GENERAL ANESTHESIABy DR. ANINDYA

2nd YEAR PG OMFS

INTRODUCTION

General anesthetics (GAs) are drugs which:

Reversible loss of all sensations and consciousness.

Loss of memory and awareness with insensitivity to painful stimuli, during a surgical procedure.

Amne

sia-

hypn

osis

Analgesia

Areflexia

Definition

GENERAL ANESTHESIA: It is a controlled state of unconsciousness, accompanied by partial or complete loss of

protective reflexes, including the inability to independently maintain an airway or respond purposefully to verbal command.

CONCIOUS SEDATION: It is a state of mind obtained by IV administration of combination of anxiolytics, sedatives and

hypnotics &/or analgesic that render the patient relaxed, yet allows the patient to communicate, maintain patent airway and ventilate adequately.

DEEP SEDATION: It is a depressed level of consciousness with some blunting of protective reflex, although it

remains possible to arouse the patient. IATRO SEDATION:

A general term used for any technique of anxiety reduction in which no drugs are given Relief of anxiety through the doctor’s behavior - it is one of the form of psychosedation

Ether synthesized in 1540 by cordus General anesthesia was absent until the mid-1800s. Ether used as anesthetic in 1842 by dr. Crawford W.Long 1846 – Oliver Wendell Sr. “Anesthesia”

meaning: Insensibility during surgery produced by inhalation of ether.

William T. G. Morton (dentist) was the first to publicly demonstrate the use of ether during surgery(1846).

Chloroform used as anesthetic in 1853 by dr. John snow 1860 – Albert Niemann Cocaineas. Endotracheal tube discovered in 1878 Thiopental first used in 1934 Curare first used in 1942 - opened the “Age of anesthesia”

HISTORICALBACK GROUND

PROPERTIES OF AN IDEAL ANAESTHETIC

For the patient – Should be pleasant, Non irritating, Should not cause nausea or vomiting. Induction and recovery should be fast with no after

effects. For the surgeon –

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.

BALANCED ANESTHESIA

It is a term used to describe the multidrug approach to managing the patient needs. Balanced anesthesia takes advantage of drug’s beneficial effects while minimizing each agent’s adverse qualities.

Intraoperatively, an ideal anesthetic drug:

• would induce anesthesia smoothly, rapidly • permit rapid recovery as soon as administration ceased.

A ‘balanced anesthesia’ is achieved by a combination of I.V and inhaled anesthesia and Preanesthetic medications

SIGNS & STAGES OF ANAESTHESIA (GUEDEL’S Signs) 

Guedel (1920) described four stages with ether anaesthesia, dividing the III stage into 4 planes.

The order of depression in the CNS is: Cortical centers→basal ganglia→spinal cord→medulla

Stage of Analgesia

• analgesia and amnesia, the patient is conscious and conversational. 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 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

Stages of anesthesia

Guedel (1920) described four stages with ether anesthesia, dividing the III stage into 4 planes. The order of depression in the CNS is:1. Cortical centers2. Basal ganglia3. Spinal cord4. Medulla

Mechanisms of GA

The unitary theory of anesthesia – Meyer-Overton rule (1901)

Lipid : water partition coefficient

GA (gases) are highly lipid soluble and therefore can easily enter in neurones

After entry causes disturbances in physical chemistry of neuronal membranes – fluidization theory

Finally, obliteration of Na+ channel and refusal of depolarization

The unitary theory has been discarded now!

Modern theory on Mechanism of General Anesthesia

Major targets – ligand gated ion channels Important one – GABAA receptor gated Cl¯ channel

• GABAA receptors - 4 transmembrane (4-TM) ion channel– 5 subunits arranged around a central pore: 2 alpha, 2 beta, 1

gamma– 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

GABAA Receptor gated Cl¯ Channel Normally, GABAA receptor mediates the effects of

gamma-amino butyric acid (GABA), the major inhibitory neurotransmitter in the brain

GABAA receptor found throughout the CNS most abundant, fast inhibitory, ligand-gated ion channel in the

mammalian brain located in the post-synaptic membrane Ligand binding causes conformational changes leading to

opening of central pore and passing down of Cl- along concentration gradient

Net inhibitory effect reducing activity of Neurones

General Anaesthetics bind with these channels and cause opening and potentiation of these inhibitory channels – leading to inhibition and anesthesia

General Anesthesia

Inhalational

Gas

Nitrous oxideZenon

Volatile liquids

EtherHalothaneEnfluraneIsofluraneDesfluraneSevoflurane

Methoxyflurane

Intravenous

Slower acting

Dissociative anesthesia

Ketamine

Opioid analgesia

Fentanyl

Benzodiazepines

DiazepamLorazepamMidazolam

Inducing agents

Thiopentone sod.Methohexitone sod.

PropofolEtomidateDroperidol

Inhalation anesthetics• Common features of inhaled anesthetics

– Modern inhalation anesthetics are nonflammable, nonexplosive agents.

– Decrease cerebrovascular resistance, resulting in increased perfusion of the brain

– Cause bronchodilation, and decrease both minute ventilation and hypoxic pulmonary vasoconstriction

• MAC (potency): The alveolar concentration of an anesthetic gas needed to eliminate movement among 50% of patients challenged by a standardized painful stimulus (skin incision). – MAC is the ED50 of the anesthetic.

– the inverse of MAC is an index of potency of the anesthetic.

uptake and distribution of inhalation anesthetics The movement of these agents from the lungs to the different body

compartments depends upon their solubility in blood and tissues as well as on blood flow.

Because gases move from one compartment to another within the body according to partial pressure gradients, a steady state (SS) is achieved when the partial pressure in each of these compartments is equivalent to that in the inspired mixture.

Factors Determine the time course for attaining Steady State:

Anesthetic concentration in the inspired air (Alveolar wash-in): replacement of the normal lung gases with the inspired anesthetic mixture. The time required for this process is

directly proportional to the functional residual capacity of the lung, inversely proportional to the ventilatory rate; it is independent of the physical properties of the gas.

Anesthetic uptake: is the product of gas solubility in the blood, cardiac output, and the alveolar to venous partial pressure gradient of the anesthetic. Solubility in the blood: called the blood/gas partition coefficient. The solubility in blood is ranked in the following order: halothane > enflurane > isoflurane > sevoflurane > desflurane >

n2o. An inhalational anesthetic agent with low solubility in blood shows fast induction and also recovery time (e.g., N2O), and an

agent with relatively high solubility in blood shows slower induction and recovery time (e.g., halothane).

Wash out: when the administration of anesthetics discontinued, the body now becomes the “source” that derives the anesthetic into the

alveolar space. The same factors that influence attainment of steady-state with an inspired anesthetic determine the time course of clearance of the drug from the body. Thus N2O exits the body faster than halothane.

Inhalation sedation Indication

Uncooperative patient Mildly apprehensive patient Medically compromised patient Patient with gaging reflex

Contraindication Patient with extreme anxiety Nasal obstruction, sinus problem, common

cold URTI Serious psychiatry disorder COPD patient

o Advantageo Easy to administero Rapid onseto Rapid uptakeo Wide margin of safetyo Nausea-Vomiting uncommon

Disadvantage Expensive equipment Occupational hazards from

Nitrous Oxide leakage

Nitrous oxide (N2O) “laughing gas” It is a potent analgesic but a weak general anesthetic.

Rapid onset and recovery: Does not depress respiration, and no muscle relaxation. No effect on CVS or on increasing cerebral blood flow The least hepatotoxic, Teratogenic, bone marrow depression.

Second gas effect: N2O can concentrate the halogenated anesthetics in the alveoli when

they are concomitantly administered because of its fast uptake from the alveolar gas.

Diffusion hypoxia: speed of N2O movement allows it to retard oxygen uptake during

recovery.

Ether

Known as diethyl ether. Prepared by Cordus in1540 – sweet oil of vitriol Blood gas partition coefficient is 15 Guedel stage of anesthesia is described on ether anesthesia On induction – analgesia > excitement > anesthesia Increase CSF pressure, blood glucose level Postoperative nausea and vomiting in 50 % of patient

Halothane

ADVANTAGE Potent anesthetic, rapid induction & recovery Neither flammable nor explosive, sweet smell,

non irritant Low incidence of post operative nausea and

vomiting. Not hepatotoxic in pediatric patient, and

combined with its pleasant odor, this makes it suitable in children for inhalation induction

DISADVANTAGE Weak analgesic (thus is usually coadministerd

with N2O, opioids) Is a strong respiratory depressant Is a strong cardiovascular depressant Hypotensive effect Cardiac arrhythmias: if serious hypercapnia

develops due to hypoventilation and an increase in the plasma concentration of catecholamines

Malignant hyperthermia

 (2-bromo-2-chloro-1,1,1-trifluoroethane)

Synthesized in 1951 Blood gas partition coefficient 2.5

Malignant hyperthermia:

It is an autosomal dominant genetic disorder of skeletal muscle that occurs in susceptible individuals undergoing general anesthesia with volatile agents and muscle relaxants (eg, succinylcholine).

The malignant hyperthermia syndrome consists of the• rapid onset of tachycardia• hypertension, • severe muscle rigidity, • hyperthermia,• hyperkalemi • acid-base imbalance.

Rx Dantroline

ENFLUREN

ADVANTAGE Less potent than halothane, but produces rapid

induction and recovery ~2% metabolized to fluoride ion, which is

excreted by the kidney Has some analgesic activity Differences from halothane:

Fewer arrhythmias, less sensitization of the heart to catecholamines greater potentiation of muscle relaxant

DISADVANTAGE CNS excitation at twice the MAC, Can induce

seizure

ISOFLUREN ADVANTAGE

A very stable molecule that undergoes little metabolism

Not tissue toxic Does not induce cardiac arrhythmias Does not sensitize the heart to the action of

catecholamines Produces concentration-dependent

hypotension due to peripheral vasodilation It also dilates the coronary vasculature,

increasing coronary blood flow and oxygen consumption by the myocardium, this property may make it beneficial in patients with IHD.

Desflurane:

• Rapidity of induction and recovery: outpatient surgery• Less volatility (must be delivered using a special vaporizer) • Like isoflurane, it decreases vascular resistance and perfuses all major tissues

very well.• Irritating cause apnea, laryngospasm, coughing, and excessive secretions

Sevoflurane:

• Has low pungency, not irritating the airway during induction; making it suitable for induction in children

• Rapid onset and recovery: • Metabolized by liver, releasing fluoride ions; thus, like enflurane, it may prove to

be nephrotoxic.

Methoxyflurane

• The most potent and the best analgesic anesthetic available for clinical use. Nephrotoxic and thus seldom used.

Intravenous sedation

Advantage Highly effective technique Rapid onset of action Patent vein is a safety factor Control of salivary secretion Nausea vomiting less common

Disadvantage Venepuncture is necessary Venepuncture complications

Infiltration Hematoma thrombophlebitis

Intensive monitoring required Delayed recovery

Intravenous anestheticsBarbiturates (thiopental, methohexital) Potent anesthetic but a weak analgesic High lipid solubility; Quickly enter the CNS and depress function, often in less

than one minute. Redistribution occur very rapidly as well to other body

tissues, including skeletal muscle and ultimately adipose tissue (serve as a reservoir).

Thiopental has minor effects on the CVS but it may cause sever hypotension in hypovolemic or shock patient

All barbiturates can cause apnea, coughing, chest wall spasm, laryngospasm, and bronchospasm

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Intravenous anesthetics/PropofolPhenol derivativeIt is an IV sedative-hypnotic used in the induction and or maintenance of anesthesia. Onset is smooth and rapid (40 seconds)It is occasionally accompanied by excitatory phenomena, such as muscle twitching, spontaneous movement, or hiccups.Rate of Infusion – 30 mg/kg/min – amnesic

- 10 to 50 mg/kg/min – sedative doseFull orientation occur with in 5 to 10 minute after stopping of infusion.

Decrease BP without depressing the myocardium, it also reduce intracranial pressure. It is widely used and has replaced thiopental as the first choice for anesthesia

induction and sedation, because it produces a euphoric feeling in the patient and does not cause post anesthetic nausea and vomiting.

Poor analgesia

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Intravenous anesthetics/Etomidate Is used to induce anesthesia, it is a hypnotic

agent but lacks analgesic activity. Induction is rapid, short acting It is only used for patients with coronary artery

disease or cardiovascular dysfunction, No effect on heart and circulation Adverse effects: a decrease in plasma cortisol

and aldosterone levels which can persist for up to eight hours. This is due to inhibition of 11-B-hydroxylase

05/01/2023

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ketamine

Ketamine (phencyclidine derivative) Non-barbiturate hypnotic 1-2mg/kg – IV or 8-10 mg/kg - IM A short acting anesthetic (up to 15 min) induces

a dissociated state in which the patient is unconscious but appear to be awake and does not fell pain.

Profound analgesia, less vomiting Provides sedation, amnesia, and immobility Interacts with NMDA receptor,

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ketamine Sympathomimetic effect:

stimulates the central sympathetic outflow, causes stimulation of the heart and increased BP and COP.

This property is especially beneficial 1. in patients with either hypovolemic or cardiogenic shock, 2. as well as in patients with asthma. Ketamine is therefore

used when circulatory depression is undesirable. BP is often increased.

It increases cerebral blood flow and induces postoperative hallucinations “nightmares” particularly in adults,

No M. relaxation

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Adjuvants/Opioids (fentanyl, sufentanil)

Benzodiazepine (midazolam, lorazepam and diazepam) Are used in conjunction with anesthetics to sedate the patient.Opioids: Analgesic, not good amnesic, used together with anesthetics. They are administered either I.V, epidurally, or intrathecally All cause hypotension, respiratory depression and muscle rigidity as well as

post anesthetic nausea and vomiting, antagonized by naloxone.Neuroleptanesthesia:

Is a state of indeffernce and immobilization (analgesia and amnesia) produced when patient become analgesic, deeply seated and partially or wholly amnesic but yet remain capable of obeying commands and answering simple question.

it occurs while fentanyl is used with droperidol and N2O, Is suitable for burn dressing, endoscopic examination

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Properties of Intravenous Anesthetic AgentsDrug Induction and

RecoveryMain Unwanted

EffectsNotes

thiopental Fast onset (accumulation occurs, giving slow recovery) Hangover

Cardiovascular and respiratory depression

Used as induction agent declining. ↓ CBF and O2 consumptionInjection pain

etomidate Fast onset, fairly fast recovery

Excitatory effects during induction Adrenocortical suppression

Less cvs and resp depression than with thiopental, Injection site pain

propofol Fast onset, very fast recovery

cvs and resp depression Pain at injection site.

Most common induction agent. Rapidly metabolized; possible to use as continuous infusion. Injection pain. Antiemetic

ketamine Slow onset, after-effects common during recovery

Psychotomimetic effects following recovery, Postop nausea, vomiting ， salivation

Produces good analgesia and amnesia. No injection site pain

midazolam Slower onset than other agents

Minimal CV and resp effects.

Little resp or cvs depression. No pain. Good amnesia.

35Non-barbiturate induction drugs effects on BP and HR

Drug Systemic BP Heart Rate

propofol ↓ ↓

etomidate No change or slight ↓

No change

ketamine ↑ ↑

Surgical Period and GA protocol

Pre-anesthetic evaluation

Use pre-anesthetic medication↓

Induce by I.V thiopental or suitable alternative↓

Use muscle relaxant↓

Intubate↓

Use, usually a mixture of N2O and a halogenated hydrocarbon→maintain and monitor.

↓

Withdraw the drugs → recover

Pre-Anesthetic Evaluation

Meet the patient personally. Choose the right technique by the

preferences, case and patient. Goal

Increase Quality of preoperative care

Reduce Morbidity and mortality of surgery

Reduce Cost of preoperative care

Reduce Anxiety

1. Patient’s History2. History of use of

anestheticsor drugs

3. Pre-operative labs4. Physical

examination & Problem Identification

5. Risk Assessment6. Plan of

Anesthetic Management

7. Pre-anaesthetic Instructions

Use the ASA and GOLDMAN scale for anaesthetic risk.

Physical Examination: General examination Airway assessment Respiratory system Cardiovascular system System related problems identified from the history

MALLAMPATI TEST

PATIENT DOCTOR

Upright, maximal jaw opening, tongue protrusion without

phonation

Class I = visualize the soft palate, uvula, anterior and posterior pillars.

Class II = visualize the soft palate and uvula.

Class III = visualize the soft palate and the base of the uvula. Class IV = soft palate is not visible at all.

Mallampati Classification

ULBT (Upper Lip Bite Test)

Class 1:Lower incisors can bite upper lip above vermillion line.

Class 2:Lower incisors can bite upper lipbelow vermillion line.

Class 3:Lower incisors cannot bite the upper lip.

Interincisor distance (IID)

Generally greater than 2.5 to 3fingerbreadths (depending on observers fingers)

Less than or equal to 4.5 cm is

considered a potentially difficult intubation.

Thyromental distance(TMD)

Upright, neck extension, mouth closed, Distance < 6.5cm difficult intubation

Sternomental Distance(SMD)

Extended head and neck, mouth closed, distance <12.5cm is a difficult intubation

medical status mortalityASA I Normal healthy patient without organic, biochemical, or

psychiatric disease0.06-0.08%

ASA II Mild systemic disease with no significant impact on daily activity e.g. mild diabetes, controlled hypertension, obesity .

Unlikely to have an impact

0.27-0.4%

ASA III Severe systemic disease that limits activity e.g. angina, COPD, prior myocardial infarction

Probable impact 1.8-4.3%

ASA IV An incapacitating disease that is a constant threat to life e.g. CHF, unstable angina, renal failure ,acute MI, respiratory failure requiring mechanical ventilation

Major impact 7.8-23%

ASA V Moribund patient not expected to survive 24 hours e.g. ruptured aneurysm

9.4-51%

ASA Physical Status Classification System

For emergent operations, you have to add the letter ‘E’ after the classification.

GOLDMAN RISK ASSESMENT SCALE (1977)Factors ValueHistory Age > 70 years (5 point)

Myocardial infection with in 6 month (10 points)Cardiac Exam Signs of CHF: ventricular gallop or JVD (11 points)

Significant aortic stenosis (3 points)Electrocardiogram Arrhythmia other than sinus or premature atrial contractions (7

points)5 or more PVC's per minute (7 points)

General Medical Conditions

PO2 < 60; PCO2 > 50; K < 3; HCO3 < 20; BUN > 50; Creat > 3; elevated SGOT; chronic liver disease; bedridden (3 points)

Operation Emergency (4 points)Intraperitoneal, intrathoracic or aortic (3 points)

0-5 Points: Class I 1% Complications

6-12 Points: Class II 7% Complications

13-25 Points: Class III 14% Complications

26-53 Points: Class IV 78% Complications

Recommended test Guidelines For Asymptomatic Patient

Age up to 49 yrs CBC

Age 50-64yrs CBC,ECG

Age > 65 yrs CBC, ECG, CXR

Urine analysis, LFT, BUN/ Cr, Electrolyte,Blood Sugar

INGESTED MATERIAL

MINIMUM FASTING PERIOD, APPLIED TO ALL AGES (hr)

Clear liquids 2Breast milk 4Infant formula 6Nonhuman milk 6Light meal (toast and clear liquids)

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Fasting Recommendations

PRE-ANAESTHETIC MEDICATIONS

PREANAESTHETIC MEDICATION

“It is the term applied to the administration of drugs prior to general anaesthesia so as to make anaesthesia safer for the patient”

Ensures comfort to the patient & to minimize adverse effects of anesthesia

PRE-ANAESTHETIC MEDICATIONS

Serve to Relief of apprehension or anxiety Sedation Analgesia Amnesia of perioperative events Antisialogogue effect Reduction of stomach acidity Prevention of nausea and vomiting Vagolytic action Facilitation of anesthetic induction Prophylactic against allergies

Preanesthetic Medicine: • Benzodiazepines; midazolam or diazepam: Anxiolysis &

Amnesia.• Barbiturates; pentobarbital: sedation• Diphenhydramine: prevention of allergic reactions:

antihistamines• H2 receptor blocker- ranitidine: reduce gastric acidity.

Anti-anxiety drugs Provide relief from apprehension & anxietyPost-operative amnesia

Benzodiazepine anxiolytics but no analgesia – should not be given with opioids

Midazolam Iv – 0.05-0.1 mg/kg (2 to 5 mg in 0.5 mg increment) – return to normal

within 4 hr Intra-nasal dose – 0.6 mg/kg

Diazepam Gold standard Oral doses – 5-10 mg With opioid can produce respiratory and cardiovascular depression

Flumezanil Drug antagonized the sedative and amnestic effect of midazolam 0.1 -0.5 mg Short acting – preferably given in infusion form

SEDATIVES-HYPNOTICS Barbiturates

Priorly used but now generally no use Replaced by benzodiazepine Doses – 50-200 mg orally Action within 15 to 20 minute – duration last – 2 to 4 hr

Butyrophenon Mainly antiemetic but can produce sedation Doses – IV/IM – 2.5 to 7.5 mg

Phenothiazine Sedation, anticholinergic and antio emetic effect Always used with opioids Lytic cocktail – 50 mg pethidine + 25 mg promethazine + 10 mg chlorpromazine

Promethazine Antisialogogue + antihistaminic + sedative Doses – Orally – 10 – 25 mg

Trimeperezine tartrate Doses – 3-4 mg/kg – 2 hr preoperatively

ANALGESIC AGENT Morphine

Well absorbed after IM injection Onset – 15 to 30 minute Peak effect – 45 to 90 minute Lasting for 4 hr May cause – orthostatic hypotension, respiratory distress, addiction

Fentanyl (preferred most now a days/ given just before induction) 50 to 125 times potent than morphine Respiratory depression is high Dose – 1-2umg/kg Onset – 30 to 60 second Route – intranasally, orally, transdermally

Pethidine Doses – 50 to 100 mg – IM / IV – single dose lasts for 2 to 4 hour

Buprenorphine Highly potent drug 3 to 6 umg/kg – IM/IV Respiratory depression

ANTICHOLINERGIC AGENTS Actions

Vagolytic Increase heart rate by blocking acetylcholine on muscarinic

receptor in SA node Atropine is more effective than glycopyrolate / scopolamine Useful in preventing intraoperative bradycardia resulting from

vagal stimulation or carotid sinus stimulation Atropine (0.5mg IM) also helps in preventing vasovagal attack

Antisialogogue Induce drying of salivary, gastric, tracheobronchial and sweat

gland secretion Glycopyrolate (0.1-0.3 mg IM) is more potent – long acting drying

effect Should be given 30 minute prior to the procedure

Sedation and amnetia Atropine and scopolamine cross blood-brain barrier Atropine cause delirium in elderly Scopolamine has good sedative and amnesic effect

Side Effects Pupillary dilatation

Tachycardia, cardiac arrhythmia

Delirium, confusion, restlessness

Increase body temperature

Antiemetics- - Metoclopramide (10mg i.m.) used as antiemetic & as prokinetic gastric emptying

agent prior to emergency surgery – 30-60 minute prior to surgery - Domperidone (10mg oral) more preferred (does not produce extrapyramidal side

effects) - Ondansetron (4-8mg i.v.), a 5HT3 receptor antagonist, found effective in preventing

post-anaesthetic nausea & vomiting Drugs reducing acid secretion - - Ranitidine (150-300mg oral) or Famotidine (20-40mg oral) given night before & in morning along

with Metoclopramide reduces risk of gastric regurgitation & aspiration pneumonia - Proton pump inhibitors like Omeprazole (20mg) with Domperidone (10mg) is preferred nowadays

DIFFERENT ASPECTS OF PREMEDICATION For OUT PATIENT DENTAL SURGERY

Atropine/ Glycopyrolate – 30 min prior to surgery Diazepam (0.25mg/kg) – orally night before procedure For longer procedure – Midazolam (0.05-0.1mg/kg) – IM- 30 min prior to

surgery If pt. having pain – fentanyl (100mg) may be added to midazolam

For MAJOR MAXILLOFACIAL SURGERY Atropine / Glycopyrolate + Pethidine + Promethazine – 30 min prior to surgery Promethazine act for drying secretion + Sedation + prevent Histamine release

For PEDIATRIC / CHILD PATIENT Vagus activity more predominant with small air passage Presence of secretion may cause deleterious effect Anticholinergic mandatory IM/IV Syrup TRIMEPERAZINE / Promethazine (0.6mg/kg) – to sedate Ketamine can also be given

CONCURRENT DRUG THERAPYTo be continued To be modified To be discontinued

Antiarrythmics Insulin Diuretic- on the day of surgery

Antiasthmatic Oral-anticoagulant Oral hypoglycemicAntibiotics Steroid cover Aspirin – 1 wk priorAntiepileptic Mono Amine Inhibitor – 2 wk prior to

surgery

B-blocker Oral contraceptive – 1 mnth cycle

Ca channel blockerEye dropsSedative/anxiolyticimmunosuppressant

ANESTHETIC EQUIPMENT Anesthesia & Resuscitation

equipment Anesthesia machine Breathing circuit Anesthetic mask Laryngoscope Endotracheal tube Airways Magill’s forceps Mouth prop Resuscitation bag

Monitoring equipment Blood pressure monitor Cardioscope Pulse oximeter Capnometer Respiratory gas monitor

Oxygen therapy Equipment Oxygen cylinder Oxygen flowmeter Oxygen mask Nasal catheter/ prongs

Intravenous infusion equipment

Scalp needle Intravenous cannula Bivalve (three way) Infusion set Intravenous fluids

Anesthesia Machine To deliver a desired concentration of a mixture of anesthetic

agents in an inhalation form with oxygen and/or air – act as a vehicle to carry this mixture to the outlet of the equipment.

Consist of Cylinder of gases Flow meter Vaporizer Oxygen flush / emergency oxygen knob Working platform and tray

Two type Intermediate flow (Walton 5 machine) Continuous flow (Boyle machine)

Intermediate machine Gas flows on patient demand through DEMAND

VALVE – now a days obsolete

Continuous flow machine Oxygen/ nitrous oxide – individual flow meter Vaporizer – meant for setting desired percentage

of anesthetic agent

Disadvantage Delivery of hypoxic gas mixture Lead to – brain damage / coma/ cardiac arrest/

death To avoid newer anesthetic machine has – hypoxic

gas mixture alarm

Breathing system Component

Reservoir bag Excursion (rhythmical inflation + deflation) – allows visual monitoring of

patient breathing

Long corrugated breathing tube Flexible Prevent kinking Plastic body – light weight – less drag on mask

Expiratory valve Spring loaded valve (Heidbrink Valve) Non-rebreathing valve

Types Magill’s system – a single corrugated tubing Bain’s system – coaxial tubing Closed circuit – double tubing – inspiratory / expiratory

Anesthetic mask Allows administration of gases

from breathing unit Type

Face mask Nasal mask

Parts Connector / mount Body Edge / seal

Size 1,2,3,4,5

Laryngoscope Designed for doing direct laryngoscopy Parts

Handle Blade with light

Size Neonate Pediatric Adult Extra large

Type MacIntosh Miller’s

Method of insertion Patient in supine position with neck flexon and head

extension Entered through right – tongue pushed to left –

extended till valecula

AIRWAY TUBES Oropharyngeal airway

Nasopharyngeal airway

LMA (Laryngeal Mask Airway)

Esophageal tracheal combi-tube

Endotracheal tube

Nasotracheal tube

Flexo-matalic tube

Ring Adair Ellwyn (RAE) South pole North pole

Tracheal intubation Intubation after induction of GA

Oral – OROTRACHEAL intubation Nasal – NASOTRACHEAL intubation

Awake intubation Blind oral Blind nasal Retrograde – rail road technique Fiberoptic scope

Resuscitation Bag

Consisting of Self inflating bag Non-breathing valve facemask

Verities With reservoir bag Without reservoir bag

Size Infant Child adult

Monitoring Equipment Blood pressure monitor

Generally monitor on the right / left upper arm Types-

Simple sphygmomanometer / aneroid dial Noninvasive automatic blood pressure monitor Invasive blood pressure monitor

Cardioscope Help to monitor

ECG Heart rate, rhythm Type of arrhythmia It may be either 3 lead or 12 lead

Pulse oximeter Non invasive equipment to monitor the oxygen

saturation of the patient A small probe attached on any of the finger/ toes/

ear lobule It is important because hypoxia can occur from

anesthetic gas mixture/ breathing circuit got disconnected

Hypoxia can lead to brain death , coma and even cardiac arrest

Capnometer/ capnograph Equipment that continuously record CO2

tension (in mm Hg or %) of expired gas

Value – 35-45 mm Hg

Also known as End Tidal CO2 monitor.

Help anesthesiologist to decide Pt breathing adequately Whether tube is in trachea or oesophagus Breathing circuit is in position or not

Oxygen Therapy Equipment

Oxygen Cylinder Oxygen flowmeter Oxygen Mask Nasal Catheter

Intravenous Infusion Equipment

Scalp needle Intravenous cannula Bivalve ( three way) Infusion set IV fluid

Induction of anesthesia the period of time from the onset of administration of the anesthetic to the

development of effective surgical anesthesia in the patient. It depends on how fast effective concentrations of the anesthetic drug reach

the brain. During induction it is essential to avoid the dangerous excitatory phase (stage II

delirium) that was observes with the slow onset of action of some earlier anesthetics.

GA is normally induced with an I.V thiopental, which produces unconsciousness within 25 seconds after injection. At that time, additional inhalation or IV drugs comprising the selected anesthetic combination (skeletal M. relaxants) may be given to produce the desired depth of surgical stage III anesthesia.

Inhalation induction: For children without IV access, non pungent agents, such as halothane or sevoflurane, are used to induce GA.

Maintenance of anesthesia Anesthesia is usually maintained by the administration of volatile

anesthetics, because these agents offer good minute-to-minute control over the depth of anesthesia.

Opioids such as fentanyl are often used for pain along with inhalation agents, because the later are not good analgesics.

Usually: N2O + volatile agent (halothane, isoflurane) Less often N2O + I.V Opioid analgesic (fentanyl, morphine,

pethidine + N.M blocking agents

Recovery the time from discontinuation of administration of the anesthesia

until consciousness and protective physiologic reflexes are regained.

It depends on how fast the anesthetic drug diffuses from the brain.

For most anesthetic agents, recovery is the reverse of induction; that is, redistribution from the site of action (rather than metabolism) underlies recovery.

Postoperative period

N.M blocking agents and Opioids induced respiratory depression have either worn off or have been adequately reversed by antagonists.

Regained consciousness and protective reflex restored

Relief of pain: NSAIDs Postoperative vomiting: metoclopramide,

prochlorperazine

Pre - Per- Post operative

complications of GA

Complications

Cause Management

Coughing Irritation of airways, secretion By deepening of anesthesia / induce muscle relaxant

Hiccup Afferent impulse from abdominal/ thoracic viscous via vagus

Deepen anesthesia / induce muscle relaxant

Wheezing Reflex under light anesthesia, ETT inserted too far, aspiration

Rule out mechanical obstructionDeepen the level of anesthesiaAminophyline IV 250-500 mg Adrenaline IV 1-3 ml (1:10000)Salbutamol IV 250mg / 2.5mg inhalation

Cyanosis Misplaced ETTDisconnectionAirway obstructionOxygen supply failure

Properly position ETTConnect circuit properlyCheck gas supplyMonitor ET CO2 SaO2

Hypertension Light anesthesiaHypoventilationHypercarbia

Use vasodilatorDeep anesthesia levelVentilate properly

Hypotension Due to anesthetic drugBlood lossB-blockers

Volume loadIV AtropineIV Vasopressor (dopamine)

hypoxemia Failed oxygen deliveryObstructed airwayEsophageal intubation

Ventilate with self inflating bagRule out disconnectionCheck ETT position

Complications Management

Nausea & Vomiting Keep patient supinePromethazine 12.5 mg- 25 mg IM/IVMetaclopromide 10-20 mg orallyRanitadine 50 mg IV

Postoperative hypertension

Passage of urineOxygenate properlyChlorpromazine 2-5 mg IV Sodium nitro preside infusion

Respiratory inadequacy

Ventilate adequately with 100% oxygen Asses neuromascular block – IV Atropine/ Neostigmine (not more than 5 mg)Naloxane administer if narcotics used (0.4 mg dilute to 4 ml – 0.1 mg increament)

Respiratory obstruction

Clear the airwayVentilate with bag and maskOxygenateIf require intubate SOS / Tracheostomy

Postoperative shivering

OxygenationWarm the patientStop any blood infusion

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