Hospital Surveys by the Centers for Medicare and Medicaid Services: An Analysis of More Than 34,000 Deficiencies.

OBJECTIVES: The aims of the study were to analyze hospital deficiencies reported by the Centers for Medicare and Medicaid Services (CMS) for a 10-year period (2007-2017) and thereby determine the specific conditions of participation (CoP) cited in each deficiency. METHODS: Deficiency data from the CMS Web site was downloaded and analyzed. A determination was made regarding the CoP assigned to each deficiency. In addition, deficiencies were analyzed according to the presence or absence of an immediate jeopardy (the most serious potential risk) and whether there was state-to-state variation. RESULTS: A total of 30,808 of 34,522 deficiencies were assigned specific "tags" related to a COP, with 77% of the A tags assigned to the following six CoP: patient rights, nursing services, quality improvement, medical records, governing body, and emergency services. Immediate jeopardy was assigned in 730 tags, and a patient death was more likely to be associated with the determination of immediate jeopardy; actual patient deaths were associated with 21% of surveys that resulted in immediate jeopardy. Survey rates varied state-to-state; 14.3 surveys per 1 million population at the 80th percentile and 6.0 surveys per million at the 20th percentile, respectively. Utah and Vermont had the least (1.7) and greatest (70.3) rates, respectively, a 41-fold difference. CONCLUSIONS: These data indicate that (a) hospital surveys result in most deficiencies being assigned to a subset of CoP; (b) a patient death is more likely to be associated with a finding of immediate jeopardy, and (c) there is significant state-to-state variation in survey rates.

How many operating rooms are needed to manage non-elective surgical cases? A Monte Carlo simulation study.

BACKGROUND: Patients often wait to have urgent or emergency surgery. The number of operating rooms (ORs) needed to minimize waiting time while optimizing resources can be determined using queuing theory and computer simulation. We developed a computer program using Monte Carlo simulation to determine the number of ORs needed to minimize patient wait times while optimizing resources. METHODS: We used patient arrival data and surgical procedure length from our institution, a tertiary-care academic medical center that serves a large diverse population. With ~4800 patients/year requiring non-elective surgery, and mean procedure length 185 min (median 150 min) we determined the number of ORs needed during the day and evening (0600-2200) and during the night (2200-0600) that resulted in acceptable wait times. RESULTS: Simulation of 4 ORs at day/evening and 3 ORs at night resulted in median wait time = 0 min (mean = 19 min) for emergency cases requiring surgery within 2 h, with wait time at the 95th percentile = 109 min. Median wait time for urgent cases needing surgery within 8-12 h was 34 min (mean = 136 min), with wait time at the 95th percentile = 474 min. The effect of changes in surgical length and volume on wait times was determined with sensitivity analysis. CONCLUSIONS: Monte Carlo simulation can guide decisions on how to balance resources for elective and non-elective surgical procedures.

Optimizing the OR: a bottom-up approach.

Efficiency in the operating room (OR) has important implications on finances, access, and patient and staff satisfaction. UC Davis Medical Center (UCDMC) launched an initiative to increase OR efficiency by using multidisciplinary staff-based teams. The initiative freed up 5,500 annual hours-about 1 hr per operating room per day-in the OR by improving the percentage of first case on-time starts, reducing OR turnover times, improving scheduling predictability and reducing the number of controllable cancellations. Importantly, the process also engrained a continuous quality improvement mentality into the medical center's culture.

Effect of high-frequency alternating current on spinal afferent nociceptive transmission.

OBJECTIVE: The study was performed to test the hypothesis that high-frequency alternating current (HFAC) ranging from 2 to 100 kHz delivered to the spinal dorsal roots reduces activity of spinal wide dynamic range (WDR) dorsal horn neurons (DHNs) during noxious peripheral stimulation. MATERIALS AND METHODS: This hypothesis was tested in both small and large animal in vivo preparations. Single-unit extracellular spinal DHN recordings were performed in seven adult rats and four adult goats while testing various parameters of HFAC delivered to the nerve roots or dorsal root entry zone using various electrode types. Frequencies tested ranged from 2 to 100 kHz but focused on the 3 to 50 kHz range. This study investigated the ability of HFAC to inhibit WDR neuronal activity evoked by noxious mechanical (pinch), and electrical stimuli was tested but was primarily focused on electrical stimulation. RESULTS: Rat Study: Effects of HFAC were successfully tested on 11 WDR neurons. Suppression or complete blockade of evoked activity was observed in all 11 of these neurons. Complete data sets for neurons systematically tested with 15 baseline and post-HFAC stimulus sweeps were obtained in five neurons, the nociceptive activity of which was suppressed by an average of 69 ± 9.7% (p < 0.0001). Goat Study: HFAC was successfully tested on 15 WDR neurons. Conclusive suppression or complete nociceptive blockade was observed for 12/15 and complete data sets with at least 20 baseline and post-HFAC stimulus sweeps were obtained from eight DHNs. For these neurons the mean activity suppression was 70 ± 10% (p < 0.005). CONCLUSIONS: Delivery of HFAC to the region of epidural nerve root or nerve root entry inhibited afferent nociceptive input and therefore may have potential to serve as an alternative to traditional spinal cord stimulation without sensory paresthesia as neuronal activation cannot occur at frequencies in this range.

Propofol and etomidate depress cortical, thalamic, and reticular formation neurons during anesthetic-induced unconsciousness.

BACKGROUND: The sites where anesthetics produce unconsciousness are not well understood. Likely sites include the cerebral cortex, thalamus, and reticular formation. We examined the effects of propofol and etomidate on neuronal function in the cortex, thalamus, and reticular formation in intact animals. METHODS: Five cats had a recording well and electroencephalogram screws placed under anesthesia. After a 5-day recovery period, the cats were repeatedly studied 3 to 4 times per week. Neuronal (single-unit) activity in the cerebral cortex (areas 7, 18 and 19), thalamus (ventral posterolateral and ventral posteromedial nuclei and medial geniculate body), and reticular formation (mesencephalic reticular nucleus and central tegmental field) was recorded before, during, and after infusion of either propofol or etomidate. Cortical neuronal action potentials were analyzed separately as either regular spiking neurons or fast spiking neurons. RESULTS: Propofol and etomidate decreased the spontaneous firing rate of cortical neurons by 37% to 41%; fast spiking neurons and regular spiking neurons were similarly affected by the anesthetics. The neuronal firing rate in the thalamus and reticular formation decreased 30% to 49% by propofol and etomidate. The electroencephalogram shifted from a low-amplitude, high-frequency pattern to a high-amplitude, low-frequency pattern during drug infusion suggesting an anesthetic effect; peak power occurred at 12 to 13 Hz during propofol infusion. There were 2 major peaks during etomidate anesthesia: one at 12 to 14 Hz and another at 7 to 8 Hz. The cats were heavily sedated, with depressed corneal and whisker reflexes; withdrawal to noxious stimulation remained intact. CONCLUSION: These data show that neurons in the cortex, thalamus, and reticular formation are similarly depressed by propofol and etomidate. Although anesthetic depression of neuronal activity likely contributes to anesthetic-induced unconsciousness, further work is needed to determine how anesthetic effects at these sites interact to produce unconsciousness.

Perioperative hypotension and myocardial ischemia: diagnostic and therapeutic approaches.

Although perioperative hypotension is a common problem, its true incidence is largely unknown. There is evidence that postoperative outcome, including the incidence of myocardial adverse events, may be linked to the prolonged episodes of perioperative hypotension. Despite this, there are very few comprehensive resources available in the literature regarding diagnosis and management of these not so uncommon clinical occurrences, especially during non-cardiac surgery. Most anesthesia providers consider intraoperative hypotension to be caused by systemic vasodilatation and relative hypovolemia and so treat it empirically. The introduction of new monitoring devices including transesophageal echocardiography and arterial pressure waveform based stroke volume measurement have provided additional tools to narrow the differential diagnoses and initiate optimal treatment measures. Understanding the basic pathophysiology of hypotension and myocardial ischemia can further assist in providing goal directed management. This article serves as a comprehensive guide for anesthesiologists to diagnose and treat hypotension and myocardial ischemia. A summary of available techniques to monitor perioperative myocardial ischemia and their limitations are also discussed.

Perioperative pharmacology in elderly patients.

PURPOSE OF REVIEW: Populations across the world are getting older and requiring more surgery. Elderly patients present unique challenges to the anesthesiologist and anesthesia-care team. This review addresses some concerns when caring for an elderly patient. Specifically, we discuss postoperative cognitive decline (POCD) and postoperative delirium, perioperative beta-blockade and use of newer drugs, as well as older drugs. RECENT FINDINGS: POCD has emerged as a new concern for anesthesiologists and their older patients. Several recent studies indicate that POCD is common after noncardiac surgery, with an incidence approaching 30-40% at discharge, although this incidence declines at 3 months. Some data suggest that POCD imparts risk for death. However, there is conflicting evidence. With regard to beta-blocker therapy, there has been growing concern about widespread use of beta-blocker therapy in the perioperative period, especially because such therapy might increase the risk for stroke. SUMMARY: Elderly patients require focused diligent care. They are particularly sensitive to the many drugs that are administered in the perioperative period. Recent data suggest that POCD is a real concern, but it is unclear what, if anything, can be done to prevent this complication. Beta-blocker therapy is beneficial in select patients but its widespread use cannot be supported.

Nitrous oxide-induced analgesia does not influence nitrous oxide's immobilizing requirements.

BACKGROUND: Nitrous oxide (N(2)O) acts on supraspinal noradrenergic neurons to produce analgesia, but it is unclear if analgesia contributes to N(2)O's immobilizing effects. We tested the hypothesis that N(2)O minimum alveolar anesthetic concentration (MAC) is unchanged after selective ablation of supraspinal noradrenergic neurons, or in naïve animals at N(2)O exposure timepoints when analgesia is absent. METHODS: We determined tailflick latency (TFL) and hindpaw withdrawal latency (HPL) under 70% N(2)O, N(2)O MAC, and isoflurane MAC before and after intracerebroventricular injections of anti-dopamine-beta hydroxylase conjugated to saporin (SAP-DBH; n = 7), or a control antibody conjugated to saporin (n = 5). In a separate group of naive rats (n = 8), N(2)O MAC was determined at 25-45 min after initiation of N(2)O exposure (during peak analgesia) and again at 120-140 min (after TFL and HPL returned to baseline). RESULTS: After 30 min of N(2)O exposure, TFL and HPL increased significantly but declined back to baseline within 120 min. N(2)O did not produce analgesia in rats that received SAP-DBH. However, N(2)O and isoflurane MAC were not significantly different between SAP-DBH and control-injected animals (Mean +/- sd for N(2)O: 1.7 +/- 0.1 atm vs 1.7 +/- 0.2 atm; isofurane: 1.6 +/- 0.2% vs 1.7 +/- 0.2%). In naïve animals, N(2)O MAC was not different at the 30 min period compared with the 120 min period (1.8 +/- 0.1 atm vs 1.8 +/- 0.2 atm). CONCLUSIONS: Destroying brainstem noradrenergic neurons or prolonged exposure to N(2)O removes its analgesic effects, but does not change MAC. The immobilizing mechanism of N(2)O is independent from its analgesic effects.

Modeling the effects of midazolam on cortical and thalamic neurons.

Controversy exists regarding the site where anesthetics act in the brain to produce sedation and unconsciousness. Actions in the cerebral cortex and thalamus are likely, although the relative importance of each site is unclear. We used in computo modeling to investigate the sensitivity of cortical and thalamic neurons to midazolam (MDZ) at concentrations that produce unconsciousness. The GABA(A) receptor conductance of the model was manipulated to simulate the effects of MDZ at free-drug plasma concentrations ranging from 8 nM to 100 nM; sleepiness to complete unconsciousness occurs in humans in the 10-40 nM range. Prolongation of phasic inhibition was simulated by increasing the decay time constant and tonic inhibition was simulated by introducing a tonic current; the extent of phasic and tonic inhibition was appropriate for each simulated MDZ concentration. Phasic and tonic inhibition was simulated in cortex, and phasic inhibition was simulated in thalamus. Simulation of MDZ effect decreased cortical neuronal firing rate. For example, the mean cortical neuronal firing rate decreased by 15% (P<0.01) and 26% (P<0.01) at MDZ concentrations of 10 nM and 40 nM, respectively. However, thalamic firing rate did not change. In computo modeling of the thalamocortical system indicates that MDZ-induced GABAergic inhibition of cortical neurons plays a significant role in the transition from waking to unconsciousness. Although MDZ produces phasic inhibition in the thalamus, computer simulation suggests it is not significant enough to decrease thalamic neuronal firing. Thus, based on in computo modeling, MDZ at sedative/hypnotic concentrations produces its effects by decreasing cortical neuronal firing.

Rat dorsal horn nociceptive-specific neurons are more sensitive than wide dynamic range neurons to depression by immobilizing doses of volatile anesthetics: an effect partially reversed by the opioid receptor antagonist naloxone.

BACKGROUND: The mechanism and site of action within the spinal cord by which volatile anesthetics produce immobility are not well understood. Little work has been done directly comparing anesthetic effects on neurons with specific functional characteristics that mediate transfer of nociceptive information within the spinal cord. METHODS: Adult male rats were anesthetized and prepared for extracellular single-unit recordings from the lumbar dorsal horn. Nociceptive-specific (NS) and wide dynamic range (WDR) neurons were identified and noxious heat-evoked neuronal spike rates evaluated at 0.8 and 1.2 anesthetic minimum alveolar anesthetic concentration (MAC) halothane or isoflurane. In another group, noxious heat-evoked responses from NS neurons were evaluated at 0.8, 1.2 MAC halothane, and 1.2 MAC halothane plus IV naloxone (0.1 mg/kg). RESULTS: Increasing halothane from 0.8 to 1.2 MAC reduced the heat-evoked neuronal responses of NS neurons (n = 9) from 827 +/- 122 (mean +/- se) to 343 +/- 48 spikes/min (P < 0.05) but not WDR neurons (n = 9), 617 +/- 79 to 547 +/- 78 spikes/min. Increasing isoflurane from 0.8 to 1.2 MAC reduced the heat-evoked neuronal response of NS neurons (n = 9) from 890 +/- 339 to 188 +/- 97 spikes/min (P < 0.05) but did not alter the response of WDR neurons (n = 9) in which evoked spike rate went from 576 +/- 132 to 601 +/- 119 spikes/min. In a separate group, the response of NS neurons went from 282 +/- 60 to 74 +/- 32 spikes/min (P < 0.05) when halothane was increased from 0.8 to 1.2 MAC. IV administration of naloxone increased the heat-evoked response to 155 +/- 46 spikes/min (P < 0.05). CONCLUSIONS: NS but not WDR neurons in the lumbar dorsal horn are depressed by peri-MAC increases of halothane and isoflurane. This depression, at least with halothane, can be partially reversed by the opioid antagonist naloxone. Given that opioid receptors are not likely involved in the mechanisms by which volatile anesthetics produce immobility, this suggests that, although the neuronal depression is of substantial magnitude and occurs concurrent to the production of immobility, it may not play a major role in the production of this anesthetic end point.

Propofol produces immobility via action in the ventral horn of the spinal cord by a GABAergic mechanism.

BACKGROUND: We investigated the actions of propofol and isoflurane on nociceptive responses of neurons in the spinal cord. METHODS: We determined nociceptive responses of lumbar neurons in the dorsal horn (<1200 microm) and ventral horn (>1200 microm) of decerebrate rats before and during propofol (1 effective dose, ED(50)) or isoflurane (1 minimum alveolar concentration) anesthesia. During recording of ventral horn neurons, we administered picrotoxin by infusion to determine whether isoflurane and propofol differed in their effects at the gamma aminobutyric acid (GABA) Type A receptors. We also determined whether decerebration altered propofol requirements to produce immobility. RESULTS: Decerebration did not affect propofol requirements. The ED(50) for propofol was 497 +/- 58 microg x kg(-1) x min(-1) in intact rats and 420 +/- 65 microg x kg(-1) x min(-1) in decerebrated rats (P > 0.05), with corresponding propofol blood concentrations of 8.1 +/- 1.1 microg/mL and 7.3 +/- 1.1 microg/mL, respectively (P > 0.05). Propofol did not significantly depress dorsal horn neurons, but isoflurane depressed the responses to 56% of control (P < 0.05). Propofol depressed ventral horn neurons to 47% of control, whereas isoflurane depressed ventral horn neurons to 20% of control. Picrotoxin significantly reversed the depressant effect of propofol on ventral horn neuronal responses (79% of control, not significantly different from control). Pic- rotoxin, however, had no effect on isoflurane's depression of ventral horn neuronal responses (26% of control). CONCLUSIONS: Propofol acts in the spinal cord to produce immobility. This depressive effect occurs in the ventral horn and is mediated mainly by GABA(A) receptors. Isoflurane also depresses neurons in the ventral horn; however, isoflurane actions at the GABA(A) receptor are either weak or overridden by other effects in the ventral horn.

Perioperative drug therapy in elderly patients.

Advances in modern medicine and public health have resulted in increased longevity, which in turn has resulted in more elderly patients (arbitrarily defined as aged 65 yr or older) coming to the operating room for a variety of surgical procedures. Even in the absence of comorbidities, these patients, as compared with their younger cohorts, respond differently to various perioperative physiologic trespasses and pharmacologic interventions. In this clinical commentary, we focus on the altered pharmacologic responses elderly patients have during the perioperative period. In many instances, elderly patients are more sensitive to drugs, and for the purposes of this clinical commentary, we use the word sensitivity in its general clinical meaning, i.e., an enhanced response for a given dose of drug that might have a pharmacokinetic or pharmacodynamic explanation.

Proprioceptive function is more sensitive than motor function to desflurane anesthesia.

BACKGROUND: Evaluating the effects of sub-immobilizing anesthetic doses on movement will identify target neural circuits for investigation as sites of action for anesthetic-induced immobility. METHODS: Eleven pithed Northern Leopard frogs received 0, 0.4, 0.8, and 1.2 times the 50% effective dose for production of immobility (ED(50)) of desflurane and a further 7 received 0 and 0.4 ED(50) desflurane in random order. An electric stimulus applied to the forelimb elicited a hindlimb wiping reflex that was captured on video for later analysis. Isometric tension developed in the hindlimb during the 30 s stimulus application was measured. RESULTS: Compared to 0 ED(50), 0.4 ED(50) desflurane significantly increased latency to wipe 0.8 (0.1, 4.0) to 17.3 (0.4, 30.0) s (median [min max]), distance traveled by the hindfoot 0.42 (0.09, 1.82) to 0.89 (0.16, 4.82) m, and proximity of the hindfoot to stimulus 1 (0, 5) to 7 (1, 40) mm. It did not alter hindlimb maximum velocity or isometric tension but significantly reduced total hindlimb force 7.3 (1.7, 23.6) to 3.2 (1.4, 13.8) N. s proportionate to a reduced number of movements from 12 (3, 28) to 8 (2, 14). From 0.4 to 0.8 ED(50,) motor depressant effects of desflurane became apparent with significant reductions in maximum tension from 2.0 (0.6, 5.5) to 0.8 (0.1, 1.6) N and total force from 3.2 (1.4, 13.8) to 0.9 (0.0, 2.5) N.s. CONCLUSIONS: Proprioceptive function is more sensitive to anesthetic-induced depression than motor function in frogs. This suggests that the most anesthetic-sensitive component of the spinal neural circuitry underlying movement generation in response to noxious stimulus is prior to the level of the motoneuron.

Modeling the GABAergic action of etomidate on the thalamocortical system.

BACKGROUND: We have used a computational model of the thalamocortical system to investigate the effects of a GABAergic anesthetic (etomidate) on cerebral cortical and thalamic neuronal function. We examined the effects of phasic and tonic inhibition, as well as the relative importance of anesthetic action in the thalamus and cortex. METHODS: The amount of phasic GABAergic inhibition was adjusted in the model to simulate etomidate concentrations of between 0.25 and 2 microM, with the concentration range producing unconsciousness assumed to be between 0.25 and 0.5 microM. In addition, we modeled tonic inhibition separately, and then phasic and tonic inhibition together. We also introduced phasic and tonic inhibition into the cerebral cortex and thalamus separately to determine the relative importance of each of these structures to anesthetic-induced depression of the thalamocortical system. RESULTS: Phasic inhibition decreased cortical neuronal firing by 11%-18% in the 0.25-0.5 microM range and by 38% at 2 microM. Tonic inhibition produced similar depression (11%-21%) in the 0.25-0.5 microM range but 65% depression at 2 microM; phasic and tonic inhibition combined produced the most inhibition (76% depression at 2 microM). When the thalamus and cortex were separately subjected to phasic and tonic inhibition, cortical firing rates decreased less compared to when both structures were targeted. In the 0.25-0.5 microM range, cortical firing rate was minimally affected when etomidate action was simulated in the thalamus only. CONCLUSIONS: This computational model of the thalamocortical system indicated that tonic GABAergic inhibition seems to be more important than phasic GABAergic inhibition (especially at larger etomidate concentrations), although both combined had the most effect on cerebral cortical firing rates. Furthermore, etomidate action in the thalamus, by itself, does not likely explain etomidate-induced unconsciousness.

Increases in spinal cerebrospinal fluid potassium concentration do not increase isoflurane minimum alveolar concentration in rats.

BACKGROUND: Previous studies demonstrated that MAC for isoflurane directly correlates with the concentration of Na(+) in cerebrospinal fluid surrounding the spinal cord, the primary site for mediation of the immobility produced by inhaled anesthetics. If this correlation resulted from increased irritability of the cord, then infusion of increased concentrations of potassium (K(+)) might be predicted to act similarly. However, an absence of effect of K(+) might be interpreted to indicate that K(+) channels do not mediate the immobility produced by inhaled anesthetics whereas Na(+) channels remain as potential mediators. Accordingly, in the present study, we examined the effect of altering intrathecal concentrations of K(+) on MAC. METHODS: In rats prepared with chronic indwelling intrathecal catheters, we infused solutions deficient in K(+) and with an excess of K(+) into the lumbar space and measured MAC for isoflurane 24 h before, during, and 24 h after infusion. Rats similarly prepared were tested for the effect of altered osmolarity on MAC (accomplished by infusion of mannitol) and for the penetration of Na(+) into the cord. RESULTS: MAC of isoflurane never significantly increased with increasing concentrations of K(+) infused intrathecally. At infused concentrations exceeding 12 times the normal concentration of KCl, i.e., 29 mEq/L, rats moved spontaneously at isoflurane concentrations just below, and sometimes at MAC, but the average MAC in these rats did not exceed their control MAC. At the largest infused concentration (58.1 mEq/L), MAC significantly decreased and did not subsequently return to normal (i.e., such large concentrations produced injury). Infusions of lower concentrations of K(+) had no effect on MAC. Infusion of osmotically equivalent solutions of mannitol did not affect MAC. Na(+) infused intrathecally measurably penetrated the spinal cord. CONCLUSIONS: The results do not support a mediation or modulation of MAC by K(+) channels.

The effects of aromatic anesthetics on dorsal horn neuronal responses to noxious stimulation.

BACKGROUND: Gamma-aminobutyric acid type A receptor potentiation and/or N-methyl-d-aspartate (NMDA) receptor inhibition might explain the anesthetic properties of fluorinated aromatic compounds. We hypothesized that depression of dorsal horn neuronal responses to noxious stimulation would correlate with the magnitude of effect of benzene (BNZ), o-difluorobenzene, and hexafluorobenzene (HFB) on NMDA receptors. METHODS: Rats were anesthetized with desflurane. A T13-L1 laminectomy allowed extracellular recording of neuronal activity from the lumbar spinal cord. After discontinuing desflurane administration, MAC for each aromatic anesthetic was determined. A 5-s noxious mechanical stimulus was then applied to the hindpaw receptive field of nociceptive dorsal horn neurons, and single-neuron responses were recorded at 0.8 and 1.2 MAC. These responses were also recorded in decerebrate rats receiving BNZ and HFB at 0-1.2 MAC. RESULTS: In intact rats, depression of responses of dorsal horn neurons to noxious stimulation by peri-MAC increases in BZN, o-difluorobenzene, and HFB correlated directly with their in vitro capacity to block NMDA receptors. In decerebrate rats, 1.2 MAC BNZ depressed nociceptive responses by 60%, with a further percentage decrease continuing from 0.8 to 1.2 MAC approximately equal to that found in intact rats. In decerebrate rats, HFB caused a progressive dose-related decrease in MAC (maximum 25%), but in intact rats, an increase from 0.8 to 1.2 neuronal response caused an (insignificant) increase in neuronal response. CONCLUSIONS: The findings in intact rats suggest that NMDA blockade contributes to the depression of dorsal horn neurons to nociceptive stimulation by fluorinated aromatic anesthetics. These results, combined with the additional findings in decerebrate rats, suggest that supraspinal effects (perhaps on gamma-aminobutyric acid type A receptors) may have a supraspinal facilitatory effect on nociception for HFB.

Immobilizing doses of halothane, isoflurane or propofol, do not preferentially depress noxious heat-evoked responses of rat lumbar dorsal horn neurons with ascending projections.

BACKGROUND: The spinal cord is an important site where volatile anesthetics decrease sensation and produce immobility. Beyond this knowledge, our understanding of a site of anesthetic action is limited. Previous evidence suggests that dorsal horn neurons with ascending projections may be more susceptible to depression by general anesthetics than local spinal interneurons. In this study we evaluated the effects of volatile and injectable general anesthetics on lumbar dorsal horn neurons with and without ascending projections. METHODS: Thirty-seven adult male rats underwent laminectomies at C1, for placement of a stimulating electrode, and T13/L1, for extracellular recording from the spinal cord dorsal horn. Neuronal responses to heat were evaluated under two doses of halothane, isoflurane, or propofol anesthesia. RESULTS: Under both halothane and isoflurane anesthesia, increasing the dose from 0.8 to 1.2 minimum alveolar concentration (MAC) had no significant effect on heat-evoked responses in neurons that had ascending projections identified via antidromic stimulation (AD) or those without ascending projections (nAD). Heat responses in AD neurons 1 min after i.v. administration of 3 and 5 mg/kg of propofol were reduced to 60% +/- 18% (mean +/- SE) and 39% +/- 14% of control respectively. Similarly, in nAD neurons responses were reduced to 56% +/- 14% and 50% +/- 10% of control by 3 and 5 mg/kg propofol respectively. CONCLUSIONS: Our findings suggest, at peri-MAC concentrations, these general anesthetics do not preferentially depress lumbar dorsal horn neurons with ascending projections compared to those with no identifiable ascending projections.