating a clinically significant drop in SaO2after administering 75 % N20 and thiopental to both animals and humans. The level of N20used in these studies is considerably higher than that typically used in dentistry. Quarnstrom and coworkers12 stated that the results of these studies could be explained by the compromisingeffects of thiopental, which is knownto cause respiratory depression in some patients. Numerousstudies have questioned whether diffusion hypoxiais clinically significant. Fruminand Edelist, 13 who found that alveolar dilution caused by N20diffusion in healthy patients producedclinically insignificant changes in SaO2, concluded that diffusion hypoxia did not occur clinically. In their study, 18 surgical patients were changed from breathing 79%NaOto room air. Arterial blood was withdrawn periodically and blood gas determinations were made by radiometer electrode. Of the patients with-
out 2 respiratory obstruction, only two demonstrated SaO values < 90%,but persistent significant shunting was suspected in those cases. Other studies also have concluded that diffusion hypoxiais clinically insignificant whenres1~-17 piratory ventilation is adequate. In a study of 42 children who underwent minor outpatient surgery, the ratio of NzOto Oz wasas high as 70 %, but no clinically significant episodes of hypoxia were observed. 18 Weare unaware of published studies assessing hypoxia attributed to NzOadministration in children undergoing routine dental care. WhenNzOis used in outpatient dental care, drugs other than local anesthetics rarely are administered, and the ratio of NzOto Oz is lower than that used in general anesthesia. Quarnstrom and lz noted that for these reasons, the use of NaOin coworkers surgery is not directly comparableto its use in outpatient dental care. Their study of adult dental patients indicated that diffusion hypoxia is extremelyrare; no cases occurred among104 adults (95% confidence interval upper limit, 2.84%). To assess the significance of hypoxia attributed to N20 diffusion and elimination in pediatric dental patients, we compared two methods of discontinuing NzO/ Oz administration: 1) breathing 100%z for 5 min after th e procedure and, 2) breathing roomair for 5 min.
Methodsand materials Clinical procedures Werecruited 24 children ages 41 to 113 months (mean 67.2_+ 20 SDmonths) from the Medical College of Georgia Hospital and Schoolof Dentistry Clinics. All children were healthy, ASAClass I patients whorequired at least two visits for completion of dental treatment and whowere scheduled to receive NzO/ Oz analgesia for mild to moderate anxiety. Procedures were expected to last less than 60 min. The parents were fully informed and gave written consent for their children to participate in the study, which met all requirements of the institution’s HumanAssurance Committee. Parents were instructed not to give the children anything by mouth for at least 2 hr prior to the procedure to reduce the risk of nausea and vomiting. Dental treatment was rendered by five pediatric dental residents whowere calibrated in administration of NzO/ O2. N20 was administered to a maximumconcentration of ® N20/O machine and 40% in Oz using a Fraser MDM z scavenging nasal mask (Matrix Medical, Inc., Orchard Park, NY). The flow rate was individually adjusted to maintain proper reservoir bag inflation. The gas mixture was adjusted from 100%to a minimumof 60%Oz in 10% increments; each step lasted at least 20 sec. At the end of 2the procedure, the patient recovered in room air or O based on prior random assignment in a crossover design. Because of the narrow criteria for entry into the study (mild to moderate anxiety), behavior was not a factor the randomization scheme. WhenOz was to be received, the reservoir bag was flushed and the flow immediately
changed to 100%Oz. Whenroom air was to be received the flow of gases was discontinued, and the mask was removed. The reservoir bag was flushed with Oz and the maskwas retained dose to the patient for emergencyuse. Oxygenation of each patient was monitored throughout the procedure by using a Nellcor N-100*pulseoximeter (Nellcor, Inc., Hayward,CA)with the probe attached the index finger. SaO z was recorded at 30-sec intervals five times before the nasal maskwas placed. During the procedure, SaO z was recorded at 5-min intervals. At the end of the procedure, the SaOz was recorded for 5 min at 15-sec intervals. Recording was done by one of three individuals who did not know the post-treatment procedure being used. Parents were instructed to report any post-treatment symptoms that might indicate adverse effects of sedation.
Statisticalanalysis Weanalyzed five, three, and 21 measurements from periods before, during, and after NaO/ 02 administration, respectively. Only the first three measurements taken during sedation were used because for several patients the procedures required only 10 min. For each patient, the mean measurementwas calculated for the first two periods (before and during) and for each 1-min subdivision the third period (after), for a total of seven meanvalues. Summarystatistics by post-treatment method were generated. One-samplet-tests were employedto evaluate the differences in SaOz between each post-treatment measurement (minutes 1-5) and the pretreatment value within each method (NzO or room air). The crossover design allowed the use of one-samplet-tests of the differences in the differences between pretreatment and post-treatment SaO2 values across the two post-treatment methods. To detect experimental design problems, analysis of variance was used to test for differences by methodin SaOz before and during treatment. Analysis of covariance was used to test for the effect of methodon the response values recorded after treatment, while controlling for the values before treatment, the crossover design, and the length of the procedure.
Results Procedures lasted from 10 to 60 min. The mean procedure length when Oz was used postoperatively was 28.8 (+ 10.9 SD) min and 28.3 (+ 12.4 SD) min when room was used. The difference by post-treatment method in meanlength of procedure was not statistically significant. Fig I displays frequency distributions of the numbersof subjects by procedure length for each post-treatment method. A preliminary model (using analysis of covariance) evaluating the effect of procedure duration indicated no significant effect (P > 0.25). The NzOdelivery protocol employedin this study ensured that administration of NzOwas consistent for all procedures. The mean and standard deviation of the SaOz was determined for each study segment by post-treatment Pediatric Dentistry: March/April, 1993 -Volume15, Number 2 89
method (Fig 2). The mean difference between each posttreatment value and the pretreatment value is given in the Table for both post-treatment methods. When02 was used postoperatively, all differences betweenthe pretreatment SaO2 level and the given post-treatment levels were significantly different from zero (Table). Whenroomair
,,1 I 10
II II 20
25 30 35 40 45 50 Duration of Procedure (minutes)
[~ Oxygen ~ Air
Fig 1. Distributionof numbers of childrenby durationof procedure for eachpost-treatment method.
was used, the pre- and post-treatment SaO2 levels were significantly different only for the first post-treatment minute; subsequent post-treatment levels returned to baseline. The actual post-treatment levels for the two methods were also compared. The first post-treatment values were not significantly different between the two methods; subsequent values were significantly higher for the 02 post-treatment method. The post-treatment SaO2 levels for the 02 method were equivalent to levels observed during the dental procedure. The mean post-treatment SaO2 values for the room air method did not drop below the mean pretreatment values. No parents reported adverse post-treatment signs or symptoms.All patients met the criteria outlined by the AmericanAcademyof Pediat2° ric Dentistry for discharge following sedation. Analysis of variance detected no group effect on SaO 2 before and during treatment (P > 0.22; P > 0.31). The results of analysis of covariance were consistent with those of the paired t-test of the differences (Table), and offered no additional insight into the data. These analyses were performed to detect design and randomization problems in our study. Nonewas found. Because duration of procedure was not a significant factor, only the t-tests are reported. Discussion
SaO2 did not drop below 95% for any measurement taken during any procedure. Our results suggest that hypoxia attributed to N20 elimination and diffusion maynot be clinically significant for healthy pediatric dental pa99.0 " tients, whether they receive room air or oxygen postoperatively. Noneof the untoward clinical side effects of 98.0diffusion hypoxia and N20/O 2 sedation after dental procedures were reported when room air was breathed. The 97.0crossover design controlled for any differences in behavOxygen ior between the post-treatment group assignments, be96.0’ cause every patient received both post-treatment meth95.0 ods. Assumingthat no child’sbehavior changeddrastically, Be;ore Du;ing Po~tl ~ :~ the effect of behavior and any other transient confounders Measurement Period were controlled by the experimental design. If, in fact, Fig2. Mean oxygen saturation of patientsbefore,during,and there was a learning effect, this also was controlled by the after breathing nitrousoxide/oxygen by post-treatment method. random assignment of patients to room air or 02 as the Errorbarsindicatestandard deviation. first or second treatment session. A preliminary analysis Table. Mean(SD) difference in oxygen saturation between pretreatment and five post-treatment periods
detected no effect for session order. Crying was a rare event, and behavior did not affect the N20delivery protocol. The large standard deviations in the raw SaO2 scores (Fig 2) indicate that no child was in danger of hypoxia. Whenchildrenbreathed 100%O2 postoperatively, posttreatment SaO2 was higher than their preoperative level. Whenchildren breathed roomair postoperatively, no difference in SaO 2 was noted between the pretreatment level and the second or later post-treatment measurement.Thus, the SaO2, which reached a meanof nearly 100%during the procedures, rapidly returned to the pretreatment level when patients breathed room air. The 5-min monitoring period after N20 cessation was sufficient to include the excretion of 99%of the inspired N20.9In studies that have reported diffusion hypoxia, it occurredduring the first 4 min in the majority of cases. It is possible, thoughunlikely, that SaO 2 could have continued to decline after 5 min of breathing room air. Re1° ported drops in SaO 2 of 5 to 10% lasting several minutes should be detectable by the Nellcor~ pulse oximeter. Young et al. 21 reported pulse oximeter response times of 17 to 150 sec in detecting a sudden 10%decrease in SaO2. The mean reaction time of the Nellcor oximeter with a finger probe to this change was less than the meanreaction time for the 11 oximeters tested. Weare confident that measurements every 15 sec over the 5-min post-treatment period would have detected significant diffusion hypoxia. The duration of treatment and concentration of were typical of pediatric dental procedures. The concentration of N20 in O2 used in dentistry is generally low comparedwith that used for general anesthesia, in which higher levels of N20are often combinedwith other drugs that may have synergistic or independent effects on the physiology of respiration. Diffusion hypoxia was not found to be a problemat the N20levels used in this study, which were consistent with pediatric dental practice and consid9ered optimal for most patients. These findings are not meant to convince clinicians to discontinue the use of oxygen in the immediate posttreatment period. In fact, use of a scavengingsystem that removesexpired gas before it enters the office environmentis an indication for post-treatment 02 administration by nasal mask. The importance of this study lies in its additional documentation of the safety of N20/O 2 sedation.
Conclusions 1. SaO2 did not fall below 95%at any measurement. 2. During N20/O2 administration, mean SaO2 increased slightly but statistically significantly from baseline levels to nearly 100%. 3. Meanpost-treatment SaO2 was sustained at nearly 100%when participants breathed 100%02. 4. Whenparticipants breathed room air postopera-
tively, the mean SaO 2 at the second post-treatment minute and the mean pretreatment value did not differ, whichindicates that no clinically detectable diffusion hypoxia occurred. 5. Nountoward effects were reported by any participant regardless of the post-treatment method (02 or roomair). Wethank Drs. Isabel Lorenzo, Alicia Mize Rix, Shirin Yasrebi, and Sally Zifer for treating patients, and Mr. David Idles for assistance in recording data. Use of trade namesis for identification only and does not constitute endorsement by the Public Health Service or the U.S. Department of Health and HumanServices. Dr. Dunn-Russe]l is in private practice in Atlanta, Ga. Dr. Adair is associate professor and chairman, Dr. Samsis assistant professor, and Dr. Barenie is professor, Department of Pediatric Dentistry, Medical College of Georgia, Augusta, Ga. Dr. Russell is statistician, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control, Augusta, Ga. 1. Weinstein P, DomotoPK, Holleman E: The use of nitrous oxide in the treatment of children: results of a controlled study. J AmDent Assoc 112:325-31, 1986. 2. Nathan JE, VenhamLL, West MS, Werboff J: The effects of nitrous oxide on anxious young pediatric patients across sequential visits: a double-blind study. ASDC J Dent Child 55: 220-30, 1988. 3. Neidle EA, Yagiela JA: Pharmacology and Therapeutics forDentistry, 3rd ed. St. Louis: CVMosbyCo 1989, pp. 263-64. 4. Sorenson HW,Roth GI: A case for nitrous oxide-oxygen inhalation sedation: Anaid in the elimination of the child’s fear of the "needle". Dent Clin North Am17:51-66, 1973. 5. HogueD, Ternisky M, Iranpour B: The responses to nitrous oxide analgesia in children. J Dent Child 38:129-33, 1971. 6. Duncan GH, Moore P: Nitrous oxide and the dental patient: a review of adverse reactions. J AmDent Assoc 108:213-19, 1984. 7. Houck WR, Ripa LW: Vomiting frequency in children administered nitrous oxide-oxygen in analgesic doses. ASDC J Dent Child 30:404-6, 1971. 8. LangaH: Relative analgesia in dental practice: inhalation analgesia with nitrous oxide. Philadelphia: W.B.Saunders Co., 1968, p. 164. 9. MalamedSF: Sedation: A Guide to Patient Management, 2nd ed. St. Louis, CVMosbyCo, 1989, pp. 172, 185-86. 10. Fink BR: Diffusion anoxia. Anesthesiology 16:511-19, 1955. 11. Fanning GL, Colgan FJ: Diffusion hypoxia following nitrous oxide anesthesia. Anesth Analg 50:86-91, 1971. 12. Quarnstrom FC, Milgrom P, Bishop MJ, DeRouen TA: Clinical study of diffusion hypoxia after nitrous oxide analgesia. Anesth Prog 38:21-23, 1991. 13. Frumin MJ, Edelist G: Diffusion anoxia: a critical reappraisal. Anesthesiology 31:243-49, 1969. 14. Selim D, Markello R, Baker JM: The relationship of ventilation to diffusion hypoxia. Anesth Analg 49:437~t0, 1970. 15. Milles M, KohnG: Nitrous oxide sedation does not cause diffusion hypoxia in healthy patients. J Dent Res 70:469 (Abstr 1627), 1991. 16. Stubbing JF, SweeneyBP: Diffusion hypoxia, does it exist? A study in ASAI patients. CanJ Anaesth 36:$67-8, 1989. 17. Brodsky JB, McKlveenRE, Zelcer J, Margary JJ: Diffusion hypoxia: a reappraisal using pulse oximetry. J Clin Monit 4:244-46, 1988. 18. MurphyIL, Splinter WM:The clinical significance of diffusion hypoxia in children. Can J Anaesth 37:$40, 1990. 19. Mueller WA,DrummondJN, Pfibisco TA, Kaplan RF: Pulse oxim-
Pediatric Dentistry: March/April, 1993 - Volume15, Number 2 91
etry monitoring of sedated pediatric dental patients. Anesth Prog 32:237-40, 1985. 20. American Academy of Pediatric Dentistry and American Academyof Pediatrics: Guidelines for the elective use conscious sedation, deep sedation, and general anesthesia in pediatric patients.
92 Pediatric Dentistry: March/April, 1993 - Volume16, Number 2
Pediatr Dent 7:334-37, 1985. 21. YoungD, Jewkes C, Spittal M, Blogg C, WeissmanJ, Gradwell D: Response time of pulse oximeters assessed using acute decompression. Anesth Analg 74:189-95, 1992.