Search

The purpose of this review is to present a comprehensive assessment of the anesthesia workforce during the past decade and attempt forecasting the future based on present knowledge. The supply of anesthesiologists has gradually recovered from a deficit in the mid to late 1990 s. Current entry rates into our specialty are the highest in more than a decade, but are still below the level they were in 1993. These factors along with slower surgical growth and less capital available for expanding anesthetizing locations have resulted in greater availability of anesthesiologists in the labor market. Despite these recent events, the intermediate-term outlook of a rapidly aging population and greater access of previously uninsured patients portends the need to accommodate increasing medical and surgical procedures requiring anesthesia, barring disruptive industry innovations. Late in the decade, nationwide surveys found shortages of anesthesiologists and certified registered nurse anesthetists to persist. In response to increasing training program output with stagnant surgical growth, compensation increases for these allied health professionals have moderated in the present. Future projections anticipate increased personnel availability and, possibly, less compensation for this group. It is important to understand that many of the factors constraining current demand for anesthesia personnel are temporary. Anesthesiologist supply constrained by small graduation growth combined with generation- and gender-based decrements in workforce contribution is unlikely to keep pace with the substantial population and public policy-generated growth in demand for service, even in the face of productivity improvements and innovation.

We randomized 74 patients to either a lower Bispectral Index (BIS) regimen (median BIS, 38.9) or a higher BIS regimen (mean BIS, 50.7) during the surgical procedure. Preoperatively and 4-6 wk after surgery, the patients' cognitive status was assessed with a cognitive test battery consisting of processing speed index, working memory index, and verbal memory index. Processing speed index was 113.7 +/- 1.5 (mean +/- se) in the lower BIS group versus 107.9 +/- 1.4 in the higher BIS group (P = 0.006). No difference was observed in the other two test battery components. Somewhat deeper levels of anesthesia were therefore associated with better cognitive function 4-6 wk postoperatively, particularly with respect to the ability to process information.

Verification of appropriate precordial Doppler probe position over the anterior chest wall is crucial for early detection of venous air embolism. We studied responses to normal saline (NS) and carbon dioxide (CO2) test injections at various probe locations during elective craniotomy. All patients received four IV injections (10 mL of NS and 1 mL of CO2 via central and peripheral venous catheters). Doppler sounds were simultaneously recorded with two separate probes. In Group A, probes were placed in left and right parasternal positions. In Group B, the left probe was intentionally malpositioned as far laterally over the left precordium as was compatible with an audible signal. In Group A (n = 23), a left parasternal Doppler signal was easily obtainable in 23 of 23 patients, versus 18 of 23 patients for the right parasternal probe (P < 0.05). In Group B (n = 17), central CO2 injection yielded a positive right parasternal response rate of 88% compared with 29% over the far left precordium (P < 0.015), where central NS injections yielded a 76% response rate (P < 0.015 versus central CO2 injection). Left parasternal placement is at least as sensitive to clinical venous air embolism events as right parasternal placement. Peripheral saline injection represents a viable alternative (83% response rate). Vigorous central injection of 10 mL of NS however, risks false positive verification of left lateral precordial probe placement.

§§Departments of *General Anesthesiology, †Department of Orthopedic Surgery, ‡Department of Urology, §Department ofBiostatistics & Epidemiology, The Cleveland Clinic Foundation; Cleveland Clinic Foundation Health Science Center of theOhio State University; ¶Department of Pathology, Ohio State University, Cleveland; #Department of Medicine, University ofWisconsin, Madison; **Division of Vascular Surgery, University of Arkansas for Medical Sciences, Little Rock; ††BaxterHemoglobin Therapeutics, Boulder, Colorado; ‡‡Pfizer Global Research and Development, New York City; and §§RichardPrielipp, MD, Bowman Gray School of Medicine; Gerald Fulda, MD, Christiana Health Care Services; Irwin Gratz, DO, CooperHospital/UMC; Michael Salem, MD, George Washington University Medical Center; Ronald Kline, MD, Harper Hospital;Benjamin Guslits, MD, Henry Ford Hospital; Michael Pasquale, MD, Lehigh Valley Hospital; Lauraine Stewart, MD, McGuireVA Medical Center; Larry Hollier, MD, Mt. Sinai Medical Center; Bhatar Desai, MD, St. Anthony Hospital; Marc J. Shapiro,MD, St. Louis University Hospital; Ronald Pearl, MD, Stanford University Medical Center; Michael J. Williams, MD, ThomasJefferson University; Dennis Doblar, PhD, MD, University of Alabama-Birmingham; Marc Hudson, MD, University of PittsburghMedical Center; Michael P. Eaton, MD, University of Rochester Medical Center; Lewis Gottschalk, MB, University of Texas-HoustonHealth Sciences Center; Mali Mathru, MD, University of Texas Medical Branch; Daniel Herr, MD, Washington Hospital CenterIn this randomized, prospective, double-blinded clinicaltrial, we sought to investigate whether diaspirin-crosslinked hemoglobin (DCLHb) can reduce the periop-erativeuseofallogeneicbloodtransfusion.One-hundred-eighty-one elective surgical patients were enrolled at 19clinical sites from 1996 to 1998. Selection criteria includedanticipated transfusion of 2–4 blood units, aortic repair,and major joint or abdomino-pelvic surgery. Once a deci-sion to transfuse had been made, patients received ini-tially up to 3 250-mL infusions of 10% DCLHb (

UNLABELLED Reports of anesthesia personnel shortages in 2001 led to the first comprehensive analysis of labor supply and demand for anesthesiologists since 1993. We now update this analysis and forecast, incorporating newly available data about residency composition, American Board of Anesthesiology and Certified Registered Nurse Anesthetist certification, the 2002 residency match, surgical facilities, and the US physician workforce. In addition, US residency programs were surveyed; national health care utilization and economic data were reviewed. Adjusted for the new information, our model still shows an anesthesiologist shortfall in 2002, projected to continue through 2005. We now estimate a current shortage of 1100-3800 anesthesiologists in 2002, on the basis of past service demand growth assumptions of 2%-3%, respectively. By 2005 this number is expected to be 500-3900, depending on a future service demand growth of 1.5%-2%, respectively. To avoid a surplus of anesthesiologists in 2006-2010, our model suggests that the number of graduates should level out at 1600 yearly, with a 1.5% service demand growth. To forecast the anesthesia personnel market more accurately, thereby helping supply match demand, substantially better quantification of future demand for anesthesia services is needed. If sustained growth in service demand >1.5% is likely, entry into the specialty should be encouraged beyond the current level. IMPLICATIONS With updates from training programs, surgical activity, and other sources, our previously described model estimates a continuing shortfall of 1000-3800 anesthesiologists in 2002 and 500-3900 in 2005, assuming that service demand growth is 1.5% or 2% annually. If service growth >1.5% is likely, entry into the specialty should be encouraged beyond current levels.

After craniotomy, hypertension may contribute to intracerebral hemorrhage.We studied whether scalp infiltration with bupivacaine during craniotomy reduces postoperative pain and hypertension. In a double-blind fashion, 36 adult patients (ASA physical status II or III) undergoing elective craniotomy were randomly assigned to receive scalp infiltration with either bupivacaine (0.25%) and epinephrine (1:200,000) or saline/epinephrine (1:200,000) for skeletal fixation, skin incision, and wound closure. Heart rate (HR) and mean arterial pressure (MAP) were measured after anesthesia induction, after skull-pin insertion, after scalp infiltration, during dural closure, during skin closure, on admission to postanesthesia care unit (PACU), and 1 h after admission. Visual analog pain scores were recorded in the PACU. MAP was significantly greater in the saline group at scalp infiltration. HR was significantly faster in the saline group at dural and skin closure. The bupivacaine group reported significantly less pain than the saline group at PACU admission and 1 h after admission. Pain scores did not correlate with hemodynamic measurements. We conclude that scalp infiltration with 0.25% bupivacaine with 1:200,000 epinephrine blunts certain intraoperative hemodynamic responses and reduces postoperative pain but has no effect on postoperative hemodynamics. Implications: We sought to evaluate whether scalp infiltration with bupivacaine and epinephrine at the beginning and end of craniotomy would afford more intra- and postoperative hemodynamic stability and influence immediate postoperative pain. We found that intraoperative hemodynamics were not influenced greatly; however, craniotomy patients do have significant postoperative pain, which does not seem to have an influence on hemodynamics in the postanesthesia care unit. (Anesth Analg 1998;87:579-82)

Our overall goal was to investigate the mechanism by which fentanyl attenuates acetylcholine-induced contraction in porcine coronary artery. We tested the hypothesis that fentanyl attenuates muscarinic coronary contraction via sigma receptor activation. Left coronary artery vascular rings were isolated from porcine hearts and were suspended in organ chambers for isometric tension recording. In untreated coronary vascular rings, acetylcholine administration resulted in dose-dependent contraction. Fentanyl attenuated acetylcholine-induced contraction. The sigma ligands--(+)-pentazocine, (+)-cyclazocine, haloperidol, and 1,3-di-o-tolylguanidine--also inhibited acetylcholine-induced contraction. In contrast, the selective sigma ligand, (+)-3-(3-hydroxyphenyl)-N-(1-propyl) piperidine failed to have an inhibitory effect on acetylcholine-induced contraction. Moreover, metaphit (1-[1(3-isothiocyanatophenyl)cyclohexyl]piperidine), which causes irreversible acylation of sigma receptors, only inhibited acetylcholine-induced contraction when it was present in the organ chamber. We also assessed the effects of inhibiting various points in the signal transduction pathway distal to naloxone-sensitive opioid receptor activation on acetylcholine-induced contraction. Selective (glybenclamide) and nonselective (tetraethylammonium) K(+)-channel inhibition, guanosine triphosphate-binding protein inactivation (pertussis toxin), and Type 1 and Type 2 dopamine receptor inhibition all failed to alter the attenuating effect of fentanyl on acetylcholine-induced contraction. Thus, neither sigma or opioid receptor activation is a prerequisite for fentanyl-induced inhibition of muscarinic coronary contraction.

The effect of propofol on the electroencephalogram (EEG) in patients with epilepsy is still unclear. Case reports with electroencephalographic documentation highlight pro- and anticonvulsant effects and beta activation of the EEG. This prospective study sought to determine the effect of propofol in 17 patients undergoing cortical resection for intractable epilepsy. Each patient received 2 mg/kg of propofol intravenously and the EEG was recorded from chronically implanted subdural electrodes placed during a previous craniotomy. Frequency of interictal spikes, time to burst suppression, and appearance of beta activation were recorded. The median frequency of interictal spikes decreased significantly from 2 spikes/min before to 0 spikes/min after propofol (P = 0.001). Seizure activity did not increase after propofol. Profound burst suppression and an increase in beta activity were noted consistently. The use of propofol in patients with epilepsy seems to be safe but may interfere with the recording of EEG spikes.

This study was undertaken to define the effect of acute hypocapnia on intraoperatively recorded somatosensory evoked potentials (SSEPs). Median nerve SSEPs were studied in ten anesthetized neurologically normal adult patients undergoing elective nonneurologic surgery. End-tidal carbon dioxide tension (ETCO2) was allowed to stabilize for 15 min before SSEP recordings were obtained during normocapnia (N) (ETCO2 = 39.9 +/- 1.45 mm Hg), hypocapnia (H) (ETCO2 = 20.6 +/- 1.07 mm Hg), and after return to normocapnia (NR). Although a trend toward a reduction in the latencies of all SSEP components was evident, only the cervical (CII), and cortical (N1 and P1) latencies decreased significantly with H when compared to N. Mean latencies for CII, N1, and P1 (+/- SD) were, respectively, 14.80 +/- 1.14, 20.93 +/- 1.50, and 25.17 +/- 2.88 msec during N, and 14.50 +/- 1.13, 20.25 +/- 1.49, and 24.23 +/- 2.52 msec during H. On return to normocapnia, latencies were unchanged from N. Cortical latencies were affected to a greater extent than subcortical ones. Aside from a small but statistically significant increase in CII amplitude at H (2.05 +/- 0.55 microV vs 1.83 +/- 0.49 microV at N), SSEP amplitudes were unaffected by hypocapnia. The authors conclude that acute hypocapnia in neurologically normal patients results in a small reduction of SSEP latencies. The magnitude of the change is such that it is unlikely to interfere with recording or interpretation of intraoperative SSEPs.