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Only inorganic anesthetic gas in clinical use.
Vapor pressure: --------
Blood/Gas Solubilities: 0.47
Colorless and essentially odorless
Non-explosive and nonflammable, is as capable as oxygen of supporting combustion.
Gas at room temperature and ambient pressure
Increases cerebral blood flow, producing mild elevation of intracranial pressure.
Increases cerebral oxygen consumption (CMRO2).
Levels below MAC provide analgesia in dental surgery and other minor procedures.
Stimulates the sympathetic nervous system
Arterial BP, CO, HR are essentially unchanged or slightly elevated because of stimulation of
Myocardial depression may be unmasked in patients with CAD or severe hypovolemia. The
resulting decrease in arterial BP may occasionally lead to myocardial ischemia.
Constriction of pulmonary vascular smooth muscle increases pulmonary vascular resistance
® of right atrial pressure
Peripheral vascular resistance is not significantly altered.
Nitrous oxide increases endogenous catecholamine levels, may be associated with a higher
incidence of epinephrine-induced dysrhythmias.
Does not provide significant muscle relaxation
Probably not a triggering agent of MH.
Implicated in postoperative nausea and vomiting presumably as result of activation of the
chemoreceptor trigger zone and vomiting center in the medulla.
Increases respiratory rate (tachypnea) and decreases TV as a result of CNS stimulation and
perhaps activation of pulmonary stretch receptors.
Net effect – minimal change in minute ventilation and resting arterial CO2 levels.
Hypoxic drive is markedly depressed by even small amounts of nitrous oxide.
Appears to decrease renal blood flow by increasing renal vascular resistance ® a drop in GFR and
Hepatic blood flow probably falls but to a lesser extent than with other volatile agents.
During emergence almost all nitrous oxide is eliminated by exhalation. Small amount diffuses
Bio-transformation is limited to the less than 0.01% that undergoes reductive metabolism in the GI
tract by anaerobic bacteria.
Prolonged exposure to anesthetic concentrations of nitrous oxide can result in bone marrow
depression (megaloblastic anemia) and neurologic deficiencies.
Because of possible teratogenic effects, it is often avoided in pregnant patients.
May also alter immunologic responses to infection.
It is 35 more times soluble than nitrogen in blood, tends to diffuse into air-containing cavities
More rapidly than nitrogen is absorbed by the bloodstream.
Avoid with conditions of: air embolus, pneumothorax, acute intestinal obstruction, intracranaial
air (tension pneumoencephalus following dural closur or pneumoencephalography),
pulmonary air cysts, intraocular air bubbles, and tympanic membrane grafting.
Will even diffuse into ET tube cuffs, increasing pressure against tracheal mucosa.
Should be avoided with patients with pulmonary hypertension
It is of limited value in patients requiring high inspired oxygen concentrations.
Because of its relatively high MAC, it prevents it use as a complete general anesthetic. It is
frequently used in combination with more potent volatile agents. The addition of nitrous oxide
decreases the requirements of these other agents.
It does attenuate the circulatory and respiratory effects of volatile anesthestics in adults.
Potentiates neuromuscular blockade, but less so than the volatile agents.
The concentration of N2O flowing through a vaporizer can influence the concentration of volatile
anesthetic delivered. Example: Decreasing N2O concentration (increasing oxygen
concentration) increases the concentration of volatile agent despite a constant vaporizer
setting. This is due to the relative solubilities of N2O and oxygen in liquid volatile anesthetics
(the second gas effect).
750 psig until all liquid vaporized, then pressure drops in tank
Halothane (Fluthane) 1956
Vapor pressure: 243
Blood/Gas Solubilities: 2.4
Fat/blood Coefficient: 60
Carbon-fluoride bonds responsible for its nonflammable and nonexpolsive nature.
Stored in amber/brown bottle
Sweet, pleasant odor
Dilates cerebral vessels, which lowers cerebral vascular resistance and increases cerebral blood
flow. Autoregulation, maintainence of constant cerebral blood flow during changes in
arterial pressure, is blunted.
Concomitant rises in intracranial pressure can be prevented by establishing hyperventilation prior
to halothane administration. Cerebral activity is decreased leading to modest reductions in
metabolic oxygen requirements.
Dose dependent reduction of arterial blood pressure is due to direct myocardial depression;
2.0 MAC of halothane results in 50% decrease of BP and CO. Cardiac interference with
intracellular calcium utilization , causes an increase in right atrial pressure. Coronary blood
flow decreases due to the drop in systemic arterial pressure. Adequate myocardial perfusion is
usually maintained since oxygen demand also drops. Halothane blunts baroreceptor response.
Slowing of SA node conduction may result in junctional rhythm or bradycardia.
Halothane prolongs QT interval (like other volatile agents).
Sensitizes the heart to the dysrhythmogenic effects of epinephrine, so doses of epinephrine above
1.5 m g/kg should be avoided. May result in halothane interfering with slow calcium
Systemic vascular resistance is unchanged.
Relaxes skeletal muscles and potentiates non-depolarizing neuromuscular blocking drugs.
It is a triggering agent of MH.
Causes rapid, shallow breathing. The increased respiratory rate is not enough to counter the
decreased TV, so alveolar ventilation drops and resting PaCO2 is elevated. Apneic threshold,
the highest PaCO2 at which a patient remains apneic, also rises because the difference between
it and resting PaCO2 is not altered by general anesthesia.
Halothane limits the increase in minute ventilation that normally accompanies a rise in PaCO2.
Halothane’s ventilatory effects are probably due to central (medullary depression) and peripheral
(intercostal muscle dysfunction) mechanisms. These are exaggerated by preexisting lung
disease and attenuated by surgical stimulation.
The increase in PaCO2 and the decrease in intrathoracic pressure that accompany spontaneous
ventilation with halothane partially reverse the CO, arterial BP, and HR depression.
Hypoxic drive is severely depressed by even low concentrations of halothane (0.1 MAC).
Potent bronchodilator, often reverses asthma-induced bronchospasm. This is not inhibited by
propranolol (b -adrenergic blocking agent).
Depresses clearance of mucous from the respiratory tract, promoting postoperative hypoxia
Causes hepatic blood flow to decrease in proportion to the depression of cardiac output.
Could have minor liver transaminase elevations.
Profound effect. Inhibits myo-uterine tone – profound bleeding.
Only use if need to relax uterus.
Metabolism and clearance of some drugs (eg, fentanyl, phenytoin, verapamil) appeared to be
impaired by halothane.
Oxidized in the liver to its principal metabolite, trifluoroacetic acid.
Bio-transformation in liver – cP450 system.
Halothane hepatitis –extremely rare (1 per 35,000 cases). Patients exposed to multiple halothane
anesthetics at short intervals, middle-aged obese women, and persons with a familial
presdisposition to halothane toxcity or personal history are considered at increased risk.
Centrilobular necrosis – implies hepatic damage from reductive metabolites or hypoxia. Could
also be related to an immune mechanism. This has implicated liver microsomal proteins
that have been modified by trifluoroacetic acid as the triggering antigens.
Withhold halothane from patients with unexplained liver dysfunction following previous
exposure. Halothane hepatitis appears to affect primarily adults and children past puberty.
Should be used with caution in patients with intracranial mass lesions because of the possibility
of intracranial hypertension.
Hypovolemic patients and some patients with severe cardiac disease (aortic stenosis) may not
tolerate halothanes’s negative inotropic effects.
Sensitization of the heart to catecholamines limits the usefulness of halothane when exogenous
epinephrine is administered or in patients with pheochromocytoma.
Myocardial depression seen with halothane is exacerbated by b -adrenergic blocking agents
(eg, propranolol) and calcium channel-blockig agents (eg, verapamil).
Tricyclic antidepressants and MAO inhibitors have been associated with BP fluctuations and
dysrhythmias, although neither represents fluctuations an absolute contraindication.
Combination of halothane and aminophylline has resulted in serious ventricular dysrhythmias.
Vapor pressure: 175
Blood/Gas Solubilities: 1.9
Mild, sweet, ethereal odor and is nonflammable at clinical concentrations.
Increases cerebral blood flow and intracranial pressure.
Has been shown to increase the secretion of CSF and the resistance to CSF outflow.
Hyperventilation is not recommended to attenuate enflurane-induced intracranial hypertension.
Deep enflurane anesthesia can culminate in frank tonic-clonic seizures.
Cerebral metabolic requirements are decreased by enflurane unless seizure activity is initiated.
Depresses myocardial contractility. This negative inotropic action appears to involve depression
of calcium influx and SR release during myocardial membrane depolarization.
Arterial BP, CO, and myocardial oxygen consumption are lowered.
Decreases SVR; HR usually rises.
Sensitizes the heart to the dysrhythmic effects of epinephrine, but doses up to 4.5 m g/kg are
usually well tolerated.
Relaxes skeletal muscle.
Decrease amount of non-depolarizing muscle relaxant (1/3 to ˝). Enhance and prolong effects.
Decrease minute ventilation despite an increase in RR and increased resting PaCO2, decreased
response to hypercapnia, abolishment of hypoxic drive, depressed mucociliary function,
Decrease in hepatic blood flow is similar to that caused by equipotent doses of other volatile
RBF, GFR, and urinary output fall during enflurane anesthesia. A metabolite of enflurane is
Metabolized in liver. Biotranformation - microsomal
Should be avoided in patients with pre-existing disease even though deterioration in renal function
Should also choose another agent for patients with seizure disorders.
Precautions concerning intracranial hypertension, hemodynmic instability, and MH are the same
as those associated with halothane.
Isoniazid induces enflurane defluorination. May be clinically significant in so-called rapid
Acetylators (patients with an autosomal trait that increases the rate of hepatic acetylation).
Isoflurane (Forane) 1981
Chemical isomer of enflurane, it has different physiochemical properties.
Vapor pressure: 240
Blood/Gas Solubilities: 1.4
Characteristics: Nonflammable, pungent ethereal odor.
At concentrations greater than 1 MAC, increases cerebral blood flow and intracranial pressure.
The effects are thought to be less pronounced than with halothane or enflurane and are reversed
by hyperventilation. The hyperventlation does not have to be instituted prior to the use of
isoflurane to prevent intracranial hypertension (unlike halothane).
It reduces cerebral metabolic oxygen requirements and at 2 MAC produces an electrically silent
Causes minimal cardiac depression. CO is maintained by a rise in HR due to partial preservation
of carotid baroreflexes.
Mild b -adrenergic stimulation increases skeletal muscle flow, decreases SVR, and lowers
Rapid increases in isoflurane concentration lead to increases in HR, arterial BP, and plasma
levels of norepinephrine.
Dilates coronary arteries (discussion of coronary steal syndrome). Usually avoided in patients
with coronary artery disease.
Relaxes skeletal muscle.
Respiratory depression resembles that of other volatile anesthetics, except that tachypnea is less
pronounced. The net effect is a more pronounced fall in minute ventilation.
Low levels of isoflurane (0.1 MAC) blunt the normal ventilatory response to hypoxia and
Considered a good bronchodilator.
Total hepatic blood flow is reduced. Hepatic oxygen supply may be better maintained with
isoflurane because hepatic artery perfusion is maintained.
Liver function tests are minimally affected.
Uterus: In high doses – uterine relaxation.
Metabolized to 1/10 of the extent of enflurane. Trifluoroacetic acid is the principal end product.
Nephrotoxcity is unlikely.
Presents no unique contraindications other than the controversy of possible coronary steal.
Patients with severe hypovolemia may not tolerate its vasodilating effects.
Epinephrine can be safely administered in doses up to 4.5 m g/kg.
Non-depolarizing muscle relaxants are potentiated by isoflurane.
Desflurane (Suprane) 1992
Structure is very similar to that of isoflurane. Only difference is a substitution of a fluorine atom for isoflurane’s chlorine atom. Has profound effects on physical properties of drug.
Vapor pressure: 681 (boils at room temperature)
Blood/Gas Solubilities: 0.42 Rapid wash-in and wash-out of anesthestic. Alveolar concentration will tend
to approach inspired concentrations much more rapidly than other volatile agents, giving tighter
control over anesthetic level. Wake up times are approximately half as long as those observed
High vapor pressure, ultra-short duration of action, and moderate potency – most characteristic
Special vaporizer needed.
Decreases cerebral vascular resistance, increases cerebral blood flow, and is associated with an
increase in ICP at normotension and normocapnia.
Cerebral vasculature remains responsive to changes in PaCo2, so that intracranial pressure can be
lowered by hyperventilation.
Cerebral oxygen consumption is decreased. During periods of desflurane induced hypotension
MAP=60 mmHg), cerebral blood flow is adequate to maintain aerobic metabolism despite a
low cerebral perfusion pressure.
Similar to those of isoflurane. Increasing the dose is associated with a decline in SVR that leads
to a fall in arterial BP.
CO remains relatively unchanged or slightly depressed at 1-2 MAC.
There is a moderate rise in HR, CVP, and pulmonary artery pressure that may not be apparent at
Rapid increases in desflurane concentration lead to transient elevations in HR, BP, and
catecholamine levels more pronounced than isoflurane.
Does not increase coronary blood flow.
Associated with a dose-dependent decrease in the response to train-of-four and tetanic
peripheral nerve stimulation.
Hepatic function tests are unaffected.
Causes a decrease in TV and an increase in respiratory rate.
There is an overall decrease in alveolar ventilation that causes a rise in resting PaCO2.
Depresses the ventilatory response to increasing PaCO2.
Pungency and airway irritation during induction can be manifested by salivation, breath-holding
coughing, and laryngospasm.
No evidence of any nephrotoxic effects.
Undergoes minimal metabolism in humans.
Shares many of the contraindications of other modern volatile anesthetics: severe hypovolemia,
MH, and intracranial hypertension.
Poteniates non-depolarizing muscle relaxants to the same extent as isoflurane.
Epinephrine can be safely administered in doses up to 4.5 m g/kg – desflurane does not sensitize
the myocardium to the dysrhythmogenic effects of epinephrine.
Sevoflurane (Ultane) 1995
Halogenated with fluorine.
Vapor pressure: 160
Blood/Gas Solubilities: 0.65
Potency slighty less than enflurane.
Nonpungency and rapid increases in alveolar concentration make sevoflurane an excellent choice for
Causes slight increases in cerebral blood flow an intracranial pressure at normocarbia.
Cerebral metabolic oxygen requirements decrease, and no seizure activity has been reported.
Mildly depresses myocardial contractility. SVR and arterial BP decline slightly less than with
isoflurane or desflurane.
Because of little if any rise in HR, CO is not well maintained as with isoflurane or desflurane.
No evidence associating it with coronary steal syndrome.
Produces adequate muscle relaxation for intubation of children following an inhalational
Depresses respiration and reverses bronchospasm to an extent similar to isoflurane.
Decreases portal vein blood flow, but increases hepatic artery blood flow, maintaining total
hepatic blood flow and oxygen delivery.
Liver microsomal enzyme P450 metabolizes sevoflurane at a rate similar to enflurane and may be
induced with ethanol or phenobarbital pretreatment.
Decreases renal blood flow – its metabolism to fluoride has been associated with impaired renal
tubule function. There is potential nephrotoxicity of the resulting rise in inorganic fluoride (F-).
Should be avoided in patients with impaired kidney function.
Alkali such as soda lime can degrade sevoflurane, producing nephrotoxic end product (compound
A, an olefin). Accumulation of compound A increases with increased respiratory gas
temperature,low-flow anesthesia, dry barium hydroxide absorbent, high sevoflurane
concentrations, and anesthetics of long duration. Determination of whether sevoflurane
anesthesia achieves toxic concentrations of compound A is yet to be determined. Fresh gas
flows less than 2 liters/min are not recommended.
Include severe hypovolemia, susceptibility to MH, and intracranial hypertension.
Potentiates non-depolarizing muscle relaxants. It does not sensitize heart to catecholamine-
Molecular Structures of Inhaled Anesthetics
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Last Updated 04/10/00 12:26:56 PM
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