Measuring contributions to the clinical mission of medical schools and teaching hospitals.

This is the final report of a panel convened as part of the Association of American Medical College's (AAMC's) Mission-based Management Program to examine the use of metrics (i.e., measures) in assessing faculty and departmental contributions to the clinical mission. The authors begin by focusing on methods employed to estimate clinical effort and calculate a "clinical full-time equivalent," a prerequisite to comparing productivity among faculty members and departments. They then identify commonly used metrics, including relative-value units, total patient-care gross charges, total net patient fee-for-service revenue, total volume per CPT (current procedural terminologies) code by service category and number of patients per physician, discussing their advantages and disadvantages. These measures reflect the "twin pillars" of measurement criteria, those based on financial or revenue information, and those based on measured activity. In addition, the authors urge that the assessment of quality of care become more highly developed and integrated into an institution's measurement criteria. The authors acknowledge the various ways users of clinical metrics can develop standards against which to benchmark performance. They identify organizations that are sources of information about external national standards, acknowledge various factors that confound the interpretation of productivity data, and urge schools to identify and measure secondary service indicators to assist with interpretation and provide a fuller picture of performance. Finally, they discuss other, non-patient-care, activities that contribute to the clinical mission, information about which should be incorporated into the overall assessment. In summary, the authors encourage the use of clinical productivity metrics as an integral part of a comprehensive evaluation process based upon clearly articulated and agreed-upon goals and objectives. When carefully designed, these measurement systems can provide critical information that will enable institutional leaders to recognize and reward faculty and departmental performance in fulfillment of the clinical mission.

Anesthesiologist direction and patient outcomes.

BACKGROUND: Anesthesia services for surgical procedures may or may not be personally performed or medically directed by anesthesiologists. This study compares the outcomes of surgical patients whose anesthesia care was personally performed or medically directed by an anesthesiologist with the outcomes of patients whose anesthesia care was not personally performed or medically directed by an anesthesiologist. METHODS: Cases were defined as being either "directed" or "undirected," depending on the type of involvement of the anesthesiologist, as determined by Health Care Financing Administration billing records. Outcome rates were adjusted to account for severity of disease and other provider characteristics using logistic regression models that included 64 patient and 42 procedure covariates, plus an additional 11 hospital characteristics often associated with quality of care. Medicare claims records were analyzed for all elderly patients in Pennsylvania who underwent general surgical or orthopedic procedures between 1991-1994. The study involved 194,430 directed and 23,010 undirected patients among 245 hospitals. Outcomes studied included death rate within 30 days of admission, in-hospital complication rate, and the failure-to-rescue rate (defined as the rate of death after complications). RESULTS: Adjusted odds ratios for death and failure-to-rescue were greater when care was not directed by anesthesiologists (odds ratio for death = 1.08, P < 0.04; odds ratio for failure-to-rescue = 1.10, P < 0.01), whereas complications were not increased (odds ratio for complication = 1.00, P < 0.79). This corresponds to 2.5 excess deaths/1,000 patients and 6.9 excess failures-to-rescue (deaths) per 1,000 patients with complications. CONCLUSIONS: Both 30-day mortality rate and mortality rate after complications (failure-to-rescue) were lower when anesthesiologists directed anesthesia care. These results suggest that surgical outcomes in Medicare patients are associated with anesthesiologist direction, and may provide insight regarding potential approaches for improving surgical outcomes. (Key words: Anesthesiologists; anesthesia care team; quality of care; mortality; failure-to-rescue; complication; Medicare; general surgery; orthopedics.)

Functional evidence for inward-rectifier potassium channels in rat cremaster muscle arterioles.

Moderate increases in extracellular K(+) produce vasodilation in fourth order cremasteric arterioles in the anesthetized rat. We studied the contribution of different subtypes of K(+) channels to this response. Cremaster muscle arteriolar diameters were observed during superfusion with buffer containing 5-30 mM K(+) in the absence (control) and presence of barium (Ba(2+), 50 microM), glibenclamide (GLIB, 1 microM), or iberiotoxin (IBTX, 100 nM) to block inward-rectifier, ATP-sensitive, or Ca(2+)-activated K(+) channels, respectively. Under control conditions, vessels dilated in response to 10-25 mM K(+) and constricted at higher concentrations. At 5 mM K(+), vessel diameters were significantly decreased by GLIB and Ba(2+), but not IBTX, suggesting that basal diameter was regulated by inward-rectifier and ATP-sensitive K(+) channels. In contrast, Ba(2+), but not GLIB or IBTX, prevented K(+)-induced dilation. The data indicate that the inward-rectifier K(+) channel (blocked by low concentrations of Ba(2+), but not GLIB or IBTX) was most likely responsible for the K(+)-induced arteriolar dilation.

Cerebellar nitric oxide is increased during isoflurane anesthesia compared to halothane anesthesia: a microdialysis study in rats.

BACKGROUND: This study examined the influences of isoflurane versus halothane anesthesia on basal and agonist-stimulated nitric oxide in the cerebellum of intact rats. Nitric oxide was measured using the hemoglobin-trapping method in an in vivo microdialysis technique. This method uses the stoichiometric reaction of nitric oxide with oxyhemoglobin to produce methemoglobin and nitrate; the change in methemoglobin concentration is measured spectrophotometrically to estimate nitric oxide concentration. METHODS: Male Wistar rats were anesthetized with isoflurane (1.4%) or halothane (1.2%), mechanically ventilated and paralyzed (intravenous pancuronium, 1 mg/kg). Microdialysis probes were implanted into the cerebellum. Bovine oxyhemoglobin dissolved in artificial cerebrospinal fluid was pumped through the probe (2 microl/min) and assayed at 15-min intervals. The glutamatergic agonist, kainic acid (KA, 5 mg/kg, intraarterially), was used to stimulate nitric oxide production. NG-nitro L-arginine methyl ester (L-NAME, 40 mg/kg, intravenously) was used to inhibit nitric oxide synthase. RESULTS: Unstimulated cerebellar nitric oxide concentrations were stable and greater during anesthesia with isoflurane (532+/-31 nM; mean +/- SEM) than with halothane (303+/-23 nM). L-NAME pretreatment reduced nitric oxide concentrations during isoflurane, but not halothane, anesthesia. Infusion of KA increased nitric oxide in both groups; however, the increase in nitric oxide was significantly greater during isoflurane anesthesia. Pretreatment with L-NAME inhibited the response to KA in both groups. CONCLUSIONS: Nitric oxide production in the cerebellum, monitored by microdialysis, was greater during isoflurane anesthesia than during halothane anesthesia. Increased nitric oxide production during isoflurane anesthesia would be expected to impact central neuronal function and cerebral blood flow and vascular resistance.

Resuscitation after hemorrhage using recombinant human hemoglobin (rHb1.1) in rats: effects on nitric oxide and prostanoid systems.

OBJECTIVES: Hemoglobin-based oxygen carriers are designed to replace blood volume and to increase oxygen delivery to tissues after blood loss. The goals of the present study were two-fold: a) to determine the systemic and regional vascular effects of resuscitation with recombinant human hemoglobin (rHb1.1) in rats during controlled hemorrhage; and b) to determine whether nitric oxide (NO) or prostaglandins were involved in the observed responses. DESIGN: Paralyzed, ventilated rats were hemorrhaged (18 mL blood/kg body weight) during halothane anesthesia and allowed to stabilize for 30 mins. Systemic and regional hemodynamics and oxygen delivery were monitored at three time points, using the radioactive microsphere method. Microspheres were first infused at the end of the hemorrhage stabilization period (t=0 min). rHb1.1 (1 g/kg body weight) or rHb1.1 diluent (phosphate buffered saline, 36 mL/kg body weight) were infused over 20 mins and microspheres were administered again, 30 mins later (t=50 mins). Saline (0.5 mL), indomethacin (5 mg/kg to inhibit cyclooxygenase), or NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg, to inhibit NO synthase) were then infused in rHb1.1-treated rats and microspheres injected once more (t=80 mins). SETTING: Research laboratory. SUBJECTS: Male Wistar rats (n=37). INTERVENTIONS: Recombinant human hemoglobin (rHb1.1), rHb1.1 diluent (phosphate buffered saline) resuscitation of hemorrhaged rats. Saline, L-NMMA, or indomethacin treatment after resuscitation. MEASUREMENTS AND MAIN RESULTS: Resuscitation with rHb1.1 increased mean arterial pressure (MAP), cardiac output, and systemic oxygen delivery significantly when compared with diluent. After rHb1.1 resuscitation, regional blood flows were significantly increased in skin, kidney, spleen, and heart compared with diluent resuscitation. Compared with saline treatment after rHb1.1 resuscitation, L-NMMA increased MAP and regional resistances in virtually all tissues; indomethacin did not alter MAP, but increased resistance in the brain. CONCLUSIONS: These data indicate that rHb1.1 resuscitation was more effective than diluent in improving systemic and regional hemodynamics and oxygen delivery, suggesting that rHb1.1 may be of benefit in the treatment of acute blood loss. Increased resistance after L-NMMA in the presence of rHb1.1 indicated that rHb1.1 resuscitation did not eliminate NO dependent circulatory control. Increased resistance after indomethacin in brain indicated that vasodilator prostanoids were important in regulating vascular resistance in these tissues after rHb1.1 resuscitation.

Anesthetics alter relative contributions of NO and EDHF in rat cremaster muscle microcirculation.

The contributions of the vasodilators nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF) were investigated in the rat cremaster muscle microcirculation during halothane, isoflurane, or ketamine anesthesia. After inhibition of prostaglandin synthesis with indomethacin, changes in diameter of fourth-order arterioles to acetylcholine (ACh) or bradykinin (BK) were studied in the presence or absence of NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, and/or 20 mM K+, an inhibitor of EDHF action. L-NMMA inhibited ACh- and BK-induced vasodilation during isoflurane but not halothane or ketamine anesthesia. Superfusion of the muscle with buffer containing 20 mM K+ dilated arterioles. EDHF was responsible for most of the NO-independent response to ACh, because 20 mM K+ unmasked ACh-stimulated, NO-dependent relaxation during halothane or ketamine anesthesia. However, 20 mM K+ did not inhibit BK-induced vasodilation during halothane or ketamine anesthesia. Our data suggest that anesthetics can alter the balance between NO and EDHF vasodilation in the microcirculation and that NO-dependent mechanisms are enhanced and EDHF action inhibited during isoflurane anesthesia.

Halothane inhibits bradykinin-stimulated prostacyclin production in endothelial cells.

BACKGROUND: Halothane and isoflurane alter signal transduction and function in several cell types. Vascular responses to these anesthetics may be attributable to agent-specific effects on vasoactive mediator production. This study investigated the effects of halothane and isoflurane on basal and agonist-stimulated prostacyclin production by endothelial cells. METHODS: Prostacyclin production by cultured bovine aortic endothelial cells was monitored by radioimmunoassay of 6-keto-prostaglandin F1 alpha, the stable breakdown product of prostacyclin. RESULTS: Neither halothane nor isoflurane (0.3-1 mM), altered prostacyclin production. Bradykinin (1 microM), adenosine triphosphate (ATP) (10 microM), and melittin (1 microgram.ml-1) stimulated prostacyclin production. Isoflurane had no effect on responses to bradykinin, ATP, or melittin. Halothane inhibited the response to bradykinin but not the response to ATP or melittin. Pretreatment with pertussis toxin (100 ng.ml-1), to inhibit the function of the guanosine triphosphate-binding protein G alpha i, did not alter the response to bradykinin in the presence or absence of halothane. Pretreatment with phorbol 12-myristate 13-acetate (100 nM), to stimulate protein kinase C activity, did not alter bradykinin-stimulated prostacyclin production and prevented the inhibition of the response to bradykinin by halothane. CONCLUSIONS: Isoflurane had no effect on the increase in prostacyclin production stimulated by bradykinin. Halothane inhibited the bradykinin-stimulated prostacyclin production but not that stimulated by ATP or melittin. These results suggest that the halothane-mediated inhibition of bradykinin-stimulated prostacyclin production does not involve a pertussis toxin-sensitive G-protein and may result from an interaction of halothane at some other step in the signal transduction pathway, including the inhibition of protein kinase C.

A demonstration of validity for certification by the American Board of Anesthesiology.

PURPOSE: To investigate the validity of the certification process of the American Board of Anesthesiology. Specifically, does board certification in anesthesiology identify physicians judged to be clinically superior by evaluators who are not part of the certification process? METHOD: All 154 U.S. anesthesiology program directors (or faculty members they chose to represent them), unaware of the study's intent, were asked whether they would permit each of their residents completing training in 1991 to administer three increasingly complex anesthetic regimens to the directors themselves. This clinical skills rating was compared with the residents' performances in the certification process in 1992. A list of personal characteristics was also provided to the directors so they could identify reasons for less-than-optimal clinical skills ratings. A total of 1,310 residents participated in the certification process in 1992. RESULTS: A total of 146 programs responded. The directors would have accepted anesthetic care for all three increasingly complex operations from 828 (63.2%) of their own residents; for only the two less complex procedures, from 262 (20%); and for only the least complex procedure, from 127 (9.7%). In addition, 93 residents (7.1%) would not have been accepted to administer anesthesia to their directors for any of these operations. Certification success rates for these groups were 74.6%, 53.8%, 44.9%, and 49%, respectively (p < .00001). The personal characteristics believed important to the practice of anesthesiology were strongly linked to the clinical skills ratings; these included motivation, adaptability, clinical judgment, manual dexterity, several work habits, response to criticism, and handling of stressful situations. CONCLUSION: These data support validity for certification in anesthesiology and identify characteristics considered necessary for high-quality practice of the specialty.

Alteration of calcium mobilization in endothelial cells by volatile anesthetics.

Halothane and isoflurane have different effects on the peripheral vasculature. Halothane decreases blood pressure primarily by decreasing cardiac contractility, whereas isoflurane acts primarily as a peripheral vasodilator. These peripheral vascular actions may result from different effects of the anesthetics on endothelial cell function and the release of endothelium-derived vasoactive mediators. The ability of these agents at clinically relevant concentrations to alter agonist-induced calcium mobilization in single cultured bovine aortic endothelial cells was tested using the fluorescent indicator fura-2. Neither halothane (0.3, 0.5, and 2 mM) or isoflurane (0.5 and 2 mM) altered basal calcium ([Ca]i = 49 +/- 5 nM); however, the calcium transient normally elicited by 10 nM bradykinin (peak [Ca]i = 307 +/- 22 nM) was inhibited significantly by halothane but not isoflurane. Neither anesthetic altered the calcium response to ATP (10 microM). These findings suggest that anesthetics may have specific effects on receptor-mediated endothelial cell functions that could influence hemodynamics.

Marked regional heterogeneity in the magnitude of EDRF/NO-mediated vascular tone in awake rats.

The systemic and regional hemodynamic effects of inhibition of endothelium-derived relaxing factor/nitric oxide (EDRF/NO) were studied in awake, indomethacin-treated rats. The radiolabeled microsphere method was used to determine the cardiac output, systemic vascular resistance (SVR), and regional blood flows and regional vascular resistances in 12 tissues before and after infusion of the EDRF/NO synthesis inhibitor, NG-monomethyl-L-arginine (NMMA, 100 mg/kg), and after reversal of NMMA by infusion of L-arginine (300 mg/kg). NMMA infusion resulted in increases in the blood pressure and SVR. After NMMA, blood flows were decreased to the cerebrum, heart, kidney, spleen, gastrointestinal tract, skin, ear, and white fat, whereas flow in the hepatic artery was increased. Vascular resistances were increased in every tissue studied except the hepatic artery, in which the resistance decreased after NMMA. L-arginine restored the vascular resistance to control values in 8 of the 12 tissues. The magnitude of the increase in the regional resistance was not uniform among the organs studied, and ranged from a maximum of 253% in brown fat to 22% in heart. These results indicate that EDRF/NO is an important mediator of regional hemodynamic control in numerous tissues of the intact rat. The marked heterogeneity in the magnitude of basal EDRF/NO-dependent tone suggests that the mechanisms mediating this cardiovascular control system are regulated locally.

The influence of hemorrhage on organ perfusion during deliberate hypotension in rats.

There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.

Endothelium-dependent circulatory control--a mechanism for the differing peripheral vascular effects of isoflurane versus halothane.

Several studies have suggested that halothane and isoflurane modify responses to endothelium-dependent vasodilators, indicating that the differing circulatory effects of these anesthetics may be, in part, attributable to alterations in endothelial cell control of vascular tone. This study was designed to determine the contribution of endothelium-derived relaxing factor (EDRF/NO) to circulatory control in indomethacin-treated rats anesthetized with equipotent concentrations (1 MAC) of either isoflurane (n = 6) or halothane (n = 8). Using radiolabelled microspheres, systemic and regional hemodynamics were measured in cerebrum, cerebellum, heart, kidney, gastrointestinal tract, spleen, liver, skeletal muscle, skin, ear, and white and brown fat. Cardiac output, mean arterial pressure (MAP), systemic vascular resistance (SVR), regional blood flows, and regional vascular resistances were determined before (control) and after administration of NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg) to inhibit EDRF/NO synthesis, and following L-arginine (300 mg/kg) to reverse the effects of L-NMMA. In both anesthetic groups, L-NMMA decreased cardiac output and increased MAP, SVR, and regional resistances in brain, heart, kidney, spleen, gastrointestinal tract, hepatic artery, skeletal muscle, skin, and white fat. L-arginine returned SVR and MAP to or below control values in both groups, although cardiac output remained decreased. During isoflurane as compared to halothane anesthesia, L-NMMA caused significantly greater increases in blood pressure (54 +/- 7% vs. 24 +/- 2%) and SVR (143 +/- 22% vs. 79 +/- 11%). In addition, rats anesthetized with isoflurane had significantly greater increases in vascular resistance in heart, kidney, gastrointestinal tract, hepatic artery, and skin after L-NMMA than did rats anesthetized with halothane.(ABSTRACT TRUNCATED AT 250 WORDS)

Inhibition of endothelium-derived relaxing factor-dependent circulatory control in intact rats.

The effects of the endothelium-derived relaxing factor (EDRF) inhibitors NG-monomethyl-L-arginine (L-NMMA) and methylene blue (MB) on resting hemodynamics and responses to vasodilators were studied in the intact rat anesthetized with pentobarbital sodium. L-NMMA infusions (100 mg/kg) significantly increased mean blood pressure by 48%; this effect was rapidly reversed by L-arginine (300 mg/kg). MB (50 mg/kg) decreased mean blood pressure by 24%. Both MB and L-NMMA significantly attenuated the vasodepressor responses to acetylcholine, ATP, and adenosine. By use of radiolabeled microspheres, it was determined that the blood pressure increase after L-NMMA was due to a marked increase in systemic vascular resistance (SVR; from 1.3 +/- 0.1 to 3.1 +/- 0.3 mmHg.ml-1.min-1) and decreased cardiac output. L-NMMA increased vascular resistance in brain, cerebellum, skin, skeletal muscle, ear, white and brown fat, kidney, spleen, hepatic artery, and gastrointestinal tract. Flow decreased in the skin, kidneys, ear, white and brown fat, gastrointestinal tract, portal venous circulation, and liver in response to L-NMMA. In contrast, MB decreased heart rate, blood pressure, and SVR significantly. MB increased blood flow and decreased vascular resistance in several organs, including the brain, and skeletal muscle. These results indicate that both MB and L-NMMA can inhibit agonist-induced EDRF-mediated vasodepressor responses. However, inhibition of agonist-induced responses did not predict the general and regional hemodynamic responses to L-NMMA or MB infusion.

Effects of hypoxemia on regional blood flows during anesthesia with halothane, enflurane, or isoflurane.

Hypoxemia during anesthesia can cause severe morbidity and mortality. To determine how the volatile anesthetics alter the normal hemodynamic compensation for hypoxemia, we investigated the effects of various anesthetics on regional blood flows during normoxemia and during normocapnic hypoxemia (FIO2 0.12 for 20 min) in rats. Using the radioactive microsphere method, organ blood flows were determined in animals anesthetized with 1 MAC of halothane, enflurane, or isoflurane and in awake animals. Brain blood flow increased significantly with hypoxemia in awake animals. However, brain blood flow decreased in all anesthetized animals that were hypoxemic. Coronary blood flow also increased significantly with hypoxemia in awake animals. In the presence of volatile anesthetics, coronary blood flow decreased, a decrease that was unchanged with hypoxemia. Thus, there was a large difference in brain and coronary blood flows between awake hypoxemic and anesthetized hypoxemic animals. Hypoxemia did not alter the magnitude of renal, gastrointestinal tract, or total hepatic blood flows in awake animals. However, all three blood flows decreased significantly in anesthetized hypoxemic animals. We conclude that volatile anesthetics modify the compensatory responses to hypoxemia that occur in awake animals, resulting in decreased blood flow to vital organs.