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Volatile agents

Carbon monoxide is a stable gas. Metal carbonyls are relatively unstable and sensitive to light and moderately high temperatures. They may spontaneously ignite on contact with air. Volatile agents are stored in steel cylinders otherwise, agents are stored in steel or glass containers. Metal carbonyls may be stored under an inert gas blanket, such as nitrogen, to prevent contact with the air. [Pg.256]

If low volatility agent aerosols or metal fumes have been released, all foodstuffs in the area should be considered contaminated. Unopened items packaged in glass, metal, or heavy duty plastic may be used after decontamination of the container. Opened or unpackaged items, or those packaged only in paper or cardboard, should be destroyed. [Pg.267]

Animals exposed to volatile pulmonary agents do not require decontamination. If low volatility agent aerosols have been released, animals can be decontaminated with shampoo/soap and water (see Section 10.5.3). If the animals eyes have been exposed to the agent, they should be irrigated with water or saline solution for a minimum of 30 minutes. [Pg.267]

If low volatility agent aerosols or metal fumes have been released, the topmost layer of unprotected feedstock (e.g., hay or grain) should be destroyed. The remaining material should be quarantined until tested for residue. It is unlikely that sufficient residue would remain on leaves of forage vegetation to pose a significant threat. [Pg.267]

Many irritating and lachrymatory agents are nonvolatile and produce negligible amounts of vapor. Vapors of volatile agents have a density greater than air and tend to collect in low places. [Pg.405]

Inhalation in the form of an aerosol (p. 12), a gas, or a mist permits drugs to be applied to the bronchial mucosa and, to a lesser extent, to the alveolar membranes. This route is chosen for drugs intended to affect bronchial smooth muscle or the consistency of bronchial mucus. Furthermore, gaseous or volatile agents can be administered by inhalation with the goal of alveolar absorption and systemic effects (e.g inhalational anesthetics, p. 218). Aerosols are formed when a drug solution or micron-ized powder is converted into a mist or dust, respectively. [Pg.14]

Induction of anesthesia - Administer at an infusion rate of 0.5 to 1 mcg/kg/min with a hypnotic or volatile agent for the induction of anesthesia. If endotracheal intubation is to occur less than 8 minutes after the start of infusion of remifentanil, then an initial dose of 1 mcg/kg may be administered over 30 to 60 seconds. [Pg.874]

Bearing in mind the technical difBculties arising from volatile organic solvents as precipitants, we also looked for ribosomes that are stable under high salt concentrations they could perhaps be crystallized using conventional precipitants such as ammonium sulfate or other non-volatile agents. Thus the crystals could be handlai with less difficulties and mounted in the conventional way in X-ray capillaries. [Pg.63]

Nitrous oxide is used for induction and maintenance of anaesthesia. It is widely used as carrier gas for other volatile agents in general anaesthesia. The usual concentra-... [Pg.61]

No interactions with volatile agents or gases No binding... [Pg.52]

Figure 3.1 Graph showing the ratio between inspired (FJ) and alveolar (FA) end-tidal concentrations of the agents shown. The least soluble agents approach equilibrium (FA/FI=1) the most rapidly. Also, since both inhalation and intravenous anaesthetic drugs tend to reduce cardiac output, they facilitate the uptake of volatile agents. It follows that any inhaled anaesthetic drug must be given with great caution to patients in shocked states, e.g. hypovolaemia, arrhythmias, myocardial infarction. Figure 3.1 Graph showing the ratio between inspired (FJ) and alveolar (FA) end-tidal concentrations of the agents shown. The least soluble agents approach equilibrium (FA/FI=1) the most rapidly. Also, since both inhalation and intravenous anaesthetic drugs tend to reduce cardiac output, they facilitate the uptake of volatile agents. It follows that any inhaled anaesthetic drug must be given with great caution to patients in shocked states, e.g. hypovolaemia, arrhythmias, myocardial infarction.
The stability of modern volatile agents is the result of the heavy fluorination of the ether molecule. The effect is most pronounced for CF3 and CF2 moieties. In the case of desflurane, of the eight available binding sites for halogens, six are occupied by fluorine atoms. Similarly, sevoflurane has seven fluorine atoms out of a possible ten. The lack of hydrogen atoms reduces both flammability and potency. [Pg.55]

The pharmacodynamic effects of all volatile agents on body systems may be modified by surgical stimulation depending on the depth of anaesthesia. The pharmacological properties of the drugs described below are those of the agents in the absence of surgical stimulation unless otherwise stated. [Pg.56]

Isoflurane has a dose-dependent depressant effect on the myocardium. In vitro studies indicate that it reduces myocardial contractility to a similar extent as halothane. In vivo, isoflurane appears to be less of a cardiovascular depressant than other volatile agents. [Pg.56]

There is a dose-dependent decrease in systemic blood pressure during isoflurane anaesthesia. This is mainly the result of a marked reduction in peripheral vascular resistance. In contrast, the decrease in arterial blood pressure during halothane anaesthesia appears to be mainly the result of a reduction in myocardial contractility. Isoflurane, in common with other volatile agents, has little effect on pulmonary artery pressure or pulmonary vascular resistance. [Pg.57]

Isoflurane, like other volatile agents, causes a transient reduction in renal blood flow, glomerular filtration rate and urinary output, but there is no evidence that these changes are harmful to the healthy kidney. Similarly, there is no evidence that isoflurane has any undesirable effects on the transplanted kidney. In... [Pg.59]

Sevoflurane, in common with all volatile agents, reduces cardiac output and systemic blood pressure. It does so mainly through a reduction in peripheral vascular resistance. Although it is a systemic vasodilator it does not appear to produce significant dilatation of small coronary vessels and there is no possibility of coronary steal as hypothesised for isoflurane. A small increase in heart rate may be observed. This is less pronounced than with isoflurane and desflurane and is almost certainly the result of reflex activity secondary to the reduction in peripheral vascular resistance. Sevoflurane is associated with a stable heart rhythm and does not predispose the heart to sensitisation by catecholamines. In children, halothane causes a greater decrease in heart rate, myocardial contractility and cardiac output than sevoflurane at all concentrations. For these reasons sevoflurane is advocated for use in outpatient dental anaesthesia, especially in children. [Pg.60]

Like other volatile agents, sevoflurane causes dose-related respiratory depression. In healthy patients this results in a decrease in tidal volume and an increase in respiratory rate with a net decrease in minute ventilation. At anaesthetic concentrations the degree of depression is greater than that seen with halothane or isoflurane. There is a decline in the slope of the carbon dioxide response curve. Sevoflurane produces the same degree of bronchodilation as isoflurane and enflurane. [Pg.61]

Desflurane does not have a marked bronchodilator effect and in cigarette smokers it is associated with significant bronchoconstriction. In clinical practice, both humidification of inspired gases and opioids are thought to reduce airway irritability but even at moderate concentrations (2 MAC), desflurane is more likely to cause coughing than sevoflurane. In common with other volatile agents, desflurane causes dose-related respiratory depression. Tidal volume is reduced and respiratory rate increases, initially. As inspired concentrations of desflurane increase, the trend is to hypoventilation and hypercardia and apnoea is to be expected at concentrations of 1.5 MAC or greater. [Pg.62]

The chemical structures of the currently available inhaled anesthetics are shown in Figure 25-2. The most commonly used inhaled anesthetics are isoflurane, desflurane, and sevoflurane. These compounds are volatile liquids that are aerosolized in specialized vaporizer delivery systems. Nitrous oxide, a gas at ambient temperature and pressure, continues to be an important adjuvant to the volatile agents. However, concerns about environmental pollution and its ability to increase the incidence of postoperative nausea and vomiting (PONV) have resulted in a significant decrease in its use. [Pg.536]

MAC values of the inhaled anesthetics are additive. For example, nitrous oxide (60-70%) can be used as a carrier gas producing 40% of a MAC, thereby decreasing the anesthetic requirement of both volatile and intravenous anesthetics. The addition of nitrous oxide (60% tension, 40% MAC) to 70% of a volatile agent s MAC would yield a total of 110% of a MAC, a value sufficient for surgical anesthesia in most patients. [Pg.546]

With the exception of nitrous oxide, all inhaled anesthetics in current use cause a dose-dependent decrease in tidal volume and an increase in respiratory rate. However, the increase in respiratory rate is insufficient to compensate for the decrease in volume, resulting in a decrease in minute ventilation. All volatile anesthetics are respiratory depressants, as indicated by a reduced response to increased levels of carbon dioxide. The degree of ventilatory depression varies among the volatile agents, with isoflurane and enflurane being the most depressant. All volatile anesthetics in current use increase the resting level of Paco2 (the partial pressure of carbon dioxide in arterial blood). [Pg.547]

Inhaled anesthetics decrease the metabolic rate of the brain. Nevertheless, the more soluble volatile agents increase cerebral blood flow because they decrease cerebral vascular resistance. The increase in cerebral blood flow is clinically undesirable in patients who have increased intracranial pressure because of a brain tumor or head injury. Volatile anesthetic-induced increases in cerebral blood flow increase cerebral blood volume and further increase intracranial pressure. [Pg.547]

Of the inhaled anesthetics, nitrous oxide is the least likely to increase cerebral blood flow. At low concentrations, all of the halogenated agents have similar effects on cerebral blood flow. However, at higher concentrations, the increase in cerebral blood flow is less with the less soluble agents such as desflurane and sevoflurane. If the patient is hyperventilated before the volatile agent is started, the increase in intracranial pressure can be minimized. [Pg.547]

Halothane, isoflurane, and enflurane have similar depressant effects on the EEG up to doses of 1-1.5 MAC. At higher doses, the cerebral irritant effects of enflurane may lead to development of a spike-and-wave pattern and mild generalized muscle twitching (ie, myoclonic activity). However, this seizure-like activity has not been found to have any adverse clinical consequences. Seizure-like EEG activity has also been described after sevoflurane, but not desflurane. Although nitrous oxide has a much lower anesthetic potency than the volatile agents, it does possess both analgesic and amnesic properties when used alone or in combination with other agents as part of a balanced anesthesia technique. [Pg.547]

In addition to the analysis of arson crime scene evidence, thermal desorption has been used for the analysis of residual volatile agents in street drugs and the analysis of stains on forensic evidence. Samples are heated to volatilize water and organic compounds. The organic analytes may then be separated by gas chromatography (Figure 22.2). [Pg.403]


See other pages where Volatile agents is mentioned: [Pg.409]    [Pg.836]    [Pg.534]    [Pg.5]    [Pg.367]    [Pg.361]    [Pg.55]    [Pg.56]    [Pg.57]    [Pg.57]    [Pg.59]    [Pg.61]    [Pg.63]    [Pg.67]    [Pg.75]    [Pg.535]    [Pg.548]    [Pg.93]    [Pg.271]    [Pg.11]    [Pg.534]    [Pg.17]   


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