Cardiac output nitrous oxide

The alveolar rate of rise toward the inspired concentration (Fa/Fi) is accelerated by an increase in alveolar ventilation from 2 to 4 and from 4 to 8 liters per minute (constant cardiac output). The increase is greatest with the more soluble agent, halothane, and smaller with the least soluble anesthetic, nitrous oxide. (Reprinted with permission from Eger El II [ed.]. Anesthetic Uptake and Action. Baltimore Williams Wilkins, 1974.)... 

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. 

An increase in pulmonary blood flow (increased cardiac output) slows the rate of rise in arterial tension, particularly for those anesthetics with moderate to high blood solubility. This is because increased pulmonary blood flow exposes a larger volume of blood to the anesthetic thus, blood "capacity" increases and the anesthetic tension rises slowly. A decrease in pulmonary blood flow has the opposite effect and increases the rate of rise of arterial tension of inhaled anesthetics. In a patient with circulatory shock, the combined effects of decreased cardiac output (resulting in decreased pulmonary flow) and increased ventilation will accelerate the induction of anesthesia with halothane and isoflurane. This is not likely to occur with nitrous oxide, desflurane, or sevoflurane because of their low blood solubility. 

In contrast to isoflurane and desflurane, sevoflurane tends not to increase the heart rate, and is usually well tolerated for induction of anesthesia in young children. However, profound bradycardia was reported in four unpremedicated children aged 6 months to 2 years during anesthesia induction with sevoflurane 8% and nitrous oxide 66% (7). The episodes were not associated with loss of airway or ventilation. In three of the children there was spontaneous recovery of heart rate when the sevoflurane concentration was reduced the other child received atropine because of evidence of significantly reduced cardiac output. In a previous study of sevoflurane induction of anesthesia in children with atropine premedication there was also a low incidence of this complication (8), which is probably due to excessive sevoflurane concentrations. 

CNS depressants (e.g., hypnotics/sedatives, inhalational anesthetics, narcotics) can increase the CNS depression induced by propofol. Morphine premedication with nitrous oxide decreases the necessary propofol maintenance infusion rate and therapeutic blood concentrations when compared to nonnarcotic (e.g., lorazepam) premedication. In addition, the induction dose requirements of propofol may be reduced in patients with IM or IV premedication, particularly with narcotics alone or in combination with sedatives. These agents may increase the anesthetic effects of propofol and may also result in more pronounced decreases in systolic, diastolic, and mean arterial pressures and cardiac output. 

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. 

In normal volunteers, inhalation of Ento-nox (a 50 50 mixture of nitrous oxide and oxygen) leads to depression of cardiac output (SED VIII). Caution in its use in patients with myocardial infarction is therefore necessary, but recently Kerr et al. (12 ) have reported that after the use of Entonox they did not find any change in cardiac rhythm or haemodynamic status . 

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