Intracranial dysfunctions: stupor and coma

Coma and stupor are pathologic neural states whose signs arise from either massive cortical or brainstem disease or toxicity. A variety of pathological processes can cause brain disease. Often one has to begin treatment before the diagnosis of the cause of the problem is made. At all stages of treatment, great care must be taken to avoid precipitating an intracranial crisis. The physiological derangements that may aid in the diagnosis include arousability, pupil reactivity, various reflexes, breathing patterns, and cardiovascular function. The treatment needs to be both specific and general; i.e., the condition itself must be treated, if possible, and the intracranial pressure must be lowered if it has been raised by the condition. Treatments for raised intracranial pressure include hyperventilation, diuretics, corticosteroids, avoidance of jugular vein compression, coughing, and any change of the position of the head and neck from normal. When sedating or anesthetizing these patients, one should avoid drugs that increase cerebral blood flow such as ketamine and inhaled anesthetics, using instead drugs that lower cerebral blood flow such as thiopental, lidocaine, and narcotics (with ventilation).     

Cardiopulmonary effects of enflurane and isoflurane in the dog.

The cardiopulmonary effects of 2 new inhalant anesthetics, enflurane and isoflurane, were studied in nonsedated, previously instrumented, awake dogs. Base line values were determined, and anesthesia was induced and maintained with the drug being studied. Enflurane depressed cardiopulmonary function to a greater extent than isoflurane. The depression of cardiopulmonary function from both agents increased with increasing depth of anesthesia. Enflurance produced muslce twitching, but isoflurane did not.     

Precautions when using alpha-2 agonists as anesthetics or anesthetic adjuvants.

Alpha-2 adrenergic agonists have some unique properties that could theoretically make them useful in the perianesthetic period: they reduce the MAC of inhaled anesthetics, and they are reversible. They also have properties that may limit their usefulness, such as marked decreases in cardiac output. Their clinical utility awaits further studies.     

Anesthetic depth: the undefinable.

With many modern anesthetic drugs and combinations, the traditional signs of anesthetic depth as a continuum of increasing depression are often incorrect. The concept of "adequate anesthetic depth" is difficult to define because it depends on the end points chosen to define "adequate." Because both central nervous system excitant and depressant drugs can induce a stage of anesthesia, it is vital that those using these agents be keenly aware of the specific type of anesthetic agent or agents being used, and their effects.