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Background: Although approximately 2,000 medical practice guidelines have been proposed, few have been successfully implemented and sustained. We hypothesized that we could develop and institute practice guidelines to promote more appropriate use of costly anesthetics, to generate and sustain widespread compliance from a large physician group, and to decrease costs without adversely affecting clinical outcomes., Methods: A prospective before and after comparison study was performed at a tertiary care medical center. Clinical outcomes data and times indicative of perioperative patient flow were collected on the first of two sets of patients 1 month before discussion of practice guidelines. Practice guidelines were developed by the physicians and their associated care team for the intraoperative use of anesthetic drugs. A drug distribution process was developed to aid compliance. Clinical outcomes data and times indicative of perioperative patient flow were collected on the second set of patients 1 month after institution of practice guidelines. Hospital drug costs and adherence to guidelines were noted throughout the study period and for each of the following 9 months by querying the database of an automated anesthesia record keeper., Results: A total of 1,744 patients were studied. Drug costs decreased from 56 dollars per case to 32 dollars per case as a result of adherence to practice guidelines. Perioperative patient flow was minimally affected. Time (mean +/- SD) from end of surgery to arrival in the post-anesthesia care unit (PACU) increased from 11 +/- 7 min before the authors instituted practice guidelines to 14 +/- 8 min after practice guidelines (P < 0.0001). Admission of inpatients to the PACU receiving monitored anesthesia care increased from 6.5 to 12.9% (P < 0.02). Perioperative patient flow and clinical outcomes were not otherwise adversely affected. Compliance and cost savings have been sustained., Conclusions: This study is an example of a successful physician-directed program to promote more appropriate utilization of health care resources. Cost savings were obtained without any substantial changes in clinical outcomes. Institution of similar practice guidelines should result in pharmaceutical savings in the range of 50% at tertiary care centers around the country, with a slightly smaller degree of savings expected at institutions with more ambulatory surgery.

Cardiac arrest causes a rapid loss of cerebral adenosine triphosphate [corrected] (ATP) and a decrease in cerebral intracellular pH (pHi). Depending on the efficacy of cardiopulmonary resuscitation (CPR), cerebral blood flow levels (CBF) ranging from near zero to near normal have been reported experimentally. Using 31P magnetic resonance spectroscopy, the authors tested whether experimental CPR with normal levels of cerebral blood flow can rapidly restore cerebral ATP and pHi despite the progressive systemic acidemia associated with CPR. After 6 min of ventricular fibrillation in six dogs anesthetized with fentanyl and pentobarbital, ATP was reduced to undetectable concentrations and pHi decreased from 7.11 +/- 0.02 to 6.28 +/- 0.09 (+/- SE) as measured by 31P magnetic resonance spectroscopy. Application of cyclic chest compression by an inflatable vest placed around the thorax and infusion of epinephrine (40 micrograms/kg bolus plus 8 micrograms/kg/min, intravenously) maintained cerebral perfusion pressure greater than 70 mmHg for 50 min with the dog remaining in the magnet. Prearrest cerebral blood flows were generated. Cerebral pHi recovered to 7.03 +/- 0.03 by 35 min of CPR, whereas arterial pH decreased from 7.41 +/- 0.4 to 7.08 +/- 0.04 and cerebral venous pH decreased from 7.29 +/- 0.03 to 7.01 +/- 0.04. Cerebral ATP levels recovered to 86 +/- 7% (+/- SE) of prearrest concentration by 6 min of CPR. There was no further recovery of ATP, which remained significantly less than control. Therefore, in contrast to hyperemic reperfusion with spontaneous circulation and full ATP recovery, experimental CPR may not be able to restore ATP completely after 6 min of global ischemia despite restoration of CBF and brain pHi to prearrest levels.

Cerebral blood flow (CBF) (radiolabelled microspheres) and oxygen consumption (CMRO2) were studied in nine dogs during 30 min of either neck vein compression or application of positive end-expiratory pressure (PEEP) ventilation. With the animal in the prone position, elevation of the head from horizontal to 30 cm above the heart markedly decreased cisterna magna (PCSF) and dorsal sagittal sinus pressure (PCV). With the head elevated, compression of neck veins using neck tourniquet (pressure 40 mmHg) increased PCSF and PCV from 3.6 +/- 2.2 to 6.8 +/- 4.8 and -2.5 +/- 2.7 to 2.3 +/- 2.3 mmHg (mean +/- SE, P less than 0.05), respectively, while total or regional CBF and CMRO2 remained unchanged. Application of PEEP (15 cm H2O) increased right atrial pressure (-4.7 +/- 1.7 to -0.1 +/- 3.4 mmHg, P less than 0.05), but did not affect PCSF or PCV (3.4 +/- 3.3 to 3.3 +/- 3.7 and -3.5 +/- 2.6 to -4.1 +/- 2.4 mmHg, respectively, P greater than 0.05). Total or regional CBF and CMRO2 were also unaffected. These data demonstrate that, although neither maneuver affects CBF or CMRO2, neck vein compression elevates PCV above atmospheric pressure, but PEEP does not. In patients at risk for cerebral venous embolism, intermittent neck vein compression should be used as a prophylactic measure to prevent air embolism.

Utilizing 31phosphorus nuclear magnetic resonance (NMR) spectroscopy, the authors tested the two hypotheses that the negative inotropic action of halothane is the result of: 1) myocardial intracellular acidosis, and 2) a decrease in myocardial high-energy phosphates. In isolated, paced, Langendorff-perfused rabbit hearts, halothane (1.5 vol %) dissolved in the coronary perfusate produced a 48 +/- 2% decrease (P less than 0.01) in left ventricular developed pressure. In contrast, halothane administration had no significant effect on myocardial intracellular pH (7.18 +/- 0.04 at control vs 7.21 +/- 0.02 during halothane). Halothane exposure decreased (P less than 0.01) the forward rate constant of the creatine kinase reaction by 32 +/- 6%, as measured using saturation transfer NMR, suggesting a decline in the rate of high-energy phosphate metabolism. This was further indicated by a concomitant decrease (P less than 0.05) in myocardial oxygen consumption (20 +/- 5%). During the halothane-induced reduction in left ventricular developed pressure, only small decreases in the myocardial steady state concentrations of phosphocreatine (7 +/- 1%; P less than 0.01) and beta ATP (12 +/- 4%; P less than 0.05), and an increase in Pi (18 +/- 6%; P less than 0.05) were observed. However, similar changes in steady-state high-energy phosphate metabolites were also measured in time-control hearts not exposed to halothane. These results indicate that the negative inotropic action of halothane is not mediated by myocardial intracellular acidosis. Moreover, these findings do not support the concept that the negative inotropic action of halothane is the result of a reduction in myocardial high-energy phosphates.

Intracranial pressure measurements were made during nitroglycerin-induced hypotension in the cat anesthetized with halothane. A total of 48 individual observations were made in eight animals. The administration of sufficient nitroglycerin to decrease mean arterial pressure from a control value of 87 +/- 7 torr by 12 +/- 4 torr resulted in an increase in mean intracranial pressure from a control value of 7 +/- 2 torr to 12 +/- 2 torr. Larger decreases in mean blood pressure were associated with larger increases in intracranial pressure. The increase in intracranial pressure was similar to that previously reported for nitroprusside, and greater as well as more reproducible than that reported for trimethaphan. Thus, nitroglycerin may produce significant increases in intracranial pressure, and this may be a limiting factor in its clinical use.

Intravenous nitroglycerin (NTG) and sodium nitroprusside (SNP) were compared as hypotensive agents in anesthetized children and adolescents. The drugs were studied in a prospective, randomized, double-blind fashion in 14 patients anesthetized with nitrous oxide: oxygen, morphine, and thiopental. NTG in doses as high as 40 micrograms X kg-1 X min-1 was ineffective at decreasing mean arterial pressure (MAP) below 55 mmHg or causing a decrease in MAP greater than one-third of baseline values. SNP was uniformly successful at inducing hypotension in all patients, including those patients in whom NTG failed. The dose of SNP required to induce hypotension was 6-8 micrograms X kg-1 X min-1. Both NTG and SNP decreased systemic vascular resistance, although SNP did so to a much greater degree than NTG (64% vs. 29%; P less than 0.01). Only SNP increased cardiac index significantly (2.27 +/- 0.35 to 4.44 +/- 1.36; P less than 0.003). Both drugs reflexly increased heart rate, necessitating the use of intravenous propranolol (range from 1 to 3 mg) in all patients. Both drugs produced small decreases in arterial oxygen tension and increases in the average alveolar-arterial oxygen tension gradient (SNP, 44 +/- 13 vs. NTG, 41 +/- 6). SNP use was associated with a slight metabolic acidosis (pH = 7.38 +/- 0.01; base excess [BE] = -6 +/- 1). Neither drug produced any other untoward reaction. SNP appears to be the agent of choice for the reliable and sustained induction of deliberate hypotension in children and adolescents.

Using the radiolabeled microsphere technique, the authors studied hemodynamic variables and regional blood flow to multiple peripheral organs during conventional positive-pressure ventilation (CV) and high-frequency ventilation (HFV) at low and high mean airway pressure (Paw). Twenty supine anesthetized, paralyzed dogs were ventilated using CV (14-16 breaths/min) and HFV (rate = 10 Hz) in random order. In the first group (low Paw, n = 10), Paw was maintained at 3 cmH2O during CV and HFV. In the second group (high Paw, n = 10), Paw was increased to 13 cmH2O during CV and HFV. Pulmonary capillary wedge pressure and right atrial pressure remained constant during low and high Paw trials. No differences in heart rate, systemic arterial pressure, intracranial pressure, or cardiac output were noted during CV and HFV within the low and high Paw groups. In addition, blood flow to multiple peripheral organs during CV and HFV remained constant within each Paw group, except for a small decrease in cerebellar blood flow during HFV at high Paw trials showed a significant decrease in hepatic arterial and outer kidney cortical flow at high Paw. Total cerebral blood flow was decreased at high Paw, as were regional flows to diencephalon, midbrain, pons, medulla, and cerebellum. However, these differences were not attributable to differences in cerebral perfusion pressure or intracranial pressure, and cerebral oxygen delivery was not different between high Paw and low Paw groups. It is concluded that under conditions of similar Paw in anesthetized dogs, HFV does not significantly alter hemodynamic patterns or regional circulation relative to CV.