Use of Nitrous = Oxide in Anaesthesia =96 to Abandon

Use of Nitrous Oxide in Anaesthesia =96 to=20 Abandon

DR.P.SELVAKUMAR

CONSULTANT CARDIAC & NEURO = ANAESTHESIOLOGIST=20

APOLLO SPECIALITY = HOSPITALS

MADURAI

Nitrous Oxide is among = the most=20 ubiquitous anaesthetics used in the world today. Since its successful=20 introduction into anesthetic practice in 1848, more anaesthetist have = used=20 nitrous oxide than any other substances for inducing analgesia. Nitrous = oxide=20 does have limitations and, like any other drug utilized in anaesthetic = practice,=20 it must be used with respect to its effect on the various body systems. = Current=20 data and recommendations will provide to enable us to make a decision = whether=20 (or) not to include this drug in a given anaesthetic = plan.

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Nitrous oxide, by its = very nature=20 is an inhaled anaesthetic and, as such, has multiple effects. Until = rather=20 recently, nitrous oxide was considered by many to be essentially inert = and to=20 have minimal, if any biologic effect. This point of view now has been = shown to=20 be largely incorrect. Indeed the use of this anaesthetic substance under = appropriate conditions can have profound influence.

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Effects of Nitrous Oxide on the=20 Heart

=20 Lappas et al=20 studied the effects of nitrous oxide on ventricular performance and = pulmonary=20 circulation. They found that 50% nitrous oxide significantly decreased = mean=20 arterial pressure, cardiac index, stroke index, LVSWI and rate pressure = product=20 (RPP). Mean pulmonary artery pressure and pulmonary artery resistance = increased,=20 when nitrous oxide was discontinued, all variables returned to control = except=20 mean pulmonary artery pressure. They concluded that nitrous oxide = depresses left=20 ventricular performance and increases pulmonary vascular resistance due = to ά =96=20 adrenergic effects.

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In order to eliminate any = confounding effects of other inhalational anaesthetics Smith performed = this=20 study in subjects who were breathing room air and recorded cardiac = function with=20 BCG (Ballisto Cardiogram). After base line recordings were taken, 40% = nitrogen=20 and then 40% nitrous oxide in oxygen were administered. Second portion = of the=20 study involved invasive monitoring and the determination of cardiac = output. The=20 investigators found a steady and apparently direct depression of = myocardial=20 function (up to 20% on BCG) during 30 minutes of nitrous oxide in = oxygen=20 breathing.

Effects of Nitrous Oxide on the Coronary=20 Artery

a) = Lone=20 et al did show that regional dysfunction in compromised myocardium in = the form=20 of post systolic shortening occurs with introduction of nitrous=20 oxide.

b) =20 Second study showed that = nitrous=20 oxide administration caused regional dysfunction in canine myocardium, = supplied=20 by a critical left anterior descending artery, whether administered = gradually or=20 abruptly and at concentrations as low as 40%.

c) = Cahealn and colleagues = evaluated=20 the effect of nitrous oxide when it was given in presence of fentanyl=20 anaesthesia. Two groups- Nitrogen 60% and Nitrous oxide = 60%- were=20 monitored by the very sensitive TEE. No new segmental wall motion = abnormality=20 was seen during the inhalation of either test gas. They concluded that = nitrous=20 oxide does not induce myocardial ischemia when used as an adjunct to = fentanyl=20 anaesthesia in patients with severe coronary artery disease and normal = left=20 ventricular function.

d) =20 Nitrous oxide had = deleterious=20 effects in patients with pulmonary hypertension undergoing cardiac=20 surgery.

It has long been = considered that=20 nitrous oxide has little influence on cardiac rhythm, despite minor but=20 significant sympathetic stimulation, but Roizen at the University of = Chicago=20 observed that the administration of nitrous oxide may be responsible for = some=20 episodes of atrio-ventricular junctional rhythm in the presence of = narcotic (or)=20 volatile anesthetic agent.

Cont..2

Effects on Respiratory = System

1) = Airway conductance fell = with the=20 administration of nitrous oxide and despite the lack of any evidence of = induced=20 bronchoconstriction, it may increase work of breathing = .

2) = Depress mucociliary = action =96 causes=20 increased incidence of atelectasis in post-operative=20 thoracotomy and upper abdominal procedures.

The recommendation might = be that in=20 patients who will undergo respiratory compromise, whether from=20 broncoconstrictive disease (or) from the procedure itself (upper = abdominal=20 /thoracic) nitrous oxide should not be used casually. Indeed, = supplementation=20 with narcotics to an air/oxygen combination in conjunction with a = judicious=20 amount of potent inhalation agent (to take advantage of the broncho = dilation=20 effect) might be more prudent.

A final mention = concerning the=20 second gas effect is appropriate here. Potential harmful effects are = avoided by=20 administering oxygen for a few minutes before removing the face mask = (or)=20 endotracheal tube.

Neurophysiological effects of Nitrous=20 Oxide

=20 The = patients=20 were anaesthetized and examined for difference in cerebral blood = flow=20 (CBF), cerebro vascular resistance = (CVR), and=20 cerebral metabolic rate. The analysis reveals statistical increase in = CBF but no=20 significant change in CMRO2 . The vasodilatation caused by nitrous oxide = when=20 administered with iIsoflurane was not due to activation of the CMR but = rather=20 was more likely due to direct vasodilatation properties of nitrous = oxide.=20 Henricksen and Jorgensen demonstrated that hyperventilation could alter = the=20 amount of cerebral blood flow significantly and that the nitrous=20 oxide effect could be =93Hidden=94. Several points of = significant=20 clinical importance are still unanswered. How much hyperventilation is = required=20 before the nitrous oxide effects are blocked? Can the effect be = completely=20 blocked? The question of whether nitrous oxide has seizure-generation = capability=20 has not been fully investigated. In the literature there is one case = report=20 involving one patient, this patient had seizures in response to both=20 halothane=96nitrous oxide and nitrous oxide alone but not to halothane=20 alone.

Cont..3

When neurosurgical = patient are=20 operated upon in the sitting position, the possibility of pneumocephalus = is a=20 definite consideration. When the patient is breathing a nitrous oxide=20 combination, this mixture will equilibrate with air in any air=96filled = space,=20 since it is 34 times more soluble than nitrogen this will result in a = net=20 increase of gas molecules in the space. =20 As a result there is an increase in volume (or) pressure. A = tension=20 pneumochepahalus may result, causing altered consciousness, seizure or=20 neurological deficits.

Toxic Effects

In 1978 Layer reported a = series of=20 15 patients referred to him for work up all of whom had prolonged = exposure to=20 nitrous oxide. The patients who had been working in poorly ventilated = areas had=20 symptoms like loss of balance, leg weakness, gait ataxia, impotence and=20 sphincter disturbances.

Neurological examination = showed=20 sensorymotor polyneuropathy which was combined with signs of posterior = and=20 lateral column spinal cord involvement, electromyography showed = incidence of=20 denervation. They felt that nitrous oxide produces a reversible = dysfunction in=20 the nervous system similar to that produced by vitamin B12 deficiency. = Nitrous=20 oxide has been shown to inhibit methionine synthetase activity, by = inactivating=20 the co-factor cyanocobalamin(B12). Anaesthesiologists are exposed to = higher=20 concentrations than dentists and the procedures involved generally are = some what=20 longer. There are various means of scavenging, each designed to conform = to the=20 different machines used in the work areas. The National Institute of=20 Occupational Safety and Health has proposed that nitrous oxide = concentration in=20 the atmosphere should be less than 25 ppm = and typical=20 health codes mandate frequent air changes.

Effects on Closed = Spaces

Nitrous oxide enters a = closed space=20 more quickly than does nitrogen due to the fact that it is 34 times more = soluble. Eger and Saidman in 1964 studied the hazards of = pneumothorax=20 and bowel obstruction when nitrous oxide was administered. = They=20 found intestinal gas volume increased 75% to 100% in 2 hours and 100 to = 200% in=20 4 hours, similarly air placed in the pleural space doubled in volume in = 10=20 minutes and tripled in 45 minutes.

Cont..4

The presence of = pneumothorax is an=20 absolute contraindication to the use of nitrous oxide. Hunter in 1955 = found that=20 patients with pneumothorax, pneumoperitoneum or pneumopericardium = worsened with=20 nitrous oxide administration and subsequently found that the gas had = diffused=20 into these spaces, increasing the local pressure. In middle ear surgery = it is=20 known that middle ear pressure may become excessive if eustachian tube = function=20 is compromised by illness. Induced tympanic membrane rupture has been = attributed=20 to this mechanism. It is obvious that in a situations in which the = volume of gas=20 can double in 2 hours in colon, cause high pressure in the middle ear = and double=20 in the pleural space in 10 minutes nitrous oxide is strongly=20 contraindicated.

Nausea and Vomiting

Nitrous oxide can cause = emetic=20 symptoms via several mechanisms, both peripheral and central. If = diffuses in to=20 the gastro intestinal tract more quickly than nitrogen can diffuse out = resulting=20 in bowel distention which can lead to nausea and vomiting. It can = diffuse into=20 the middle ear greatly increasing pressure there. It also can interact = centrally=20 with the endogenous opioid receptor system, thereby stimulating nausea = and=20 vomiting at this level.

Nitrous Oxide and = Pregnancy

=20 Since = nitrous=20 oxide is a small non polar molecule, it is relatively easy for this = agent to=20 cross the placenta and enter the fetal circulation Dutta et al reported = that the=20 neonates consistently had Apgar scores of less than 7 when anesthetized = for more=20 than 10 minutes. The presence of nitrous oxide in high concentration in = fetal=20 blood results in partial pressures of the gas in the neonates alveoli, = which=20 interferes with oxygenation. This occurs whether or not the fetus is = depressed.=20 However it should be noted carefully that the rate of washout in the = newborn is=20 significantly less than that of the mother. While diffusion hypoxia is = perhaps a=20 theoretical issue, those data and prudence strongly indicate that the = baby=20 should be given oxygen until there is clinical evidence that there is no = more=20 hypoxemia.

Cont..5

The Parturient and Fetus =96 Teratogenic=20 Effects

&nbs= p; =20 Result of the American Dental Association and National Institute = of=20 Occupational Safety and Health study indicated that females exposed to = nitrous=20 oxide had statistically significant increase in the incidence of = neurological=20 disease, congenital malformations in their children and spontaneous = abortion=20 rates. It is prudent then not to administer this agent during the first=20 trimester and to consider using, when possible, regional anaesthesia or = a high=20 dose narcotic/ muscle relaxant techniques when general anaesthesia must = be=20 administered. There is accumulating laboratory evidence that nitrous = oxide may=20 possess neuro degenerative effects on the developing brain, it may be = prudent to=20 omit it from a general anesthetic technique in developing=20 infants.

MESSAGE

&nbs= p; =20 These recent investigations and reports of adverse CNS effects of = nitrous=20 oxide serve to highlight its potential for harm in the patients. It is = unlikely=20 that the therapeutic margin of nitrous oxide will ever become small = enough to=20 preclude its use altogether.