Inhaled Anesthetics II

Inhaled Anesthetics
Part II
Roxanne Jeen L. Fornolles, M.D.
MAC
 MAC is the alveolar concentration of an anesthetic at one atmosphere (in

volume%) that prevents movement in response to a surgical stimulus in 50% of
patients.
AGENT POTENCY
Halothane most
Isoflurane
Enflurane
Sevoflurane
Desflurane
N20 least
MAC decreases
with age approx.
6% per decade,
22% from age 40-
80 yrs and 27%
decrease from 1-
40 yrs.
 MAC-awake is the alveolar concentration of anesthetic at which a patient
opens his or her eyes to command, and it varies from 0.15 to 0.5 MAC.
 MAC-BAR is the alveolar concentration of anesthetic that blunts adrenergic
responses to noxious stimuli. It has been approximated at 50% higher than
standard MAC.
Alterations in Neurophysiology
 N20 administered without volatile anesthetics causes cerebral vasodilation and increased
cerebral blood flow.
 Volatile anesthetics decrease CRMO2. In normocapnic humans, these volatile anesthetics
cause cerebral vasodilation at concentrations above 0.6 MAC. At concentrations in excess
of MAC 1.0, vasodilating effects predominate and cerebral blood flow increases.
 Increase in CBF with increasing anesthetic dose occurs despite decreases in CMRO2-
uncoupling.
 In general, ICP will increase or decrease in proportion to changes in CBF.
 Postoperative Cognitive Dysfunction- impairment to the mental processes of perception,
memory, and information processing. These alterations are associated with increased
morbidity and mortality in the first year after surgery
Circulatory System
 A common effect of the potent volatile anesthetics has been to decrease BP

in a dose-related fashion with essentially no differences noted between the
volatile anesthetics at equianesthetic concentrations.
 Their primary mechanism to decrease BP is via a potent effect to relax
vascular smooth muscle leading to decreases in regional and systemic vascular
resistance. They have only minimal effects on cardiac output.
 1 MAC sevoflurane and desflurane reduced contractility, assessed as dp/dtmax
 Functional reserve of the heart was not impaired by the volatile anesthetic
 When comparing sevoflurane and desflurane to propofol in cardiac patients
with impaired ventricular function after CABG surgery, the volatile
anesthetics preserved and propofol worsened ventricular responses to acute
increases in preload.
 Isoflurane (and most other potent volatile anesthetics) increases coronary
blood flow beyond that of the myocardial oxygen demand, thereby creating
potential for “steal”
 Steal is the diversion of blood from a myocardial bed with limited or
inadequate perfusion to a bed with more adequate perfusion.
Cardioprotection from Volatile
Anesthetics
 Ischemic preconditioning consists of early and late phase protection.
 The early phase, lasting approximately 2 hours, is mediated by the release of
adenosine, inducing a protective signal through the activation of
mitochondrial potassium channels (KATP) and opioid and bradykinin receptor.
 The late phase, while not as strong as the early phase, provides additional
myocardial protection for 24 to 72 hours. This delayed effect relates to
induction of nitric oxide synthase, superoxide dismutase, and heat-shock
proteins.
 Preconditioning effects of sevoflurane are noted at a minimum of 1 MAC with
a dose of 1.5 MAC needed for full efficacy.
 Sulfonylurea oral hyperglycemic drugs close KATP channels, abolishing
anesthetic preconditioning.
Autonomic Nervous System
 Anesthetic mediated, dose dependent decreases in reflex control of

sympathetic output are most prominent at the 1 MAC or greater of the
volatile anesthetics.
 With increasing steady state concentrations of desflurane, there is a
progressive increase in resting sympathetic nervous system activity and
plasma norepinephrine levels.
Pulmonary System
 All volatile anesthetics decrease tidal volume and increase respiratory rate.
 The respiratory depression can be partially antagonized during surgical
stimulation where respiratory rate and tidal volume have been shown to
increase, resulting in a decrease in the PaCO2.
 FRC is decreased during general anesthesia.
 All of the inhaled anesthetics produce a dose-dependent depression of the
ventilatory response to hypercarbia.
 It is generally 4 to 5 mmHg below the prevailing resting PaCO2 in a
spontaneously breathing patient.
 Inhaled anesthetics, including N2O, also produce a dose-dependent
attenuation of the ventilatory response to hypoxia
 Bronchoconstriction can result:
(1) from direct stimulation of the laryngeal and tracheal areas,
(2) from the administration of adjuvant drugs that cause histamine release
(3) from noxious stimuli activating vagal afferent nerves.
 Volatile anesthetics and N2O reduce ciliary movement and alter the
characteristics of mucus.
 Smokers have impaired mucociliary function, and the combination of a
volatile anesthetic in a smoker who is mechanically ventilated sets up a
scenario for inadequate clearing of secretions, mucus plugging, atelectasis,
and hypoxemia.
 Volatile anesthetics have the potential to attenuate hypoxic pulmonary
vasoconstriction (HPV).
Hepatic Effects
 The mechanism for this severe injury is immunologic, requiring prior exposure to
a volatile anesthetic.
 Halothane, isoflurane, and desflurane all undergo oxidative metabolism by
cytochrome P-450 enzymes to produce trifluoroacetate.
 The trifluoroacetate can bind covalently to hepatocyte proteins. The
trifluoroacetyl-hepatocyte moieties can act as haptens.
 Subsequent exposure to any anesthetic capable of producing trifluoroacetate
may provoke an immune response, leading to severe hepatic necrosis.
 Sevoflurane is metabolized to hexafluoroisopropanol, a compound that does not
have the equivalent antigenic behavior as trifluoroacetate
Neuromuscular System and Malignant
Hyperthermia
 Actions:
(1) they directly relax skeletal muscle through a dose-dependent effect and
(2) they potentiate the action of neuromuscular blocking drugs
 Relaxation of skeletal muscle is most prominent for potent volatile
anesthetics above 1.0 MAC, with an effect enhanced by 40% in patients with
myasthenia gravis.
 While the mechanism of volatile anesthetic potentiation of the neuromuscular
blocking drugs is not entirely clear, it appears to be largely because of a
postsynaptic effect at the nicotinic acetylcholine receptor located at the
neuromuscular junction.
 Specifically, at the receptor level, the volatile anesthetics act synergistically
with the neuromuscular blocking drugs to enhance their action.
Genetic Effects, Obstetric Use and
Effects on Fetal Development
 Volatile anesthetics can be teratogenic in animals but do not cause
teratogenicity in humans.
 N2O decreases the activity of vitamin B12-dependent enzymes, methionine
synthetase (MS) and thymidylate synthetase.
 Uterine smooth muscle tone is diminished by volatile anesthetics in similar
fashion to the effects of volatile anesthetics on vascular smooth muscle.
 There is a dose-dependent decrease in spontaneous myometrial contractility
that is consistent among the volatile anesthetics. Desflurane and sevoflurane
also inhibit the frequency and amplitude of myometrial contractions induced
by oxytocin in a dose-dependent manner.
 In terms of neonatal effects from general anesthesia, Apgar scores and acid–
base balance are not affected by anesthetic technique, such as spinal versus
general.
 More sensitive measures of neurologic and behavioral function, such as the
Scanlon Early Neonatal Neurobehavioral Scale and the Neurologic and
Adaptive Capacities Score (NACS) indicate some transient depression of scores
following general anesthesia that resolves at 24 hours after delivery.
Anesthetic Degradation by Carbon
Dioxide Absorbers
 Compound A
 Sevoflurane undergoes base-catalyzed degradation in carbon dioxide absorbents to
form a vinyl ether called compound A.
 Dessicated barium hydroxide lime produces more compound A than soda lime and
this can be attributed to slightly higher absorbent temperature during CO2
extraction.
 Carbon Monoxide and Heat
 Carbon dioxide (CO2) absorbents degrade sevoflurane, desflurane, and isoflurane to
carbon monoxide (CO) when the normal water content of the absorbent (13% to
15%) is markedly decreased to less than 5%.
Clinical Utility of Volatile Anesthetics
 Induction
 Clinical studies indicate that stage two excitation is avoided with high
concentrations of sevoflurane.
 typical time to loss of consciousness is 60 seconds when delivering 8% sevoflurane
via the face mask
 The gas induction technique is improved by pretreatment with benzodiazepines
worsened with opioid pretreatment because of apnea
 Maintenance
 easily administered via inhalation, they are readily titrated
 high safety ratio in terms of preventing recall, and the depth of anesthesia can be
quickly adjusted in a predictable way
Thank you

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Inhaled Anesthetics

 MAC is the alveolar concentration of an anesthetic at one atmosphere (in

 A common effect of the potent volatile anesthetics has been to decrease BP

 Anesthetic mediated, dose dependent decreases in reflex control of

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