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Biomedical subjects

Stephan M Jakob

Publications and source records attributed to Stephan M Jakob.

At least 19 recordsLinked to original sources

Incidence of low central venous oxygen saturation during unplanned admissions in a multidisciplinary intensive care unit: an observational study.

INTRODUCTION: It has been shown that early central venous oxygen saturation (ScvO2)-guided optimization of hemodynamics can improve outcome in septic patients. The early ScvO2 profile of other patient groups is unknown. The aim of this study was to characterize unplanned admissions in a multidisciplinary intensive care unit (ICU) with respect to ScvO2 and outcome. METHODS: Ninety-eight consecutive unplanned admissions to a multidisciplinary ICU (median age 63 [range 19 to 83] years, median Simplified Acute Physiology Score [SAPS II] 43 [range 11 to 92]) with a clinical indication for a central venous catheter were included in the study. ScvO2 was assessed at ICU arrival and six hours later but was not used to guide treatment. Length of stay in ICU (LOSICU) and in hospital (LOShospital) and 28-day mortality were recorded. RESULTS: ScvO2 was 70% +/- 12% (mean +/- standard deviation) at admission and 71% +/- 10% six hours later (p = 0.484). Overall 28-day mortality was 18%, LOSICU was 3 (1 to 28) days, and LOShospital was 19 (1 to 28) days. Patients with an ScvO2 of less than 60% at admission had higher mortality than patients with an ScvO2 of more than 60% (29% versus 17%, p < 0.05). Changes in ScvO2 during the first six hours were not predictive of LOSICU, LOShospital, or mortality. CONCLUSION: Low ScvO2 in unplanned admissions and high SAPS II are associated with increased mortality. Standard ICU treatment increased ScvO2 in patients with a low admission ScvO2, but the increase was not associated with LOSICU or LOShospital.

Adult↗

Decreasing gut wall glucose as an early marker of impaired intestinal perfusion.

OBJECTIVE: The aim of this study was to assess the microcirculatory and metabolic consequences of reduced mesenteric blood flow. DESIGN: Prospective, controlled animal study. SETTING: The surgical research unit of a university hospital. SUBJECTS: A total of 13 anesthetized and mechanically ventilated pigs. INTERVENTIONS: Pigs were subjected to stepwise mesenteric blood flow reduction (15% in each step, n = 8) or served as controls (n = 5). Superior mesenteric arterial blood flow was measured with ultrasonic transit time flowmetry, and mucosal and muscularis microcirculatory perfusion in the small bowel were each measured with three laser Doppler flow probes. Small-bowel intramucosal Pco2 was measured by tonometry, and glucose, lactate (L), and pyruvate (P) were measured by microdialysis. MEASUREMENTS AND MAIN RESULTS: In control animals, superior mesenteric arterial blood flow, mucosal microcirculatory blood flow, intramucosal Pco2, and the lactate/pyruvate ratio remained unchanged. In both groups, mucosal blood flow was better preserved than muscularis blood flow. During stepwise mesenteric blood flow reduction, heterogeneous microcirculatory blood flow remained a prominent feature (coefficient of variation, approximately 45%). A 30% flow reduction from baseline was associated with a decrease in microdialysis glucose concentration from 2.37 (2.10-2.70) mmol/L to 0.57 (0.22-1.60) mmol/L (p < .05). After 75% flow reduction, the microdialysis lactate/pyruvate ratio increased from 8.6 (8.0-14.1) to 27.6 (15.5-37.4, p < .05), and arterial-intramucosal Pco2 gradients increased from 1.3 (0.4-3.5) kPa to 10.8 (8.0-16.0) kPa (p < .05). CONCLUSIONS: Blood flow redistribution and heterogeneous microcirculatory perfusion can explain apparently maintained regional oxidative metabolism during mesenteric hypoperfusion, despite local signs of anaerobic metabolism. Early decreasing glucose concentrations suggest that substrate supply may become crucial before oxygen consumption decreases.

Animals↗

Membrane microdialysis: Evaluation of a new method to assess splanchnic tissue metabolism.

OBJECTIVE: Measuring peritoneal lactate concentrations could be useful for detecting splanchnic hypoperfusion. The aims of this study were to evaluate the properties of a new membrane-based microdialyzer in vitro and to assess the ability of the dialyzer to detect a clinically relevant decrease in splanchnic blood flow in vivo. DESIGN: A membrane-based microdialyzer was first validated in vitro. The same device was tested afterward in a randomized, controlled animal experiment. SETTING: University experimental research laboratory. SUBJECTS: Twenty-four Landrace pigs of both genders. INTERVENTIONS: In vitro: Membrane microdialyzers were kept in warmed sodium lactate baths with lactate concentrations between 2 and 8 mmol/L for 10-120 mins, and microdialysis lactate concentrations were measured repeatedly (210 measurements). In vivo: An extracorporeal shunt with blood reservoir and roller pump was inserted between the proximal and distal abdominal aorta, and a microdialyzer was inserted intraperitoneally. In 12 animals, total splanchnic blood flow (measured by transit time ultrasound) was reduced by a median 43% (range, 13% to 72%) by activating the shunt; 12 animals served as controls. MEASUREMENTS AND MAIN RESULTS: In vitro: The fractional lactate recovery was 0.59 (0.32-0.83) after 60 mins and 0.82 (0.71-0.87) after 90 mins, with no further increase thereafter. At 60 and 90 mins, the fractional recovery was independent of the lactate concentration. In vivo: Abdominal blood flow reduction resulted in an increase in peritoneal microdialysis lactate concentration from 1.7 (0.3-3.8) mmol/L to 2.8 (1.3-6.2) mmol/L (p = .006). At the same time, mesenteric venous-arterial lactate gradient increased from 0.1 (-0.2-0.8) mmol/L to 0.3 (-0.3 -1.8) mmol/L (p = .032), and mesenteric venous-arterial Pco2 gradients increased from 12 (8-19) torr to 21 (11-54) torr (p = .005). CONCLUSIONS: Peritoneal membrane microdialysis provides a method for the assessment of splanchnic ischemia, with potential for clinical application.

Animals↗

Reversible encephalopathy complicating post-streptococcal glomerulonephritis.

We describe a 15-year-old boy with acute transient encephalopathy complicating poststreptococcal glomerulonephritis. Based on advanced magnetic resonance imaging, cerebral alterations were related to cerebrovascular autoregulatory dysfunction (ie, a vasogenic edema) and vasculitis was excluded. These insights into the pathophysiology improve patient management and argue against the therapeutic immunosuppression postulated by some authors.

Adolescent↗

Effects of low abdominal blood flow and dobutamine on blood flow distribution and on the hepatic arterial buffer response in anaesthetized pigs.

Low cardiac output impairs the hepatic arterial buffer response (HABR). Whether this is due to low abdominal blood flow per se is not known. Dobutamine is commonly used to increase cardiac output, and it may further modify hepatosplanchnic and renal vasoregulation. We assessed the effects of isolated abdominal aortic blood flow changes and dobutamine on hepatosplanchnic and renal blood flow. Twenty-five anesthetized pigs with an abdominal aorto-aortic shunt were randomized to 2 control groups [zero (n = 6) and minimal (n = 6) shunt flow], and 2 groups with 50% reduction of abdominal blood flow and either subsequent increased abdominal blood flow by shunt reduction (n = 6) or dobutamine infusion at 5 and 10 microg kg(-1) min(-1) with constant shunt flow (n = 7). Regional (ultrasound) and local (laser Doppler) intra-abdominal blood flows were measured. The HABR was assessed during acute portal vein occlusion. Sustained low abdominal blood flow, by means of shunt activation, decreased liver, gut, and kidney blood flow similarly and reduced local microcirculatory blood flow in the jejunum. Shunt flow reduction partially restored regional blood flows but not jejunal microcirculatory blood flow. Low-but not high-dose dobutamine increased gut and celiac trunk flow whereas hepatic artery and renal blood flows remained unchanged. Neither intervention altered local blood flows. The HABR was not abolished during sustained low abdominal blood flow despite substantially reduced hepatic arterial blood flow and was not modified by dobutamine. Low-but not high-dose dobutamine redistributes blood flow toward the gut and celiac trunk. The jejunal microcirculatory flow, once impaired, is difficult to restore.

Abdomen↗

Effects of prolonged endotoxemia on liver, skeletal muscle and kidney mitochondrial function.

INTRODUCTION: Sepsis may impair mitochondrial utilization of oxygen. Since hepatic dysfunction is a hallmark of sepsis, we hypothesized that the liver is more susceptible to mitochondrial dysfunction than the peripheral tissues, such as the skeletal muscle. We studied the effect of prolonged endotoxin infusion on liver, muscle and kidney mitochondrial respiration and on hepatosplanchnic oxygen transport and microcirculation in pigs. METHODS: 20 anesthetized pigs were randomized to receive endotoxin or saline infusion for 24 hours. Muscle, liver and kidney mitochondrial respiration was assessed. Cardiac output (thermodilution), carotid, superior mesenteric and kidney arterial, portal venous (ultrasound Doppler) and microcirculatory blood flow (laser Doppler) were measured, and systemic and regional oxygen transport and lactate exchange were calculated. RESULTS: Endotoxin infusion induced hyperdynamic shock and impaired the glutamate- and succinate-dependent mitochondrial respiratory control ratio (RCR) in the liver (glutamate: endotoxemia: median [range] 2.8 [2.3-3.8] vs. controls: 5.3 [3.8-7.0]; p<0.001; succinate: endotoxemia: 2.9 [1.9-4.3] vs. controls: 3.9 [2.6-6.3] p=0.003). While the ADP:O ratio was reduced with both substrates, maximal ATP production was impaired only in the succinate-dependent respiration. Hepatic oxygen consumption and extraction, and liver surface laser Doppler blood flow remained unchanged. Glutamate-dependent respiration in the muscle and kidney was unaffected. CONCLUSIONS: Endotoxemia reduces the efficiency of hepatic but neither skeletal muscle nor kidney mitochondrial respiration, independent of regional and microcirculatory blood flow changes.

Animals↗

The effects of dexmedetomidine/remifentanil and midazolam/remifentanil on auditory-evoked potentials and electroencephalogram at light-to-moderate sedation levels in healthy subjects.

Avoidance of excessively deep sedation levels is problematic in intensive care patients. Electrophysiologic monitoring may offer an approach to solving this problem. Since electroencephalogram (EEG) responses to different sedation regimens vary, we assessed electrophysiologic responses to two sedative drug regimens in 10 healthy volunteers. Dexmedetomidine/remifentanil (dex/remi group) and midazolam/remifentanil (mida/remi group) were infused 7 days apart. Each combination of medications was given at stepwise intervals to reach Ramsay scores (RS) 2, 3, and 4. Resting EEG, bispectral index (BIS), and the N100 amplitudes of long-latency auditory-evoked potentials (ERP) were recorded at each level of sedation. During dex/remi, resting EEG was characterized by a recurrent high-power low-frequency pattern which became more pronounced at deeper levels of sedation. BIS Index decreased uniformly in only the dex/remi group (from 94 +/- 3 at baseline to 58 +/- 14 at RS 4) compared to the mida/remi group (from 94 +/- 2 to 76 +/- 10; P = 0.029 between groups). The ERP amplitudes decreased from 5.3 +/- 1.3 at baseline to 0.4 +/- 1.1 at RS 4 (P = 0.003) in only the mida/remi group. We conclude that ERPs in volunteers sedated with dex/remi, in contrast to mida/remi, indicate a cortical response to acoustic stimuli, even when sedation reaches deeper levels. Consequently, ERP can monitor sedation with midazolam but not with dexmedetomidine. The reverse is true for BIS.

Acoustic Stimulation↗

Comparison of continuous and intermittent renal replacement therapy for acute renal failure.

BACKGROUND: Mortality rates of critically ill patients with acute renal failure (ARF) requiring renal replacement therapy (RRT) are high. Intermittent and continuous RRT are available for these patients on the intensive care units (ICUs). It is unknown which technique is superior with respect to patient outcome. METHODS: We randomized 125 patients to treatment with either continuous venovenous haemodiafiltration (CVVHDF) or intermittent haemodialysis (IHD) from a total of 191 patients with ARF in a tertiary-care university hospital ICU. The primary end-point was ICU and in-hospital mortality, while recovery of renal function and hospital length of stay were secondary end-points. RESULTS: During 30 months, no patient escaped randomization for medical reasons. Sixty-six patients were not randomized for non-medical reasons. Of the 125 randomized patients, 70 were treated with CVVHDF and 55 with IHD. The two groups were comparable at the start of RRT with respect to age (62+/-15 vs 62+/-15 years, CVVHDF vs IHD), gender (66 vs 73% male sex), number of failed organ systems (2.4+/-1.5 vs 2.5+/-1.6), Simplified Acute Physiology Scores (57+/-17 vs 58+/-23), septicaemia (43 vs 51%), shock (59 vs 58%) or previous surgery (53 vs 45%). Mortality rates in the hospital (47 vs 51%, CVVHDF vs IHD, P = 0.72) or in the ICU (34 vs 38%, P = 0.71) were independent of the technique of RRT applied. Hospital length of stay in the survivors was comparable in patients on CVVHDF [median (range) 20 (6-71) days, n = 36] and in those on IHD [30 (2-89) days, n = 27, P = 0.25]. The duration of RRT required was the same in both groups. CONCLUSION: The present investigation provides no evidence for a survival benefit of continuous vs intermittent RRT in ICU patients with ARF.

Acute Kidney Injury↗

Severe acute pancreatitis: case-oriented discussion of interdisciplinary management.

The clinical course of an episode of acute pancreatitis varies from a mild, transitory illness to a severe often necrotizing form with distant organ failure and a mortality rate of 20-40%. Patients with severe pancreatitis, representing about 15-20% of all patients with acute pancreatitis, need to be identified as early as possible after onset of symptoms allowing starting intensive care treatment early in the disease process. An episode of severe acute pancreatitis progresses in two phases. The first 10-14 days are characterized by a systemic inflammatory response syndrome maintained by the release of various inflammatory mediators. The second phase, beginning about 10-14 days after the onset of the disease is dominated by sepsis-related morbidity due to infected peripancreatic and pancreatic necrosis. This state is associated with septic multiple organ systemic failure. The importance of infection on the outcome of necrotizing pancreatitis has been clearly delineated and the pre-emptive use of broad-spectrum antibiotics that achieve effective tissue concentrations is considered standard management of patients with severe necrotizing pancreatitis, especially if associated with organ failure or extended necrosis. Patients with infected necrosis should undergo a surgical intervention. The standard open technique consisting of an organ preserving necrosectomy followed by a postoperative concept of lavage and/or drainage to evacuate necrotic debris occurring during the further course has recently been challenged by various minimally invasive approaches.

Acute Disease↗

Siglec-9 transduces apoptotic and nonapoptotic death signals into neutrophils depending on the proinflammatory cytokine environment.

We report about new apoptotic and non-apoptotic death pathways in neutrophils that are initiated via the surface molecule sialic acid-binding immunoglobulin-like lectin (Siglec)-9. In normal neutrophils, Siglec-9 ligation induced apoptosis. Inflammatory neutrophils obtained from patients with acute septic shock or rheumatoid arthritis demonstrated increased Siglec-9, but normal Fas receptor-mediated cytotoxic responses when compared with normal blood neutrophils. The increased Siglec-9-mediated death was mimicked in vitro by short-term preincubation of normal neutrophils with proinflammatory cytokines, such as granulocyte/macrophage colony-stimulating factor (GM-CSF), interferon-alpha (IFN-alpha), and IFN-gamma, and was demonstrated to be caspase independent. Experiments using scavengers of reactive oxygen species (ROS) or neutrophils unable to generate ROS indicated that both Siglec-9-mediated caspase-dependent and caspase-independent forms of neutrophil death depend on ROS. Interestingly, the caspase-independent form of neutrophil death was characterized by cytoplasmic vacuolization and several other nonapoptotic morphologic features, which were also seen in neutrophils present in joint fluids from rheumatoid arthritis patients. Taken together, these data suggest that apoptotic (ROS- and caspase-dependent) and nonapoptotic (ROS-dependent) death pathways are initiated in neutrophils via Siglec-9. The new insights have important implications for the pathogenesis, diagnosis, and treatment of inflammatory diseases such as sepsis and rheumatoid arthritis.

Antigens, CD↗

Does fluid loading influence measurements of intestinal permeability?

INTRODUCTION: Urinary recovery of enterally administered probes is used as a clinical test of intestinal mucosal permeability. Recently, evidence has been provided that the recovery of some but not all sugar probes is dependent on the amount of diuresis and renal function. The aim of this study was to assess the effect of fluid loading on the urinary recovery of sugar probes in healthy volunteers. METHODS: In a cross-over study, 10 healthy volunteers ingested 100 ml of a solution containing 0.2 g of 3-O-methyl-D-glucose (3-OMG), 0.5 g of D-xylose, 1.0 g of L-rhamnose, and 5.0 g of lactulose on two different days. The volunteers were randomized to receive either 2 litres of Ringer acetate or no fluid during the following 3 hours. The sugar concentrations were measured in 5-hour urine samples period. RESULTS: Fluid loading increased urine production and urinary recovery of xylose. Fluid loading did not influence the urinary recovery of 3-OMG, L-rhamnose, or lactulose. Neither the lactulose/rhamnose ratio nor the 3-OMG/rhamnose ratio changed. CONCLUSION: Fluid loading increases mediated carbohydrate transport but not the lactulose/rhamnose ratio, after oral sugar administration in healthy volunteers. It remains to be determined whether sugar probes are handled differently in response to fluids in patients with organ dysfunctions.

Adult↗

Blood pressure and vessel recanalization in the first hours after ischemic stroke.

BACKGROUND AND PURPOSE: Transient elevation of arterial blood pressure (BP) is frequent in acute ischemic stroke and may help to increase perfusion of tissue jeopardized by ischemia. If this is true, recanalization may eliminate the need for this BP elevation. METHODS: We analyzed BP in 149 patients with acute ischemic stroke on admission to the hospital and 1 and 12 hours after intraarterial thrombolysis. BP values of patients with adequate recanalization were compared with BP values of patients with inadequate recanalization. Recanalization was determined on cerebral arteriography after thrombolysis using thrombolysis in myocardial infarction grades. RESULTS: Systolic, mean, and diastolic arterial BP decreased significantly from admission to 12 hours after thrombolysis in all patients (P<0.001). Before thrombolysis, patients with adequate and inadequate recanalization showed equal systolic (147.4 and 148.0 mm Hg), mean (102.1 and 104.1 mm Hg), and diastolic (79.5 and 82.1 mm Hg) BP values. Twelve hours after thrombolysis, patients with adequate recanalization had lower values than those with inadequate recanalization (systolic BP, 130 versus 139.9 mm Hg; mean BP, 86.8 versus 92.2 mm Hg; and diastolic, BP 65.2 versus 68.3 mm Hg). Two-way repeated ANOVA analysis showed a significant group x time interaction for systolic BP, indicating a larger systolic BP decrease when recanalization succeeded (P=0.019). CONCLUSIONS: The course of elevated systolic but not diastolic BP after acute ischemic stroke was found to be inversely associated with the degree of vessel recanalization. When recanalization failed, systolic BP remained elevated longer than when it succeeded.

Adult↗

Estimation of central venous pressure by ultrasound.

INTRODUCTION: Increasing blood volume and cardiac output is one of the most commonly needed intervention in the primary care of traumatized and severely ill patients. Although cardiac filling pressures have severe limitations in assessing the preload, central venous pressure (CVP) is the invasive measure most frequently used in clinical practice for the assessment of volume status and cardiac preload. We combined ultrasound and tissue pressure measurement for non-invasive jugular and brachial venous pressure estimation. MATERIALS AND METHODS: CVP was measured invasively and non-invasively using the new technique in 32 critically ill patients. In six volunteers, increasing PEEP was used for the assessment of changes in non-invasive CVP. RESULTS: Non-invasive CVP increased linearly with increasing PEEP, independent of the investigator. Median (range) coefficient of variation (CV) for five consecutive measurements performed by three investigators in volunteers was 15% (6-31%), 14% (4-31%), and 21% (8-42%). Absolute differences between the average non-invasive CVP between investigators was 1.7 cm H2O (0.4-6.6 cm H2O), and the inter-examiner CVP was high (182%, 40-415%). In patients, invasive CVP was 10 mmHg (5-18 mmHg), and the corresponding non-invasive venous pressures were 8 mmHg (3-14 mmHg, basilic vein, p<0.01) and 6 mmHg (3-13 mmHg, jugular vein, p<0.01). The coefficients of variation were 4% (<1%-64%, invasive CVP), 22% (5%-51%, non-invasive basilic vein pressure), and 17% (7%-34%, non-invasive jugular vein pressure). CONCLUSION: Ultrasound-based, non-invasive measurement of venous pressure provides a relatively easy method rapid estimation of changes in CVP, although absolute values may differ substantially from invasive CVP and between different investigators.

Adult↗

Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion.

OBJECTIVE: To assess the effects of low hepatosplanchnic blood flow on regional blood flow control and oxygenation. DESIGN: Three randomized, controlled animal experiments. SETTING: Two university experimental research laboratories. SUBJECTS: Pigs of either gender. INTERVENTIONS: Isolated abdominal blood flow reduction: An extracorporeal shunt with reservoir and roller pump was inserted between proximal and distal aorta in 11 pigs. Abdominal aortic blood flow was reduced by 50% by activating the shunt. Mesenteric ischemia: In seven pigs, superior mesenteric arterial flow was reduced to 4 mL.kg.min for 4 hrs. Cardiac tamponade: In 12 pigs, aortic blood flow was reduced by cardiac tamponade to 50 mL (moderate tamponade) and further to 30 mL.kg.min (severe tamponade) for 1 hr each. In each experimental condition, the same number of control animals was used. MEASUREMENTS AND MAIN RESULTS: Abdominal blood flow reduction, acute mesenteric ischemia, and moderate tamponade resulted in a portal venous flow (QPV) reduction to 51 +/- 23%, 52 +/- 18%, and 61 +/- 25% (mean +/- sd) of baseline flow, respectively. During abdominal blood flow reduction, QPV and hepatic arterial flow (QHA) decreased proportionally, whereas in moderate tamponade and acute mesenteric ischemia QPV reduction was associated with an increase in QHA of 30 +/- 39% and 102 +/- 108%, respectively (p = .001 and .018). Prolonged mesenteric ischemia restored total hepatic blood flow (Qliver) completely. During all conditions, decreasing mesenteric oxygen consumption was partly prevented by increased mesenteric oxygen extraction (p < .001 for all conditions). In contrast, decreasing hepatic oxygen delivery was associated with increased oxygen extraction in tamponade (p = .009) but not in abdominal blood flow reduction. CONCLUSIONS: Blood flow redistribution can restore Qliver totally when mesenteric blood flow is reduced selectively, partially when cardiac output is reduced, and not at all during abdominal blood flow reduction. Since hepatic oxygen extraction does not increase in abdominal blood flow reduction, hepatic oxygenation is at risk in this condition.

Animals↗

Preconditioning with monophosphoryl lipid A improves survival of critically ischemic tissue.

In this study we sought to assess the effects of preconditioning with monophosphoryl lipid A on critically ischemic wound margins and on systemic and local hemodynamics and oxygenation during prolonged anesthesia with volatile anesthetics and narcotics. Twenty large white pigs were randomly assigned to receive either monophosphoryl lipid A 35 mug/kg IV or saline 24 h before dissection of a buttock flap. The animals were anesthetized with isoflurane (end-tidal concentration approximately 1.25%) for surgery and subsequent monitoring of hemodynamics and oxygenation both systemically and in the flap tissue for 6 h. Preconditioning resulted in increased cardiac index and oxygen delivery (both P < 0.05) and in decreased central venous pressure and systemic vascular resistance (both P < 0.01). In the preconditioned flap tissue, microcirculatory blood flow (laser Doppler flowmetry) and partial tissue oxygen tension (polarographic microprobes) were up to 2.5-fold higher compared with control (both P < 0.05) and flap necrosis was reduced by 20% on postoperative day 14 (P < 0.05). Our results suggest that preconditioning with a single dose of monophosphoryl lipid A may attenuate ischemia-related wound healing complications, which may be related to an improvement in perfusion and oxygenation of this tissue. Furthermore, preconditioning exerted a systemic cardiovascular stabilization effect during prolonged isoflurane anesthesia.

Anesthesia, General↗

N100 auditory potential and electroencephalogram discriminate propofol-induced sedation levels.

OBJECTIVE: In the present study, we evaluated the electroencephalogram (EEG) and auditory N100 potential (N100) before and during propofol-induced sedation. The aim was to test whether using EEG and N100 the level of sedation may be evaluated. METHODS: Twenty-nine cardiac surgery patients were studied. The EEG signal and the N100 potential were recorded at awake one day before the cardiac operation and two times after the operation, when the clinical level of postoperative propofol sedation was considered deep (Ramsay Score 6) and moderate (Ramsay Score 4). Discriminant analysis was used to select those spectral EEG and/or N100 variables which would predict the correct level of sedation best. The final classification was based on canonical discriminant functions and Mahalanobis' distance. RESULTS: The spectral EEG variables (slow/fast-ratio, delta, and beta2 powers) predicted the correct level of sedation with 81% (canonical discriminant functions) and 80% (Mahalanobis' distance) accuracy. Similarly, the N100 (amplitude, latency, and the first principal component) predicted the correct level of sedation with 91% and 92% accuracy, and the combination of the EEG and N100 with 96% and 93% accuracy. CONCLUSIONS: Our findings suggest that the combined use of EEG and N100 may help to differentiate the propofol-induced sedation levels, and thus be a useful compliment to clinical sedation scales.

Consciousness↗

Midlatency auditory-evoked potentials in the assessment of sedation in cardiac surgery patients.

OBJECTIVES: Midlatency auditory-evoked potentials (MLAEPs) may provide an objective measure of depth of sedation. The aim of this study was to evaluate MLAEPs for measuring sedation in cardiac surgery patients. DESIGN: Prospective study. SETTING: Intensive care unit of a university hospital. PARTICIPANTS: Twenty-two patients scheduled for elective coronary artery bypass grafting. INTERVENTIONS: MLAEPs were obtained at 5 time points: the day before surgery (baseline), 1 hour before surgery, after premedication, postoperatively during deep (Ramsay 6) and moderate (Ramsay 4) sedation, and the day after surgery. MEASUREMENTS AND MAIN RESULTS: The latency of the Nb MLAEP component increased from 44 ms (38-60 ms; median, range) at baseline to 49 ms (41-64 ms) after premedication (p = 0.03) and further to 63 ms (48-80 ms) during deep sedation after surgery (P < 0.01). Although a decreasing clinical level of sedation after rewarming was not associated with a significant change in Nb latency (61 ms [42-78 ms]), the MLAEP NaPa amplitude increased from 0.9 muV (0.4-1.6 microV) to 1.3 muV (0.8-3.9 microV; p = 0.01). Nb latency remained increased the day after surgery (49 ms [37-71 ms]) as compared with baseline (p < 0.01). CONCLUSIONS: MLAEP latencies can reflect subtle changes in auditory perception, while amplitudes seem to change with transition between deep levels of sedation.

Adult↗