David E. Longnecker

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.

Lidocaine constricts or dilates rat arterioles in a dose-dependent manner

The microvascular effects of varying concentrations of lidocaine were evaluated with the use of videomicroscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane and breathed room air spontaneously. Mean areterial pressure and heart rate were measured via a carotid artery cannula. The cremaster muscle was suffused with a balanced electrolyte solution and pH, temperature, Po2, Pco2, and osmolarity were controlled. Internal diameters of fourth-order arterioles in the cremaster muscle were measured with an electronic vernier system. In one group of animals (n = 7), arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of lidocaine hydrochloride, and a 10-min recovery period. Lidocaine hydrochloride, 100, 101, 102, 103, or 104 μg·ml−1, produced changes in arteriolar diameters to 88.9 ± 0.9, 79.0 ± 1.3, 67.5 ± 2.4, 60.1 ± 3.4, and 127.1 ± 7.2 per cent of control, respectively (P < 0.001). In a second group of animals (n = 4), fourth-order arteriolar diameters were measured during administration of intravenous lidocaine, 1.2 mg·kg−1 bolus plus 0.3 mg·kg−1 · min−1. Vasoconstriction to 91.3 ± 0.9% of control was observed (P < 0.001). These results demonstrate a biphasic dose-dependent response to lidocaine. At lesser concentrations, including those that occur in the plasma of patients during intravenous infusion or nerve blocks, dose-related vasoconstriction occurred. Lidocaine, 104 μg · ml−1, a concentration similar to that which occurs at the site of injection during infiltration, nerve block, or epidural anesthesia, produced vasodilation. It appears likely that the observed effects are a result of peripheral rather than central actions of the drug.

Anesthesiologist Board Certification and Patient Outcomes

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.

Anesthetic Influences on Regional Hemodynamics in Normal and Hemorrhaged Rats

Forty-six male Sprague-Dawley rats were divided in five groups: awake animals and those receiving ketamine, halothane, enflurane, or isoflurane anesthesia. Cannulae were inserted into the left femoral artery and vein and the left ventricle. Inspired concentrations of the volatile anesthetics were adjusted to achieve the minimal alveolar concentration (MAC) of each drug. Ketamine, 125 mg·kg−1, was injected intraperitoneally and then infused at a rate of 1 mg·kg−1·min−1. All animals breathed spontaneously throughout the experiment (Flo2 = 0.3). Following a 2-h stabilization period, 30% of estimated blood volume was withdrawn gradually over 10 min. Immediately before and 20 min after hemorrhage, cardiac output and regional blood flows were measured by the microsphere method (85Sr, 141Ce-labeled 15-μm microspheres, respectively). Arterial blood samples were analyzed for Po2, Pco2, pH, lactate, and pyruvate at these times also. Prior to hemorrhage, cardiac output (CO) values were similar in awake rats and those receiving ketamine or isoflurane, but CO was reduced moderately by enflurane and to a greater extent by halothane. After hemorrhage, CO was greatest in awake animals and those receiving isoflurane, and awake rats tended to have the greatest organ blood flows. Values of lactate/pyruvate and excess lactate were least in awake animals. Overall results suggested that, in terms of cardiac output and regional blood flows, ketamine approximates the awake state most closely in normovolemic animals, whereas isoflurane anesthesia is most like the awake condition after hemorrhage.

Minimum alveolar concentrations in man on awakening from methoxyflurane, halothane, ether and fluroxene anesthesia: MAC awake.

Alveolar anesthetic concentrations at the first response to command and those concentrations just preventing the response were determined in man during recovery from methoxyflurane, halothane, ether and fluroxene anesthesia. The authors assumed equilibration of cerebral anesthetic concentration with alveolar concentration after alveolar concentration had been kept constant for at least 15 minutes. The anesthetic concentration midway between the value permitting the response and that just preventing the response was defined as “MAC awake.” MAC awake values were 0.081 ± 0.021 (SD) per cent methoxyflurane, 0.41 ± 0.05 per cent halothane, 1.41 ± 0.22 per cent ether, and 2.20 ± 0.49 per cent fluroxene. MAC awake-to-MAC ratios were fairly close for the four agents, being 0.52, 0.52, 0.67, and 0.60 for methoxyflurane, halothane, ether, and fluroxene, respectively. When the alveolar concentrations were allowed to fall spontaneously, falsely low MAC awake values were obtained for halothane and fluroxene, while MAC awake for methoxyflurane was unchanged from that found at constant alveolar concentration.

Photodegradation of sodium nitroprusside: biologic activity and cyanide release.

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 μW·cm−2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 μW·cm−2 produced 100% apparent photodegradation after 2 h exposure. At 100% 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 μM and 0.09 to 3.2 μM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 μW·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.

Dose-dependent Effects of Bupivacaine on Rat Muscle Arterioles

The dose-dependent actions of bupivacaine on the microvasculature were evaluated by television microscopy in an in vivo rat cremaster muscle preparation. Animals were anesthetized with chloralose and urethane. Mean arterial pressure was measured via a carotid artery cannula; heart rate was calculated from the phasic pressure trace. The cremaster muscle was suffused with a balanced electrolyte solution that was controlled for temperature, pH, PO2, PCO2, and osmolarity to provide a physiologic environment. Internal diameters of fourth-order arterioles were measured with an electronic vernier displayed on the video monitor. Arteriolar diameters were measured every 30 s during a 10-min control period, a 10-min period of topical application of bupivacaine hydrochloride, and a 30-min recovery period. Bupivacaine 10−1, 100, 101, and 102 μg · ml−1 produced progressive vasoconstriction to 82.7 ± 2.9%, 75.0 ± 5.6%, 71.0 ± 7.0%, and 65.7 ± 9.4% of control (P ≤ 0.05 for each), respectively. Bupivacaine, 103 and 2.5 X 103 μg · ml−1, did not alter arteriolar diameters significantly, although there was a tendency for vasodilation. In a second group of animals, arteriolar diameters were measured during intravenous bupivacaine infusion that produced stable plasma concentrations of 2.3 ± 0.2 μg · ml−1. Vasoconstriction of 91.4 ± 2.2%, of control (P ≤ 0.01) was observed. These results demonstrate that dose-dependent arteriolar constriction occurs even with blood bupivacaine levels that are at the upper limits of those expected to occur during regional anesthesia.

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, indo-methacin-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 Regulatory Function of the Renin–Angiotensin System during General Anesthesia

Variation of plasma renin activity has been shown to occur during anesthesia, but its significance remains obscure. The recent development of a specific angiotensin II antagonist, saralasin, allows the delineation of the role of the renin-angiotensin system in blood pressure control during anesthesia. Twenty-seven rats were divided into four groups: awake, halothane (1 MAC), ketamine (125 mg/kg), and fluroxene (1 MAC). Arterial pressure was recorded continuously and plasma renin activity was determined by radioimmunoassay at the end of a two-hour awake control period, after one hour of anesthesia, and after half an hour of saralasin infusion. A similar protocol for enflurane with 1.75 vol per cent was also followed in seven anesthetized rats, but renin analysis was not performed. Anesthesia resulted in decreases in mean arterial pressure from 123.0 ± 1.3 torr to 95.2 ± 2.2 torr for ketamine, 91.6 ± 3.9 torr for halothane, 96.9 ± 7.9 torr for fluroxene, and 84.5 ± 3.8 torr for enflurane. Renin activity did not change significantly from control (4.33 ± 0.51 ng/ml/hr). When saralasin was infused only the rats anesthetized with halothane or enflurane had significant decreases in mean blood pressure, to 75.0 ± 4.8 and 66.1 ± 3.4 torr, respectively. It is concluded that the anesthetic agents studied do not cause a detectable increase in plasma renin activity. However, through the use of a competitive inhibitor of angiotensin II, a significant role for the maintenance of blood pressure by the renin-angiotensin system during halothane and enflurane anesthesia has been demonstrated.

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)