ANESTHETICS DRUGS

ENNY ROHMAWATY

Depart. of Pharmacology and Therapy

Faculty Of Medical -Padjadjaran University
 HISTORY OF ANESTHESIA

Ancient Egypt : Narcotics

China : Canabis indica, traumatic
1776 : the first gas anesthetic (N2O)
1795 : Ether
 TERMINOLOGY

ANESTHETICS :
Drugs that caused anesthesia
ANESTHESIA :
No pain sensation

TWO GROUPS OF ANESTHESIA :

1. General Anesthetics
2. Local Anesthetic
 THEORY OF ANESTHESIA

1. No stimuli from perifer

2. Stimuli + Block at Gg. cervicalis sup
3. Stimuli +
No block at Gg. Cervicalis sup
No interpretation
4. Stimuli +
No block
interpretation +
No response
 GENERAL ANESTHESIA

Analgesic, amnesic, unconscious state

Muscle relaxation
Suppresion of undesirable reflexes

BALANCED ANESTHESIA
PRE ANESTHETIC MEDICATION

SKELETAL MUSCLE RELAXANTS

 PRE ANESTHETIC MEDICATION

SERVES TO :
Calm the patient
Relieve pain
Protect against undesirable effects of the subsequently
administered anesthetic or the surgical procedures

INCLUDING :
Hipnotic sedatives, anti histamines, anti emetics, opioids,
anti cholinergics
 STAGES OF ANESTHESIA

STAGE I Analgesia
STAGE II Excitement
violent combative behavior BP
Respiratory rate
Reflexes
Hyper secretion
 STAGES OF ANESTHESIA

STAGE III Surgical anesthesia

Regular respiration
Skeletal muscles relaxation
Eye reflexes
Eye movements
Fixed pupil
STAGE IV Medullary paralysis
 STAGES OF ANESTHESIA

PLANE I PLANE II PLANE III PLANE

IV
EYE Roving midconstriction middilatation dilatation
movment of
eye ball.
Myotic pupil
REFLEXES

MUSCLE Small Large muscles All muscles All

RELAXATION muscles muscles
RESPIRATION Thoracal > Thoracal = Abdominal >
Abdominal Abdominal Thoracal
 EVALUATION

Rhythm and automatization of respiration

Conjunctival reflexes
Gradually loss of Mm. Intercostales activity
Fixated eye

DEEP ANESTHESIA
GENERAL ANESTHESIA

INHALATIONAL ANESTHETICS

INTRAVENOUS ANESTHETICS
 INHALATIONAL ANESTHETICS
MECHANISM OF ACTION

Non selective action

Their clinically important effect on the CNS
also alter the function of various peripheral
cell types
Site of action :Reticular activating system
and cortex cerebri (controlling the overall
state consciousness and response to sensory
stimuli)
 INHALATIONAL ANESTHETICS
THE POTENCY
Defined quantitatively as the MINIMUM ALVEOLAR
CONCENTRATION (MAC)
MAC :
The concentration of gas anesthetic needed to eliminate
movement among 50% of patient challenged by a
standardized skin incision
MAC is small for potent anesthetics and large for the less one
The more lipid soluble an anesthesia, the lower the
concentration of anesthetics needed to produce anesthesia
 THE PHARMACOKINETICS OF
INHALATIONAL ANESTHETICS
Partial pressure of anesthetic gas driving
force moves the anesthetics into the
alveolar space blood brain and body
compartment

Steady state :
The partial pressure in each of these compartments
is equivalent to that in inspired mixtures
 THE PHARMACOKINETICS OF
INHALATIONAL ANESTHETICS

The steady state depends on :

Alveolar wash-in
Solubility in blood
Blood-gas partition coefficient
halothane > enflurane > isoflurane > N20
solubility faster achievement of steady state
Tissue uptake
Wash-out
 COMMON FEATURES OF
INHALATIONAL ANESTHETICS

Decrease cerebrovascular resistance resulting

in increased perfusion of the brain
Bronchodilation and decrease minute
ventilation
Potency does correlate with their solubility in
lipid
Recovery is due to redistribution from the
brain
 HALOTHANE

Weak analgesic effect

Vagomimetic, atropine-sensitive bradycardi
Cardiac output , hipotension
Cardiac arrhytmia, esp. to whom with hipercapnia
and high concentration of blood catecholamine
Toxic metabolites (trifluoroethanol + bromide ion)
No hepatotoxic effect for children
DOC for pediatric patient
 ENFLURANE
Less potent than halothane
Rapid induction and recovery
The metabolite (fluoride ion) excreted by kidney, so its contra
indicated in patient with renal failure
Some differences from halothane:
Fewer arrhytmia
less heart sensitization to catecholamines
greater potentiation of muscle relaxants
Intra ocular pressure
Disadvantage : CNS excitation
 ISOFLURANE

Low biotransformation and low organ

toxicity
Doesnt induce cardiac arrhytmia
No heart sensitization to catecholamine
Less fluoride ion is produced
 METHOXYFLURANE

High solubility in lipid

Not for prolonged adminiostration (toxic
effect to the kidney)
Indication : obstetrical practice (does not
relax the uterus)
 NITROUS OXIDE

Potent analgesic, weak general anesthetic

No respiration depression
Less effect on CVS
Increasing cerebral blood flow
Less hepatotoxic effect
 INTRAVENOUS ANESTHETIC
BARBITURATES

Quickly enter the CNS depress function

diffusion out of the brain
redistribution to other body tissue
Not significant analgesic
ADR : apnea, coughing, chest wall spasm,
laryngospasm, bronchospasm
 BENZODIAZEPINES

Lorazepam and Midazolam are more potent

than diazepam
Facilitate amnesia while causing sedation
Etomidate : No analgesic effect
uncontrolled skeletal muscle activity
 OPIOIDS

Analgesic effect
Amnesic effect <
BP decreased, respioratory depression,
muscle rigidity, post anestetic nausea and
vomiting.
Fentanyl, morphine
Antagonis: Naloxone
 NEUROLEPTANESTHESIA

Neuroleptic : adrenergik blocking as well as

sedative, antiemetic and anticonvulsant
properties
Contraindicated in Parkinsons patient
INNOVAR : Fentanyl + droperidol
 LOCAL ANESTHETICS

IDEAL LOCAL ANESTHETIC:

No tissue irritation
No permanently nerve fiber damage
Wide margin of safety
Long duration of action
Water soluble
Stable
Sterilable without agent changing
 MECHANISM OF ACTION

Inhibition of impuls production and

conduction
DOA depends on:
contact period with nerve fiber
the act that localized drug

Site of action : cell membrane

Small fibers and unmyelinated are more
sensitive to the stimuli
 Loss of sensation: pain cold hot
tactile deep pressure
Anesthesia due to nerve fiber pressure :
tactile hot cold pain
The conduction of local anesthetic could be
inhibite by changing the pH to 7 or 9,5 (most
of local anestheticin the form of cation )
 EFFECT OF
VASOCONSTRICTOR
Early OOA and longer DOA
Epinefrin (1 : 200,000) and Nor epinefrin
(1: 100,000)
ADR : takikardi, palpitation, chest pain,
delayed wound healing, udem or necrosis
 CLASSIFICATION

AMIDE LINKAGE :
LIDOCAINE
DIBUCAINE
ESTER LINKAGE :
PROCAINE
MEPIVACAINE
COCAINE
PRILOCAINE
TETRACAINE
BENZOCAINE
 COCAINE

Source : Erythroxylon coca

Very strong stimulation on cortex cerebri and medullary
Bradicardia (low dose), tachycardia (high dose). Systemic
administration will cause hipotension after hypertension
strong pyrogenous effect
Pharmacokinetics:
absorpsi: from almost tissue
detoxication : liver
excretion : urine
SYNTHETIC LOCAL ANESTHETIC
PROCAINE

PHARMACODYNAMIC :
Systemic analgesia
Procaine-sulfonamide antagonism

PHARMACOKINETIC:
fast absorption from site of injection
LIDOCAINE

Strong local anesthetic

Widely use as topical and injection agents
faster, stronger, longer, and more
extensive effect than procaine
indication:
anesthetic

antiarrhytmia