Anestesi Umum Dan Lokal

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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