Halogenated hydrocarbons halothane

Poa polarographic electrode "error" due to halogenated hydrocarbons (eg, Halothane)... 

The mechanism of action of inhalational anesthetics is unknown. The diversity of chemical structures (inert gas xenon hydrocarbons halogenated hydrocarbons) possessing anesthetic activity appears to rule out involvement of specific receptors. According to one hypothesis, uptake into the hydrophobic interior of the plasmalemma of neurons results in inhibition of electrical excitability and impulse propagation in the brain. This concept would explain the correlation between anesthetic potency and lipophilicity of anesthetic drugs (A). However, an interaction with lipophilic domains of membrane proteins is also conceivable. Anesthetic potency can be expressed in terms of the minimal alveolar concentration (MAC) at which 50% of patients remain immobile following a defined painful stimulus (skin incision). Whereas the poorly lipophilic N2O must be inhaled in high concentrations (>70% of inspired air has to be replaced), much smaller concentrations (<5%) are required in the case of the more lipophilic halothane. 

Inhalation anesthetics still in use include nitrous oxide and the halogenated hydrocarbon inhalation anesthetics such as halothane, isoflurane, methoxyflurane and sevoflurane. 

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. 

Similar disturbances in intracranial pressure and coronary blood flow occur with most of the halogenated hydrocarbons. In addition, renal blood flow, filtration, and urine output decrease with the use of halothane. These changes also occur with other inhalational agents that reduce arterial blood pressure. 

Halothane and all other halogenated hydrocarbons cause some relaxation of skeletal muscle. The relaxation is not adequate when muscle paralysis is a requirement of the operative procedure, but halothane s action will... 

E. Reduced peripheral vascular resistance occurs with most halogenated hydrocarbons, and reflex tachycardia may be a concern. Halothane may be the clearest exception, since there appears to be a balance between relaxation and constrictor influences in various vascular beds with this agent so that total peripheral resistance changes very little. Halothane is the agent of concern when sensitization of the myocardium to catecholamine-induced arrhythmias may be important, such as during incidences of hypercapnia. Sevoflurane does not directly influence sympathetic function. However, reflex tachycardia can occur. Reflex sympathetic... 

In the nucleus accumbens of rats the dopamine concentration was increased by both cyclopropane and halothane anesthesia cyclopropane, but not halothane, also increased the dopamine concentration in the caudate nucleus halothane, but not cyclopropane, significantly reduced the dopamine concentration in the ventral nucleus of the thalamus (4). It has been suggested that potentiation of the actions of dopamine could occur with cyclopropane or halogenated hydrocarbon anesthetics, but there is no direct evidence that this interaction occurs in humans. 

Since halogenated hydrocarbons are viewed as relatively inert, it is not surprising that up to 80% of the inspired (and absorbed) halothane that is exhaled is unchanged. Most of the remainder is also excreted unchanged. However, a small fraction is reductively dehalo-genated. As expected, it is the weaker C-Cl and C-Br bonds that yield their halides as ions. The C-F bond appears undaunted. Thus trifluoroacetic acid (from the acid chloride) is identified in the urine (Eq. 12.4). However, in the case of enflurane and its analog isoflu-rane, trace quantities of F have been also identified. 

Figure 23-18 presents typical absorption spectra with the essential bands of COj, NjO, anesthetic agents, and water vapor. Halogenated hydrocarbons such as Halothane, Ethrane, and Isoflurane are used as anesthetic agents [19]. 

The measurement of halogenated hydrocarbons such as Halothane, Enflurane, and Isoflurane, which are used as vaporized anesthetic agents, is of moderate clinical relevance. The main applications are monitoring of over- and underdosing, to control anesthesia depth, brain perfusion, or blood pressure during speciHc phases of the surgical procedure [19, 24]. In addition, this type of measurement is used to determine malfunctions of anesthetic agent vaporizers. 

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 ... 

Katz RL, Matteo RS, Rapper EM. The injection of epinephrine during general anesthesia with halogenated hydrocarbons and cyclopropane in man. 2. Halothane. Anesthesiology (1962) 23, 597-600,... 

It seems possible that the general adverse hepatotoxic effects of halothane can slow the normal rate of phenytoin metabolism. One suggested explanation for the increased adverse effects on the liver is that, just as in animals, pre-treatment with phenobarbital and phenytoin increases the rate of drug metabolism and therefore the hepatotoxicity of halogenated hydrocarbons, including carbon tetrachloride and halothane. As well as increased metabolism, the halothane-rifampicin interaction might also involve additive hepatotoxicity. 

Many hydrocarbon TIC also have a direct effect on the conducting system of the heart causing dysrhythmias. This is sometimes seen in general anaesthesia, particularly with halogenated hydrocarbon compounds such as halothane. 

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