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Background Opioid addiction therapy includes successful detoxification, rehabilitation, and sometimes methadone maintenance. However, the patient may have physical, mental, and emotional pain while trying to achieve abstinence. A new detoxification technique that incorporates general anesthesia uses a high-dose opioid antagonist to compress detoxification to within 6 h while avoiding the withdrawal. Methods After Institutional Review Board approval and detailed informed consent, 20 patients, American Society of Anesthesiologists status I-II, addicted to various opioids underwent anesthesia-assisted rapid opioid detoxification. After baseline hemodynamics and withdrawal scores were obtained, anesthesia was induced. After testing with 0.4 mg intravenous naloxone, 4 mg nalmefene, was infused over 2 to 3 h. After emergence, severity of withdrawal was scored before and after administration of 0.4 mg intravenous naloxone. After 24 h, patients began outpatient follow-up treatment while taking oral naltrexone. Results All 20 patients were successfully detoxified with no adverse anesthetic events. After the first post-treatment test dose of 0.4 mg naloxone, 13 of 20 patients had no signs of withdrawal and hemodynamic changes were minimal. Withdrawal scores were always very low and similar before and after detoxification. Three of 17 patients (18%) available for follow-up have remained abstinent from opioids since treatment (< or = 18 months). Four other patients are clean after brief relapses. Conclusions Anesthesia-assisted opioid detoxification is an alternative to conventional detoxification.

Fine-screen filters were studied in a simulated clinical situation wherein ten units of outdated concentrated erythrocytes were rapidly transfused per filter to determine flow rates and effectivenesses of debris removal. Preliminary studies to evaluate flow rates with outdated whole blood indicated

The cardiovascular effects of 3 and G per cent alveolar concentrations of diethyl ether in nine healthy young volunteers during the first and fifth hours of anesthesia were studied. Pac* was maintained at 35–39 torr and esophagcal temperature at 36 ± 0.5 C. Cardiac output was unchanged or increased at 3 and 6 per cent ether during the first hour; heart rate increased while stroke volume fell. During the fifth hour of anesthesia, cardiac output increased at both 3 and 6 per cent ether, heart rate increased further, and stroke volume rose to the awake value. Total peripheral resistance was initially unchanged but fell with duration of anesthesia. The ratio of cardiac output to oxygen consumption was unchanged at one hour and increased at five hours. Base excess fell slightly initially and slightly more by five hours.

Acute isovolemic anemia in dogs reduced orterial oxygen content (Cao2) without changing Pao- and AP. Halothane requirement (MAC) remained normal despite reducton of hematocrit to 10 per cent (Cao2 4.3 vol per cent). Tissue oxygenation was not compromised, as evidenced by the absence of metabolic aci

The clinical signs of anesthetic depth (heart rate, mean arterial pressure, pupil diameter, pupil reactivity to light, tearing, and eye movement) were correlated with anesthetic dose in healthy young volunteers. During halothane, halothane—nitrous oxide, Forane, or Forane–nitrous oxide anesthesia at normal PaCO2 (controlled ventilation), only hypotension in the first hour of anesthesia correlated with anesthetic dose. After five hours of halothane or halothane–nitrous oxide, blood pressure remained constant as anesthetic concentration increased. During cyclopropane, diethyl ether, and fluroxene anesthesia, only pupillary dilatation and reduced pupil reactivity to light correlated with anesthetic dose. When nitrous oxide was added to halothane, ether, or fluroxene, mean arterial pressure rose and pupils dilated. During halothane–oxygen anesthesia with spontaneous ventilation, the rise in PaCO2 allowed less hypotension and increased heart rate. Tidal volume decreased and respiratory rate increased as anesthesia deepened. During Forane–oxygen anesthesia with spontaneous respiration, mean arterial pressure, tidal volume, and minute ventilation decreased as anesthesia deepened. In healthy surgical patients anesthetized with halothane or Forane only, incision of the skin modified the clinical signs significantly. While surgery continued, this change in clinical signs persisted during Forane anesthesia, but returned to control during halothane anesthesia.

The effects of 0.75 to 2 per cent end-tidal halothane on cardiovascular and respiratory responses to hypoxia were quantitated. Moderate hypoxia (Pa02. 45 torr) caused stimulation of ventilation and cardiac output at all levels of halothane anesthesia. Although severe hypoxia (Pa02 30 torr) further stimulated ventilation and cardiac output at 0.75 to 1.25 per cent halothane, increasing the halothane concentration to 1.0–1.5 per cent rapidly converted hyperventilation and elevated cardiac output to respiratory or cardiac arrest. Oxygen transport did not meet oxygen consumption requirements; hence, severe metabolic acidosis developed during severe hypoxia. Within narrow limits, the dose of halothane is most important in determining the physiologic response to severe hypoxia.

The cardiac and peripheral vascular effects of 15–20 per cent, 25–30 per cent, and 35–40 per cent alveolar concentrations of cyclopropane were determined in each of 11 nonmedicated human volunteers at normal Pacos and body temperature during controlled ventilation. Compared with awake values during controlled ventilation, cyclopropane caused little change in cardiac output (Q), heart rate (HR) or stroke volume (SV), while mean right atria! pressure (MRAP) increased markedly. Large increases in mean arterial pressure (AP), total peripheral resistance and forearm vascular resistance suggested arterial constriction. A profound decrease in venous compliance contributed to the elevated MRAP. Cutaneous blood flow increased 560 per cent. Rapid reduction of cyclopropane led to immediate increase in Q, SV, and at a lower MRAP within two minutes. After eight additional minutes at the lower cyclopropane concentration, Q, SV, and returned to the previous values (i.e., before reduction of cyclopropane), but at even lower MRAP.

Using the anesthetic requirement for halothane (MAC) to follow central nervous system depression in dogs, acute hypoxia reduced MAC starting at Pao2 38 mm Hg. The decrease in MAC related to both arterial oxygen content (Cao2) and arterial pH (group 1). Therefore, acute hypoxia to Pao2 30 mm Hg was induced in two groups of dogs during hypocapnia (group 2) and normocapnia (group 3). MAC decreased far more rapidly during normocapnic hypoxia than during hypocapnic hypoxia. Respiratory alkalosis maintained pH at 7.39 in group 2, and Cao2 remained at 10 vol per cent In group 3, arterial pH fell progressively, reducing Cao2 to 7.4 vol per cent at a constant Pao2 of 30 mm Hg. Significant regression lines correlated arterial and mixed venous oxygen contents, arterial oxygen transport, and arterial pH with the decreases in MAC in groups 2 and 3. Serial CSF pH determinations in both groups correlated poorly with the reductions in MAC.

No standard outcome measures exist to evaluate the effect of interventions intended to improve the quality of anesthesia care. The authors established a clinically practical definition of outcome, and used it to assess the effect of feedback of information about complications and the effect of pulse oximetry on the rate and severity of important anesthesia-related problems encountered in the operating room (OR) and recovery room (RR). On admission to the RR, the patient's anesthetist documented Recovery-Room-Impact Events (RRIE), defined as an "unanticipated, undesirable, possibly anesthesia-related effect that required intervention, was pertinent to recovery-room care, and did or could cause at least moderate morbidity." Following a control period with no feedback of data, intense feedback of grouped (anonymous) RRIE rates was provided. Later, pulse oximeters were introduced to all anesthetizing locations. Among 12,088 patients (71% of all RR admissions), 18% had at least one RRIE in the OR or RR. The most common RRIEs were hypotension (4.4%), arrhythmia (3.9%), hypertension (1.5%), intubation difficulties (0.8%), hypoventilation (0.8%), and hypovolemia (0.6%). Feedback of information produced no demonstrable change in the rate of RRIEs. Although significantly fewer patients experienced RRIEs (15.6% vs. 12.4%, P less than 0.0001), hypotensive RRIEs (5.2% vs. 3.8%, P = 0.0003), and hypovolemic RRIEs (0.88% vs. 0.42%, P = 0.0017) following the introduction of pulse oximetry in the OR, confounding factors prevent establishment of a cause-and-effect relationship. Quality assurance may require more direct intervention and individual feedback to be effective. Still, the RRIE measure requires minimal effort at low cost and encourages improved transmission of information at the time of admission to recovery-room care.

Succinylcholine-induced muscle fasciculations may be prevented by pretreatment with small doses of nondepolarizing muscle relaxants. Such pretreatment, however, may increase the difficulty of tracheal intubation by antagonizing succinylcholine (SCh) depolarization. To determine which drugs and doses