SEMINAR TOPIC General Anesthesia

DEPARTMENT OF ORAL AND MAXILLOFACIAL SURGERY

SEMINAR MODERATOR Dr. Suhas S. Godhi Dr. Rajesh Kalra

PRESENTER Dr. ASHOK KUMAR M.D.S (FIRST YEAR)

CONTENTS 1- Introduction and History of General anesthesia 2- Properties of ideal General anesthetic 3- Classification of General anesthetic agents 4- Mechanism of Anesthesia 5- Stages of Anesthesia 6- Inhalation anesthetic agents 7- Intravenous anesthetic agents 8- Techniques of inhalation of anesthetics 9- Induction, Maintenance and Extubation 10- Anaesthetic Machine (Boyle’s 12- Preanesthetic medication 13- General anesthesia- facts and fiction equipment) 11- Complications of General anesthesia

GENERAL ANESTHETICS
• General anaesthetics (GAs) are drugs which produce reversible loss of all senations and consciousness. Or, • General anaesthetics (GAs) are a class of drugs used to depress the CNS to a sufficient degree to permit the performance of surgery and other noxious or unpleasant procedures.

• Triad of General Anesthesia” – need for unconsciousness – need for analgesia – need for muscle relaxation

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 •

• 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 the “Age of Anesthesia”

Properties of an ideal anaesthetic A. For the patient - It should be pleasant, nonirritating, should not cause nausea or vomiting. Induction and recovery should be fast with no after effects. B. For the surgeon - It should provide adequate analgesia, immobility and muscle relaxation. It should be noninflammable and nonexplosive so that cautery may be used. C. 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 Inhalational Intravenous Gas Inducing agents Slower acting Nitrous oxide Thiopentone sod. Benzodiazepines Liquids Methohexitone sod. Diazepam Ether Propofol Lorazepam Halothane Etomidate Midazolam Enflurane Dissociative anaesthesia Isoflurane Ketamine Desflurane Neurolept analgesia Sevoflurane Fentanyl + droperidol

MECHANISM OF ACTION OF ANAESTHESIA The mechanism of action of GAs is not precisely known. A wide variety of chemical agents produce general anaesthesia. Therefore, GA action had been related to some common physicochemical property of the drugs.

Minimal alveolar concentration (MAC) is the lowest concentration of the anaesthetic in pulmonary alveoli needed to produce immobility in response to a painful stimulus (surgical incision) in 50% individuals.

It is accepted as a valid measure of potency of inhalational GAs because it remains fairly constant for a given species even under varying conditions. MAC reflects capacity of the anaesthetic to enter into CNS and attain sufficient concentration in neuronal membrane. Mayer and Overton (1901) proposed that the anaesthetic by dissolving in the membrane lipids increases the degree of disorder in their structure favouring a gel-liquid transition (fluidization) which secondarily affects the state of membrane bound functional proteins, or expands the membrane disproportionately (about 10 times their molecular volume) closing the ion channels. Different anaesthetics may be acting through different molecular mechanisms. Many inhalational anaesthetics, barbiturates, benzodiazepines and propofol potentiate the action of the inhibitory transmitter GABA at the GABAA receptor. Certain fluorinated anaesthetics and barbiturates in addition inhibit the neuronal cation channel gated by nicotinic cholinergic receptor. As such, the receptor operated ion channels appear to be a major site of GA action. Unlike local anaesthetics which act primarily by blocking axonal conduction, the GAs appear to act by depressing synaptic transmission

SIGNS & STAGES OF ANAESTHESIA (GUEDEL’S Signs) GAs cause an irregularly descending depression of CNS, i.e. the higher functions are lost first and progressively lower areas of the brain are involved, but in the spinal cord lower segments are affected somewhat earlier than the higher segments. The vital centres located in the medulla are paralysed the last as the depth of anaesthesia increases. Guedel (1920) described four stages with ether anaesthesia, dividing the III stage into 4 planes. • I. Stage of Analgesia Starts from beginning of anaesthetic inhalation and lasts upto the loss of consciousness. Pain is progressively abolished during this stage. Patient remains conscious, can hear and see, and feels a dream like state. Reflexes and respiration remain normal. • Though some minor and even major operations can be carried out during this stage, it is rather difficult to maintain - use is limited to short procedures. II. Stage of Delirium From loss of consciousness to beginning of regular respiration. Apparent excitement is seen - 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 stimulus should be applied or operative procedure carried out during this stage. This stage can be cutshort by rapid induction, premedication etc. and is inconspicuous in modern anaesthesia.

• • •

III. 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. IV. 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.

Four stages of general Anesthesia

Inhalational Anesthetic Agents
Inhalational anesthesia refers to the delivery of gases or vapors from the respiratory system to produce anesthesia.

Nitrous Oxide

It is prepared by Priestly in 1776 Anesthetic properties described by Davy in1799 Characterized by inert nature with minimal metabolism Colorless, odorless, tasteless, and does not burn Simple linear compound, not metabolized. It is the only anesthetic agent that is inorganic Major difference is low potency MAC value is 105% Weak anesthetic, powerful analgesic Needs other agents for surgical anesthesia Low blood solubility (quick recovery) Nitrous oxide is generally used as a carrier and adjuvant to other anaesthetics. A mixture of 70% N20 + 25-30% 02 + 0.2-2% another potent anaesthetic is employed for most surgical procedures. As the sole agent, N20 has been used with 02 for dental and obstetric analgesia. It is nontoxic to liver, kidney and brain. Metabolism of N20 does not occur; it is quickly removed from body by lungs. It is cheap and very commonly used Nitrous Oxide Systemic Effects Minimal effects on heart rate and blood pressure May cause myocardial depression in sick patients Little effect on respiration Safe, efficacious agent

Nitrous Oxide Side Effects Manufacturing impurities toxic Hypoxic mixtures can be used Large volumes of gases can be used Beginning of case: second gas effect End of case: diffusion hypoxia Inhibits methionine synthetase (precursor to DNA synthesis) Inhibits vitamin B-12 metabolism Dentists, OR personnel, abusers at risk

Halothane

Synthesized in 1956 by Suckling Halogen substituted ethane Volatile liquid easily vaporized, stable, and nonflammable Most potent inhalational anesthetic MAC of 0.75% Efficacious in depressing consciousness

Very soluble in blood and adipose Prolonged emergence It is currently one of the most popular anaesthetics because of nonirritant, noninflammable, pleasant and rapid action. Its deficiencies in terms of poor analgesia and muscle relaxation are compensated by concomitant use of N20 or opioids and neuromuscular blockers. Inhibits sympathetic response to painful stimuli Inhibits sympathetic driven baroreflex response (hypovolemia) Halothane Systemic Effects Decreases respiratory drive 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 -Malignant Hyperthermia-- 1/60,000 with succinylcholine to 1/260,000 without halothane in 60%, succinylcholine in 77%. Rapid rise in body temperature, muscle rigidity, tachycardia, rhabdomyolysis, acidosis, hyperkalemia. most common masseter rigidity

Ether (Diethyl ether) It is a highly volatile liquid, produces irritating vapours which are inflammable and explosive. Ether is a potent anaesthetic, produces good analgesia and marked muscle relaxation by reducing ACh output from motor nerve endings. It is highly soluble in blood - induction is prolonged and unpleasant with struggling, breath holding, salivation and marked respiratory secretions. Recovery is slow; post-anaesthetic nausea, vomiting and retching are marked. It does not sensitize the heart to Adr and is not hepatotoxic. Ether was very popular in the past, but not used now because of its unpleasant and inflammable properties.

Enflurane

Developed in 1963 by Terrell, released for use in 1972 Stable, nonflammable liquid Pungent odor MAC 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 Enflurane Side Effects Metabolism one-tenth that of halothane-- does not release quantity of hepatotoxic metabolites Metabolism releases fluoride ion-- renal toxicity Isoflurane

Synthesized in 1965 by Terrell, introduced into practice in 1984 Not carcinogenic

Nonflammable,pungent Less soluble than halothane or enflurane 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. 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
Low solubility in blood-- produces rapid induction and emergence Minimal systemic effects-- mild respiratory and cardiac suppression Few side effects Expensive

Intravenous Anesthetic Agents
First attempt at intravenous anesthesia by Wren in 1656-opium into his dog Use in anesthesia in 1934 with thiopental INDUCING AGENTS These are drugs which on i.v. injection produce loss of consciousness in one arm-brain circulation time (-11 sec); are generally used for induction because of rapidity of onset of action. Anaesthesia is then usually maintained by an inhalational agent. They also serve to reduce the amount of maintenance anaesthetic. Supplemented with analgesics and muscle relaxants, they can also be used as the sole anaesthetic.

1. Thiopentone sod.
It is an ultrashort acting thiobarbiturate, highly soluble in water yielding a very alkaline solution, which must be prepared freshly before injection.

Extravasation of the solution or inadvertent intraarterial injection produces intense painnecrosis and gangrene may occur. Injected i.v. (3-5 mg/kg) as a 2.5% solution, it produces unconsciousness in 15-20 sec. Its undissociated form has high lipid solubility - enters brain almost instantaneously. Initial distribution depends on organ blood flow - brain gets large amounts. Thiopentone is a poor analgesic. Painful procedures should not be carried out under its influence unless an opioid or N20 has been given, otherwise the patient may struggle, shout and show reflex changes in BP and respiration. It is a weak muscle relaxant BP falls immediately after injection, but recovers rapidly. Cardiovascular collapse may occur if hypovolemia, shock or sepsis are present. Thiopentone is the commonest inducing agent used. It can be employed as the sole anaesthetic for short operations that are not painful. Thiopental Side Effects Laryngospasm- Can be prevented by atropine premedication and administration of succinylcholine immediately. Succinylcholine and thiopentone react chemically - should not be mixed in the same syringe. Shivering and delirium may occur during recovery. Post-anesthetic nausea and vomiting are uncommon.

Propofol Rapid onset and short duration of action Myocardial depression and peripheral vasodilation may occur-- baroreflex not suppressed Not water soluble-- painful (50%) Minimal nausea and vomiting Unconsciousness after propofol injection occurs in 1545 sec and lasts -15 min. It distributes rapidly (distribution t1/2 2-4 min) and elimination is much shorter than thiopentone due to rapid metabolism. It is particularly suited for out patient surgery because residual impairment is less marked and incidence of post operative nausea and vomiting is low. Dose:2mg/kg bolus i.v. for induction; 9 mg/kg/hr for maintenance. Etomidate Structure similar to ketoconozole 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

Slower Acting Drugs
Benzodiazepines Produce sedation and amnesia Potentiate GABA receptors 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 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 Water soluble Ketamine Interrupts cerebral association pathways -- “dissociative anesthesia”

Stimulates central sympathetic pathways Ketamine Systemic and Side Effects Characteristic of sympathetic nervous system stimulation-increase HR, BP. Maintains laryngeal reflexes and skeletal muscle tone Emergence can produce hallucinations and unpleasant dreams (15%) TECHNIQUES OF INHALATION OF ANAESTHETICS Different techniques are used according to facility available, agent used, condition of the patient, type and duration of operation. 1. Open drop method -Liquid anaesthetic is poured over a mask with gause 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 requires no special apparatus. Ether is the only agent used by this method, specially in children. 2. 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 by the anaesthetist (a) 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 drug is consumed. However, inhaled 02 and anaesthetic concentration can be accurately measured. (b) 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.

(c) Semiclosed system - Partial rebreathing is allowed through a partially closed valve. Conditions ·are intermediate with moderate flow rates

Induction, Maintenance and Extubation
Patients are premedicated with oral diazepam 10mg on night before surgery. Injection glycopyrrolate 0.2mg I/V should be given before induction. Patients are induced with thiopentone sodium 4-7 mg/kg body weight after adequate preoxygenation. Succinylcholine 1-2 mg/kg body weight should be given to facilitate laryngoscopy and intubation. Anaesthesia is maintained with N2O + O2 mixture. 0.5% halothane along with nondepolarizing muscle relaxant like vecuronium bromide are also used in maintenance. Neostigmine (0.05-.08 mg/kg body weight) and glycopyrrolate are used for extubation.

Anaesthetic Machine (Boyle’s equipment)
The anaesthetic machine • Gas source- either piped gas or supplied in cylinders • Flow meter • Vaporisers • Delivery System or circuit

A continuous flow (Boyle’s) anaesthetic machine

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 (2000 psi). Nitrous oxide is compressed at a pressure of about 44 bar (600 psi). They are made entirely out of steel that meets certain chemical and physical requirements or out of a chrome molybdenum mixture that is 20% lighter than steel. 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 not match and the cylinder will not fit. Therefore it is not possible with this system to fit a nitrous oxide cylinder to an oxygen yoke or vice versa. THE FLOWMETER The gases pass from the reducing valve, via pressure tubing, to the flowmeter calibrated for each gas.

The flowmeters record the volume of gas flowing to the patient per minute. There are various designs for the flowmeters. We will describe those used in the Boyle's machine. The flowmeter in the Boyle’s 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 are 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.

COMPLICATIONS OF GENERAL ANAESTHESIA
A. During anaesthesia 1. Respiratory depression and hypercarbia. 2. Salivation, respiratory secretions -less now as non-irritant anaesthetics are mostly used. 3. Cardiac arrhythmias, asystole. 4. Fall in BP 5. Aspiration of gastric contents: acid pneumonitis. 6. Laryngospasm and asphyxia. 7. Delirium, convulsions. Excitatory effects are generally seen with i.v. anaestheticsspecially if phenothiazines or hyoscine have been given in premedication. These are suppressed by opioids. 8. Fire and explosion - rare now due to use of noninflammable agents. B. After anaesthesia 1. Nausea and vomiting. 2. Persisting sedation: impaired psychomotor function. 3. Penumonia, atelectasis. 4. Organ toxicities: liver, kidney damage. 5. Nerve palsies - due to faulty positioning. 6. Emergence delirium.

PREANAESTHETIC MEDICATION
Preanaesthetic medication refers to the use of drugs before anaesthesia to make it more pleasant and safe. 1. Opioids 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. 2. Antianxiety drugs Benzodiazepines like diazepam (5-10 mg oral) or lorazepam (2 mg i.m.) have become popular drugs for preanaesthetic medication because they produce tranquility and smoothen induction; there is loss of recall of intaoperative 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. Midazolam is a good amnesic with potent and shorter action; it is also better suited for injection 3. 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. 4. Anticholinergics Atropine or hyoscine (0.6 mg i.mJi.v.) have 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 reflexly due to certain surgical procedures), and prophylaxis of laryngospasm 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 acting atropine substitute. It is a potent anti secretory and antibradycardiac drug; acts rapidly and is less likely to produce central effects 5. H2 blockers Patients undergoing prolonged operations, caesarian section, obese patients are at increased risk of gastric regurgitation and aspiration pneumonia. 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. 6. 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) has been found to be highly effective in reducing the incidence of post anaesthetic nausea and vomiting.

General Anesthesia: Facts and Fiction

“Anesthetic awareness”? Only occurs under general anesthesia Medication given to render patient unconscious fails May recall some or all events during surgery May or may not feel pain or pressure Occurs infrequently: 1 in 1,000 cases

Duration and severity vary Extreme awareness experiences are very uncommon. Patients Need Not be Afraid! Anesthesia today nearly 50 times safer than it was just 20 years ago. Causes of awareness --Inadequate anesthesia --Equipment failure or misuse Awareness might not be completely avoidable in the following types of surgery: Cardiac Emergency C-section Trauma

“Awake” movie
Released in November 2007 Exploits anesthesia awareness as plot device “Awake” movie

Irresponsible: Movie ads claim 1 in 700 patients under general anesthesia are awake for entire surgery

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

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