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)
6
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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