Local anesthetics (VK)


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  • Common digital nerve block
  • Have a student read this slide out loud to the rest of the class
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  • NONE
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  • Local anesthetics (VK)

    1. 1. LocaL anesthetics
    2. 2. Local Anesthetic  A local anesthetic is an agent that interrupts pain impulses in a specific region of the body without a loss of patient consciousness. Normally, the process is completely reversible.
    3. 3. History  The first local anesthetic introduced into medical practice Cocaine, was isolated from coca leaves by Albert Niemann in Germany in the 1860s.  The very first clinical use of Cocaine was in 1884 by Sigmund Freud who used it to wean a patient from morphine addiction.  Freud and his colleague Karl Kollar first noticed its anesthetic effect and introduced it to clinical ophthalmology as a topical ocular anesthetic.  Cocaine was used - 30 years  Einhorn (1905) synthesized procaine  Lidocaine-1943-Lofgren
    4. 4. Susceptibility of nerve fibers to local anesthetic blockade  In general, small nerve fibers are more susceptible than large fibers; however, – – – – the type of fiber degree of myelination fiber length and frequency- dependence are also important in determining susceptibility
    5. 5. Order of sensory function block 1. pain 2. cold 3. warmth 4. touch 5. deep pressure 6. motor Recovery in reverse order
    6. 6. Chemistry The LAs consists of three parts. 1.A hydrophilic amino group. 2.An intermediate chain (ester or amide). 3.A lipophilic aromatic group. • LAs are weak bases • In the body, they exist either as the uncharged base or as a cation.
    7. 7. CLASSIFICATION Based on there chemistry and duration of action LAs are classified as follows 1. AMIDE TYPE  LONG ACTING Bupivacaine, levo- Bupivacaine, Etidocaine, Ropivacaine  INTERMEDIATE ACTING Lidocaine, Mepivacaine 2. ESTER TYPE  LONG ACTING Tetracaine (Amithocaine)  INTERMEDIATE ACTING Cocaine  SHORT ACTING Procaine, Chloroprocaine, Benzocaine.
    9. 9. PHARMACOKINETICS Esters:  These include cocaine, procaine, tetracaine, and chloroprocaine.  Short duration  They are hydrolyzed in plasma by pseudo-cholinesterase. One of the by-products of metabolism is PABA - the common cause of allergic reactions seen with these agents and also antagonize the action of sulfonamides.  Rarely used for infiltration or nerve block, but are still used topically on mucus membranes
    10. 10. PHARMACOKINETICS Amides:  These include lidocaine, mepivacaine, prilocaine, bupivacaine, and etidocaine.  Produce more intense and longer lasting anesthesia  Bind to α1 acid glycoprotein in plasma  They are metabolized in the liver to inactive agents. True allergic reactions are rare (especially with lidocaine)
    11. 11. Factors affecting local anesthetic action Effect of pH  Charged (cationic) form binds to receptor site uncharged form penetrates membrane ,efficacy of drug can be changed by altering extracellular or intracellular pH
    12. 12. Factors affecting local anesthetic action Cont… Effect of lipophilicity  Lipid solubility appears to be the primary determinant of intrinsic anesthetic potency.  Chemical compounds which are highly lipophilic tend to penetrate the nerve membrane more easily, such that less molecules are required for conduction blockade resulting in enhanced potency.
    13. 13. Factors affecting local anesthetic action Cont… Effect of protein binding  increased binding increases duration of action Effect of vasodilator activity  greater vasodilator activity = decreased potency and decreased duration of action
    14. 14. Types of Local Anesthesia Infiltration Anesthesia:  Local infiltration occurs when the nerve endings in the skin and subcutaneous tissues are blocked by direct contact with a local anesthetic, which is injected into the tissue.  Local infiltration is used primarily for surgical procedures involving a small area of tissue (for example, suturing a cut).
    15. 15. Types of Local Anesthesia Cont… Surface Anesthesia:  This type of anesthesia is accomplished by the application of a local anesthetic to skin or mucous membranes.  Surface anesthesia is used to relieve itching, burning, and surface pain.  This technique is often used during examination procedures involving the respiratory tract.  The topical block easily anesthetizes the surface of the cornea and the oral mucosa.
    16. 16. Types of Local Anesthesia Cont… Conduction block anaesthesia: Two types 1. Field block:- LA is injected subcutaneously in the surrounding area of the nerves. So that all other nerves coming to a particular field are blocked. e.g. scalp and anterior abdominal walls 2. Nerve block:- LA injected around the anatomically localized nerve trunk. The block is usually described by adding the nerve name. e.g. radial nerve block, ulnar nerve block.
    17. 17. Types of Local Anesthesia Epidural Anesthesia  This type of anesthesia is accomplished by injecting a local anesthetic into the epidural space.  Widely used to provide analgesia or anesthesia in surgical and obstetric practice. Cont…
    18. 18. Types of Local Anesthesia Cont… Spinal block Anesthesia:  In spinal anesthesia, the local anesthetic is injected into the subarachnoid space of the spinal cord  Also referred as subarachnoid or intrathecal block anesthesia or spinal anesthesia.  Site- subarachnoid space between L2-L3 or L3-L4  Used to anesthetise lower abdomen, hind limbs.
    19. 19. Types of Local Anesthesia Cont… Intravenous regional anesthesia:  Also referred as Bier’s block  Used for upper limb and orthopedic procedures.
    20. 20. PROLANGATION OF ACTION BY VASOCONSTRICTORS  Vasoconstrictors decrease the rate of vascular absorption which allows more anesthetic to reach the nerve membrane and improves the depth of anesthesia.  There is variable response between LA and the location of injection as to whether vasoconstrictors increase duration of action. 1:200,000 epinephrine appears to be the best vasoconstrictor.  Felypressin a synthetic vasopressin – to avoid cardiac complications which may occur with adrenalin
    21. 21. TOXICITIES OF LOCAL ANESTHETICS  Essentially all systemic toxic reactions associated with local anesthetics are the result of over-dosage leading to high blood levels of the agent given.  Therefore, to avoid a systemic toxic reaction to a local anesthetic, the smallest amount of the most dilute solution that effectively blocks pain should be administered.
    22. 22. TOXICITIES OF LOCAL ANESTHETICS Cont… Hypersensitivity  Some patients are hypersensitive (allergic) to some local anesthetics.  Such allergies are very rare  There are two basic types of local anesthetics (the amide type and the ester type).  A patient who is allergic to one type may or may not be allergic to the other type.
    23. 23. TOXICITIES OF LOCAL ANESTHETICS Cont… Central Nervous System Toxicities  Stimulation followed by depression  Local anesthetics, if absorbed systematically in excessive amounts, can cause central nervous system (CNS) excitement or, if absorbed in even higher amounts, can cause CNS depression.
    24. 24. CNS toxicity cont.. Excitement:  Tremors, shivering, and convulsions characterize the CNS excitement. Depression:  Respiratory depression and, if enough drug is absorbed, respiratory arrest.
    25. 25. CNS toxicity cont.. Signs of toxicity are:  Tongue numbness, lightheadedness, tinnitus, visual disturbances, muscular twitching, convulsions, unconsciousness, coma, respiratory arrest, then cardiovascular collapse.
    26. 26. TOXICITIES OF LOCAL ANESTHETICS Cont… Cardiovascular Toxicities:  Depression of the cardiovascular system.  Peripheral vascular action arteriolar dilation (except cocaine which is vasoconstrictive)  Hypotension and a certain type of abnormal heartbeat (atrioventricular block) characterize such depression.  These may ultimately result in both cardiac and respiratory arrest.
    27. 27. Prevention of toxicity  Enquire about history of allergy  Cautiously in liver and myocardial damage  Select proper site –nerve block  Use minimal ED, well diluted preferably with the vasoconstrictor  Wait after injection  Observe the face for any twitching, excitement and tachycardia if any  Observe post operatively for allergic reactions
    28. 28. Lignocaine  Most commonly employed  Stable, can be stored at room temperature for long time  Can be autoclaved repeatedly  Has quick onset of action and a high degree of penetration  Also an excellent surface anesthetic  Toxicities are similar to other LA  Recommended for topical use, nerve blocks, infiltration and epidural injection and for dental analgesia  Can be used in subjects allergic to procaine and other ester type LA
    29. 29. Other uses Procaine: Forms poorly absorable salt with benzylpenicilin called procaine penicilin  Its amide derivative procainamide is used as class 1A group of antiarrhythmic  lidocaine:  I.V. for management of ventricular arrhythmias
    30. 30. General Anesthesia
    31. 31. General Anesthesia  Definition: General Anesthesia is the loss of response to & perception of all external stimuli.  General anaesthetics are the drugs which causes reversible loss of all the sensations and consciousness
    32. 32. Components of General Anesthesia:  1. Unconsciousness (Hypnosis)  2. Analgesia (Areflexia)  3. Muscle relaxation
    33. 33. Phases of Anesthesia Induction: putting the patient to sleep Maintenance: keeping the patient asleep Emergence: waking the patient up
    34. 34. STAGES OF GENERAL ANESTHESIA  STAGE 1 (Analgesia): From induction of anesthesia to loss of conciousness (loss of eyelid reflex). Pain is progressively abolished in this stage.  STAGE 2 (Delirium/Excitement): From loss of consiousness to beginning of regular respiration. Characterized by uninhibited excitation. Pupils are dilated and eyes divergent. Agitation, delirium, irregular respiration, and breatholding are commonly seen. Potentially dangerous responses can occur during this stage including vomiting, laryngospasm, HTN, tachycardia, and uncontrolled movement.
    35. 35.  STAGE 3 (Surgical Anesthesia): Regular respiration to caessation of spontaneous breathing Central gaze, constricted pupils, and regular respirations. Target depth of anesthesia is sufficient when painful stimulation does not elicit somatic reflexes or deleterious autonomic reflexes.
    36. 36. Plane 1 From the return of regular respirations to the cessation of REM. Plane 2 The Surgical Plane From the cessation of REM to the onset of paresis of the intercostal muscles. Plane 3 From the onset to the complete paralysis of the intercostal muscles. Plane 4 From the paralysis of the intercostal of this plane the patient will be apneic.
    37. 37.  STAGE 4 (Impending Death/Overdose): Onset of apnea, dilated and nonreactive pupils, and hypotension to complete circulatory failure.
    38. 38. Classic Stages of Anesthesia*  Stage 1: Analgesia – decreased awareness of pain, amnesia  Stage 2: Disinhibition – delirium & excitation, enhanced reflexes, retching, incontinence, irregular respiration  Stage 3: Surgical Anesthesia – unconscious, no pain reflexes, regular respiration, BP is maintained  Stage 4: Medullary Depression – respiratory & CV depression requiring ventilation & pharmacologic support. * Seen mainly with Ether. Not all stages are observed with modern GAs.
    39. 39. Mechanisms of Action Enhanced GABA effect on GABAA Receptors 1. – – – - Etomidate - Propofol Block nicotinic receptor subtypes (analgesia) 1. – Moderate to high conc’s of inhaled anesthetics Activate K channels (hyperpolarize ) 1. – Nitrous oxide, ketamine, xenon Inhibit NMDA (glutamate) receptors 1. – 1. Inhaled anesthetics Barbiturates Benzodiazepines Nitrous oxide, ketamine, xenon, high dose barbiturates Enhance glycine effect on glycine R’s (immobility)
    40. 40. Regional Effects  Immobilization in response to surgical incision (spinal cord)  Sedation, loss of consciousness (↓thalamic firing)  Amnesia (↓hippocampal neurotransmission)
    41. 41. CLASSIFICATION  INTRAVENOUS INDUCING AGENTS Thiopentone sodium Methohexital Propofol Etomidate SLOWER ACTING Diazepam Lorazepam Midazolam DISSOCIATIVE ANAESTHESIA Ketamine OPIOID ANALGESIA Fentanyl  INHALATIONAL GAS Nitrous oxide LIQUID Ether Halothane Enflurane Desflurane Sevoflurane
    42. 42. Parenteral Anesthetics (Intravenous)  Most commonly used drugs to induce anesthesia – – – – – Barbiturates (Thiopental* & Methohexital) Benzodiazepines (Midazolam) Opioids (Morphine & Fentanyl) Propofol* Etomidate * Most commonly used for induction
    43. 43. Barbiturates & Benzodiazepines MOA: GABA Barbiturate BZDS 1) Both bind to GABAA receptors, at different sites • Both cause increase Clinflux in presence of GABA • BNZ binding can be blocked by flumazenil. 2) Barbs at high doses - are also GABA mimetic, block Na channels NMDA/glutamate Rs
    44. 44. Dose Response Relationships Coma Barbiturates CNS Effects Medullary depression Benzodiazepines Anesthesia Hypnosis Sedation, disinhibition, anxiolysis Increasing dose Possible selective anticonvulsant & musclerelaxing activity
    45. 45. Barbiturates  Thiopental & methohexital are highly lipid soluble & can produce unconsciousness & surgical anesthesia in <1 min.  Rx: induction of anesthesia & short procedures  Actions are terminated by redistribution  With single bolus - emergence from GA occurs in ~ 10 mins  Hepatic metabolism is required for elimination
    46. 46. Opioids (Fentanyl & Remifentanil*)  GAs do not produce effective analgesia (except for ketamine).  Given before surgery to minimize hemodynamic changes produced by painful stimuli. This reduces GA requirements.  High doses can cause chest wall rigidity & post-op respiratory depression  Therapeutic doses will inhibit respiration (↑CO2)  Used for post-op analgesia, supplement anesthetic in balanced anesthesia.  Remifentanil is an ester opioid metabolized by plasma esterases. It is very potent but w/ a short t (3-10 mins).
    47. 47. Ketamine  Nonbarbiturate, rapid acting general anesthetic  Dissociated from the environment, immobile, and unresponsive to pain  Profound analgesic
    48. 48. Ketamine  Selectively blocks the associative pathways producing sensory blockade  Preserved pharyngeal-laryngeal reflexes  Normal or slightly enhanced skeletal muscle tone  Cardiovascular and respiratory stimulation
    49. 49. Ketamine (1.5mg/kg)  A “dissociative anesthetic” that produces a cataleptic state that includes intense analgesia, amnesia, eyes open, involuntary limb movement, unresponsive to commands or pain.  Increases heart rate & blood pressure (opposite of other GAs)  Can be used in shock states (hypotensive) or patients at risk for bronchospasm.  Used in children & young adults for short procedures  Side Effects: nystagmus, pupillary dilation, salivation, hallucinations & vivid dreams
    50. 50. Inhaled Anesthetics
    51. 51. Inhaled Anesthetics  Partial pressure or “tension” in inspired air is a measure of their concentration  The speed of induction of anesthesia depends on: – Inspired gas partial pressure (GA concentration) – Ventilation rate – GA solubility (less soluble GAs equilibrate more quickly with blood & into tissues such as the brain)
    52. 52. Elimination  Anesthesia is most commonly terminated by redistribution of drug from brain to the blood & out through the lungs.  The rate of recovery from anesthesia for GAs with low blood: gas PCs is faster than for highly soluble Gas.  Time is $$ in the O.R. & recovery room Blood: Gas P. Coeff – Haltothane – Desflurane – Sevoflurane 2.30 0.42 0.69  Halothane & methoxyflurane undergo hepatic metabolism & can cause liver toxicity.
    53. 53. Toxicity  Malignant Hyperthermia – Esp. when halogenated GA used with succinylcholine – Rx: dantrolene (immediately)  Halothane: – Halothane undergoes >40% hepatic metabolism – Rare cases of postoperative hepatitis occur – Halothane can sensitize the heart to Epi (arrhythmias)  Methoxyflurane – F release during metabolism (>70%) may cause renal insufficiency after prolonged exposure.  Nitrous oxide – Megaloblastic anemia may occur after prolonged exposure due to decreases in methionine synthase activity(Vit B12 deficiency).
    54. 54. PREANAESTHETIC MEDICATION  Opioids: Morphine-10 mg Pethidine 50-100mg i.m.  Sedatve antianxiety : Diazepam 5-10mg orally Lorazepam 2mg i.m.  Anticholinergics : Atropine 0.6mg i.m./ i.v Glycopyrolate 0.1-0.3mg i.m  Neuroleptics: Chlorpramazine 25mg  H2 blockers : Ranitidine 150mg Famotidine 40mg  Antiemetics : Metoclopramide 10-20mg i.m
    55. 55. Dantrolene  Interfers with the release of calcium from the sarcoplasmic reticulum through the SR calcium channel complex.  Used to prevent or reverse malignant hyperthermia (which is otherwise fatal in ~50% of cases w/o dantrolene).  Given by i.v. push at the onset of symptoms (e.g. an unexpected rise in CO2 levels)  Supportive measures & 100% O2 are also used to treat malignant hyperthermia
    56. 56. Nausea & Vomiting  General anesthetics effect the chemoreceptor trigger zone & brainstem vomiting center (cause nausea & vomiting)  Rx: - Ondansetron (5-HT3 antagonist) to prevent - Avoidance of N2O - Propofol for induction - Keterolac vs. opioid for analgesia - Droperidol, metaclopromide & dexamethasone