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GENERAL ANESTHETICS
I WAYAN SUMARDIKA Department of Pharmacology,Faculty Of Medicine, Udayana University
Introduction
The goal of general anesthesia is to create a reversible condition of comfort, quiescence, and physiological stability before, during, and after a surgical procedure.
Introduction
Characteristics of an ideal general anesthetic– Provide a smooth and rapid induction of
unconsciousness– Produce amnesia– Block troublesome reflexes– Produce skeletal muscle relaxation– Produce analgesia– Provide a smooth and rapid emergence and
recovery without long lasting adverse effects
Introduction
Combination Anesthesia– Since a single anesthetic agent will not meet the
ideal, a combination of drugs is used to take advantage of their best properties and minimize the undesirable side effects.
Preanesthetics
Preanesthetic medications – drugs given generally prior to anesthesia (may be given during or after, as well) in order to:– Decrease anxiety without producing excessive
drowsiness– Facilitate a rapid, smooth induction without
prolonging emergence– Provide amnesia for the perioperative period– Relieve pre-and post-operative pain– Minimize undesirable side effects of anesthetics
Preanesthetic AgentsDrug Classification Generic Name Desired Effect
Benzodiazepines DiazepamMidazolam
Reduce anxiety, Sedation, Amnesia, “Conscious sedation”
Antihistamines Hydroxyzine Sedation
Opioid analgesics MorphineMeperidineFentanylRemifentanil
Sedation to decrease tension, anxiety, and provide analgesia
Phenothiazines Promethazine Sedation, antihistaminic, antiemetic, decreased motor activity
Anticholinergics AtropineGlycopyrollate
Inhibit secretion, bradycardia, vomiting, and laryngospasms
GI Drugs OndansetronCimetidineMetoclopramide
Antiemetic
Decrease gastric acidity Decrease stomach contents
Signs and Stages
These signs and stages are only partly recognizable with modern balanced anesthesia.
ECG, HR, body temp, pulse oximetry, BP are routinely used to evaluate depth of anesthesia in practice. EEG now being used, too.
Stages of General Anesthesia
Stage I: Loss of pain Stage II: Excitement and hyperactivity Stage III: Surgical anesthesia Stage IV: Paralysis of the medulla
Anesthetics divide into 2 classes:
Inhalation Anesthetics
– Gasses or Vapors– Usually Halogenated
Intravenous Anesthetics
– Injections– Anesthetics or induction
agents
Inhalation Anesthetic Agents
General pharmacological effects CNS – dose dependent depression of all portions of
CNS. Order of sensitivity (most to least) is RAS and cortex → hippocampus → basal ganglia → cerebellum → spinal cord → medulla (irregularly descending anesthesia)
Autonomic nervous system
– Inhibition of sympathetics– Stimulation of parasympathetics– Nausea and vomiting
Inhalation Anesthetic Agents
General pharmacological effects Cardiovascular
– Dose related negative inotropic effect– ↓ BP– Arrhythmias– Sensitization to circulating catecholamines
Respiration
– Dose dependent depression of medullary respiratory center
Inhalation Anesthetic Agents
General pharmacological effects Hypothermia
– Altered thermoregulatory control and reduced metabolic rate
Miscellaneous
– Decrease lower esophageal sphincter tone– Malignant hyperthermia– Halothane hepatitis– Post-operative cognitive dysfunction
Inhalation Anesthetic Agents
Anesthetic gases – only one is Nitrous Oxide Volatile liquids
– Halothane (Fluothane) – Isoflurane (Forane) – commonly used anesthetic for adults– Enflurane (Ethrane) – like isoflurane, except increased risk of
seizures. Rarely used– Desflurane (Suprane) – similar to isoflurane except for more
rapid emergence, and more irritating to airway– Sevoflurane (Ultane) – similar to desflurane except not
irritating to airway
Anesthetic Agents
Intravenous agents– Barbiturates – sodium thiopental– Propofol (Diprivan) – similar to thiopental except
that it can be used for longer periods of anesthesia– Dissociative – ketamine– Benzodiazepines – diazepam, midazolam– Etomidate (Amidate)– Dexmedetomidine (Precedex)
Properties of Intravenous Anesthetic Agents
Drug Speed of Induction and Recovery
Main Unwanted Effects
Notes
Thiopental Fast (accumulation occurs, giving slow recovery) Hangover
Cardiovascular and respiratory depression
Used as induction agent declining. Decreases cerebral blood flow and O2 consumption.
Etomidate Fast onset, fairly fast recovery
Excitatory effects during induction and recovery, Adrenocortical suppression
Less cardiovascular and respiratory depression than with thiopental, Causes pain at injection site
Propofol Fast onset, very fast recovery
Cardiovascular and respiratory depression. Pain at injection site.
Most common induction agent. Rapidly metabolized; possible to use as continuous infusion.
Ketamine Slow onset, after-effects common during recovery
Psychotomimetic effects following recovery, Postoperative nausea, vomiting and salivation
Produces good analgesia and amnesia
Midazolam Slower than other agents Little respiratory or cardiovascular depression
Anesthetic Agents
Anesthetic Antagonists– Naloxone (Narcan) and nalmefene (Revex)– Flumazenil (Romazicon)
Thank you!
LOCAL ANESTHETICS
I WAYAN SUMARDIKA Department of Pharmacology,Faculty Of Medicine, Udayana University
1885 Advertisement
Techniques of administration
Topical Anesthesia Infiltration Peridural Spinal anesthesia
Classes: The rule of “i”
Amides
Lidocaine
Bupivacaine
Levobupivacaine
Ropivacaine
Mepivacaine
Etidocaine
Prilocaine
Esters
Procaine
Chloroprocaine
Tetracaine
Benzocaine
Cocaine
Mechanism of Action
Blocks the sodium channel Wide ranging effects on the nervous system
Local anesthetics blocks the channel from the intracellular side
Must enter the neuron to work increased lipophilicity is associated with increased potency Increased un-ionized fraction increases potency
– The un-ionized molecule crosses the cell membrane– Adding bicarbonate increases the un ionized fraction
Tetrodotoxin binds the sodium channel from the outside
Metabolism
Amides– Primarily hepatic– Plasma concentration
may accumulate with repeated doses
– Toxicity is dose related, and may be delayed by minutes or even hours from time of dose.
Esters– Ester hydrolysis in the
plasma by pseudocholinesterase
– Almost no potential for accumulation
– Toxicity is either from direct IV injection
tetracaine, cocaine
or persistent effects of exposure
benzocaine, cocaine
Duration of Action
Rate of systemic absorption Rate of elimination
Particularly for esters, which are metabolized locally
Dose Potency General groups:
Short: Procaine, chloroprocaine Intermediate: lidocaine, mepivicaine, prilocaine Long acting: Tetracaine, bupivacaine, etidocaine,
ropivacaine, levobupivacaine
Systemic Absorption
Dose Vascularity
– Intercostal > Caudal > Epidural > Brachial > Infiltration
pH Slower absorption if solution is alkaline, because more is
bound into the tissues.
Lipophilicity Slower absorption for more lipophilic drugs, again because
more is bound in the tissues
Epinephrine Decreases local blood flow, decreasing absorption
Drug Interactions
Esters are metabolized by pseudocholinesterase
Compete with succinylcholine for metabolism, so when given together each lasts longer
Metabolism slowed by administration of anticholinesterase (e.g., neostigmine)
Acute toxicity
Main concern is CNS and cardiac toxicity CNS
Tinnitus, dizziness, lightheadedness are early signs Anxiety disorientation loss of consciousness
seizures respiratory arrest
Cardiac Hypotension
– All local anesthetics are negative inotropes PVC wide QRS Multiform vtach vfib, or
– Pattern with bupivacaine Bradycardia asystole
– Pattern with bupivacaine + lidocaine
Allergies
Amides– True allergies to
amide anesthetics are EXCEEDINGLY rare
Esters– Uncommon– Allergic reactions are
probably related to PABA.
Common ingredient in sun-screen.
– May also be related to topical benzocaine exposure.
THANK YOU