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anesthetics

1. Intravenous Anesthesia

2. IDEAL IV ANAESTHETICS 1-Drug compatibility (water solubility) and stability in solution. 2-lake pain on injection , veno - irritation , and local tissue damage . 3-low potential to release histamine. 4-rapid and smooth onset of action without excitatory activity. 5-rapid metabolism to inactive metabolites. 6-a steep dose to minimize titratability and tissue accumulation. 7-lake of acute cardiovascular and respiratory depression. 8-decrease in cerebral metabolism and intracranial pressure. 9-rapid and smooth return to consciousness .

3. Anesthesia is produced by diffusion of drug from arterial blood across the blood brain barrier in to the brain which regulated by the following factors: -protein binding: unbound drug is free to cross BBB. -blood flow to the brain. -extracellular PH and Pka of the drug: nonionized. -solubility of the drug in lipid and water: high lipid solubility enhances transfer in to the brain.

4. -(2,6-dispropylphenol). -pain on injection 32-67% of patients. -t1/2 is 1-8 min (Barash 2009). -elimination half time 2-24 min. -metabolized in liver to sulfate and glucuronic acid which are eliminated by kidney. -extra hepatic route of elimination by lungs. -anesthesia is induced in 20-40 sec after iv administration. -we can monitor the onset by loss of verbal contact. -induction dose 1.5 – 2.5 mg/kg.

5. - propofol decrease CPF and ICP. -excitatory motor activity without EEG changes. -dose and concentration dependent cardiovascular depression. -dose dependent respiratory depression with apnea. -antiemetic effects (10-20 mg to treat nausea and emesis in the early post operative period. - antidopamenergic which lead to euphoria. -it decrease the pruritus produced by spinal opioids. -agent of choice in malignant hyperthermia suspictable pt. -Propofol syndrome : after high dose infusion of propofol for long time – myocardial failure – metabolic acidosis – rabdomyolysis .

6. Propofol has no effect on bronchial muscle tone and laryngospasm isparticularlyuncommon . The suppression of laryngeal reflex and low incidence of coughing or laryngospasm when a laryngeal mask airway (LMA) is introduced , and propofol is regarded by most anesthetists as the drug of choice for induction of anesthesia when LMA is to be used.

7. KETAMINE - Arylcyclohexylamine . -water solublecompound . -potent anesthetics and analgesic properties +amnesia . -metabolized by liver to norkitamine which excreted by kidney. -elimination half life 2-4 h . -dose dependent CNS depression + stimulation of limbics . -induction dose: 1-2 mg/kg IV. 4-8mg/kg IM. -duration of action: 10-20min –full orientation require more 60 – 90 min

8. -high incidence of psychomimetic reactions (namely , hallucination , nightmares , altered short term memory , and cognition). -ketamine increase CPF and ICP . - bronchodilatory activity - minimal respiratory depression. –Increase oral secretion. -cardiovascular stimulation + increase peripheral resistant. -not recommended in severe coronary artery disease. -increase pulmonary artery pressure (contraindicated in poor right ventricular reserve.

9. Indications: -high risk pt : shocked patients. -pediatric anesthesia. -difficult locations: site of accidents. –developing countries: where anesthetic equipment and trained staff in short supply.

10. -midazolam , lorazepam , diazepam and antagonist flumazenil. -metabolized in liver , excreted by kidney. -short acting: midazolam –flumazenil: Benzodiazepine antagonist -intermediate: diazepam. -long acting: lorazepam. -only midazolam can given by continuous infusion. -all benzodiazepines produce: anxiolytic, anterograde amnesia, sedative, hypnotic, anticonvulsant, and spinally mediated muscle relaxant properties.

11. -dose dependent respiratory depression. -it depress the swallowing reflex and depress upper airway reflex activity. -produce decrease in systemic vascular resistant and blood pressure in large doses. -specific antagonist :flumazenil