Expansion of the Acceptance Program: nitrous oxide scavenging equipment and nitrous oxide trace gas monitoring equipment.
Explore the source record for details and available documents.
American Dental Association↗
SEARCH · PubMed Health
Results for “Nitrous Oxide”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Comparison of sampling techniques for studies of nitrous oxide pollution.
The retention of nitrous oxide in samples of nitrous oxide in air held in disposable plastic syringes, glass syringes and custom-made nylon film bags was studied by means of gas chromatography at intervals of 90 min, 24, 48 and 120 h after filling the containers. After 24 h the nylon bags retained a mean concentration of 94.5% of the original concentration of nitrous oxide. The disposable plastic syringes and glass syringes were unsatisfactory and retained only 80% of the original concentration of nitrous oxide after 90 min. These values decreased to 51% and 31% of the original concentration of nitrous oxide respectively at 24 and 48 h.
Air Pollution↗
Self-administered intermittent nitrous oxide analgesia for labour. Enhancement of effect with continuous nasal inhalation of 50 per cent nitrous oxide (Entonox).
Explore the source record for details and available documents.
Anesthesia, Inhalation↗
Operating room nurses' psychomotor and driving skills after occupational exposure to halothane and nitrous oxide.
Concentrations of halothane and nitrous oxide were assayed by gas chromatography throughout a working day in three operating theatres and in the end-tidal air of 19 nurses 15 and 60 min after leaving the theatres. Perceptual, psychomotor and driving skills were measured in these nurses and in 11 younger nurses working in the wards of the same hospital. A complicated psychomotor test battery and a driving simulator were used. End-tidal air concentrations of halothane and nitrous oxide were positively correlated with the exposure level of these gases in the operating theatres. Some of the operating room nurses had greater amounts of halothane in their end-tidal air (average 15 to 10 ppm) than student volunteers 4.5 h after 3.5 min of general anaesthesia with a combination of halothanenitrous-oxide oxygen (10 ppm halothane). These volunteers had worse psychomotor and driving performances when measured than controls who had not been anaesthetized. No correlations were found between the concentrations of halothane or nitrous oxide in end-tidal air and psychomotor or driving performance. Despite their higher age and exposure to the operating room environment, the driving skills of the operating room nurses were similar to those of the ward nurses. The results suggest that tolerance to anaesthetic gases develops among operating room personnel. No impairment of driving skills can be expected after daily exposure to halothan and nitrous oxide among long-term employees in operating theatres.
Air Pollutants↗
Residual nitrous oxide in operating room personnel.
The concentrations of nitrous oxide in the blood and end-tidal air of 10 operating-room nurses were assayed by gas chromatography immediately and 1, 2, 5, and 21 h after 3 hours of exposure to an average of 380 ppm of nitrous oxide in operating-room air. In the second trial the nurses' end-tidal air concentrations of nitrous oxide were assayed on Monday, Wednesday, Friday and Sunday morning, and on Sunday afternoon and evening to reveal a possible accumulation of nitrous oxide during a routine week. After cessation of exposure there was a rapid decrease in the blood concentrations of nitrous oxide during the first hour (from 153 +/- 110 microgram/1 to 48 +/- 20 microgram/l at 1 h; means +/- s.d.), followed by a slower decrease. Small amounts (mean +/- s.d.: 18 +/- 6 microgram/l) of nitrous oxide were still measurable on the following morning 21 h after exposure. At 2 or 5 h after exposure there was an increase in blood and end-tidal air concentrations of nitrous oxide in seven and nine nurses, respectively. The end-tidal air concentrations of nitrous oxide were greater on Wednesday (22 +/- 7 microgram/l) than on Monday morning (8.4 +/- 1.5 microgram/l), but on Friday they were similar to those measured on Monday morning. The concentrations measured on Sunday, i.e. 2 days after exposure, were similar (average 15 microgram/l) to those measured during the week. It is concluded that, after cessation of exposure to nitrous oxide, there is a rapid decrease in the concentrations in blood and end-tidal air, but small amounts of nitrous oxide remain in the body for at least 3 days after cessation of exposure.
Air Pollutants↗
Cerebral effects of nitrous oxide in the dog.
The cerebral effects of nitrous oxide, 60 per cent, were examined in 27 dogs. During administration of halothane, 0.2 per cent, nitrous oxide increased cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMR02) to a maximum of 203 and 121 per cent of control, respectively. Cerebrospinal fluid pressure paralleled the change in CBF. The electroencephalogram (EEG) showed low-voltage slow-wave activity. With halothane, 0.8 per cent, nitrous oxide increased CBF and CMR02 to maximum values of 164 and 108 per cent of control, respectively. After administration of thiamylal, 8 mg/kg, intravenously, nitrous oxide did not increase CBF or CMR02 for the first 30-min period, but thereafter, CMR02 increased to 11 per cent above control. Pretreatment with reserpine, 0.5 mg/kg, intramuscularly, for two days did not modify the cerebral circulator and metabolic responses to nitrous oxide. These results indicate that nitrous oxide causes cerebral metabolic stimulation accompanied by an increase in CBF and slowing of the EEG. Sympathoadrenal stimulation would appear not to be the mechanism for the increases in CBF and CMR02. The cerebral effects of nitrous oxide are modified by the background anesthesia.
Animals↗
Nitrous oxide "analgesia": resemblance to opiate action.
Nitrous oxide produced a dose-related "analgesia" in mice (median effective dose, 55 percent). The analgesia was evaluated by means of a phenylquinone writhing test. Narcotic antagonists or chronic morphinization reduced nitrous oxide analgesia. Either nitrous oxide releases an endogenous analgesic or narcotic antagonists have analgesic antagonist properties heretofore unappreciated.
Analgesia↗
The effect of nitrous oxide on renal function in open heart surgery.
The renal function of 20 patients undergoing open-heart surgery was investigated pre-, per- and postoperatively. The patients were anaesthetized with a combination of morphine, halothane, oxygen and nitrous oxide (the nitrous oxide group), and the remaining ten with a combination of morphine, halothane, oxygen and air (the air group). The renal function tests included urine flow, sodium and potassium excretion, and creatinine and free water clearance. As a consequence of the anaesthesia, the mean arterial pressure declined half an hour after induction, being lower than the preoperative level by 15% (p less than 0.001) in the nitrous oxide group and lower by 11% (p less than 0.05) in the air group. At the same time the urine sodium/potassium ratio was 1.3 in the nitrous oxide group and 1.9 in the air group. Free water clearance was significantly (p less than 0.01) greater in the air group. During the perfusion the sodium/potassium excretion ratio was 1.7 in the nitrous oxide group and 4.1 in the air group (p less than 0.01). On the second day, creatinine clearance was significantly lower in the nitrous oxide group than in the air group (p less than 0.05). On the third day, urine flow was significantly higher and urine osmolality significantly lower (p less than 0.05) in the air group than in the nitrous oxide group.
Adolescent↗
Reduction of nitrous oxide contamination in a paediatric hospital.
Ambient nitrous oxide concentrations were recorded in an operating room during delivery of the gas at low and medium flow-rates, with and without the application of simple scavenging devices. Residual background levels of nitrous oxide were still present more than one hour after disconnection of the flowmeters and use of the room. Scavenging reduced concentrations ten-fold. Adjacent corridors and the post-anaesthetic recovery room were contaminated with nitrous oxide from the operating rooms and from patients. A vigorous programme of checking for leaks and repairing and maintaining equipment, coupled with the use of suction scavenging, can reduce atmospheric contamination with nitrous oxide below 30 p.p.m., which is well within the limit suggested by the U.S. National Institute for Occupational Safety and Health.
Air Pollution↗
"Recreational" misuse of nitrous oxide.
With the use of nitrous oxide increasing, overuse and excessive exposure to this gas are also more prevalent. Neuropathy, expressed as amnesia, aphasia or weakness, numbness, and incoordination affecting all extremities, is the common result of frequent overexposure. For optimal dental treatment, it is recommended that both patient and dentist be aware that nitrous oxide can be an exogenous toxin, damaging to neuronal structures, if used in excess.
Adult↗
Nitrous oxide and neutrophil chemotaxis in man.
Inhalation of 60% nitrous oxide in oxygen by seven adult male volunteers for 60 min was found to increase significantly polymorphonuclear leuocyte (PMN) chemotaxis, but not to influence total white or PMN blood cell counts. Also, the addition or morphine 0.2 mg kg-1 i.v. during the breathing of nitrous oxide did not alter any variable. These results indicate that nitrous oxide and nitrous oxide incombination with morphine do not depress PMN chemotaxis.
Adolescent↗
[The technique of arthroscopy with nitrous oxide insufflation (author's transl)].
Since April 1977 we have carried out more than 250 arthroscopies using a nitrous oxide insufflation device. Nitrous oxide is completely non-toxic to the tissues and is rapidly absorbed. Unlike carbon dioxide, which is the other commonly used insufflation gas, nitrous oxide does not combine with water to form an acid which can irritate the tissues. Furthermore, it is more rapidly absorbed than air. The normal insufflation pressure of 50 mm Hg is usually sufficient to expand the soft parts of the knee joint to the required degree. Interstitial nitrous oxide emphysema occurred in only 7 cases; it was of limited degree in each case and attributable to initial technical difficulties with the apparatus, selection of an excessive insufflation pressure, or additional stab incision. The nitrous oxide emphysema was always asymptomatic and, in some cases, was not even noticed by the patient. No infections of the knee joint or other serious complication followed insufflation with this device, which incorporated a bacterial filter.
Emphysema↗
Megaloblastic haemopoiesis in patients receiving nitrous oxide.
In a prospective study the incidence of megaloblastic change after ventilation with nitrous oxide for periods of up to 24 h has been determined and the cause of the altered D.N.A. synthesis studied with the deoxyuridine (dU) suppression test in 22 patients undergoing cardiac bypass surgery. 8 patients who received nitrous oxide and oxygen for 24 h had megaloblastic bone-marrow aspirates and abnormal dU suppression tests at the end of ventilation. 5 patients who received no nitrous oxide had normoblastic aspirates and normal dU suppression test. Of the remaining 9 patients, who received nitrous oxide during the operation only, 3 had abnormal dU suppression tests at 24 h. The abnormality revealed by the dU suppression tests was identical with that found in vitamin-B12 deficiency, but the patients' serum-B12 concentrations were normal. These results suggest that nitrous oxide interferes with the function of vitamin B12. Nitrous oxide oxidises vitamin B12 in vitro, and probably also in vivo when premixed 50% nitrous oxide and 50% oxygen mixture ('Entonox') is given.
Acute Disease↗
Nitrous oxide levels in operating room air with various gas flows.
Monitoring of nitrous oxide concentrations in operating rooms disclosed some leaks that had hitherto been unrecognized. Because nitrous oxide concentrations reported before 1967 had been obtained for the most part with high flows of the gas and without information concerning room air exchange, measurements were made of nitrous oxide levels during operations with an infra-red analyzer. after correction of leaks. Measurements were made at six sites in the operating-room suite, with and without scavenging. Flows that varied 0.1 to 2.5 litres of nitrous oxide were used in rooms that had 20 changes per hour of fresh air. Without scavenging, the highest time-weighted average value inhaled by any of the personnel (anaesthetists) was 31 ppm, when flow of 500 ml of nitrous oxide per minute were employed. The lowest reported deleterious concentration (unconfirmed) is 50 ppm. Lower flows produced lower values. With good scavenging, using flows as high as 2.51/min of nitrous oxide, the highest average value (anaesthetist) was 7.2 ppm. A short discussion is given concerning reasons for using low flows, including the cost of wasting agents and pollution of the entire atmosphere.
Air Pollutants↗
Peripheral vascular and cardiac effects of nitrous oxide in the bovine.
Peripheral vascular and myocardial effects of increasing concentrations of nitrous oxide (0 to 70 per cent) in oxygen were determined in 15 unanaesthetized calves before and after replacement in their natural heart (NH) with a pneumatically driven artificial heart (AH). Nitrous oxide produced concentration-related decreases in arterial and mixed venous pH and increases in minute ventilation and arterial and mixed venous carbon dioxide tensions in both NH and AH calves. Nitrous oxide resulted in significant increases in cardiac output, stroke volume and mean aortic, pulmonary artery and right atrial pressures in NH and AH calves, but did not significantly change systemic vascular resistance in either group of animals. Heart rate was increased in NH calves but was fixed in AH calves. Elevations in heart rate and cardiac output at nitrous oxide concentrations greater than 30 per cent and aortic pressure at 70 per cent nitrous oxide were significantly greater in NH than AH animals (P less than 0.05). These data demonstrate that nitrous oxide stimulates the cardiovascular system in spontaneously breathing mammals and that the changes result from improved venous return and an increase in myocardial chronotropy. Our findings also suggest that cardiovascular stimulation during nitrous oxide breathing may be related to increased concentrations of arterial and/or venous carbon dioxide.
Animals↗
Myeloneuropathy after prolonged exposure to nitrous oxide.
A neurological disorder developed after prolonged exposure to nitrous oxide in 15 patients, all but 1 of whom were dentists. 13 patients had abused nitrous oxide to some extent for periods ranging from 3 months to several years, but 2 patients were exposed to nitrous oxide only professionally, by working in poorly ventilated surgeries. Symptoms included early sensory complaints, Lhermitte sign, loss of balance, leg weakness, gait ataxia, impotence, and sphincter disturbances. Neurological examination showed sensorimotor polyneuropathy, often combined with signs of involvement of the posterior and lateral columns of the spinal cord. Electrodiagnostic tests pointed to an axonal polyneuropathy, but other laboratory results were normal, including examination of the spinal fluid. The neurological picture is similar to that of subacute combined degeneration of the spinal cord, and it is possible that nitrous oxide interferes with the action of vitamin B12 in the nervous system.
Adult↗
The influence of nitrous oxide anaesthetic on middle-ear fluid.
Nitrous oxide anaesthesia invades the middle-ear cavity, resulting in a positive pressure within this cavity. It has been suggested that the pressure may be sufficient to force open the Eustachian tube and evacuate fluid from the middle ear. This study examined the possible influence of nitrous oxide on middle-ear fluid. Pre- and intra-operative tympanograms were obtained on 39 children scheduled for myringotomy surgery. Fluid was found in 83.1% of the operated ears while the absence of fluid was noted in 16.9%. It is possible that the nitrous oxide anaesthetic did cause an evacuation of fluid from this latter group of ears prior to actual surgery.
Acoustic Impedance Tests↗
Cerebral responses to the addition of nitrous oxide to halothane in man.
Cerebral responses to the substitution of 60% nitrous oxide for nitrogen during halothane anaesthesia (0.84%, end-tidal) were studied in four patients during surgery. The mean (+/-SEM) cerebral blood flow equivalent and internal jugular venous oxygen tension during halothane anaesthesia, 17+/-3 ml blood/ml oxygen and 41+/-2 mm Hg respectively, increased significantly to 45+/-3 ml blood/ml oxygen and 54+/-3 mm Hg following the introduction of nitrous oxide. On the withdrawal of nitrous oxide, the mean cerebral blood flow equivalent and internal jugular venous oxygen tension returned gradually to the control values. Cerebral perfusion pressure and blood-gas values, other than the internal jugular venous oxygen tension, did not change significantly. Marked slowing of the e.e.g. was observed following the addition of nitrous oxide to halothane, Upon the withdrawal of nitrous oxide the e.e.g. returned to the control pattern. These results indicate that cerebral blood flow was in excess of oxygen demand during nitrous oxide/halothane anesthesia in man.
Anesthesia↗