Inhalational Agents
NITROUS OXIDE
From U of Miami School of Medicine
Description
Nitrous oxide is the only inhalational anesthetic agent used that is a not a vapor, but a true gas by definition. For anesthetic purposes, it is supplied in blue cylinders, compressed to its liquid phase.
Physical Constants
Molecular Weight........................................................44
Boiling Point..................................-88.0 deg. C @ 760 mm Hg
Vapor Pressure.................................39,000 mm Hg @ 20 deg. C
Partition Coefficients
Blood:Gas......................................................................0.47
Brain:Blood....................................................................1.1
Oil:Gas..........................................................................1.4
Potency
MAC in 100% oxygen..............................................104% atm
Pharmacokinetics
Mechanism of Action: unknown
Dosage: titrate to effect for analgesia or supplementation of general anesthesia
Onset of Action: dose dependant
Peak Effect: dose dependant
Duration of Action: dose dependant
Elimination: pulmonary, renal, GI(0.04% is reduced to nitrogen in GI tract by anaerobes)
Metabolites: free radicals may be liberated when reduced
Pharmacology
Respiratory / Airway
- Direct depression of medullary ventilatory center with concentrations greater than 50%
- Increases respiratory rate
- Decreases functional residual capacity
- Can increase pulmonary vascular resistance, especially with preexisting pulmonary hypertension
- Relaxes bronchial smooth muscle (direct effect, and decreased afferent tone)
Cardiovascular
- Direct myocardial depression at concentrations >40%
- Can lead to hypotension and decreased cardiac output when administered alone
- When combined with a volatile agent, there is usually less circulatory depression than if either agent is used alone
- Attenuates baroreceptor and vasomotor reflexes
- Enhances isoflurane-induced coronary artery vasodilation, and can lead to coronary artery steal
CNS
- Causes cerebral vasodilation and increased cerebral blood flow
- Increases intracranial pressure due to increased cerebral blood volume
Musculoskeletal / Other
- Does not cause skeletal muscle relaxation
- Weak triggering agent for malignant hyperthermia
- Chronic exposure may interfere with DNA synthesis as a result of reduced methionine synthetase activity
Principal Adverse Effects
Respiratory
Respiratory depression, apnea, diffusion hypoxia
Cardiovascular
Hypotension, arrhythmias
CNS
Dizzyness, euphoria, increased CBF/ICP, neuropathy with chronic exposure
GI
Nausea, vomiting, ileus
Other
Bone marrow depression with chronic exposure, malignant hyperthermia
Other Considerations
- Diffuses into air-containing spaces 34 times faster than nitrogen can diffuse out, and can lead to potentially dangerous airspace expansion (pneumothorax, bowel obstruction, etc)
- May cause diffusion hypoxia during emergence if supplemental oxygen is not administered
- Crosses the placenta, and can cause fetal depression
| Last Modified -
Fri, Mar 31, 2006 |
Used by Erowid without permission of author |
