10800669.ppt

Inhalational Anaesthesia
Dr.Mahmoud Al-MUSTAFA
University of Jordan
Department of Anesthesia

Basic Principles of Anesthesia
 Anesthesia defined as the abolition of
sensation
 Analgesia defined as the abolition of pain
 “Triad of General Anesthesia”
 need for unconsciousness
 need for analgesia
 need for muscle relaxation

Inhalational Anesthetic Agents
 Inhalational anesthesia refers to the
delivery of gases or vapors from the
respiratory system to produce
anesthesia
 Pharmacokinetics--uptake, distribution,
and elimination from the body
 Pharmacodyamics-- MAC value

Ideal Characteristics
 1. Be pleasant to inhale, permitting a
smooth induction and emergence.
 2. Be potent to allow the concomitant
administration of high oxygen.
 3. Rapid induction and emergence (low
solubility).
 4. Be easy to administer and analyze

Ideal Characteristics
 5. Be easily and cheaply prepared in pure
form.
 6. Be stable in storage and with soda-lime,
not flammable, not metabolized.
 7. Act at specific CNS sites to cause
unconsciousness.
 8. No CV or respiratory effects, non-toxic to
organ systems.
 9. Provide postop pain relief.

Minimum Alveolar Concentration
 Minimum Alveolar Concentration
 Eger 1969
 Minimal alveolar concentration of inhalational
agent that prevent movement in 50% of the
patients in response to surgical stimulation
(skin incision)
 Equivalent to ED50
 For the same agent, varies with age,
temperature and other drugs on board

Uptake and Distribution
 Factors which influence the rate of
uptake
 Inspired concentration
 Minute ventilation
 Cardiac output
 Solubility

Respiratory Effects
 All cause respiratory depression
 Increased respiratory rate
 Decreased tidal volume
 CO2 retention
 Decreased alveolar minute ventilation ->
 Decreased uptake
 Negative feedback

Respiratory Effects
 Abolish the hypoxic response at less
than half MAC concentrations
 Fantastic bronchodilators by direct
action on smooth muscle

Cardiovascular Effects
 All cause cardiac depression
 Cardiac depression causes an increased
rate of concentration rise
 An increased concentration causes more
cardiac depression

Cardiovascular Effects
 Isoflurane and desflurane cause increased
heart rate which may mask depression
 Systemic vascular resistance
 Isoflurane and desflurane decrease (great for
starting IVs)
 Halothane and nitrous oxide do not change
 Steal phenomena

CNS Effects
 Short time constant (2 min)
 Hypnotic, not analgesic
 Cause unconsciousness
 Spinal cord depression (lack of reflexes)

Renal Effects
 All decrease arterial pressure
 RBF and GFR will be maintained until
threshold of autoregulation, absent other
influences (sympathetic tone, renin)
 Urine output is variable, depending on ADH
and aldosterone and other humeral agents
 Enflurane ……….nephrotoxic

Nitrous Oxide
 Prepared by Priestly in 1776
 Anesthetic properties described by Davy
in 1799
 Characterized by inert nature with
minimal metabolism
 Colorless, odorless, tasteless, and does
not burn

Nitrous Oxide
 Simple linear compound
 Not metabolized
 Only anesthetic agent that is inorganic
 Week Anesthetic good analgesic agent

Nitrous Oxide
 Major difference is low potency
 MAC value is 105%
 Weak anesthetic, powerful analgesic
 Needs other agents for surgical
anesthesia
 Low blood solubility (quick recovery)

Nitrous Oxide Systemic Effects
 Minimal effects on heart rate and blood
pressure
 May cause myocardial depression in sick
patients
 Little effect on respiration
 Safe, efficacious agent

Nitrous Oxide Side Effects
 Manufacturing impurities toxic
 Hypoxic mixtures can be used
 Large volumes of gases can be used
 Beginning of case: second gas effect
 End of case: diffusion hypoxia

 Diffusion into closed spaces
……………………

 Inhibits methionine synthetase
(precursor to DNA synthesis)
 Inhibits vitamin B-12 metabolism

Halothane
 Synthesized in 1956 by Suckling
 Halogen substituted ethane
 Volatile liquid easily vaporized, stable,
and nonflammable

Halothane
 Most potent inhalational anesthetic
 MAC of 0.75%
 Efficacious in depressing consciousness
 Very soluble in blood and adipose
 Prolonged emergence

Halothane Systemic Effects
 Inhibits sympathetic response to painful
stimuli
 Inhibits sympathetic driven baroreflex
response (hypovolemia)
 Sensitizes myocardium to effects of
exogenous catecholamines-- ventricular
arrhythmias

Halothane Systemic Effects
 Decreases respiratory drive-- central
response to CO2 and peripheral to O2
 Respirations shallow-- atelectasis
 Depresses protective airway reflexes
 Depresses myocardium-- lowers BP and
slows conduction
 Mild peripheral vasodilation

Halothane Side Effects
 “Halothane Hepatitis” -- 1/10,000 cases
 fever, jaundice, hepatic necrosis, death
 metabolic breakdown products are hapten-
protein conjugates
 immunologically mediated assault
 exposure dependent

 Malignant Hyperthermia-- 1/60,000 with
succinylcholine to 1/260,000 without
 halothane in 60%, succinylcholine in 77%
 Classic-- rapid rise in body temperature,
muscle rigidity, tachycardia,
rhabdomyolysis, acidosis, hyperkalemia,
DIC
 family history

 Malignant Hyperthermia (continued)
 high association with muscle disorders
 autosomal dominant inheritance
 diagnosis--previous symptoms, increase
CO2, rise in CPK levels, myoglobinuria,
muscle biopsy
 physiology--hypermetabolic state by
inhibition of calcium reuptake in
sarcoplasmic reticulum

 Malignant Hyperthermia (continued)
 treatment--early detection, d/c agents,
hyperventilate, bicarb, IV dantrolene (2.5
mg/kg), ice packs/cooling blankets,
lasix/mannitol/fluids. ICU monitoring

Enflurane
 Developed in 1963 by Terrell, released
for use in 1972
 Stable, nonflammable liquid
 MAC 1.68%

Enflurane Systemic Effects
 Potent inotropic and chronotropic depressant
and decreases systemic vascular resistance--
lowers blood pressure and conduction
dramatically
 Inhibits sympathetic baroreflex response
 Sensitizes myocardium to effects of
exogenous catecholamines-- arrhythmias

Enflurane Systemic Effects
 Respiratory drive is greatly depressed--
central and peripheral responses
 increases dead space
 widens A-a gradient
 produces hypercarbia in spontaneously
breathing patient

Enflurane Side Effects
 Metabolism one-tenth that of
halothane-- does not release quantity of
hepatotoxic metabolites
 Metabolism releases fluoride ion-- renal
toxicity
 Epileptiform EEG patterns

Isoflurane
 Synthesized in 1965 by Terrell, introduced
into practice in 1984
 Not carcinogenic
 Nonflammable,pungent
 Less soluble than halothane or enflurane
 MAC of 1.30 %
 Steal phenomena

Isoflurane Systemic Effects
 Depresses respiratory drive and ventilatory
responses-- less than enflurane
 Myocardial depressant-- less than enflurane
 Inhibits sympathetic baroreflex response--
less than enflurane
 Sensitizes myocardium to catecholamines --
less than halothane or enflurane

Isoflurane Systemic Effects
 Produces most significant reduction in
systemic vascular resistance-- coronary
steal syndrome, increased ICP
 Excellent muscle relaxant-- potentiates
effects of neuromuscular blockers

Isoflurane Side Effects
 Little metabolism (0.2%) -- low
potential of organotoxic metabolites
 No EEG activity like enflurane
 Bronchoirritating, laryngospasm

Sevoflurane and Desflurane
 Low solubility in blood-- produces rapid
induction and emergence
 Minimal systemic effects-- mild respiratory
and cardiac suppression
 Few side effects
 Expensive
 Sevoflarane …….compound A
 Desflurane ……….Special vaporizer

10800669.ppt

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10800669.ppt