Nitrous oxide cardiovascular effects

Nitrous oxide is the only inhalation anesthetic that is a gas. It is chemically inert. Nitrous oxide has little effect on overall cardiovascular function. Disadvantages are that it has no muscle relaxing effect and that it cannot be used on its own because of high Minimal Alveolar Concentration values needed for adequate anesthesia. During recovery there is a risk for hypoxia and anesthesia should be slowly tapered off to prevent this event. 

Halogenated hydrocarbon inhalation anesthetics may increase intracranial and CSF pressure. Cardiovascular effects include decreased myocardial contractility and stroke volume leading to lower arterial blood pressure. Malignant hyperthermia may occur with all inhalation anesthetics except nitrous oxide but has most commonly been seen with halothane. Especially halothane but probably also the other halogenated hydrocarbons have the potential for acute or chronic hepatic toxicity. Halothane has been almost completely replaced in modern anesthesia practice by newer agents. 

Nitrous oxide has both a direct depressant and sympthomimetic effect on the myocardium. In healthy patients these tend to counterbalance each other, the resultant effect being minimal cardiovascular depression. In patients with car-diovascular disease or who are taking conconcurrent medication with, e.g. 3 blockers, its depressant effect may be more obvious. Nitrous oxide supplementation of high-dose opioid-based anaesthesia may result in a reduction in cardiac output and heart rate although the mechanism of this is unclear. Nitrous oxide may have a venoconstrictor effect resulting in increased pulmonary vascular resistance, particularly in the presence of pulmonary hypertension. 

Recovery is sufficiently rapid with most intravenous drugs to permit their use for short ambulatory (outpatient) surgical procedures. In the case of propofol, recovery times are similar to those seen with sevoflurane and desflurane. Although most intravenous anesthetics lack antinociceptive (analgesic) properties, their potency is adequate for short superficial surgical procedures when combined with nitrous oxide or local anesthetics, or both. Adjunctive use of potent opioids (eg, fentanyl, sufentanil or remifentanil see Chapter 31) contributes to improved cardiovascular stability, enhanced sedation, and perioperative analgesia. However, opioid compounds also enhance the ventilatory depressant effects of the intravenous agents and increase postoperative emesis. Benzodiazepines (eg, midazolam, diazepam) have a slower onset and slower recovery than the barbiturates or propofol and are rarely used for induction of anesthesia. However, preanesthetic administration of benzodiazepines (eg, midazolam) can be used to provide anxiolysis, sedation, and amnesia when used as part of an inhalational, intravenous, or balanced anesthetic technique. 

Rupp SM, Fahey MR, Miller RD. Neuromuscular and cardiovascular effects of atracurium during nitrous oxide-fentanyl and nitrous oxide-isoflurane anaesthesia. Br J Anaesth 1983 55(Suppl l) S67-70. 

Murray DJ, Mehta MP, Choi WW, Forbes RB, Sokoll MD, Gergis SD, Rudd GD, Abou-Donia MM. The neuromuscular blocking and cardiovascular effects of doxacurium chloride in patients receiving nitrous oxide narcotic anesthesia. Anesthesiology 1988 69(4) 472-7. 

Mckinney MS, Fee JP. Cardiovascular effects of 50% nitrous oxide in older adult patients anaesthetized with isoflurane or halothane. Br J Anaesth 1998 80(2) 169-73. 

Choi WW, Mehta MP, Murray DJ, Sokoll MD, Forbes RB, Gergis SD, Abou-Donia M, Kirchner J. Neuromuscular and cardiovascular effects of mivacurium chloride in surgical patients receiving nitrous oxide-narcotic or nitrous oxide-isoflurane anaesthesia. Can J Anaesth 1989 36(6) 641-50. 

Savarese JJ, Ah HH, Basta SJ, Scott RP, Embree PB, Wastila WB, Abou-Donia MM, Gelb C. The cardiovascular effects of mivacurium chloride (BW B1090U) in patients receiving nitrous oxide-opiate-barbiturate anesthesia. Anesthesiology 1989 70(3) 386-94. 

From RP, Pearson KS, Choi WW, Abou-Donia M, Sokoll MD. Neuromuscular and cardiovascular effects of mivacurium chloride (BW B1090U) during nitrous oxide-fentanyl-thiopentone and nitrous oxide-halothane anaesthesia. Br J Anaesth 1990 64(2) 193-8. 

Cardiovascular effects Most inhaled anesthetics decrease arterial blood pressure moderately. Enflurane and halothane are myocardial depressants that decrease cardiac output, while isoflurane causes peripheral vasodilation. Nitrous oxide is less likely to lower blood pressure than are other inhaled anesthetics. Blood flow to the liver and kidney is decreased by most inhaled agents. Halothane may sensitize the myocardium to the arrhythmogenic effects of catecholamines. 

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