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Halothane partial pressure

In contrast, with halothane, partial pressure in blood is low and tissue uptake is high, resulting in a much slower elimination. [Pg.218]

Increases in blood solubility without corresponding increases in tissue solubility slow the rate at which halothane increases in the alveoli. Because of the increased content of this anaesthetic in the blood flowing through the tissues, however, the halothane partial pressure in the tissues approaches equilibrium more rapidly than in the alveoli. The net consequence is that the time for induction with halothane is not greatly affected by changes in blood solubility, although the... [Pg.51]

Uptake curves for inhaled anesthetics Figure 11.6 illustrates the uptake curves for four inhalation anesthetics. The solubility in blood, as well as tissues, is in the following order halothane > enflurane > isoflurane > nitrous oxide. Because of its low solubility, the partial pressure of nitrous oxide in the inspired mixture and the body most rapidly achieves a steady-state. [Pg.123]

C. M. Coburn and E. 1. Eger. The partial pressure of isoflurane or halothane does not affect their solubility in rabbit blood or brain or human brain inhaled anesthetics obey Henry s law. Anesth. Analg., 65, 960-2 (1986)... [Pg.54]

Answer D. Saturation of the blood with inhaled anesthetics is more rapid if they have a low blood-gas partition coefficient. This results in the more rapid achievement of a partial pressure of the dissolved anesthetic molecules commensurate with their movement out of the blood into the alveolar spaces of the lung, where they are eliminated. Note that the same physicochemical characteristic is responsible for the rapid onset of the anesthetic action of sevoflurane. Although redistribution of anesthetics between tissues occurs, it is not responsible for rapid recovery. MAC values are a measure, of anesthetic potency. With the exception of halothane (and methoxyflurane), inhaled anesthetics are not metabolized to a significant extent. Naloxone is an opioid receptor antagonist. [Pg.183]

If the patient anesthetized with halothane is allowed to breathe spontaneously, an increased partial pressure of carbon dioxide in the arterial blood is common and is indicative of ventilatory depression. There also is an increased difference between the partial pressure of oxygen in the alveolar gas and in the arterial blood, indicating less efficient exchange of gas. Halothane thus influences both ventilatory control and the efficiency of oxygen transfer. To compensate for these effects, ventilation frequently is assisted or controlled by manual or mechanical means, and the concentration of inspired oxygen is increased. [Pg.319]

In clinical practice, one can monitor the equilibration of a patient with anesthetic gas. Equilibrium is achieved when the partial pressure in inspired gas is equal to the partial pressure in end-tidal (alveolar) gas. This defines equilibrium because it is the point at which there is no net uptake of anesthetic from the alveoh into the blood. For inhalational agents that are not very soluble in blood or any other tissue, equilibrium is achieved quickly (e.g., nitrous oxide, Figure 13-4). If an agent is more soluble in a tissue such as fat, equilibrium may take many hours to reach. This occurs because fat represents a huge anesthetic reservoir that will be filled slowly because of the modest blood flow to fat (e.g., halothane, Figure 13 ). [Pg.232]

A. Classification and Pharmacokinetics The agents currently used in inhalation anesthesia are nitrous oxide (a gas) and several easily vaporized liquid halogenated hydrocarbons, including halothane, desflurane. enflurane, isoflurane, sevoflurane, and methoxyflurane. They are administered as gases their partial pressure, or tension, in the inhaled air or in blood or other tissue is a measure of them concentration. Since the standard pressure of the total inhaled mixture is atmospheric pressure (760 mm Hg at sea level), the partial pressure may also be expressed as a percentage. Thus 50% nitrous oxide in the inhaled air would have a partial pressure of 380 mm Hg. The speed of induetion of anesthetic effects depends on several factors ... [Pg.230]

Figure 25-2. Why induction of anesthesia is slower with more soluble anesthetic gases and faster with less soluble ones. In this schematic diagram, solubility is represented by the size of the blood compartment (the more soluble the gas, the larger the compartment). For a given concentration or partial pressure of the two anesthetic gases in the inspired air, it will take much longer with halothane than with nitrous oxide for the blood partial pressure to rise to the same partial pressure as in the alveoli Since the concentration in the brain can rise no faster than the concentration in the blood, the onset of anesthesia will be much slower with halothane than with nitrous oxide. (Reproduced, with permission, from Katzung BG [editor] Basic Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)... Figure 25-2. Why induction of anesthesia is slower with more soluble anesthetic gases and faster with less soluble ones. In this schematic diagram, solubility is represented by the size of the blood compartment (the more soluble the gas, the larger the compartment). For a given concentration or partial pressure of the two anesthetic gases in the inspired air, it will take much longer with halothane than with nitrous oxide for the blood partial pressure to rise to the same partial pressure as in the alveoli Since the concentration in the brain can rise no faster than the concentration in the blood, the onset of anesthesia will be much slower with halothane than with nitrous oxide. (Reproduced, with permission, from Katzung BG [editor] Basic Clinical Pharmacology, 8th ed. McGraw-Hill, 2001.)...
Methoxyflurane (Penthmne) is the most potent inhala-tional agent available, but its high solubility in tissues limits its use as an induction anesthetic. Its pharmacological properties are similar to those of halothane with some notable exceptions. For example, since methoxyflurane does not depress cardiovascular reflexes, its direct myocardial depressant effect is partially offset by reflex tachycardia, so arterial blood pressure is better maintained. Also, the oxidative metabolism of methoxyflurane results in the production of oxalic acid and fluoride concentrations that approach the threshold of causing renal tubular dysfunction. Concern for nephrotoxicity has greatly restricted the use of methoxyflurane. [Pg.304]

Enflurane produces a dose-related decrease in systemic arterial blood pressure secondary to reductions in cardiac output and systemic vascular resistance. There is evidence that cardiac output is partially maintained by a compensatory increase in heart rate. This effect seems dependent on a degree of hypercardia and does not occur during controlled ventilation. Enflurane and halothane depress myocardial contractility to a similar extent and less than isoflurane. Enflurane does not sensitise the heart to the effects of catecholamines to any significant extent and adrenaline (epinephrine) may be given subcutaneously for control of bleeding. [Pg.63]


See other pages where Halothane partial pressure is mentioned: [Pg.216]    [Pg.140]    [Pg.216]    [Pg.140]    [Pg.303]    [Pg.52]    [Pg.540]    [Pg.540]    [Pg.95]    [Pg.586]    [Pg.587]    [Pg.173]    [Pg.52]    [Pg.52]    [Pg.291]    [Pg.476]    [Pg.747]    [Pg.72]   
See also in sourсe #XX -- [ Pg.51 ]




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