This commentary calls for an updated research agenda building on traditional basic science and clinical investigation to emphasize patient- and population-outcome-oriented science. The authors argue this expanded research portfolio will be important to transforming our inefficient and expensive health care system into a more evidence-based system of effective, coordinated, safe, and patient-centered care.

PurposeTo explore the roles of physician leaders who hold titles such as chief medical officer (CMO), vice president for medical affairs, and vice dean for clinical affairs in Association of American Medical Colleges (AAMC) member organizations, and to identify critical success factors for these positions.MethodAn Internet-based survey was submitted to 340 physician leaders in 281 AAMC member institutions. The survey posed questions regarding demographics, titles, reporting relationships, time commitments, scope of responsibility, accomplishments, and challenges related to recipients' positions, among other questions.ResultsResponses were received from 154 physicians representing 139 institutions (response rates 45% and 49%, respectively). Forty-nine percent of these positions had existed for 10 years or less. The most common administrative title was CMO (48%). Eighty-five percent of these individuals reported directly to the dean or CEO of their organization. The majority of administrative effort involved quality and safety (31%), coordination of clinical care (21%), and graduate medical education (9%). The remainder (39%) encompassed a broad portfolio of responsibilities ranging from information technology (6%) to nursing services (2%). Keys to job success included personal stature and relationships, clear definition of responsibilities, and the commitments of the senior administration to the position.ConclusionsTeaching hospitals and medical schools are creating or strengthening positions for physician leaders, most commonly called CMOs. CMOs' work involves numerous activities beyond the traditional areas of quality and safety. The effectiveness of these positions requires clear definition of the role throughout the organization and strong, evident support from senior executives in the organization.

BACKGROUND:Board certification is often used as a surrogate indicator of provider competence, although few outcome studies have demonstrated its validity. The aim of this study was to compare the outcomes of patients who underwent surgical procedures under the care of an anesthesiologist with or without board certification.METHODS:Medicare claims records for 144,883 patients in Pennsylvania who underwent general surgical or orthopedic procedures between 1991 and 1994 were used to determine provider-specific outcome rates adjusted to account for patient severity and case mix, and hospital characteristics. Outcomes of 8,894 cases involving midcareer anesthesiologists, 11-25 yr from medical school graduation, who lacked board certification were compared with all other cases. Midcareer anesthesiologist cases were studied because this group had sufficient time to become certified during an era when obtaining certification was already considered important, and consequently had the highest rate of board certification. Mortality within 30 days of admission and the failure-to-rescue rate (defined as the rate of death after an in-hospital complication) were the two primary outcome measures.RESULTS:Adjusted odds ratios for death and failure to rescue were greater when care was delivered by noncertified midcareer anesthesiologists (death = 1.13 [95% confidence interval, 1.00, 1.26], P < 0.04; failure to rescue = 1.13 [95% confidence interval, 1.01, 1.27], P < 0.04). Adjusting for international medical school graduates did not change these results.CONCLUSIONS:When anesthesiology board certification is very common, as in midcareer practitioners, the lack of board certification is associated with worse outcomes. However, the poor outcomes associated with noncertified providers may be a result of the hospitals at which they practice and not necessarily their manner of practice.

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.

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.)

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.

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. (Crit Care Med 1998; 26:1071-1080)

IT is an honor to join a group of distinguished colleagues who have delivered the Rovenstine lecture previously. Dr. Rovenstine has special meaning for me because he was a fellow Hoosier and graduate of Indiana University, my alma mater for both undergraduate and graduate medical education. However, I am humbled by this recognition, also. I am aware that there are many in this audience who possess more judgment and knowledge than I, and all of us would benefit from their wisdom on this occasion. Nevertheless, I accept the opportunity with enthusiasm, for I believe these are defining times for the specialty. The thoughts that follow are mine only, and they will benefit from group discussion and modification by collective wisdom. My purpose is to catalyze these discussions and stimulate action by both the leaders and the membership of this society. My title suggests an analogy between my vocation, anesthesiology, and my avocation, sailing. Both require careful route planning to reach a desired destination, so the analogy seems appropriate. My comments are divided into four sections, which are intended to define the current position of the specialty and plot a course for the future.

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.

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)

Male Wistar rats were anesthetized at 6 weeks of age and a silver clip placed around the renal artery to produce renovascular hypertension. The rats were allowed to grow on a normal sodium diet for the next 6-9 weeks. Using diethyl ether anesthesia, arterial and venous cannulae were placed and the animals allowed to awaken in restraining cages. The group of rats was divided into three groups: awake (n = 7), halothane 1.3 vol% (n = 9), and enflurane 2.2 vol% (n = 8). The protocol consisted of a 1-h control awake period, 1 h of stable anesthesia (one group received no anesthesia), and 30-min iv infusion of saralasin, a competitive inhibitor of angiotensin II. Plasma renin activity (PRA) and plasma catecholamines were measured after 1 h of stable anesthesia and after the saralasin infusion. In additional rats treated identically, radiolabelled microspheres were used to measure cardiac output and regional blood flows during halothane (n = 7) or enflurane (n = 6) anesthesia. Principal responses were as follows: mean arterial pressure (MAP) was 193 +/- 4 mmHg awake and decreased to 114 +/- 3 mmHg and 135 +/- 3 mmHg with halothane and enflurane, respectively. Saralasin decreased MAP in the awake group to 176 +/- 3 mmHg and to 69 +/- 3 mmHg and 96 +/- 5 mmHg with halothane and enflurane, respectively. PRA in the awake rats was 7.24 +/- 1.3 ng X ml-1 X h-1. PRA increased with halothane but decreased with enflurane. Plasma catecholamines were decreased markedly by saralasin and by both anesthetic agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Because the belief that cyanide is released from nitroprusside in vivo recently was challenged, the authors performed a series of experiments that examined the conditions under which nitroprusside is degraded. These experiments include an examination of the release of cyanide and nitric oxide from nitroprusside in vitro, the release of cyanide in vivo, and a comparison of the biologic activity of intact and degraded nitroprusside. Nitroprusside in aqueous solution degraded when exposed to white or blue light but not to red light. While light at 20 microW X cm-2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 microW X cm-2 produced 100% apparent photodegradation after 2 h exposure. At 10% apparent photodegradation, 10% of the nitrosyl ligand was recovered as free nitric oxide, and 0.4% of the cyanide ligand was recovered as free cyanide. Following a 2-h infusion of light-protected nitroprusside in seven patients, cyanide concentrations ranged from 1.4 to 45.5 microM and 0.09 to 3.2 microM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 microW X cm-2) for 4 h. Intact and photodegraded nitroprusside produced identical hypotensive responses in rats as would be expected, since the nitrosyl ligand was detected in solution following degradation, and it mediates this action. Cyanide was released from nitroprusside, both on its exposure to light in vitro and also in vivo. The latter was not an artifact of the assay for cyanide. Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.

The authors studied 12 patients who required deliberate hypotension for spinal fusion operations in order to investigate the efficacy of captopril for reducing dose requirement for sodium nitroprusside (SNP). Six patients, selected at random, were pretreated with captopril, 3 mg/kg po, and the remaining six patients served as controls. All patients received a similar anesthetic technique, consisting of thiopental 3 mg/kg, pancuronium 0.1 mg/kg, morphine 0.5 mg/kg, plus nitrous oxide 70% in oxygen. SNP was used to maintain mean arterial pressure (MAP) at 50-55 mmHg during deliberate hypotension lasting 140 +/- 13 minutes (mean +/- SE). Patients who received captopril required less SNP than untreated patients both early during hypotension (1.4 +/- 0.5 micrograms X kg-1 X min-1 vs. 4.8 +/- 0.8 micrograms X kg-1 X min-1, P less than 0.05), as well as late during hypotension (2.2 +/- 0.2 micrograms X kg-1 X min-1 vs. 5.6 +/- 0.6 micrograms X kg-1 X min-1, P less than 0.05). Whole blood cyanide was significantly lower in the patients pretreated with captopril than the untreated controls both early in the hypotensive period (2.7 +/- 0.6 mumol/l vs. 13 +/- 4 mumol/l, P less than 0.05) and also late in the hypotensive period (3.7 +/- 0.8 mumol/l vs. 30 +/- 10 mumol/l, P less than 0.05). MAP was reduced by captopril pretreatment both following induction of anesthesia (64 +/- 4 mmHg captopril vs. 80 +/- 4 mmHg control, P less than 0.05) and during surgery before deliberate hypotension (86 +/- 5 mmHg captopril vs. 100 +/- 4 control, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriolar diameters and tissue oxygen tensions were measured in the cremaster muscles of 68 hemorrhaged rats which were anesthetized with either intramuscular ketamine, 125 mg/kg, plus 30 mg/kg supplements as needed, or enflurane, 2.2% inspired. Animals breathed room air, or room air plus enflurane, throughout the experiments. Arterioles in the cremaster muscle were identified according to successive orders of branching, and the internal diameters of first-, third-, and fourth-order vessels were measured at 30-s intervals. Cremaster muscle oxygen tension was measured polarographically with platinum-iridium microelectrodes. Mean arterial pressure was controlled at 30-35 mmHg during 30 min of hemorrhage, and maximum shed blood volumes were similar (2.6 ml/100 g) in both groups. Principal responses to hemorrhage in rats receiving enflurane were 1) constriction in first-, third-, and fourth-order arterioles, and 2) tissue hypoxia. In hemorrhaged rats receiving ketamine, the constrictor response to hemorrhage either was diminished (first-, and third-order arterioles) or abolished (fourth-order arterioles), and tissue hypoxia did not occur. The authors conclude that ketamine, as compared with enflurane, diminishes or prevents arteriolar constriction and tissue hypoxia in the cremaster muscle of hemorrhaged rats.

The authors examined the effects of controlled hypotension induced with sodium nitroprusside (SNP) with and without propranolol on the cardiovascular, pulmonary, and renin-angiotensin systems in 10 consecutive anesthetized patients with kyphoscoliosis undergoing posterior spinal fusion. SNP infusion (4.1 microgram . kg-1 . min-1) alone decreased mean systemic arterial pressure (SAP) by 25 torr +/- 3 SE (P less than 0.001), systemic vascular resistance index (SVRI) by 1113 dyne . sec. cm-5 . m2 +/- 125 SE (P less than 0.001), mean pulmonary artery pressure (PAP) by 6 torr +/- 2 SE (P less than 0.02), pulmonary capillary wedge pressure (PCWP) by 4 torr +/- 1 SE (P less than 0.01), pulmonary vascular resistance (PVR) by 50 dyne . sec . cm-5 +/- 18 (P less than 0.05), and PaO2 by 16 torr +/- 7 SE (P less than 0.05), whereas cardiac index increased by 1.08 l . min-1 . m2 +/- 0.24 SE (P less than 0.01) and heart rate increased 16 beats/min +/- 5 SE (P less than 0.02). After 40 min of hypotension, 0.03 mg/kg propranolol was injected intravenously while the SNP infusion rate was held constant. Ten min later there was a significant decrease in the heart rate (10 beats/min +/- 4 SE, P less than 0.02) and cardiac index (0.65 l . min-1 . m-2 +/- 0.21, P less than 0.02). Plasma renin activity (PRA) increased from 2.37 ng . ml-1 . h-1 +/- 0.7 SE before anesthesia to 6.50 ng . ml-1 . h-1 +/- 1.45 SE (P less than 0.05) after 40 min of nitroprusside infusion. Forty min after propranolol there was a significant reduction in PRA to 4.07 ng . ml-1 . h-1 +/- 0.73 SE (P less than 0.05). Thus propranolol, when given during SNP hypotension, exhibits an early cardiovascular response manifested as a decrease in cardiac output and heart rate and a delayed action of the kidney resulting in an inhibition of renin release.