Diethyl ether (C2H5-O-C2H5) is one of the metabolically safe non-halogenated anesthetics . About 6% is metabolized in the liver to ethanol and acetaldehyde, thereafter to acetic acid and onto carbon dioxide and water. Examples of non-halogenated anesthetics Divinyl ether Cyclopropane Trichloroethylene Non-halogenated anesthetics are all anesthetic agents mostly inhalation agents that do not contain a hologen in their structure. Divinyl […]
The pharmacodynamics of inhaled anesthetics is discussed here in detail. The action of inhalation agents are as follows: I. Pulmonary effects 2. Cardiovascular effects 3. Metabolism 4. Toxicity Pulmonary Effects: For pharmacodynamics of inhaled anesthetics , the pulmonary effects of inhalation agents are many and important as this is the portal of entry. There are
Halogenated volatile agents are inhalational anesthesia gases used during surgeries to provide general anesthesia. They are metabolized to varying degrees. There is biotransformation in the liver resulting in cleavage and dehalogenation by the specific enzyme P450, which is a haemocytochrome present in the hepatic cell. Desflurane (CHF2-O-CHFCHF3): It is one of the halogenated volatile agents
With respect to inhalation agent anesthetic , an increase in cardiac output and the consequent increased pulmonary blood flow removes more general anesthetic from the alveoli. The alveolar venous anesthetic gradient is determined by the amount of tissue uptake of an inhalation agent anesthetic . This depends on the tissue solubility, tissue blood flow and
The exact site of mechanisms of action of inhalation anesthetics is not certain but possible sites are macroscopic (CNS-brain), microscopic (axons and synapses) and molecular (pre- and postsynaptic membranes). Hence, the possible mechanisms of action of inhalation anesthetics is varied: a) Multiple receptor sites b) Motor inhibition at spinal cord level c) Many neurotransmitters are
The pharmacokinetics of inhaled anesthetics are explained here with detail • Absorption of agent from alveoli to blood • Distribution in the body • Metabolism (liver) • Elimination (lungs mainly) Uptake and Distribution The pharmacokinetics of inhaled anesthetics depends upon: (1) Respiratory uptake, (2) Alveolar ventilation, (3) The partial pressure of the agent in the
Inhalation anesthetic mechanism of action after being administered and excreted via the lungs. The dose of the agent is defined by the fraction of inhaled concentration that equates with the blood concentration and not the total amount of drug administered. The minimum alveolar concentration (MAC) was introduced in 1963 as a comparison of potency of
Despite the rapid clearance of propofol pharmacokinetics by metabolism, there is no evidence of impaired elimination in patients with cirrhosis of the liver. Chronic alcoholism does not change the propofol pharmacokinetics significantly. Extrahepatic elimination of propofol occurs during the anhepatic phase of orthotopic liver transplantation. Renal dysfunction does not influence the clearance of propofol. Patients
The fact that total body clearance of propofol metabolism exceeds hepatic blood flow is consistent with extra hepatic clearance. Indeed hepatic clearance of propofol was approximately 60% of total body clearance.Pulmonary uptake of propofol is significant and influences the initial availability of propofol. Human lungs take part in the elimination of propofol by transforming the
It is rapidly distributed in the body with a propofol half life of only around 2 mm and has an efficient hepatic and extra hepatic clearance. Because the total body clearance may exceed liver blood flow, an extrahepatic metabolism or extrarenal elimination has been suggested. Hepatic metabolism is rapid and extensive, resulting in inactive, water-soluble
