GENERAL ANESTHESIA

Presented by: Shalakha Bhardwaj BDS final year(2007-2011)

Contents
Introduction and History of General anesthesia Properties of ideal General anesthetic Classification of General anesthetic agents Mechanism of Anesthesia Stages of Anesthesia Inhalation anesthetic agents Intravenous anesthetic agents Techniques of inhalation of anesthetics Induction, Maintenance and Extubation Anaesthetic Machine (Boyles equipment) Complications of General anesthesia Pre-anesthetic medication General anesthesia- facts and fiction

INTRODUCTION
General anaesthetics (GAs) are drugs which produce reversible loss of all sensations and consciousness. It usually involves a loss of memory and awareness with insensitivity to painful stimuli, during a surgical procedure

General anesthesia

need for unconsciousness

need for analgesia

need for muscle relaxation

 Balanced anesthesia - it is a term used to describe the

multidrug approach to managing the patient needs. Balanced anesthesia takes advantage of drugs beneficial effects while minimizing each agents adverse qualities.

Combination Anesthesia - Since a single anesthetic

agent will not meet the ideal, a combination of drugs is used to take advantage of their best properties and minimize the undesirable side effects.

HISTORY OF ANESTHESIA
Ether synthesized in 1540 by cordus Ether used as anesthetic in 1842 by dr. Crawford W.Long Ether publicized as anesthetic in 1846 by dr. William morton. Ether is no longer used in modern practice, yet considered to be the first ideal anesthetic Chloroform used as anesthetic in 1853 by dr. John snow Endotracheal tube discovered in 1878 Thiopental first used in 1934 Curare first used in 1942 - opened theAge of anesthesia

PROPERTIES OF AN IDEAL ANAESTHETIC

For the patient - It should be pleasant, non irritating,
should not cause nausea or vomiting. Induction and recovery should be fast with no after effects.

For the surgeon - It should provide adequate analgesia,

immobility and muscle relaxation. It should be noninflammable and nonexplosive so that cautery may be used.

For the anaesthetist - Its administration should be easy,

controllable and versatile.

 Margin of safety should be wide - no fall in BP. Heart, liver and other organs should not be affected. It should be potent so that low concentrations are needed and oxygenation of the patient does not suffer. Rapid adjustments in depth of anaesthesia should be possible. It should be cheap, stable and easily stored. It should not react with rubber tubing or soda lime.

CLASSIFICATION
General anesthesia

Inhalational

Intravenous
Gas

Inducing agents

Slower acting

volatile Liquids

Nitrous oxide Ether halothane enflurane isoflurane desflurane sevoflurane

Dissociative anesthesia

opiod analgesia

Benzodiazep-ines

ketamine

fentanyl

diazepam lorazepam midazolam

Thiopentone sod. methohexitone sod. propofol etomidate

MECHANISM OF ACTION OF ANAESTHESIA

Anesthesia from physical interactions with lipophilic membrane components
Anesthesia is produced by disturbance of the physical properties of cell membranes Anesthesia may be produced when anesthetics physically dissolved into the cell membranes lipid biophase MEYERS OVERTON RULE. This theory fails to explain how the proposed disturbance of the lipid bilayer would result in a dysfunctional membrane protein

Anesthesia from selective interactions of anesthetics with cellular components

GABAA Receptor (Ligand-gated ion channels) chloride channels gated by the inhibitory GABAA receptor GABAA receptor found throughout the CNS. Located in the post-synaptic membrane. GABAA Receptor mediates the effects of gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the brain

EN
c

5 subunits arranged around a central pore:2 alpha, 2 beta, 1 gamma

F
N

c F
K
c
N

Each subunit has N-terminal extracellular chain which contains the Ligand-binding site 4 hydrophobic sections cross the membrane 4 times: one extracellular and two intracellular loops connecting these regions, plus an extracellular C-terminal chain

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

Anesthetics bind to specific sites on the receptor protein.

They do not compete with GABA for its binding on the receptor. They inhibit the response to painful stimuli by interacting with beta3 subunit of GABAA receptor.

SIGNS & STAGES OF ANAESTHESIA (GUEDELS Signs)

Guedel (1920) described four stages with ether anaesthesia, dividing the III stage into 4 planes. Starts from beginning of anaesthetic inhalation and lasts upto the loss of consciousness Pain is progressively abolished Reflexes and respiration remain normal Use is limited to short procedures

Stage of Analgesia

Stage of Delirium

From loss of consciousness to beginning of regular respiration Patient may shout, struggle and hold his breath; muscle tone increases, jaws are tightly closed, breathing is jerky; vomiting, involuntary micturition or defecation may occur . Heart rate and BP may rise and pupils dilate due to sympathetic stimulation No operative procedure carried out Can be cut short by rapid induction, premedication

Surgical anaesthesia

Extends from onset of regular respiration to cessation of spontaneous breathing. This has been divided into 4 planes which may be distinguished as: Plane 1 roving eye balls. This plane ends when eyes become fixed. Plane 2 loss of corneal and laryngeal reflexes. Plane 3 pupil starts dilating and light reflex is lost. Plane 4 Intercostal paralysis, shallow abdominal respiration, dilated pupil.

Medullary paralysis

Cessation of breathing to failure of circulation and death. Pupil is widely dilated, muscles are totally flabby, pulse is thready or imperceptible and BP is very low

AMERICAN SOCIETY OF ANESTHELOGISTS CLASSIFICATION

ASA I Healthy individuals having no organic,physiological,biochemical or psychological disturbance ;pathology is localised and non systemic Mild to moderate systemic disturbance, e.g. Epileptic children on medication Severe systemic disturbance or disease, even though it may not be possible to define the degree of disability with finality e.g. Children with congenital heart disease Severe systemic disorder that are already life threating The moribund(dying) patient who is unlikely to survive without planned procedures

ASA II

ASA III

ASA IV

ASA V

PHARMACOKINETIC CHARACTERISTICS
Distribution
The rate of initial redistribution following the administration of a single iv bolus of drug is defined by the half life (t1/2a) and is generally about 8 min for most anesthetics Distribution of an anesthetic agent depends upon the blood supply of that part.

Metabolism and Excretion of Intravenous Drugs

Since drugs with long elimination half-lives (t1/2_) will have slow rates of clearance, their use by repeated IV bolus or continuous infusion to maintain anesthesia has been restricted. Long-term application with limited concern for the pharmacokinetics of the agents may lead to delayed awakening , As large quantities of these drugs may accumulate in Reservoir tissues, such as skeletal muscle and fat.

INHALATIONAL ANESTHETIC AGENTS

Inhalational anesthesia refers to the delivery of gases or vapours from the respiratory system to produce anesthesia.

NITROUS OXIDE
It is prepared by priestly in 1776 and anesthetic properties described by davy in 1799. It is characterized by inert nature with minimal metabolism. It is colorless, odorless, tasteless, and does not burn. The mac value is 105%. It is a weak anesthetic, powerful analgesic. It has low blood solubility (quick recovery)

Nitrous Oxide Systemic Effects Effects on heart rate and blood pressure May cause myocardial depression in sick patients Little effect on respiration Safe, efficacious agent Nitrous oxide concentration should be regulated during different stages of sedation as described
Induction Slow-0.5-1 lit/min Rapid-2-4 lit/min 40%nitrous oxide 60%oxygen 20-30% nitrous oxide

Maintenance

Reversal

100%oxygen

Nitrous Oxide Side Effects Manufacturing impurities toxic Beginning of case: second gas effect End of case: Diffusion hypoxia may be encountered. To avoid diffusion hypoxia, the anesthesiologist may employ 100% oxygen rather than room air after discontinuing administration of the anesthetic gas Mixture. Inhibits vitamin B-12 metabolism Dentists, OR personnel, abusers at risk

HALOTHANE
It is synthesized in 1956 by suckling. It substituted ethane. It is a volatile liquid easily vaporized, stable, and nonflammable. It is the most potent inhalational anesthetic having a mac of 0.75%.It is efficacious in depressing consciousness It is very soluble in blood and adipose.

Halothane systemic effects Inhibits sympathetic response to painful stimuli Inhibits sympathetic driven baroreflex response (hypovolemia) Sensitizes myocardium to effects of exogenous catecholamines-ventricular arrhythmias Johnson found median effective dose 2.1 mg/kg Limit dose to 300 ug over one hour Other medications decreases respiratory drive-- central response to CO2 and peripheral to O2 Respirations shallow-- atelectasis Depresses protective airway reflexes Depresses myocardium-- lowers BP and slows conduction Mild peripheral vasodilation

Halothane side effects Halothane hepatitis -- 1/10,000 cases fever, jaundice, hepatic necrosis, death metabolic breakdown products are hapten-protein conjugates immunologically mediated assault Exposure dependent Malignant hyperthermia-- 1/60,000 with succinylcholine to 1/260,000 without halothane in 60%, succinylcholine in 77% Classic-- rapid rise in body temperature, muscle rigidity, tachycardia, rhabdomyolysis, acidosis, hyperkalemia, DIC most common masseter rigidity family history high association with muscle disorders autosomal dominant inheritance Diagnosis--previous symptoms, increase CO2,rise in CPK levels, myoglobinuria, muscle biopsy Physiology--hypermetabolic state by inhibition of calcium reuptake in sarcoplasmic reticulum

Enflurane
Developed in 1963 by Terrell, released for use in 1972.It is a stable, nonflammable liquid having a pungent odor and a MAC of 1.68%.

Enflurane Systemic Effects Potent inotropic and chronotropic depressant and decreases systemic vascular resistance-- lowers blood pressure and conduction dramatically

 Inhibits sympathetic baroreflex response Sensitizes myocardium to effects of exogenous catecholamines arrhythmias Respiratory drive is greatly depressed-- central and peripheral responses increases dead space widens A-a gradient produces hypercarbia in spontaneously breathing patient Enflurane Side Effects Metabolism one-tenth that of halothane does not release quantity of hepatotoxic metabolites Metabolism releases fluoride ion-- renal toxicity Epileptiform EEG patterns

Isoflurane
Synthesized in 1965 by Terrell, introduced into practice in 1984 .it is Nonflammable having a pungent odour It is less soluble than halothane or Enflurane having a MAC of 1.30 %

Isoflurane Systemic Effects Depresses respiratory drive and ventilatory responses-- less than Enflurane Myocardial depressant-- less than Enflurane Inhibits sympathetic baroreflex response-- less than Enflurane Sensitizes myocardium to catecholamines -- less than halothane or Enflurane Produces most significant reduction in systemic vascular resistance-coronary steal syndrome, increased ICP Excellent muscle relaxant-- potentiates effects of neuromuscular blockers Isoflurane Side Effects Little metabolism (0.2%) -- low potential of organotoxic metabolites No EEG activity like Enflurane Bronchoirritating, laryngospasm

Sevoflurane and Desflurane

Desflurane has low tissue and blood solubility compared with other halogenated hydrocarbons, and its anesthetic partial pressure is thus established more rapidly. Recovery is similarly prompt when the patient is switched to room air or oxygen. Desfluranes popularity for outpatient procedures stems from its rapid onset and prompt elimination from the body by exhalation.

 Advantage-it may be used to maintain anesthesia after induction with an alternative IV or inhalational agent, preserving the advantage of rapid recovery. Disadvantage- is that Desflurane irritates the respiratory tract; thus, it is not preferred for induction of anesthesia using an inhalational technique. Sevoflurane (Ultane) it is the most recently introduced inhalation anesthetic. It has low tissue and blood solubility,which allows for rapid induction and emergence and makes it useful for outpatient and ambulatory procedures.

 Advantage- non pungent, a characteristic that permits a smooth inhalation induction, and is particularly useful in pediatric anesthesia. Disadvantage-it undergoes hepatic biotransformation (about 3% of the inhaled dose), and it is somewhat degraded by conventional CO2 absorbents. The degradation product from the absorbent has been reported to be nephrotoxic, although the report is controversial and not substantiated by more recent studies.

Intravenous Anesthetic Agents

The First attempt at intravenous anesthesia was by Wren in 1656- opium into his dog. Use in anesthesia in 1934 with thiopental. They have Appealing, pleasant experience

Thiopental
It is an ultrashort acting thiobarbiturate, highly soluble in water yielding a very alkaline solution, which must be prepared freshly before injection. Dose-3-5 mg/kg

Thiopental Systemic Effects Varied effects on cardiovascular system in people-- mild direct cardiac depression-- lowers blood pressure-- compensatory tachycardia (baroreflex) Dose-dependent depression of respiration through medullary and pontine respiratory centers Thiopental Side Effects Noncompatibility Tissue necrosisgangrene Tissue stores Post-anesthetic course

Etomidate
Its Structure similar to ketoconozole .it is a Direct CNS depressant (thiopental) and GABA agonist

Etomidate Systemic Effects Little change in cardiac function in healthy and cardiac patients

 Mild dose-related respiratory depression Decreased cerebral metabolism Etomidate Side Effects Pain on injection (propylene glycol) Myoclonic activity Nausea and vomiting (50%) Cortisol suppression

Ketamine
Structurally it is similar to PCP.it Interrupts cerebral association pathways resulting in dissociative anesthesia. It stimulates central sympathetic pathways. Dose 0.5-2mg/kg

Advantage- its potential for administration by the IM route. This is particularly useful in anesthetizing children, since anesthesia can be induced relatively Quickly in a child who resists an inhalation induction or the insertion of an IV line. Ketamine has a limited but useful role as an IM induction agent and in pediatrics. Disadvantage- ketamine and its propensity evoke excitatory and hallucinatory Phenomena as the patient emerge from anesthesia. Patients in the recovery period may be agitated, scream and cry, hallucinate, or experience vivid dreams. These episodes may be controlled to some extent by maintaining A quiet reassuring atmosphere in which the patient can awaken or if necessary by administering tranquilizing doses of diazepam.

Propofol
Rapid onset and have a short duration of action. Myocardial depression and peripheral vasodilation may occur. Insoluble in water, causing pain in 50% of patients. Side effects are Minimal (nausea and vomiting) Propofol can be used to supplement inhalational anesthesia in longer procedures. Both continuous infusion of Propofol for conscious sedation and with opioids for the maintenance of anesthesia for cardiac surgery are acceptable techniques. Dose-2-2.5mg/kg

Benzodiazepines
They Produce sedation and amnesia, Potentiate GABA receptors and have a Slower onset and emergence.

Diazepam
Often used as premedication or seizure activity, rarely for induction Minimal systemic effects- respirations decreased with narcotic usage Not water soluble- venous irritation Metabolized by liver- not redistributed Dosage-oral/rectal0.2-0.5mg/kg -IV 0.25 mg/kg

Lorazepam
Slower onset of action (10-20 minutes)-- not used for induction Used as adjunct for anxiolytic and sedative properties Not water soluble-- venous irritation

Midazolam
More potent than diazepam or lorazepam,Induction slow, recovery prolonged May depress respirations when used with narcotics Minimal cardiac effects Dosage pediatrics dose: 0.05-0.1mg/kg(iv/im)

Narcotic agonists (opioids)

Used for years for analgesic action-- civil war for wounded soldiers Predominant effects are analgesia, depression of sensorium and respirations Mechanism of action is receptor mediatedBradycardia in large doses Some peripheral vasodilation and histamine release -hypotension Side effects nausea, chest wall rigidity,

COMPLICATIONS OF GENERAL ANAESTHESIA

During anaesthesia Respiratory depression and hypercarbia. Salivation, respiratory secretions -less now as non-irritant anaesthetics are mostly used. Cardiac arrhythmias, asystole. Fall in BP Aspiration of gastric contents: acid pneumonitis.

 Delirium, convulsions. Excitatory effects are generally seen with i.v. anaesthetics especially if phenothiazines or hyoscine have been given in premedication. These are suppressed by opioids. Fire and explosion - rare now due to use of noninflammable agents. After anaesthesia Nausea and vomiting. Persisting sedation: impaired psychomotor function. Pneumonia, atelectasis. Organ toxicities: liver, kidney damage. Nerve palsies - due to faulty positioning.

General Anesthesia in pediatric dentistry

Indications
1. Patients with certain physical, mental, or medically compromising conditions. 2. Patients with dental restorative or surgical needs for whom local anesthesia is ineffective because of acute infection, anatomic variations, or allergy. 3. The extremely uncooperative, fearful, anxious, physically resistant, or uncommunicative child or adolescent with substantial dental needs for whom There is no expectation that the behavior will soon

5. Patients with immediate comprehensive oral or dental needs who otherwise would not receive comprehensive dental care. 6. Patients requiring dental care for whom the use of general anesthesia may protect the developing psyche and/or reduce medical risks.

Contraindication
Patients for whom general anesthesia is usually contraindicated include those with a medical contraindication to general anesthesia and healthy and cooperative patients with minimal dental needs.

Pretreatment documentation and assessment

A. Documentation-the practitioner must document each sedation or general anesthetic procedure in the patients record. It should include: 1. Rationale for sedation or general anesthesia: the dental surgeon should briefly document the reason for the sedation 2. informed consent: each patient, parent, or other responsible individuals entitled to be

3. Instructions

to parent or responsible individual: the dentist should provide verbal and written instructions to the parents in a language that the parent understands. It should include explicit and include an explanation of preanesthetic, potential or anticipated postoperative behaviour, and limitation of activities 4. Dietary instructions: general anesthetic agents must be proceeded by an evaluation of the patients dietary intake

Ingested food Clear liquids Breast milk Infant formula Non human milk Light meal
Fasting guidelines

Minimum fasting period 2 hours 4 hours 6 hours 6 hours 6 hours

The dental procedure must be postponed if the recommendations are not followed because of increase in risk of aspiration if there is unintended loss of protective reflexes during

B) Preoperative assement it should include: 1) Medical history  Allergies and previous allergy and adverse drug reaction  Current medication if any  disease, disorder and other physical abnormalities  Previous hospitalization, including the date, purpose and hospital course  History of previous treatment under general anesthesia and sedation and any associated complications

2) Physical evalution weight in kilograms Vital signs, including heart rate, respiratiory rate and blood pressure. Evaluation of airway patency and tonsil size. Risk assessment (Asa classification)

Important consideration for children A child is smaller than an adult so the relative surface area exposed to a drug is greater and chances of overdose are more The effect and duration of drug action can be un predictable because of prolonged retention and variable metabolism which increase the chances of toxicity The airway and nasal passages are smaller in children. The tongue, enlarged adenoid and oral secretions increase the risk of

Commonly used agents for conscious sedation in children

drugs used for concious sedation in children

systemic agents

inhalational agents

conventional - lytic cocktail - barbiturates - chloral hydrate - anyihistaminics - benzodiazepines

contemporary -newer benzodiazipnes eg:midazolam,trizolam -newer antihistaminics eg:loratidine

nitrous oxide and oxygen

Technique of general anesthesia

Preanaesthetic medication
Preanaesthetic medication refers to the use of drugs before anaesthesia to make it more pleasant and safe.
Morphine (10 mg) or pethidine (50-100 mg),i.m. allay anxiety and apprehension of the operation, produce pre and postoperative analgesia, smoothen induction, reduce the dose of anaesthetic required and supplement poor analgesic (thiopentone, halothane) or weak(N20) anaesthetics. Postoperative restlessness is also reduced.

Opioids

Antianxiety drugs

Benzodiazepines like diazepam (5-10 mg oral) or lorazepam (2 mg i.m.) produce tranquility and smoothen induction; there is loss of recall of intraoperative events (specially with lorazepam) with little respiratory depression or postoperative vomiting. They counteract CNS toxicity of local anaesthetics and are being used along with pethidine/fentanyl for a variety of minor surgical and endoscopic procedures

Sedative-hypnotics

Barbiturates like pentobarbitone, secobarbitone or butabarbitone (100 mg oral) have been used night before (to ensure sleep) and in the morning to calm the patient. However, their popularity has decreased in the recent years because they tend to depress respiration and circulation; emergence delirium is more common and they lack analgesic or antiemetic property.

Anticholinergics

Atropine or hyoscine (0.6 mg i.m i.v.) has been used, primarily to reduce salivary and bronchial secretions. The main aim of their use now is to prevent vagal Bradycardia and hypotension (which occur reflex due to certain surgical procedures), and prophylaxis ofLaryngospasm which is precipitated by respiratory secretions. They should not be used in febrile patients. Dryness of mouth in the pre and postoperative period may be distressing. Glycopyrrolate (0.1-0.3 mg i.m.) is a longer actingatropine substitute. It is a potent anti secretory and antibradycardiac drug; acts rapidly and is less likely to produce central effects

H2 blockers

Ranitidine (150 mg) or famotidine (20 mg) given night before and in the morning benefit by raising pH of gastric juice. Prevention of stress ulcers is another advantage. Now routinely used before prolonged surgery.

Antiemetics

Metoclopramide 10-20 mg i.m. preoperatively is effective in reducing post operative vomiting. By enhancing gastric emptying it reduces the chances of reflux and its aspiration. Extrapyramidal effects And motor restlessness can occur. Combined use of metoclopramide and H2 blockers is more effective. Ondansetron (4-8 mg i.v.) and Granisetron (0.1 mg) hasbeen found to be highly effective in reducing the incidence of post anaesthetic nausea and vomiting.

TECHNIQUES OF INHALATION OF ANAESTHETICS

Open drop method Liquid anaesthetic is poured over a mask with gauze and its vapour is inhaled with air. A lot of anaesthetic vapour escapes in the surroundings and the concentration of anesthetic breathed by the patient cannot be determined. It is wasteful - can be used only for cheap anaesthetics. Some rebreathing does occur in this method. However, it is simple and

Through anaesthetic machines Use is made of gas cylinders, specialized graduated vaporisers, flow meters, unidirectional. Valves, corrugated rubber tubing and reservoir bag. The gases are delivered to the patient through a tightly fitting face mask or endotracheal tube. Admmlstralton of the anaesthetic can be more precisely Controlled and in many situations its concentration determmed. Respiration can be controlled and assisted

1. Open system - The exhaled gases are allowed to escape through a valve and fresh anaesthetic mixture is drawn in each time. No rebreathing is allowed - flow rates are high - more drugs are consumed. However, inhaled 02 and anaesthetic concentration can be accurately measured. 2. Closed system -The patient rebreaths the exhaled gas mixture after it has circulated through sodalime which absorbs C02. Only as much 02 and anaesthetic as have been taken up by the patient are added to the circuit. The flow rates are low; specially useful for expensive and Explosive agents (little anaesthetic escapes in the surrounding air) e.g. Halothane, Enflurane, Isoflurane. However, determination of inhaled anaesthetic concentration is difficult. It should not be used for trichloroethylene which forms a toxic compound with sodalime.

Anaesthetic Machine (Boyles equipment)

The anaesthetic machine Gas source- either piped gas or supplied in cylinders Flow meter Vaporisers Delivery System or circuit

THE GAS SOURCE Piped gas-Piped gases are stored in a bank, remote from the operating room. The gases are piped into the operating room and connected to the anaesthetic machine via hoses with special connections to ensure that the nitrous oxide cannot be connected to the oxygen inlet and vice versa. Cylinders are fitted directly on to the anaesthetic machine by means of yokes. The cylinders contain gases under a very high pressure. Oxygen is compressed at a pressure of about 147 bar (2000psi). Nitrous oxide is compressed at a pressure of about 44bar (600 psi).

 Colour code for cylinders: There is an international standard for colour coding gas cylinders but not all countries follow it. In India nitrous oxide cylinder is of blue colour and oxygen cylinder is of black colour with white shoulder. Pin index system: An ever-present hazard in anaesthesia is the danger of attaching a cylinder to the yoke meant for a different gas. This is eliminated by the pin index system the system consists of two pins projecting from the yoke in the anaesthetic machine, designed to fit into matching holes in the body of the cylinder valve. For any one gas there is only one combination of pins and holes. Unless the correct cylinder valve is attached to the correct yoke these pins and holes will

THE FLOWMETER

The gases pass from the reducing valve, via pressure tubing, to the flow meter calibrated for each gas. The flow meters record the volume of gas flowing to the patient per minute. There are various designs for the flow meters. The flow meter in the Boyles machine is referred to as a "Rotameter". It consists of a vertical glass tube tapered at the lower end. Rotating a knob at the base of the machine permits the entry of gases into the flowmeter. In the glass tube is an indicator or a bobbin. The height of the float in the tube indicates the flow of gases through the flowmeter. The flow should be read at the top of the bobbin.

THE VAPORISER

From the flowmeters the gases pass in the direction of the vaporisers. The vaporiser enables volatile agents to be introduced into the gaseous mixture. These volatile agents are liquids at room temperature and do not need to be stored under pressure. The function of the vaporiser is to vaporise this liquid.

OTHER FEATURES OF ANAESTHETIC MACHINE Alarm devices :Designed to initiate a signal when the oxygen pressure is low. The alarm should be triggered by a low oxygen pressure and not by nitrous oxide flow. Alarm devices triggered by nitrous oxide flow will not function if the nitrous oxide and oxygen fail simultaneously or if there is prior failure of the nitrous oxide supply. Oxygen flush valves:The valve directs a very high flow of oxygen (at least 30L/min) to the outlet of the machine. The valve is useful if it is necessary to fill the reservoir bag quickly with 100% oxygen.

Patient is in a stable anesthetic condition and ready for the dental procedure. Notice the position of the precordial stethoscope, blood pressure cuff, and nasotracheal tube.

Monitoring of patient

There should be quiet environment the operatory should be equipped with suction, monitoring equipments, emergency drugs, and equipments like defibrillators and a system capable of delivering oxygen under positive pressure

 gas delivery machines should have an oxygen fail-safe system, and should be checked and calibrated periodically on a scheduled basis. an anesthesia chart should be maintained for monitoring the patient

Defibrillator

Monitoring should be done according to the following criteria: 1) Level of consciousness The response of patient to the commands during procedures performed under sedation as a guide to their level of consciousness

2) Respiration pulmonary ventilation capnometer The rate and depth of respiration should be monitored. Respiratory rate in children is 10-18/min whereas depths can b judge by movements of chest and abdomen

3) Oxygenation Clinical colour of tongue and nails help to have an idea of oxygenation of blood.pulseoximetry has revolutionized modern monitoring procedures under normal circumstances, a childs oxygen saturation is 97-100%

4)hemodynamics cardioscope Pulse rate, blood pressure and continuous ECG monitoring reduces the likelihood of adverse outcomes during the procedure.ecg monitoring should be used in all patient undergoing sedation

5) Recording of monitored parameters Vital signs and respiratory variable should be recorded before initiating sedation, after administration of medication, at a regular interval during procedure, upon initiation if recovery, and immediately before discharge.

Completion of the procedure The anesthesiologist should be notified 10 minutes before the completion of the procedure so that the child can begin to be aroused and preparations can be made for estuation. The dentist should remain in the operating room during the estuation process to assist the anesthesiologist if necessary. When the childIs transported to the recovery room, the dentist should accompany the anesthesiologist and provide assistance during the transportation.

POSTANESTHESIA CARE UNIT

When the child arrives in the postanesthesia care unit or recovery room, the dentist should inform the nursing staff of the procedures accomplished and of any special requests or instructions. If teeth have been removed, the nurse should be specifically instructed how and where to apply gauze packs for hemostasis. The nurses and other medical staff are available to deal with immediately postoperative complications if they should occur (i.e., fever, nausea, vomiting, croup, hypoxia, bleeding, and laryngospasm).

 After the dentist has confirmed that the airway is patent and the vital signs are stable, and after The anesthesiologist is confident the child is recovering well; the dentist should meet with the parents or guardian to provide a brief report of the child's condition and a review of the treatment. The parents or guardian of Inpatients should be informed of the approximate time the child will be transported to the ward. The parents or guardian of outpatients should be informed of the time to meet the child in the recovery area. Prescriptions may be Written for pain control agents (i.e., acetaminophen with codeine, or ibuprofen suspension) antibiotics (i.e., amoxicillin, clindamycin)

Post anesthesia instructions

1. After the treatment the first drink should be sips of plain water, sweet drinks can be given next 2. For elevate body temperature, patient can be given antipyretic and fluids 3. Patient should seek advice if there is;  persistent vomiting beyond 4 hoarse  increased temp above 101 f  any breathing difficulty  excessive drowsiness 4. A 24 hr contact no. of the dental surgeon or pedodontics should be given to the parents 5. Emphasize check up on the following day and essential follow up

Latest Discoveries
Explosion of new information on the structure and function of GABAa receptors. Cloning and sequencing multiple subunits-large number of different subunits allows for a great variety of different types of GABAa receptors that will likely differ in drug sensitivity. Profol delivery technology:  mechanically driven pumps  computer-controlled infusion systems  target control infusion

 Findings collectively enhance the understanding on the mechanism of action of profol Allows the medicinal chemist to rationally design analogues with the better pharmacological profiles The Wall Streat Journal: FDA wants more research on anesthesia risk to kids  anesthesia can be harmful to developing brain  prolonged changes in behaviour, memory and learning impairements

REFERENCES
The Pharmacological basis of therapeutics- Goodman & Gilman Clinical Pharmacology- Bennett & Brown Essentials of medical pharmacology- Tripathi KD Basic & Clinical Pharmacology- Katzung G Petersons Principles of oral and maxillofacial surgery

Thank you