General Anaesthetics - drdhriti


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A PowerPoint presentation on "General Anaesthetics" suitable for reading by Undergraduate medical Students.


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Presentation Transcript

Slide 1: 

2010 Wish you

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General Anesthesia

Anaesthesia : 

Anaesthesia Anesthesia – is a reversible condition of comfort, quiescence and physiological stability in a patient before, during and after performance of a procedure. General anesthesia – for surgical procedure to render the patient unaware / unresponsive to the painful stimuli. Drugs producing G. Anaesthesia – are called general anaesthetics Local anesthesia - reversible inhibition impulse generation and propagation in nerves. In sensory nerves, such an effect is desired when painful procedures must be performed, e.g., surgical or dental operations. Drugs producing L. Anaesthesia – are called local anaesthetics

Local anaesthesia : 

Local anaesthesia Some terms related to Local anaesthesia: Surface anaesthesia: Ointment / jelly / solutions applied on mucous membrane. Infiltration anaesthesia: Injection of the LA to produce analgesia over an area. Regional anaesthesia: spinal, epidural and IV regional anaesthesia. Spinal – sub-arachnoid space. Epidural – between spinal bone and dura matter. IV Regional – limited to limbs and practically upper limbs.

What are General anaesthetics ? : 

What are General anaesthetics ? General Anaesthetics are the drugs which produce reversible loss of all sensation and consciousness, or simply, a drug that brings about a reversible loss of consciousness. These drugs are generally administered by an anesthesiologist in order to induce or maintain general anesthesia to facilitate surgery. General anaesthetics are – mainly inhalation or intravenous

What are the Drugs used as GA ? (Classification) : 

What are the Drugs used as GA ? (Classification) Inhalation: Gase: Nitrous Oxide Volatile liquids: Ether Halothane Enflurane Isoflurane Desflurane Sevoflurane Intravenous: Inducing agents: Thiopentone, Methohexitone sodium, propofol and etomidate Benzodiazepines (slower acting): Diazepam, Lorazepam, Midazolam Dissociative anaesthesia: Ketamine Neurolept analgesia: Fentanyl

Essential components of GA: : 

Essential components of GA: Triad of General Anesthesia: need for unconsciousness need for analgesia need for muscle relaxation Essential components of GA: Loss of all sensations – pain Unconsciousness Amnesia Immobility and muscle relaxation Loss of somatic and autonomic reflexes

History - The Primitive techniques : 

History - The Primitive techniques Club Strangulation Alcohol Mesmerism Plants

History / Background - GA : 

History / Background - GA

History – contd. : 

History – contd. General anesthesia was absent until the mid-1800’s Original discoverer of general anesthetics Crawford Long, Physician from Georgia: 1842, ether anesthesia Chloroform introduced James Simpson: 1847 Nitrous oxide Horace Wells in 1845 19th Century physician administering chloroform

History – contd. : 

History – contd. William T. G. Morton, a Boston Dentist and medical student October 16, 1846 Gaseous ether Public demonstration gained world-wide attention Public demonstration consisted of an operating room, “the ether dome,” where Gilbert Abbot underwent surgery for removal of a neck tumour in an unconscious state at the Massachusetts General Hospital But, ether no longer used in modern practice, yet considered to be the first “ideal” anesthetic

Mechanism of GA(Potency) : 

Mechanism of GA(Potency) For inhalation anesthetics – Minimum Alveolar Concentration (MAC) – 1 (one) MAC is defined as the minimum alveolar concentration that prevents movement in response to surgical stimulation in 50% of subjects. Practically – Alveolar concentrations can be monitored continuously by measuring end-tidal anesthetic concentration using spectrometry End point (immobilization) – can me measured. Other end points – Verbal commands or memory etc. For Intravenous agents – Potency of IV agent is defined as the free plasma concentration (at equilibrium) that produces loss of response to surgical incision in 50% of subjects. Difficult to measure: no available method to measure blood or plasma concentration continuously Free concentration at site of action cannot be determined

Mechanism – contd. : 

Mechanism – contd. The unitary theory of anesthesia – Meyer-Overton rule (1901) Lipid : water partition coefficient (fluidization) Potency of a gas correlated with its solubility in olive oil (olive oil : water) – lipid bilayer as the only target for anesthetic action. Clear exceptions have been found out now. The unitary theory has been discarded now.

Modern theory on Mechanism of general anesthesia : 

Modern theory on Mechanism of general anesthesia Major targets – ligand gated ion channels. Important one – GABAA receptor gated Cl¯ channel. Examples – Many inhalation anesthetics, barbiturates, benzodiazepines and propofol Potentiate the GABA to open the Cl¯ channels

Molecular Actions: GABAA Receptor : 

Molecular Actions: GABAA Receptor Ligand-gated ion channels Chloride channels gated by the inhibitory GABAA receptor 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

GABAA receptor – contd. : 

GABAA receptor – contd. GABAA receptor is a 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 – contd. : 

GABAA receptor – contd.

GABAA receptor – contd. : 

GABAA receptor – contd. Receptor sits in the membrane of its neuron at the synapse GABA, endogenous compound, causes GABA to open Receptor capable of binding 2 GABA molecules, between an alpha and beta subunit Binding of GABA causes a conformational change in receptor Opens central pore Chloride ions pass down electrochemical gradient Net inhibitory effect, reducing activity of the neuron

Mechanism of GA – contd. : 

Mechanism of GA – contd. Other Mechanisms: Glycine – Barbiturates, propofol and others can activate in spinal cord and medulla N – methyl D- aspartate (NMDA) type of glutamate receptors - Nitrous oxide and ketamine selectively inhibit

Signs and stages of GA : 

Signs and stages of GA Guedel in 1920 described with ether – Guedel`s stages of GA. Descending depression of CNS. Higher to lower areas of brain are involved. Vital centers located in medulla are paralyzed last. But, in spinal chord lower segments are affected earlier than the higher segments.

signs & stages of GA – contd. : 

signs & stages of GA – contd.

stages of GA – contd. : 

stages of GA – contd. Stage 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. It is difficult to maintain - use is limited to short procedures only.

stages of GA – contd. : 

stages of GA – contd. Stage II: Stage of Delirium and Excitement: From loss of consciousness to beginning of regular respiration. Excitement - 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 or operative procedure carried out during this stage. Breatholding are commonly seen. Potentially dangerous responses can occur during this stage including vomiting, laryngospasm and uncontrolled movement. This stage is not found with modern anaesthesia – preanaesthetic medication, rapid induction etc.

stages of GA – contd. : 

stages of GA – contd. Stage III: Stage of Surgical anaesthesia Extends from onset of regular respiration to cessation of spontaneous breathing. This has been divided into 4 planes: 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.

stages of GA – contd. : 

stages of GA – contd. Stage IV: Medullary / respiratory paralysis Cessation of breathing failure of circulation death. Pupils: widely dilated. Muscles are totally flabby. Pulse is imperceptible BP is very low.

Phases of GA : 

Phases of GA There are 3 (three) phases: Induction Maintenance Recovery

Phases of GA – contd. : 

Phases of GA – contd. Induction: It is the period of time which begins with the beginning of administration of anaesthesia to the development of surgical anaesthesia (Induction time). Induction is generally done with IV anaesthetics like Thiopentone Sodium Maintenance: Sustaining the state of anaesthesia. Usually done with an admixture of Nitrous oxide and halogenated hydrocarbons Recovery: At the end of surgical procedure administration of anaesthetic is stopped and consciousness regains (recovery time)

Pharmacokinetics of inhalation anaesthetics: : 

Pharmacokinetics of inhalation anaesthetics: Pathway for anaesthetics:

Pharmacokinetic of inhalation GA – contd. : 

Pharmacokinetic of inhalation GA – contd. Depth of anaesthesia depends on Potency of the agent (MAC) and Partial Pressure (PP) attained in the brain. Induction and recovery depends on rate of change of PP in brain.

Pharmacokinetic of inhalation GA – contd. : 

Pharmacokinetic of inhalation GA – contd. Factors affecting PP of anaesthetics in Brain: PP of anaesthetic in the inspired gas Pulmonary ventilation Alveolar exchange Solubility of anaesthetic in blood - Blood: gas partition coefficient Solubility in tissues Cerebral blood flow

Blood : gas partition coefficient : 

Blood : gas partition coefficient Solubility of an anesthetic agent in blood is quantified as the blood : gas partition coefficient. It is the ratio of the concentration of an anesthetic in the blood phase to the concentration of the anesthetic in the gas phase when the anesthetic is in equilibrium between the two phases. Lower the blood : gas co-efficient – faster the induction and recovery – Nitrous oxide. Higher the blood : gas co-efficient – slower induction and recovery – Halothane.

Rate of Entry into the Brain: Influence of Blood and Lipid Solubility : 

Rate of Entry into the Brain: Influence of Blood and Lipid Solubility

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Agents with low solubility in blood quickly saturate the blood. The additional anesthetic molecules are then readily transferred to the brain.

Elimination of GA : 

Elimination of GA Mostly through lungs in unchanged form. Channel of absorption (lungs) become channel of elimination Enter and persists in adipose tissue for long periods – high lipid solubility and low blood flow. They are not metabolized except Halothane Second gas effect Diffusion hypoxia

Techniques of inhalation GA : 

Techniques of inhalation GA Open drop method Through anaesthetic machines - Open system - Closed system - Semi-closed system

Continuous flow (Boyle’s) anaesthetic machine : 

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

Properties of an Ideal anaesthetic agent: : 

Properties of an Ideal anaesthetic agent: For Patient: Pleasant, non-irritating and should not cause nausea or vomiting Induction and recovery should be fast For Surgeon: - analgesia, immobility and muscle relaxation - nonexplosive and noninflammable

Properties of GA – contd. : 

Properties of GA – contd. For the anaesthetist: - Margin of safety - Heart, liver and other organs - Potent - Cheap, stable and easily stored - Rubber tubing or soda lime - Rapid adjustment of depth of anaesthesia

Slide 40: 

Individual Inhalation anaesthetic agents

1. Diethyl ether (C2H5 – O – C2H5) : 

1. Diethyl ether (C2H5 – O – C2H5) Colourless, highly volatile liquid with a pungent odour. Boiling point – 35ºC Produces irritating vapours and are inflammable and explosive. Pharmacokinetics: - 85 to 90 percent is eliminated through lung and remainder through skin, urine, milk and sweat. - Can cross the placental barrier.

Ether – contd. : 

Ether – contd. Advantages - Can be used without complicated apparatus. - Potent anaesthetic and good analgesic. - Muscle relaxation. - Wide safety of margin. - Respiratory stimulation and bronchodilatation. - Does not sensitize the heart to adrenaline - No cardiac arrythmias. - Can be used in delivery. - Less likely hepato or nephrotoxicity. Disadvantages - Inflammable and explosive. - Slow induction and unpleasant -atropine. - Slow recovery – nausea & vomiting - Cardiac arrest. - Convulsion in children. - Cross tolerance – ethyl alcohol.

2. Nitrous oxide / laughing gas (N2O): : 

2. Nitrous oxide / laughing gas (N2O): NH4NO3 (s) → 2 H2O (g) + N2O (g) Colourless, odourless inorganic gas with sweet taste. Noninflammable and nonirritating, but of low potency. Very potent analgesic Carrier and adjuvant to other anaesthetics – 70% + 25-30% + 0.2-2%

Nitrous oxide – contd. : 

Nitrous oxide – contd. Advantages: - Non-inflammable and nonirritant. - Rapid induction and recovery - Very potent analgesic (low concentration) - No nausea and vomiting. - Nontoxic to liver, kiddney and brain. Disadvantages: - Not potent alone (supplementation) - Hypoxia. - Inhibits methionine synthetase (precursor to DNA synthesis). - Inhibits vitamin B-12 metabolism. - Dentists, OR personnel, abusers at risk. - Gas filled spaces - dangerous

3. Halothane: : 

3. Halothane: Fluorinated volatile liquid with sweet odour, non-irritant non-inflammable and supplied in amber coloured bottle. Potent anaesthetic, 2-4% for induction and 0.5-1% for maintenance. Boiling point - 50ºC Pharmacokinetics: 60 to 80% eliminated unchanged. 20% retained in body for 24 hours and metabolized.

Halothane – contd. : 

Halothane – contd. Advantages: Non-inflammable and non-irritant Pharyngeal and laryngeal reflexes – bronchodilatation Potent and speedy induction & recovery Controlled hypotension Inhibits intestinal and uterine contractions Disadvantages: Special apparatus Poor analgesic and muscle relaxation Respiratory depression Hypotension and arrythmia Decreased urine formation Hepatitis: 1 in 10,000 Malignant hyperthermia: Ryanodine receptor

4. Enflurane: : 

4. Enflurane: Non-inflammable, with mild sweet odour and boils at 57ºC Similar to halothane in action, except better muscular relaxation. Depresses myocardial force of contraction and sensitize heart to adrenaline. Induces seizure in deep anaesthesia and therefore not used now - Epileptiform EEG Metabolism one-tenth that of halothane-- does not release quantity of hepatotoxic metabolites Metabolism releases fluoride ion-- renal toxicity

5. Isoflurane: : 

5. Isoflurane: Isomer of enflurane and have simmilar properties but slightly more potent. Induction dose is 1.5 – 3% and maintenance dose is 1 – 2%. By special vapourizer.

Isoflurane – contd. : 

Isoflurane – contd. Advantages: Rapid induction and recovery Good muscle relaxation Good coronary vasodilatation Less Myocardial depression than no myocardial sensitization to adrenaline No renal or hepatotoxicity Low nausea and vomiting No dilatation of pupil and no loss of light reflex in deep anaesthesia No seizure and preferred in neurosurgery Uterine muscle relaxation Disadvantages: Pungent and respiratory irritant Special apparatus required Respiratory depression Maintenance only, no induction ß adrenergic receptor stimulation Costly

Intravenous Anaesthetics: : 

Intravenous Anaesthetics: For induction only Rapid induction (one arm-brain circulation time For maintenance not used Alone – analgesic and muscle relaxants Intravenous: Inducing agents: Thiopentone, Methohexitone sodium, propofol and etomidate Benzodiazepines (slower acting): Diazepam, Lorazepam, Midazolam Dissociative anaesthesia: Ketamine Neurolept analgesia: Fentanyl

1 Thiopentone sodium: : 

1 Thiopentone sodium: Barbiturate Water soluble Alkaline Dose-dependent suppression of CNS activity Dose: 3-5mg/kg iv (2.5%) solution – 15 to 20 seconds

Thiopentone sodium – contd. : 

Thiopentone sodium – contd. Pharmacokinetics: Redistribution Hepatic metabolism (elimination half-life 7-12 hrs) CNS depression persists for long (>12 hr)

Tiopentone – contd,. : 

Tiopentone – contd,. Redistribution: Blood Brain Muscle Body fat conc. of thiopentoone Time

Side effects of Thiopentone: : 

Side effects of Thiopentone: Pre-anaesthetic course - laryngospasm Noncompatibility - succinylcholine Tissue necrosis--gangrene Post-anaesthetic course - analgesic

Thiopentone – contd. : 

Thiopentone – contd. Advantages: Rapid induction Does not sensitize myocardium to adrenaline No nausea and vomiting Non-explosive and non-irritant Short operations (alone) Other uses: convulsion, psychiatric patients and narcoanalysis of criminals Disadvantages: Depth of anaesthesia difficult to judge Pharyngeal and laryngeal reflexes persists - apnoea – controlled ventilation Respiratory depression Hypotension (rapid) – shock and hypovolemia Poor analgesic and muscle relaxant Gangrene and necrosis Shivering and delirium

2. Propofol : 

2. Propofol Replacing thiopentone Oily liquid used as 1% emulsion Rapid induction (one arm-brain circulation time): 15 – 45 seconds and lasts for 5–10 minutes Rapid distribution – distribution half-life (2-4 min) Short elimination half-life (100 min) Dose: Induction - 2mg/kg bolus i.v. Maintenance - 9 mg/kg/hr i.v. Propofol is extensively metabolized 88% of an administered dose appears in the urine Metabolized by hepatic conjugation of the inactive glucuronide metabolites

Propofol – contd. : 

Propofol – contd. Advantages: Rapid induction Does not sensitize myocardium to adrenaline No nausea and vomiting Non-explosive and non-irritant Total i.v. anaesthesia Short operations (alone) Disadvantages: Induction apnoea Hypotension Braddycardia Dose dependent respiratory depression Pain during injection: local anaesthetic combination

3. Ketamine: : 

3. Ketamine: Phencyclidine derivative Dissociative anaesthesia: a state characterized by immobility, amnesia and analgesia with light sleep and feeling of dissociation from ones own body and mind and the surroundings. Site of action – cortex and subcortical areas – NMDA receptors Dose: 5-10mg/kg im or 1-2mg i.v.

Ketamine – contd. : 

Ketamine – contd. Disadvantages: Limb movements and nystagmus Emergence phenomenon – 50% patients Hypertensives Increase in IOT and ICP Uterine stimulation Psychosis and shizophrenia Rare laryngospasm Poor muscle relaxation

Ketamine – contd. : 

Ketamine – contd. Uses: Characteristics of sympathetic nervous system stimulation (increase HR, BP & CO) – hypovolumic shock In head and neck surgery In asthmatics Short surgical procedures – burn dressing, forceps delivery, breech extraction manual removal of placenta and dentistry Combination with diazepam - angiography, cardiac catheterization OPD surgical procedures

4. Fentanyl : 

4. Fentanyl Neurolept analgesia: droperidol 4-acylanilino derivative Opioid analgesic Duration of action: 30-50 min. Uses: in combination with diazepam used in diagnostic, endoscopic and angiographic procedures Adjunct to spinal and nerve block anaesthesia

Fentanyl – contd. : 

Fentanyl – contd. Advantages: Smooth onset and rapid recovery Suppression of vomiting and coughing Commanded operation Less fall in BP and no sensitization to adrenaline Disadvantages: Respiratory depression Increase tone of chest muscle Nausea, vomiting and itching during recovery

Complications of anaesthesia: : 

Complications of anaesthesia: During anaesthesia: Respiratory depression Salivation, respiratory secretions Cardiac arrhythmias Fall in BP Aspiration Laryngospasm and asphyxia Awareness Delirium and convulsion Fire and explosion After anaesthesia: Nausea and vomiting Persisting sedation Pneumonia Organ damage – liver, kidney Nerve palsies Emergence delirium Cognitive defects

Preanesthetic medication: : 

Preanesthetic medication: Definition: It is the term applied to the use of drugs prior to the administration of an anaesthetic agent to make anaesthesia safer and more agreeable to the patient. Aim: Relief of anxiety Amnesia for pre and post operative events Analgesia Decrease secretions Antiemetic effects Decrease acidity and volume of gastric juice

Preanaesthetic medication – contd. : 

Preanaesthetic medication – contd. Drugs used: Sedative-anxiolytics – diazepam or lorazepam, midazolam, promethazine etc. Opioids – Morphine and its congeners Anticholinergics – Atropine H2 blockers – ranitidine, famotidine etc. Antiemetics – Metoclopramide, domperidone etc.

The Practical approach: Protocol : 

The Practical approach: Protocol Preoperative assesment Preanaesthetic medication Induction by thiopentone or Propofol Muscle relaxants Intubation Nitrous oxide + halogenated hydrocarbon Withdraw and recovery.

Thank you : 

Thank you

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