anesth Lecture for 3rd year MBBS


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  • anesth Lecture for 3rd year MBBS

    1. 1. Types and modes of anaesthesia DR.NADIR MEHMOOD Asst professor Department ofSurgery, RMC
    2. 2. LEARNING OBJECTIVES At end of this discussion, a student will be able to, • Enumerate the types of anesthesia • Describe techniques of G/A and L/A • Enlist the advantages and indications of each type of anesthesia • Outline management plan in case of adverse effect of technique or overdose of L/A, S/A, OR Bier’s A • Technique and Video of spinal anesthesia
    4. 4. General Anaesthesia (GA) • complete loss of perception & consciousness • fundamental attributes of GA – loss of consciousness – does not block autonomic reflexes to painful stimuli (perspiration, arrhytmia, hypertension, bronchoconstriction, bronchial hypersecretion) – vegetative stabilisation – analgesia – loss of pain sensation, suppression of autonomic reactions – muscle relaxation • induction of all the GA attributes facilitated by mosaic assembly of partial effects of many substances such as anaesthetics, analgetics, tranquillizers, myorelaxants
    5. 5. Intravenous Anesthetic Agents • First attempt at intravenous anesthesia by Wren in 1656-- opium into his dog • Use in anesthesia in 1934 with thiopental • Many ways to meet requirements-- muscle relaxants, opoids, nonopoids • Appealing, pleasant experience
    6. 6. 7 Overview • General anaesthesia is a complex procedure involving : – Pre-anaesthetic assessment – Administration of general anaesthetic drugs – Cardio-respiratory monitoring – Analgesia – Airway management – Fluid management – Postoperative pain relief
    7. 7. Techniques • History and physical examination • Induction • Maintenance • Emergence
    8. 8. Types of GA according to the entry into organism • inhalational • intravenous • intramuscular • rectal – especially in children • intraperitoneal – in animals
    9. 9. 10 Pre-anaesthetic evaluation • medical history, current medications. • previous anaesthetics.History • age, weight, teeth condition. • Airway assessment, neck flexibility and head extension Examination. • Relevant to age and medical conditions.Investigations.
    10. 10. 11 Pre-anaesthetic evaluation The plan best combination , drugs and dosages and the degree of how much monitoring is required . fasting time If airway management is deemed difficult, then alternative placement methods such as fiberoptic intubation may be used.
    11. 11. GA – premedication Purpose of premedication – satisfactory rest at night before operation (premedication) – calm down – basal analgesia – supression of readines to allergic reactions – supression of vegetative reflexes (bradycardia, hypersalivation, bronchial hypersecretion) e.g: sedatives, hypnotics, anxiolytics, vagolytics (atropine), atihistaminics
    12. 12. Ideal Characteristics of Inhalational Anesthetics • Rapid & pleasant induction & recovery • Rapid changes in depth of anesthesia • Adequate relaxation of smooth muscle • Wide margin of safety • Absence of toxic effect
    13. 13. 14 Induction intravenous Faster onset avoiding the excitatory phase of anaesthesia inhalational where IV access is difficult Anticipated difficult intubation. patient preference (children)
    14. 14. 15 Maintenance • In order to prolong anaesthesia for the required duration (usually the duration of surgery), patient has to breathe a carefully controlled mixture of oxygen, nitrous oxide, and a volatile anaesthetic agent. This is transferred to the patient's brain via the lungs and the bloodstream, and the patient remains unconscious.
    15. 15. 16 Maintenance • Inhaled agents are supplemented by intravenous anaesthetics, such as opioids (usually fentanyl or morphine). • At the end of surgery the volatile anaesthetic is discontinued. • Recovery of consciousness occurs when the concentration of anaesthetic in the brain drops below a certain level (usually within 1 to 30 minutes depending upon the duration of surgery).
    16. 16. 17 Maintenance • Total Intra-Venous Anaesthesia (TIVA): this involves using a computer controlled syringe driver (pump) to infuse Propofol throughout the duration of surgery, removing the need for a volatile anaesthetic. • Advantages: faster recovery from anaesthesia, reduced incidence of post-operative nausea and vomiting, and absence of a trigger for malignant hyperthermia.
    17. 17. 18 Neuromuscular-blocking drugs • Block neuromuscular transmission at the neuromuscular junction. • Used as an adjunct to anesthesia to induce paralysis. • Mechanical ventilation should be available to maintain adequate respiration.
    18. 18. GA muscle relaxants depolarising muscle relaxants • cholinergic receptor -> depolarisation -> generation AP • fasciculations • antagonisation is not possible • e.g.: Suxametonium (succinylcholine) non-depolarising muscle relaxants • competetive block of cholinergic receptors without generation of AP • so called curariform medicaments, e.g.: Pancuronium, Atracurium • antagonist: neostigmin (decurarization)
    19. 19. 20 Monitoring • ECG • Pulse oximetry (SpO2) • Blood Pressure Monitoring (NIBP or IBP) • Agent concentration measurement • Low oxygen alarm • Carbon dioxide measurement (capnography) • Temperature measurement • Circuit disconnect alarm
    20. 20. Monitoring depth of GA • concentration inhalational anaesthetics • bispectral index (computerized EEG analysis) • vegetative response (perspiration, pupils, blood pressure, pulse rate) • clinical status, esp. waning muscle tonus (not available when muscle relaxants are used)
    21. 21. TOXICITY OF INHALATIONAL AGENTS 1. Hepatotoxic agent Isoflurane 2. Nephrotoxic agent Barbiturate 3. Cardiotoxic agent Enflurane Halothane 4. Flammable agent Ether
    22. 22. 23 Mortality rates • Overall, about five deaths per million. • Most commonly related to surgical/anesthesia factors or pre-existing medical conditions ( haemorrhage, sepsis). • Common causes of death directly related to anaesthesia include: 1- aspiration of stomach contents 2- suffocation (due to inadequate airway management) 3- allergic reactions to anaesthesia 4- human error 5- equipment failure
    23. 23. Local Anesthetics • Followed general anesthesia by 40 years • Koller used cocaine for the eye surgery in 1884 • Halsted used cocaine as nerve block • First synthetic local-- procaine in 1905 • Lidocaine synthesized in 1943
    24. 24. Local Anesthetics • Mechanism of action is by reversibly blocking sodium channels to prevent depolarization • Anesthetic enters on axioplasmic side and attaches to receptor in middle of channel
    25. 25. Mechanism of the effect of LA • blockade of the inner oriffice of sodium channel -> influenced depolarisation • non-ionized form – penetration throuhg connective tissue, myelin sheet and cell membrane, intracellularly ionization and attachment to the sodium channel (competetive antagonism) • ionizoed vs. non-ionized form ratio dependent on pH – healthy tissue: slightly alkaline pH -> more non-ionized form -> easy penetration of LA into cells -> quick effect onset – inflammatory focus: acid pH -> less non-ionized form -> -> poor penetration intracellularily -> weak LA effect • Vasoconstrictive addition agents (adrenaline/epinephrine) – reduction of absorbtion ->longer lasting effect, lowered toxicity, less bleeding
    26. 26. Classified into a. Short acting – cocaine, procaine b. Intermediate acting – lidocaine, mepivacaine, dibucaine, prilocaine c. Long acting – tetracaine, bupivacaine, etidocaine
    27. 27. Properties of a Desirable Local Anesthetic •contrary to general anaesthesia, consciousness is preserved sites of action • should not be irritating to tissues • should not cause permanent damage to nerves • have low systemic toxicity • must be effective • should have rapid onset but long duration of action
    28. 28. ROUTES OF ADMINISTRATION: 1. Topical (skin, mucosal) 2. Local Infiltration 3. Nerve Block 4. Spinal or Intrathecal injection 5. Epidural 6. Caudal LOCAL ANESTHETICS
    29. 29. Local anaesthesia topic infiltrative cunduct epidural subarachnoid scheme by J.Cendelín
    30. 30. Effects of LA on nerve fibers 1. block of sympathetic division (warming of skin) 2. loss of sensation of heat and pain 3. loss of sensation of touch and pressure 4. loss of motorics
    31. 31. Local Anesthetic Toxicity • Central nervous system – initially-- lightheadedness, circumoral numbness, dizziness, tinnitus, visual change – later-- drowsiness, disorientation, slurred speech, loss of consciousness, convulsions – finally-- respiratory depression
    32. 32. Local Anesthetic Toxicity • Cardiovascular – myocardial depression and vasodilation-- hypotension and circulatory collapse • Allergic reactions-- rare (less than 1%) – preservatives or metabolites of esters – rash, bronchospasm
    33. 33. Prevention and Treatment of Toxicity • Primarily from intravascular injection or excessive dose -- anticipation – aspirate often with slow injection – ask about CNS toxicity – have monitoring available – prepare with resuscitative equipment, CNS- depressant drugs, cardiovascular drugs – ABC’s
    34. 34. Treatment of Toxicity
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