or a short period of time (see dosage & administration ) as an aid in the prevention of elevation of arterial co2 tension during the administration of oxygen. it should not be used in conjunction with mechanical ventilation.

ese combined sources (see precautions , pediatric use). in postanesthetic use doxapram is neither an antagonist to muscle relaxant drugs nor a specific narcotic antagonist. more specific tests (eg, peripheral nerve stimulation, airway pressures, head lift, pulse oximetry, and end-tidal carbon dioxide) to assess adequacy of ventilation are recommended before administering doxapram. doxapram should be administered with great care and only under careful supervision to patients with hypermetabolic states such as hyperthyroidism or pheochromocytoma. since narcosis may recur after stimulation with doxapram, care should be taken to maintain close observation until the patient has been fully alert for ½ to 1 hour. in patients who have received general anesthesia utilizing a volatile agent known to sensitize the myocardium to catecholamines, administration of doxapram should be delayed until the volatile agent has been excreted in order to lessen the potential for arrhythmias, including ventricular tachycardia and ventricular fibrillation (see precautions, drug interactions). in drug-induced cns and respiratory depression doxapram alone may not stimulate adequate spontaneous breathing or provide sufficient arousal in patients who are severely depressed either due to respiratory failure or to cns depressant drugs, but may be used as an adjunct to established supportive measures and resuscitative techniques. in chronic obstructive pulmonary disease because of the associated increased work of breathing, do not increase the rate of infusion of doxapram in severely ill patients in an attempt to lower pco2.

ge by infusion is 4 mg/kg, or approximately 300 mg for the average adult. in the management of drug-induced cns depression (see table ii. dosage for drug-induced cns depression.) table ii. dosage for drug-induced cns depression. * mild depression class 0: asleep, but can be aroused and can answer questions. class 1: comatose, will withdraw from painful stimuli, reflexes intact. † moderate depression class 2: comatose, will not withdraw from painful stimuli, reflexes intact. class 3: comatose, reflexes absent, no depression of circulation or respiration. method one using single and/or repeat single i.v. injections give priming dose of 2 mg/kg body weight and repeat in 5 minutes. the priming dose for moderate depression is 2 mg/kg and the priming dose for mild depression is 1 mg/kg. repeat same dose q 1 to 2h until patient wakens. watch for relapse into unconsciousness or development of respiratory depression, since dopram does not affect the metabolism of cns-depressant drugs. if relapse occurs, resume injections q 1 to 2h until arousal is sustained, or total maximum daily dose (3 grams) is given. after maximum dose has been given (3 grams), allow patient to sleep until 24 hours have elapsed from first injection of dopram, using assisted or automatic respiration if necessary. repeat procedure the following day until patient breathes spontaneously and sustains desired level of consciousness, or until maximum dosage (3 grams) is given. repetitive doses should be administered only to patients who have shown response to the initial dose. failure to respond appropriately indicates the need for neurologic evaluation for a possible central nervous system source of sustained coma. method two by intermittent i.v. infusion give priming dose as in method one. if patient wakens, watch for relapse; if no response, continue general supportive treatment for 1 to 2 hours and repeat priming dose of dopram. if some respiratory stimulation occurs, prepare i.v. infusion by adding 250 mg of dopram (12.5 ml) to 250 ml of saline or dextrose solution. deliver at rate of 1 to 3 mg/min (60 to 180 ml/hr) according to size of patient and depth of coma. discontinue dopram if patient begins to waken or at end of 2 hours. continue supportive treatment for ½ to 2 hours and repeat step b. do not exceed 3 grams/day. chronic obstructive pulmonary disease associated with acute hypercapnia one vial of doxapram (400 mg) should be mixed with 180 ml of dextrose 5% or 10% or normal saline solution (concentration of 2 mg/ml). the infusion should be started at 1 to 2 mg/minute (½ to 1 ml/minute); if indicated, increase to a maximum of 3 mg/minute. arterial blood gases should be determined prior to the onset of doxapram’s administration and at least every half hour during the two hours of infusion to insure against the insidious development of co2-retention and acidosis. alteration of oxygen concentration or flow rate may necessitate adjustment in the rate of doxapram infusion. predictable blood gas patterns are more readily established with a continuous infusion of doxapram. if the blood gases show evidence of deterioration, the infusion of doxapram should be discontinued. additional infusions beyond the single maximum two hour administration period are not recommended. parenteral drug products should be inspected visually for particulate matter and discoloration prior to administration, whenever solution and container permit. diluent compatibility doxapram hydrochloride is compatible with 5% and 10% dextrose in water or normal saline. incompatibility admixture of doxapram with alkaline solutions such as 2.5% thiopental sodium, sodium bicarbonate, furosemide, or aminophylline will result in precipitation or gas formation. doxapram is also not compatible with ascorbic acid, cefoperazone sodium, cefotaxime sodium, cefotetan sodium, cefuroxime sodium, folic acid, dexamethasone disodium phosphate, diazepam, hydrocortisone sodium phosphate, methylprednisolone sodium, or hydrocortisone sodium succinate. admixture of doxapram and ticarcillin disodium results in an 18% loss of doxapram in 3 hours. when doxapram is mixed with minocycline hydrochloride, there is a loss of 8% of doxapram in 3 hours and a 13% loss of doxapram in 6 hours. dosage 1 dosage 2

iovascular diseases. 4. gastrointestinal nausea, vomiting, diarrhea, desire to defecate. 5. genitourinary stimulation of urinary bladder with spontaneous voiding; urinary retention. elevation of bun and albuminuria. 6. hemic and lymphatic hemolysis with rapid infusion. a decrease in hemoglobin, hematocrit, or red blood cell count has been observed in postoperative patients. in the presence of pre-existing leukopenia, a further decrease in wbc has been observed following anesthesia and treatment with doxapram hydrochloride.

ng doxapram administration, an increased release of catecholamines has been noted. although opiate-induced respiratory depression is antagonized by doxapram, the analgesic effect is not affected. pharmacokinetics doxapram is metabolized via ring hydroxylation to ketodoxapram, an active metabolite readily detected in the plasma.