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Edit Comment Close Premium member Presentation Transcript Prepared By: SANJAY KUMAR TALHA JAWAID MEHNAZ KAMALDEPARTMENT OF PHARMACOLOGYHYGIA INSTITUTE OF PHARMACEUTICAL EDUCATION & RESEARCH LUCKNOW : Prepared By: SANJAY KUMAR TALHA JAWAID MEHNAZ KAMALDEPARTMENT OF PHARMACOLOGYHYGIA INSTITUTE OF PHARMACEUTICAL EDUCATION & RESEARCH LUCKNOW GENERAL ANAESTHETICS Slide 2: CONTENT 1 . Definitions 2 . Principles of general anaesthesia 3 . Difference between general and local anaesthetics 4 . Different stages of general anaesthesia 5 . Classification of general anaesthetics 6 . Mechanism of action general anaesthetics 7 . Comparative study of general anaesthetics 8 . Indications 9 . Drug interaction 10. Pre-anaesthetic medication Slide 3: Definition : Anesthesia (an =without, aisthesis = sensation ) Anesthesia is medication that attempts to eliminate pain impulse from reaching the brain. In general anesthesia this is accomplished by putting the patient asleep. STREPTOKINASE STREPTOKINASE Streptokinase ANAESTHESIA Slide 4: A drug that brings about a reversible loss of all sensation and consciousness. These drugs are generally administered by an anesthesiologist in order to induce or maintain general anesthesia to facilitate surgery and unpleasant procedure. General anesthetics depress the central nervous system. It causes immobility and muscle relaxant. What Are General Anaesthetics? Slide 5: Principle of General Anaesthesia The practice of anesthesia is usually neither therapeutic nor diagnostic. The development of new anesthetic agent have been driven by three general objectives – Sustaining physiologic homeostasis during surgical procedure. That may involve – reperfusion of ischemic tissue,major blood loss,fluid shift and impaired coagulation. Minimize the potentiolly deleterous effects of anesthetic agent and technique. Improving postoperative out comes. Slide 6: Hemodynamic Effect of General Anaesthetics Decrease in arterial blood loss. The causes include direct – #. Vasodilation. #. Myocardial depression. Respiratory Effect of general anaesthetic : Respiratory Effect of general anaesthetic Decrease or eliminate both ventilatory drive and the reflexes that maintain air way potency. Slide 8: Hypothermia Temperature reduces less then 30 degree during surgery. Metabolic rate and total body oxygen consumption decreases with general anesthetis by 30% , reduce heat generation. Slide 9: Nausea And Vomitting GENERAL ANAESTHETICS post operative period Stimulate CTZ and brain stem vomiting center Nausia and vomiting Stages of anaesthesia : Stages of anaesthesia Stage I : Analgesia : Start from beginning of anesthetic administration and last upto loss of consciousness, feels a dream like state, reflexes and respiration remain normal. Stage II : Stage of delirium : From loss of consciousness to beginning of irregular respiration.Apparent excitement is seen. Muscle tone increases. Jaws are tightly closed. Heart rate and blood pressure may rise. Slide 11: Stage III : Surgical anesthesia : Extends from onset of irregular respiration to cessation of spontaneous breathing. This has been devided into 4 planes- Plane 1: This plane ends when eyes become fixed. Plane 2: Loss of corneal and laryngeal reflexes. Plane 3: Pupil start dilating and light reflexes. Plane 4: Dilated pupil, decrease muscle tone ,BP falls. Stage IV : Medullary paralysis : Respiratory and vasomotor control ceases. Lipid theory of General Anaesthetics : Lipid theory of General Anaesthetics Based on the fact the anesthetic action is correlated with the oil/gas coefficients. @. Higher the solubility of general anesthetics in oil greater is the anesthetics action. Slide 14: Minimum alveolar Concentration (MAC) MAC is the concentration necessary to prevent responding in 50% of population. Blood gas partition coefficient Lower the Blood : Gas partition coefficient the fester the induction and recovery. Slide 15: Other Theories included Binding theory: Anesthetics bind to hydrophobic portion of the ion channel Slide 17: 1. INHALATIONAL a. Gas * Nitrous oxide b. Volatile liquids * Halothane * Enflurane * Isoflurane * Desflurane * Sevoflurane 2. INTRAVENOUS * Theopentone sod. * Etomidate * Propofol * Kitamine * Methohexitone sod. Slide 18: Halothane Enflurane Isoflurane Desflurane Sevoflurane Halogenated compounds: Contain Fluorine and/or bromide Simple, small molecules Slide 19: Used in combinationwith Inhaled anesthetics to: Supplement general anesthesia Maintain general anesthesia Provide sedation Control blood pressure Slide 22: SITES OF ACTION In principle, general anesthetics could interrupt nervous system function at myriad levels, including peripheral sensory neurons, the spinal cord, the brainstem, and the cerebral cortex. Slide 23: CELLULAR MECHANISMS General anesthetics produce two important physiologic effects at the cellular level. First, inhalational anesthetics hyperpolarize neurons, possibly an important effect on neurons serving a pacemaker role and on pattern-generating circuits and in synaptic communication, since reduced excitability in a postsynaptic neuron diminishes the likelihood that an action potential will be initiated in response to neurotransmitter release. Slide 24: Second, at anesthetizing concentrations, both inhalational and intravenous anesthetics have substantial effects on synaptic transmission and much smaller effects on action-potential generation or propagation. Inhalational anesthetics inhibit excitatory synapses and enhance inhibitory synapses via effects on pre- and postsynaptic sites. Slide 25: The inhalational anesthetic isoflurane clearly can inhibit neurotransmitter release and produce a small reduction in presynaptic action potential amplitude (3% reduction at MAC concentration) that inhibits neurotransmitter release, a significant effect because the reduced action potential is amplifiedinto a larger reduction in presynaptic Ca2+ influx, and thence into an even greater reduction intransmitter release. Intravenous anesthetics produce a narrower range of physiological effects. Most of the intravenous agents act predominantly by enhancing inhibitory neurotransmission, whereas ketamine predominantly inhibits excitatory neurotransmission at glutamatergic synapses. Slide 26: Molecular mechanism of the GA : GABA –A : Potentiation by Halothane, Propofol, Etomidate NMDA receptors : inhibited by Ketamine Slide 27: Receptor sits in the membrane of its neuron at the synapse GABA, endogenous compound, causes GABA to open Receptor capable of binding 2 GABA molecules, between an alpha and beta subunit Binding of GABA causes a conformational change in receptor Opens central pore Chloride ions pass down electrochemical gradient Net inhibitory effect, reducing activity of the neuron Slide 29: Anesthetic Suppression of Physiological Response to Surgery Slide 34: Volatile liquid at room temperature. Light sensitive Halothane + oxygen = inflammable, norexplosive PHARMACOKINETICS High fat solubility => slow induction & recovery. Eliminated unchange via lungs. Metabolised in liver by Cyt-P450. Slide 35: Commonly used in children, where preoperative placement if an iv catheter can be difficult. Anesthesia is produced at end –tidal concentration of 0.7 -1%. CVS : cardiac arrhythmia,depression of myocardial contraction. CLINICAL USES SIDE EFFECTS Slide 36: >Deression of respiration. MUSCLES : Malignant hyperthermia. KIDNEY: Decrease renal blood flow and g.f.r. LIVER AND GIT: Cause-halothane induced hepatitis & nausia and vomitind. DRUG INTERACTION : Halothane + adrenaline,theophylline => arrhythmia may be precipitated. RESPIRATORY SYSTEM Slide 37: CONTRAINDICATION: Hepatic dysfunction and/or jaundice. OVER DOSE: On over dose patient move to fresh airway or inserting an emergency airway. Slide 38: THIOPENTAL Barbiturate with very high lipid solubility. Rapid action, short duration. Slowly metabolised in liver and liable to accumulate in body fat. Risk of sever vasospasm if accidently injected into artery. Intravenous Anaesthetics Slide 39: PROPOFOL Repidely metabolised. Very rapid recovery. Useful for day-case surgery. Safe for use in pregnant women. KETAMINE Analogue of phencyclidine with similar properties. Act on NMDA receptor. Slide 40: Onset of action is relatively slow(2-5 minutes). Produce dissociative anaesthesia, in which patient remain conscious though sensitive to pain. Slide 41: Nitrous oxide (50%) has been used with oxygen for dental and obstetric analgesia. Isoflurane ,Desflurane is preferred for neurosurgery. Sevoflurane is suitable both outpatient as well as inpatient. Thiopentone sod. Ocationally used for control of convulsion. Propofol : injection and perfusion is frequently used for total i.v. anaesthesia when supplemented by fentanyl. Slide 42: Ketamine have been used for operations on the head and neck. Slide 43: Kitamine is dengerous for hypertensives ,in ischemic heart disease. And Halothane is not given in liver disease. Sevoflurane is not given to sever hepatic dys function , jaundice, fever . Nitrous oxide Is contraindicated in first two trimester of pregnency because its effect on DNA production => undesirable out comes. Slide 44: It is the use of drugs prior to anesthesia to make it more safe and pleasant. To relieve anxiety – benzodiazepines. To prevent allergic reactions – antihistaminics. To prevent nausea and vomiting – antiemetics. To provide analgesia – opioids. To prevent bradycardia and secretion – atropine. Slide 45: Decrease secretions and vagal stimulation caused by anaesthetics. Decrease acidity and volume of gastric juice. Antiemetic effect extending to the post operative period. Slide 46: Sedative-anti anxiety drug => diazepam(5mg), lorazepam (2mg-0.05mg/kg). 2. Anticholinergic drugs => Atropine and hyoscine are use to reduce salivary & bronchial secretions. 3. H2 Blockers => Famotidine , & ranitidine are use to reduce the PH & gastric juice. Proton pump inhibitors => Omeperazole, Antiemitic => metoclopramide (10-20 mg) 5HT blockers => ondensetron (4-8 mg iv) Slide 47: THANK YOU You do not have the permission to view this presentation. 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