FORANE (isoflurane, USP) is an inhalation anesthetic. The MAC (minimum alveolar concentration) in man is as follows:
|| 100% Oxygen
|| 70% N20
Induction of and recovery from isoflurane anesthesia are rapid. Isoflurane
has a mild pungency, which limits the rate of induction, although excessive
salivation or tracheobronchial secretions do not appear to be stimulated. Pharyngeal
and laryngeal reflexes are readily obtunded. The level of anesthesia may be
changed rapidly with isoflurane. Isoflurane is a profound respiratory depressant.
RESPIRATION MUST BE MONITORED CLOSELY AND SUPPORTED WHEN NECESSARY. As
anesthetic dose is increased, tidal volume decreases and respiratory rate is
unchanged. This depression is partially reversed by surgical stimulation, even
at deeper levels of anesthesia. Isoflurane evokes a sigh response reminiscent
of that seen with diethyl ether and enflurane, although the frequency is less
than with enflurane.
Blood pressure decreases with induction of anesthesia but returns toward normal
with surgical stimulation. Progressive increases in depth of anesthesia produce
corresponding decreases in blood pressure. Nitrous oxide diminishes the inspiratory
concentration of isoflurane required to reach a desired level of anesthesia
and may reduce the arterial hypotension seen with isoflurane alone. Heart rhythm
is remarkably stable. With controlled ventilation and normal PaCO2,
cardiac output is maintained despite increasing depth of anesthesia, primarily
through an increase in heart rate, which compensates for a reduction in stroke
volume. The hypercapnia, which attends spontaneous ventilation during isoflurane
anesthesia further increases heart rate and raises cardiac output above awake
levels. Isoflurane does not sensitize the myocardium to exogenously administered
epinephrine in the dog. Limited data indicate that subcutaneous injection of
0.25 mg of epinephrine (50 mL of 1:200,000 solution) does not produce an increase
in ventricular arrhythmias in patients anesthetized with isoflurane.
Muscle relaxation is often adequate for intra-abdominal operations at normal
levels of anesthesia. Complete muscle paralysis can be attained with small doses
of muscle relaxants. ALL COMMONLY USED MUSCLE RELAXANTS ARE MARKEDLY POTENTIATED
WITH ISOFLURANE, THE EFFECT BEING MOST PROFOUND WITH THE NONDEPOLARIZING TYPE.
Neostigmine reverses the effect of nondepolarizing muscle relaxants in the presence
of isoflurane. All commonly used muscle relaxants are compatible with isoflurane.
Isoflurane can produce coronary vasodilation at the arteriolar level in selected
animal models1,2; the drug is probably also a coronary dilator in
humans. Isoflurane, like some other coronary arteriolar dilators, has been shown
to divert blood from collateral dependent myocardium to normally perfused areas
in an animal model (“coronary steal”)3. Clinical studies to date
evaluating myocardial ischemia, infarction and death as outcome parameters have
not established that the coronary arteriolar dilation property of isoflurane
is associated with coronary steal or myocardial ischemia in patients with coronary artery disease 4,5,6,7.
Isoflurane undergoes minimal biotransformation in man. In the postanesthesia
period, only 0.17% of the isoflurane taken up can be recovered as urinary metabolites.
1. J.C. Sill, et al, Anesthesiology 66:273-279, 1987
2. RF. Hickey, et al, Anesthesiology 68:21-30, 1988
3. C.W. Buffington, et al, Anesthesiology 66:280-292, 1987
4. S. Reiz, et al, Anesthesiology 59:91-97, 1983
5. S. Slogoff and A.S. Keats, Anesthesiology 70:179-188, 1989
6. K.J. Tuman, et al, Anesthesiology 70:189-198, 1989
7. D.T. Mangano, Editorial Views, Anesthesiology 70:175-178, 1989