A departmental policy addressing chemical substance abuse.

Substance abuse is a major socioeconomic problem. However, the ready availability of potent narcotic and sedative drugs probably constitutes a unique risk for anesthesiologists. Until recently, few anesthesia departments were prepared to recognize or safely manage afflicted colleagues. Because we felt it important to educate our staff and residents and to have a response mechanism established prior to the advent of a substance abuse problem, a departmental committee was formed to develop a Substance Abuse Policy. The policy has served to increase our general awareness and to direct our actions effectively when dealing with physician impairment. It is presented here in the belief that other departments might find it useful in tailoring their approach to this problem.

Peripheral vascular response to potassium administration during cardiopulmonary bypass.

Potassium (K+) is often administered to patients during cardiopulmonary bypass (CPB). The effects of rapid K+ administration during CPB were studied in 30 adult patients. Each patient received one bolus dose (2, 4, 8, 12, or 16 mEq) of potassium chloride (KCl) (2 mEq/ml) during CPB. Serum K+ was significantly increased from baseline values at KCl doses of 8 mEq and larger (p less than 0.05). All increases in serum K+ returned to clinically acceptable levels within 5 minutes after the bolus. Mean arterial pressure (MAP) (torr) and total peripheral resistance (TPR) (dynes sec cm-5) changes were biphasic; after an initial transient decrease, maximal with the 16 mEq K+ bolus (MAP -21 +/- 6, TPR - 315 +/- 135), these parameters increased (8 mEq K+ bolus, MAP + 15 +/- 16, TPR + 301 +/- 90; 12 mEq K+ bolus, MAP + 43 +/- 9, TPR + 998 +/- 250; 16 mEq bolus, MAP + 51 +/- 9, TPR + 1,216 +/- 120) with a peak at 3 minutes after the bolus. Hypertension, in nine of 18 patients receiving a KCl bolus of 8 mEq or larger, was of such magnitude (range 132 to 196 torr) as to require rapid therapeutic intervention to lower blood pressure. When KCl supplementation is required on CPB and slow infusion rates seem unreasonable, bolus doses of less than 8 mEq may be administered without vascular effect.

Physostigmine-atropine solution fails to reverse diazepam sedation.

Patients undergoing dental extraction under intravenous diazepam sedation were studied to determine whether physostigmine, a cholinesterase inhibitor, reverses diazepam-induced sedation. A modified Bender-Gestalt Dot Test was used to measure psychomotor function. Patient self-assessment of recovery and a surgeon's independent assessment of recovery were scored on a 0 to 10 measured scale before and after administration of either a physostigmine-atropine mixture (nine patients) or saline (12 patients). The physostigmine-atropine mixture did not significantly speed recovery or improve psychomotor function when compared with normal saline. The results indicate that, in contradiction to previous case report, the analeptic effect of physostigmine may be specific for anticholinergic drugs.

Sodium bicarbonate and systemic hemodynamics in volunteers anesthetized with halothane.

The cardiovascular effects of acute metabolic alkalosis (NaHCO3) in normal male volunteers anesthetized with halothane were measured. Pure metabolic alkalosis was studied by maintaning the end-tidal carbon dioxide tension at 40 torr. In each subject, cardiac index increased and total peripheral resistance decreased after each dose of NaHCO3. The increased cardiac index was associated with increased central blood volume, left ventricular minute work index, stroke index, and heart rate. Systolic time intervals showed increased myocardial performance. NaHCO3 administered to volunteers whose hearts were depressed by halothane appeared to cause peripheral vasodilation, volume expansion, and myocardial stimulation. The authors conclude that NaHCO3 administered during halothane anesthesia decreases total peripheral resistance and may lead to severe hypotension.