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Anesthesia
The document provides a history of anesthetics from primitive techniques to modern discoveries. It discusses Crawford Long using ether anesthesia in 1842, followed by chloroform and nitrous oxide. In 1846, William Morton demonstrated ether anesthesia publicly at Massachusetts General Hospital, considered the beginning of modern anesthesia. The document also describes different types of anesthesia including general, regional, and local, and their mechanisms of action and uses. It discusses various anesthetic drugs and their properties.
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Anesthesia
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- 2. History - ThePrimitive techniques • Club • Strangulation • Alcohol • Mesmerism • Plants
- 3. 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
- 4. 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, no longer used in modern practice, yet considered to be the
- 5. They did itfor a better tomorrow!
- 6. Analgesics Analgesics is sometimesconfused with anesthesia. Below is the difference between them
- 7. Anesthetic A medication thatcauses loss of sensation. This is sometimes used to alleviate pain or for loss of consciousness for surgical procedures. It relieves pain by numbing nerve impulses. Its action is reversible when right dose is administered
- 8. Anesthesia Loss of consciousness Analgesia(loss of pain sensation) Adequate muscle relaxation Analgesia •Loss of sensation to pain
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- 10. GENERAL ANESTHESIA They induceunconsciousness and eliminate pain by blocking the general body innervation usually administered by IV inhalation for the purpose of In ophthalmology general anesthesia is rarely used but does have a place in physically or emotionally traumatic surgeries and in non co-operative children. General anesthesia need for unconsciousness ‘Amnesia-hypnosis’ need for analgesia ‘Loss of sensory and autonomic reflexes’ need for muscle relaxation
- 11. REGIONAL ANESTHESIA Regionalanesthesia is an injection of a local anesthetics around nerves or into the trunk of a nerve so that all the areas supplied by these nerves will not send pain signals to the brain. They anesthetized area is usually larger than the area affected by local anesthesia. Eg: retrobulbar injection to numb all eye movents by targeting the oculomotor nerve
- 12. LOCAL ANAESTHESIA Itis an anesthetic agent given to temporarily stop the sense of pain in a particular area of the body. The entire area supplied by a nerve is not be anesthetized. Only a certain branches does. Patient remains conscious during a local anesthetic. Giving ametocaine to numb the cornea (only axons of the ophthalmic division are severed)
- 13. Mechanism of action GENERALANESTHESIA General anesthetics have two main routes: Inhalation Most general anesthetics target GABAA receptor channel Intravenous
- 14. General anesthesia Inhalational Gas Nitrous oxide Zenon Volatileliquids Ether halothane enflurane isoflurane desflurane Sevoflurane methoxyflurane Intravenous Slower acting Dissociative anesthesia ketamine opiod analgesia fentanyl Benzodiazepines diazepam lorazepam midazolam Inducing agents Thiopentone sod. methohexitone sod. propofol Etomidate droperidol
- 15. Inhaled anesthetics Twomain drugs used are Gases eg Nitrous oxide, cyclopropane Halogenated anesthetics e.g. halothanes, isoflurane, desflurane and influrane Inhaled anesthetics have varying potency in proportion to their lipid solubility. Every inhaled anesthetic has a specific MAC value.
- 16. A MAC (minimalalveolar anesthetic concentration) is defined as the concentration of inhaled anesthetic as a % of inspired air, at which 50% of patients will be anesthetized. MAC is a measure of potency: ED50.
- 17. Comparison between NitrousOxide and the Halothanes
- 18. Facts about inhaledanesthetics Rates of onset and recovery depend on the blood-gas ratio: a. The more soluble the anesthetic in the blood, the slower the anesthesia. b. Anesthetics with high blood-gas ratios are associated with slow onset. c. Anesthetics with high blood-gas ratios are associated with slow recovery. d. Anesthetics with low blood-gas ratios have fast onset and recovery.
- 19. Intravenous anesthetics Theironset of action faster than the fastest of the gaseous agents so they are used for induction of anesthesia.
- 20. 1. Thiopental Barbiturateused for induction Highly lipid soluble; rapid onset; short-acting due to redistribution Disadvantage: Severe vasospasm Cardiovascular depression Hypersensitivity reactions
- 21. Midazolam Benzodiazepine usedfor: Preoperative sedation Anterograde amnesia Induction Outpatient surgery Depresses respiratory function
- 22. Propofol (Michael Jackson'sKiller) Used for induction and maintenance of anesthesia Antiemetic CNS and cardiac depressant It can induce prolonged sedation. Similar to thiopentone, but more rapidly metabolized (rapid induction and recovery) so it is suitable for one day surgery. Lacks tendency to induce involuntary movement and adrenocortical suppression.
- 23. Propofol (Michael Jackson'sKiller) Propofol. The onset of its action begins after 30 s. After a single dose patient recovers after 5 min with a clear head and no hangover.
- 24. Fentanyl Opiate usedfor induction and maintenance of anesthesia Depresses respiratory function – be careful of your asthma patient
- 25. Ketamine Dissociative anesthetic NMDA-receptor antagonist Induction of anesthesia Emergent delirium, hallucinations Cardiovascular stimulation increases intracranial pressure Disadvantages: Cerebral hemorrhage Dysphoria and hallucinations
- 30. Mechanism of actionof general anesthetics Most injectable and inhaled anesthetic agents produce anesthesia by enhancing GABA-mediated neuronal transmission, primarily at GABAA receptors. GABA is an inhibitory neurotransmitter found throughout the CNS. Some inhaled anesthesia may also act by inhibiting such excitatory ion channels as neuronal nicotinic and glutamate receptors. Note: Ketamine does not affect GABAA it antagonizes glutamic acid on NMDA receptor
- 31. 4 (Four) Stagesand signs !!! • Traditional Description of signs and stages of GA - Also called Guedel`s sign • Typically seen in case of Ether
- 32. Stages of GA StageI: 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
- 33. Stage II: Stageof 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.
- 34. Stage III: Stageof 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.
- 35. 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.
- 36. Local anesthetics Drugs usedto provide local anesthesia are also used to achieve regional anesthesia. Regional anesthesia is an injection of a local anesthetics around nerves so that the area supplied by these nerves will not send pain signals to the brain. They anesthetized area is usually larger than the area affected by local anesthesia.
- 37. Mechanism of action Mechanisms: Nonionized form crosses axonal membrane - From within, ionized form blocks the inactivated Na+ channel - Slows recovery and prevents propagation of action potentials When local anesthetics are applied to the area that they numb, they need to get to the axon by crossing to the membrane. Only non ionized forms R-NH2 can enter the axon through the membrane. Upon entering the axon, only the ionized forms can block the sodium channels which causes depolarization of the sodium channel consequently numbing the area. Ionized form RNH3+
- 39. Classification of LocalAnesthetics based on chemical group - Esters: procaine, cocaine, benzocaine are metabolized by plasma and tissue esterases - Amides: lidocaine, bupivacaine, mepivacaine are metabolized by liver amides
- 40. Esters Two types 1. Estersof benzoic acid (BA) 2. Esters of para amino benzoic acid.( PABA)
- 41. Esters of benzoicacid Butacaine Cocaine Ethyl aminobenzoate (benzocaine) Hexylcaine Piperocaine Tertracaine
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- 43. Amides Articaine Bupivacaine Dibucaine Etidocaine Lidocaine Mepivacaine Prilocaine Roppivacaine
- 44. May also beclassified into a. Short acting – cocaine, procaine b. Intermediate acting – lidocaine, mepivacaine, dibucaine, prilocaine c. Long acting – tetracaine, bupivacaine, etidocaine
- 45. Metabolism Esters are metabolizedby the plasma by enzymes esterase amides are metabolized by liver by the enzyme hepatic amidases
- 46. Clinical note Don’tgive amides to patients with poor liver function. Eg. patient with any form of hepatitis! WHY? the amides will pile up due inability of the liver to metabolize. Hence elicit a complete history in your patient. In cases where patients have liver problem; your local anesthesia should be an ester.
- 47. How do weknow which cocaine derivative is an amides or ester? The trick: the letter i in almost all cases if an i precedes the “caine” sound, the drug is an amide but if not, it is an ester.
- 48. Amides Esthers Articaine Bupivacaine Dibucaine Etidocaine Lidocaine Mepivacaine Prilocaine Roppivacaine Butacaine Cocaine Ethyl aminobenzoate (benzocaine) Hexylcaine Tertracaine Cloroprocaine Procaine propoxycaine
- 49. Limiting local anesthetics All local anesthetics should be co-administered with alpha-1 agonist. E.g. phenylephrine, metoximine. WHY? Reason; The alpha-1 agonist will cause a powerful vasoconstriction and limit the access of surrounding tissues to the local anesthetics.
- 50. The Cocaine saga Iam the only local anesthetics that does not need an alpha-1 agonist. WHY? ANS: I am a NEP re-uptake blocker. NOTE: it causes NEP build up in the synapsis. From the synapsis NEP binds to the alpha-1 receptors and causes vasoconstriction in the surrounding tissues. Therefore you don’t need an alpha-1 agonist after administration of cocaine.
- 51. Side effect Localanesthetics can cause allergies especially the ester groups because they form PABA. All PABA containing compounds can always cause allergic reactions. Therefore check your creams that you buy on the market.
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- 53. Injection: amide + longeracting ester = longer-acting motor and sensory anesthesia.
- 54. Targets of injectableagents muscle cone of the orbit-blocks all motor and sensory nerves of eye directly into orbicularis muscles into CNVII stylomastoid foramen –these two cause a complete loss of facial nerve on that side of face
- 55. Topical anesthesia Anytest requiring contact with the cornea is made more comfortable if topical anesthetic is used first Indeed, some of these tests would be nearly impossible for the patient to endure if the cornea was not numbed first. In addition to numbing the cornea and conjunctiva for testing, topial anesthetic is required in procedures such as removal of a foreign body or scraping a corneal lesion
- 56. Tetracaine is the mostpopular topical anesthetic. Tetracaine is unpreserved.
- 57. Proparacaine and benoxinate contain preservatives and are effective in anesthetizing the corneal nerve endings through topical application. These formulations are highly osmotic and therefore sting and burn when applied.
- 58. Home use? never prescribedfor a patient to use at home. Frequent use interferes with the healing process and can cause corneal melting
- 59. Please don’t rubyour eyes! the cornea now lacks sensation, the patient could conceivably rub hard enough to cause a corneal abrasion.
- 60. Toxicity Potential .All anesthetics have a potential to become toxic in higher doses. Individuals may experience lightheadedness, ringing in their ears, or blurred vision. At even higher doses, respiratory arrest can occur, as well as convulsions, coma and death.
- 61. punctual occlusion When topicalanesthetic is used, punctual occlusion can reduce the amount of drug that is absorbed into the system
- 62. MUSCLE RELAXANTS Used mainlyin anesthesia protocols (EMERGENCIES) or in the (Intensive Care Unit) ICU to afford muscle relaxation and/or immobility. Used to relieve symptoms such as spasms ,pain and hyperreflexia Muscle relaxants interact with nicotinic ACh receptors at the neuromuscular junction.
- 63. MECHANISM NORMAL CHOLINERGICTRANSMISSION Normally, a nerve impulse arrives at the motor nerve terminal, initiating an influx of calcium ions, which causes the exocytosis of synaptic vesicles containing acetylcholine. Acetylcholine then diffuses across the synaptic cleft. It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate. The binding of two acetylcholine molecules results in a conformational change in the receptor that opens the sodium-potassium channel of the nicotinic receptor. This allows Na + and Ca 2+ ions to enter the cell and K+ ions to leave the cell, causing a depolarization of the end plate, resulting in muscle contraction.
- 64. Normal end platefunction can be blocked by two mechanisms. 1.Nondepolarizing agents (competetive), such as tubocurarine, block the agonist , acetylcholine, from binding to nicotinic receptors and activating them, thereby preventing depolarization.
- 65. Major Non-depolarizing MRs Atracurium Rapid recovery Safe in hepatic or renal impairment Spontaneous inactivation to laudanosine ,Laudanosine can cause seizures Mivacurium Very short duration Metabolized by plasma cholinesterases
- 66. 2.depolarizing agents, (noncompetitive) Alternatively, depolarizing agents such as succinylcholine, are nicotinic receptor agonists which mimic Ach, block muscle contraction by depolarizing to such an extent that it desensitizes the receptor and it can no longer initiate an action potential and cause muscle contraction
- 67. MRs mainly in anesthesia protocols(EMERGENCIES) or in the (Intensive Care Unit)
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Editor's Notes
- #3 MESMERISE to have someone's attention completely so that they cannot think of anything else
- #5 Cardiac and hepatic toxicity limited the usefulness of chloroform (out of date!).
- #16 The lipophilicity character of the drug determines how much it can cross the highly lipophilic membranes of the nerves.
- #18 Blood-gas ratio: ratio of concentration of the soluble form of drug in the blood to the concentration of the form of the drug that still remains a gas and can be distributed to other tissues.
- #19 Blood-gas ratio: ratio of concentration of the soluble for of drug in the blood to the concentration of the form of the drug that still remains a gas and can be distributed to other tissues.
- #20 This is many degrees faster than inhalation n route. Hence IV is much applied in surgeries. This is faster than the fastest
- #21 Barbiturate: drugs that act as CNS depressant and can therefore produce a wide spectrum of effect from mild sedation to total anesthesia. It has analgesic effect.
- #22 Anterograde Amnesia: inability to form or create new memories after the incident causing the amnesia. Hence long term memories before incident is intact but recent things after cannot be recalled
- #23 Antiemetic: a drug that is effective against vomiting and nausea Propofol. The onset of its action begins after 30 s. After a single dose patient recovers after 5 min with a clear head and no hangover.
- #24 Antiemetic: a drug that is effective against vomiting and nausea
- #26 In dissociative anesthetic the patient is not totally unconscious but the brain no longer feels the pain as if the brain is dissociated from the other parts of the body. Ketamine:It works as an NMDA receptor antagonist. Ketamine is the only IV anesthetic with analgesic property. Emergent delirium- where a patient recovering or emerging soon from anaesthesia undergoes a psychomotor agitation or excitement Dysphoria a profund state of unease, restlessness ,anxiety and generalized dissatisfaction with life!-it can even be gender dysphoria
- #31 Gamma Amino Butyric ACID N-METHYL D-ASPARTATE
- #40 Both esters and amides are derivatives of cocaine the difference is the chemical structure
- #52 PARA AMINO BENZOIC ACID
- #54 directly into the muscle cone of the orbit, blocking the motor and sensory nerves of the eye. Injection of anesthetic can also be given directly into the orbicularis muscles of the eyelid, into the seventh cranial nerve as it crosses the maxillary bone, for a nerve block directly into the stylomastoid foramen, for complete motor block of the facial muscles on the facial muscles on that side