Lipocalin-2 serum levels are increased in acute hepatic failure.

Lipocalin-2 (LCN-2), which is expressed in immunocytes as well as hepatocytes, is upregulated in cells under stress from infection or inflammation with increase in serum levels. We sought to investigate the relevance of LCN-2 in the setting of acute hepatic failure, particularly when addressed with the molecular adsorbent recirculating system (MARS). We measured serum LCN-2 concentrations with enzyme-linked immunosorbent assay (ELISA) in 8 patients with acute-on-chronic-liver failure (ACLF) and acute liver failure (ALF) who were treated with MARS. The controls were 14 patients with stable chronic hepatic failure (CHF). LCN-2 was determined immediately before and after the first MARS session. Baseline LCN-2 serum concentrations were significantly increased among ACLF and ALF patients as compared with CHF (P = .004 and P = .0086, respectively). There was no significant difference between the ALF and ACLF group. Moreover, serum LCN-2 levels did not change significantly during the MARS treatment. Serum LCN-2 levels, therefore, may be useful to discern acute from chronic hepatic failure and to monitor the course as well as the severity of the disease.

The effect of the molecular adsorbent recirculating system on moxifloxacin and meropenem plasma levels.

BACKGROUND: Adequate plasma antibiotic concentrations are necessary for effective elimination of invading microorganism; however, extracorporeal organ support systems are well known to alter plasma concentrations of antibiotics, requiring dose adjustments to achieve effective minimal inhibitory concentrations in the patient's blood. METHODS: A mock molecular adsorbent recirculating system (MARS) circuit was set using 5000 ml of bovine heparinized whole blood to simulate an 8-h MARS treatment session. After the loading dose of 400 mg of moxifloxacin or 2 g of meropenem had been added, blood was drawn from the different parts of the MARS circuit at various time points and analyzed by high-performance liquid chromatography. The experiments were performed in triplicate. Additionally, meropenem concentrations were determined in the plasma of one patient treated with MARS suffering from acute liver failure due to an idiosyncratic reaction to immunosuppressive medication. RESULTS: In our single-compartment model, a significant decrease in the quasi-systemic concentration of moxifloxacin and meropenem could be detected as early as 15 min after the commencing of the MARS circuit. Moreover, within 60 min the moxifloxacin and meropenem concentrations were less than 50% of the initial value. The activated charcoal removed the majority of moxifloxacin and meropenem in the albumin circuit. In our patient, the meropenem concentrations in the return line after MARS were constantly lower than in the access line, indicating a likely removal of meropenem through MARS. CONCLUSION: Our data provide evidence that moxifloxacin and meropenem are effectively removed from the patient's blood by MARS, leading to low plasma levels. Dose adjustments of both antibiotic compounds may be required.

Nucleosome serum levels in acute hepatic failure and MARS treatment.

Serum nucleosomes have been suggested to be markers for cell death and apoptosis. Increased hepatocyte apoptosis can be demonstrated in acute liver failure (ALF) as well as acute-on-chronic liver failure (ACLF). We investigated the relevance of nucleosomes in the setting of acute hepatic failure. Further, we studied the effects of the molecular adsorbent recirculating system (MARS) on this marker of cell death. We measured serum nucleosome concentrations with ELISA in 12 patients with ACLF and 7 patients suffering from ALF, with 14 patients experiencing stable chronic hepatic failure (CHF) as controls. In a subset of 8 ACLF and ALF patients treated with MARS, nucleosomes were determined immediately before and after the first MARS session. Baseline nucleosome serum concentrations were significantly increased in ACLF and ALF patients as compared with CHF patients (P = .0161 and P = .0037, respectively). There was no significant difference between the ALF and ACLF groups. Moreover, serum nucleosome levels did not change significantly during MARS treatment in ALF and ACLF patients. Serum nucleosome levels therefore may be useful to discern acute from chronic hepatic failure or to monitor the course and the severity of the disease. Our results, however, warrant further larger clinical studies regarding the clearance of nucleosome in artificial liver-assist devices and to assess their role in acute hepatic failure.

Evaluation of stroke volume variation obtained by arterial pulse contour analysis to predict fluid responsiveness intraoperatively.

BACKGROUND: Fluid management guided by oesophageal Doppler monitor has been reported to improve perioperative outcome. Stroke volume variation (SVV) is considered a reliable clinical predictor of fluid responsiveness. Consequently, the aim of the present trial was to evaluate the accuracy of SVV determined by arterial pulse contour (APCO) analysis, using the FloTrac/Vigileo system, to predict fluid responsiveness as measured by the oesophageal Doppler. METHODS: Patients undergoing major abdominal surgery received intraoperative fluid management guided by oesophageal Doppler monitoring. Fluid boluses of 250 ml each were administered in case of a decrease in corrected flow time (FTc) to <350 ms. Patients were connected to a monitoring device, obtaining SVV by APCO. Haemodynamic variables were recorded before and after fluid bolus application. Fluid responsiveness was defined as an increase in stroke volume index >10%. The ability of SVV to predict fluid responsiveness was assessed by calculation of the area under the receiver operating characteristic (ROC) curve. RESULTS: Twenty patients received 67 fluid boluses. Fifty-two of the 67 fluid boluses administered resulted in fluid responsiveness. SVV achieved an area under the ROC curve of 0.512 [confidence interval (CI) 0.32-0.70]. A cut-off point for fluid responsiveness was found for SVV > or =8.5% (sensitivity: 77%; specificity: 43%; positive predictive value: 84%; and negative predictive value: 33%). CONCLUSIONS: This prospective, interventional observer-blinded study demonstrates that SVV obtained by APCO, using the FloTrac/Vigileo system, is not a reliable predictor of fluid responsiveness in the setting of major abdominal surgery.

Pro-inflammatory interleukin-18 and Caspase-1 serum levels in liver failure are unaffected by MARS treatment.

BACKGROUND: The pro-inflammatory cytokine IL-18 and its activator Caspase-1 are involved in acute liver failure and acute-on-chronic-liver-failure. In acute liver failure and acute-on-chronic-liver-failure, the MARS system has been used to support liver function. Enhancement of IL-18, as seen in other extracorporeal-support systems like hemodialysis might thus have mitigated beneficial effects of the MARS system in acute hepatic failure. PATIENTS AND METHODS: We measured serum concentrations of IL-18 and Caspase-1 in 10 patients with acute liver failure and 10 patients suffering from acute-on-chronic-liver-failure, who were all treated with MARS. Thirteen patients suffering from chronic hepatic failure and 15 healthy individuals served as controls. Data are given as mean with 95% CI. RESULTS: Baseline IL-18 serum concentrations were significantly increased in acute liver failure and acute-on-chronic-liver-failure patients as compared to chronic hepatic failure (P=0.0039 and P=0.0011, respectively) and controls (P=0.0028 and P=0.0014, respectively). Caspase-1 serum concentrations were as well significantly elevated in the acute liver failure and acute-on-chronic-liver-failure groups as compared to chronic hepatic failure patients (P=0.0039 and P=0.0232, respectively) and controls P<0.0001 and P<0.0007, respectively). IL-18 and Caspase-1 did not change significantly during MARS treatment in acute liver failure and acute-on-chronic-liver-failure patients. CONCLUSIONS: MARS had no effect on IL-18 and Caspase-1 serum concentrations in acute liver failure and acute-on-chronic-liver-failure, providing no evidence of harmful effects by the increase of these potentially hepatocidal cytokines.

Plasma disappearance rate of indocyanine green in liver dysfunction.

The presence of hepatic dysfunction significantly affects the length of hospital stay and the outcome in critically ill patients. Considering the important partial hepatic functions of metabolism, synthesis, detoxification, and excretion, the worse clinical course of patients suffering from hepatic dysfunction is not surprising. The most often used indicator of hepatic dysfunction is bilirubin. However, bilirubin and other commonly used static laboratory tests provide only indirect measures of hepatic function. In contrast to these static tests, dynamic liver tests, such as indocyanine green (ICG) disappearance rate should provide better direct measures of the actual functional state of the liver at the time of assessment. The ICG is a water-soluble inert compound that is injected intravenously. It mainly binds to albumin in the plasma. ICG is then selectively taken up by hepatocytes, independent of adenosine triphosphate (ATP), and later excreted unchanged into the bile via an ATP-dependent transport system. The ICG is not metabolized; it does not undergo enterohepatic recirculation. Thus, ICG excretion rate in bile reflects the hepatic excretory function and hepatic energy status. Because of these features, ICG has been found to be useful to assess liver function in liver donors and transplant recipients, in patients with chronic liver failure, and as a prognostic factor in critically ill patients. Further trials concerning liver dysfunction have applied the noninvasive bedside assessment of ICG among other clinical variables to monitor the progress and/or the reversal of liver dysfunction.

Heightened levels of circulating 20S proteasome in critically ill patients.

BACKGROUND: Recently, circulating proteasome core particles (20S proteasome) have been suggested as a marker of cell damage and immunological activity in autoimmune diseases. Aberrant leucocyte activation and increased lymphocyte apoptosis with consecutive T-cell unresponsiveness is deemed to play a pivotal role in the sepsis syndrome. Moreover sepsis-induced muscle proteolysis mainly reflects ubiqutin proteasome-dependent protein degradation. We therefore sought to investigate serum levels of 20S proteasome in critical ill patients. MATERIAL AND METHODS: Case-control-study at a university hospital intensive care unit; 15 patients recruited within 24-48 h of diagnosis of sepsis, 13 trauma patients recruited within 24 h of admission to the ICU, a control group of 15 patients who underwent abdominal surgery, and 15 healthy volunteers. ELISA was used to measure the concentration of 20S proteasome in the sera of the patients and controls. Data are given as mean +/- SEM. Mann-Whitney U-test was used to calculate significance and a P-value of 0.05 was considered to be statistically significant. RESULTS: Marked increase of 20S proteasome was detected in the sera of septic patients (33 551 +/- 10 034 ng mL-1) as well as in trauma patients (29 669 +/- 5750 ng mL-1). In contrast, significantly lower concentrations were found in the abdominal surgery group (4661 +/- 1767 ng mL-1) and in the healthy control population (2157 +/- 273 ng mL-1). CONCLUSION: Detection of 20S proteasome may represent a novel marker of immunological activity and muscle degradation in sepsis and trauma patients, and may be useful in monitoring the clinical effect of proteasome-inhibitors.

Perioperative kinetics of heat shock protein 60 in serum during orthotopic liver transplantation.

INTRODUCTION: Heat shock proteins (HSP) play essential roles in the synthesis, transport, and folding of proteins. During ischemia/reperfusion (I/R) injury to orthotopic liver transplants (OLT), disassembly of oligomeric complexes and unfolding of proteins are likely to occur, producing a major burden on HSP to prevent and/or reverse these events. To date, all studies have evaluated HSP expression in tissues after an I/R injury. No data are available on HSP serum levels during I/R injury in liver graft recipients. PATIENTS AND METHODS: We evaluated the intraoperative and perioperative kinetics of HSP60 in the serum of 25 liver graft recipients. RESULTS: We observed a significant increase in serum levels of HSP60 at 4 hours compared with 30 minutes after reperfusion of the graft (P = .028). The perioperative HSP60 kinetics in serum neither correlated with the cold ischemia time nor the indocyanin green clearance. The type of preservation solution had no effect on serum HSP60 levels. CONCLUSION: This first study provides evidence for increased serum levels of HSP60 after reperfusion in OLT. The perioperative kinetics of HSP60 in serum may result from suppressed protein synthesis caused by a reduced energy charge of hepatocytes during early reperfusion, impaired transcription, and/or corticosteroid treatment. Further studies are needed to clarify the role of HSP60 under clinical conditions including immunosuppressive medications in human OLT.

Perioperative cytokines during orthotopic liver transplantation without venovenous bypass.

UNLABELLED: Since most of studies investigating cytokine levels during human orthotopic liver transplantation used venovenous bypass (VVB), it may be difficult to distinguish between the increase in proinflammatory mediators induced by VVB, by ischemia-reperfusion injury or by splanchnic venous congestion in the anhepatic phase. The goal of this investigation was to assess the levels of interleukin-6 (IL-6) and soluble interleukin-2 receptors (sIL-2r) during OLT procedures routinely performed without VVB. PATIENTS AND METHODS: Twenty-one consecutive patients underwent OLT with cross clamping of the inferior caval vein without VVB. Soluble IL-2r concentrations were measured by means of luminescence enzyme immunometric assay and IL-6 by means of a sequential immunometric assay. Time points (TP) of sampling were before induction of anesthesia (TP1), after cross-clamping of the inferior vena cava (TP2), 15 minutes after reperfusion (TP3), and 24 hours after the transplant procedure (TP4). RESULTS: Soluble IL-2r increased significantly 24 hours after transplantation (P =.02) compared to TP1, TP2, and TP3. IL-6 increased significantly during the anhepatic period (TP2 vs TP1, P =.003) and again in the reperfusion period (TP2 vs TP3, P =.002). Twenty-four hours after surgery IL-6 declined significantly (TP3 vs TP4, P =.001), but remained significantly higher (P = 0.04) compared to TP1. Furthermore, we examined the relative changes (DeltaTP %) in perioperative levels of cytokines compared with those previously published in studies using VVB. We observed higher values of DeltaTP % of IL-6 in TP2 and TP4 among our group of patient without VVB. The data on sIL-2r were similar, suggesting no major effects of the operative technique on sIL-2r levels. CONCLUSION: The two interleukins showed different perioperative trends. Our data suggest that cross clamping contributes more to cell activation, namely, increased release of IL-6 in the anhepatic phase than the use of VVB. However, no major differences were observed during the reperfusion period. The extent of clinical effect on graft function of higher IL-6 levels in the anhepatic period among recipients not supported with VVB remains to be clarified.

Comparison of lactate or BE during out-of-hospital cardiac arrest to determine metabolic acidosis.

During cardiopulmonary resuscitation, pH and base excess (BE) decrease to a variable degree due to metabolic acidosis. The main cause has been shown to be lactate, which cannot be eliminated sufficiently because of low perfusion during cardiac massage. Both BE and lactate can be measured in the prehospital phase. The aim of the study was to determine if BE and lactate are comparable variables during cardiopulmonary resuscitation (CPR) and if the measurement of lactate level alone would be sufficient to determine the patient's metabolic status and sufficiently reliable to determine the administration of buffer solutions. During the observation period, we registered 31 patients (21 males, ten females) who were resuscitated according to European Resuscitation Council recommendations, who had blood gas analysis and lactate levels measured in blood taken by arterial puncture or arterial line. The first measurement from each patient was taken after primary resuscitation (within 5-20 min). The mean lactate level was 9.85+/-2.98 (range, 4.1-18.7) mmol/l, and the mean BE was -15.0+/-5.98 (range, 5.5 to -24.3). There were statistically significant correlations between the lactate level and BE and pH (linear correlation, r=-0.673, P<0,001 and r=-0,683, P<0,001, respectively), but not with pO2 and pCO2. The receiver-operated curve analysis showed that a cut-off point of 7.0 mmol/l lactate indicates a BE below -10 with a sensitivity of 96% and a specificity of 67%. Lactate measurement is a valuable tool to determine metabolic acidosis during CPR and may be able to replace blood gas analysis in this situation.

Influence of aortic blood flow velocity on changes of middle cerebral artery blood flow velocity during isoflurane and sevoflurane anaesthesia.

BACKGROUND AND OBJECTIVE: We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia. METHODS: Forty patients (age: isoflurane 24-62 years; sevoflurane 24-61 years; ASA I-III) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50-60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspiratory and end-expiratory concentrations of 0.75, 1.00, and 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvI). CSvI of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity. RESULTS: Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvI decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 +/- 25%/81 +/- 23%, 1.0 MAC: 79 +/- 19%/74 +/- 16%, 1.25 MAC: 71 +/- 16%/79 +/- 21%; [mean +/- SD] P = 0.0001). CONCLUSIONS: The reduction of the CSvI vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.

Aggressive warming reduces blood loss during hip arthroplasty.

UNLABELLED: We evaluated the effects of aggressive warming and maintenance of normothermia on surgical blood loss and allogeneic transfusion requirement. We randomly assigned 150 patients undergoing total hip arthroplasty with spinal anesthesia to aggressive warming (to maintain a tympanic membrane temperature of 36.5 degrees C) or conventional warming (36 degrees C). Autologous and allogeneic blood were given to maintain a priori designated hematocrits. Blood loss was determined by a blinded investigator based on sponge weight and scavenged cells; postoperative loss was determined from drain output. Results were analyzed on an intention-to-treat basis. Average intraoperative core temperatures were warmer in the patients assigned to aggressive warming (36.5 degrees +/- 0.3 degrees vs 36.1 degrees +/- 0.3 degrees C, P< 0.001). Mean arterial pressure was similar in each group preoperatively, but was greater intraoperatively in the conventionally warmed patients: 86+/-12 vs 80+/-9 mm Hg, P<0.001. Intraoperative blood loss was significantly greater in the conventional warming (618 mL; interquartile range, 480-864 mL) than the aggressive warming group (488 mL; interquartile range, 368-721 mL; P: = 0.002), whereas postoperative blood loss did not differ in the two groups. Total blood loss during surgery and over the first two postoperative days was also significantly greater in the conventional warming group (1678 mL; interquartile range, 1366-1965 mL) than in the aggressively warmed group (1,531 mL; interquartile range, 1055-1746 mL, P = 0.031). A total of 40 conventionally warmed patients required 86 units of allogeneic red blood cells, whereas 29 aggressively warmed patients required 62 units (P = 0.051 and 0.061, respectively). We conclude that aggressive intraoperative warming reduces blood loss during hip arthroplasty. IMPLICATIONS: Aggressive warming better maintained core temperature (36.5 degrees vs 36.1 degrees C) and slightly decreased intraoperative blood pressure. Aggressive warming also decreased blood loss by approximately 200 mL. Aggressive warming may thus, be beneficial in patients undergoing hip arthroplasty.

Comparable postoperative pulmonary atelectasis in patients given 30% or 80% oxygen during and 2 hours after colon resection.

BACKGROUND: High concentrations of inspired oxygen are associated with pulmonary atelectasis but also provide recognized advantages. Consequently, the appropriate inspired oxygen concentration for general surgical use remains controversial. The authors tested the hypothesis that atelectasis and pulmonary dysfunction on the first postoperative day are comparable in patients given 30% or 80% perioperative oxygen. METHODS: Thirty patients aged 18-65 yr were anesthetized with isoflurane and randomly assigned to 30% or 80% oxygen during and for 2 h after colon resection. Chest radiographs and pulmonary function tests (forced vital capacity and forced expiratory volume) were obtained preoperatively and on the first postoperative day. Arterial blood gas measurements were obtained intraoperatively, after 2 h of recovery, and on the first postoperative day. Computed tomography scans of the chest were also obtained on the first postoperative day. RESULTS: Postoperative pulmonary mechanical function was significantly reduced compared with preoperative values, but there was no difference between the groups at either time. Arterial gas partial pressures and the alveolar-arterial oxygen difference were also comparable in the two groups. All preoperative chest radiographs were normal. Postoperative radiographs showed atelectasis in 36% of the patients in the 30%-oxygen group and in 44% of those in the 80%-oxygen group. Relatively small amounts of pulmonary atelectasis (expressed as a percentage of total lung volume) were observed on the computed tomography scans, and the percentages (mean +/- SD) did not differ significantly in the patients given 30% oxygen (2.5% +/- 3.2%) or 80% oxygen (3.0% +/- 1.8%). These data provided a 99% chance of detecting a 2% difference in atelectasis volume at an alpha level of 0.05. CONCLUSIONS: Lung volumes, the incidence and severity of atelectasis, and alveolar gas exchange were comparable in patients given 30% and 80% perioperative oxygen. The authors conclude that administration of 80% oxygen in the perioperative period does not worsen lung function. Therefore, patients who may benefit from generous oxygen partial pressures should not be denied supplemental perioperative oxygen for fear of causing atelectasis.

[Preclinical blood gas analysis. 1. The value of preclinical blood gas analysis]. / Die präklinische Blutgasanalyse Teil 1: Der Stellenwert der präklinischen Blutgasanalyse.

UNLABELLED: Prehospital blood gas analysis is a new method in out-of-hospital emergency care. In a prospective pilot study we evaluated the feasibility of prehospital compensation of severe acidosis relying on different monitoring systems to evaluate patients oxygen, carbon dioxide or acid-base status, respectively. METHODS: With the help of arterial blood gas checks taken at the site of the emergency, the acid base status of patients undergoing out of hospital cardiopulmonary resuscitation was analysed. The values derived from the first arterial puncture were used to determine the presence and the type of acidosis. The data of the arterial blood gas checks were set into relation with the time elapsed since the beginning of resuscitation and they were compared with end-tidal CO2. RESULTS: During the observation period 26 blood gas analyses from patients who had out-of-hospital resuscitation because of cardiac arrest were done. Twenty three patients had severe acidosis (pH range < 6.9 to 7.31), one had alkalosis (pH 7.51). Only two had an arterial pH within normal range. The pCO2 was variable (range: 24 to 97 mm Hg). The correlation of pH with time from the beginning of resuscitation to arterial puncture was poor (r = 0.407, p < 0.05). There was no correlation between pH and BE (r = 0.267) or pH and pCO2, (r = 0.016) respectively. Prehospital capnometry had a poor correlation with arterial pCO2 in most emergency patients. Only patients with respiratory disturbances of extrapulmonary origin showed a good correlation between end-tidal CO2 and the arterial pCO2. In severely ill patients the arterio-alveolar CO2-difference was unexpectedly high (> 15 mm Hg). In four patients resuscitation was not successful until compensation of an unexpectedly severe acidosis based upon the findings from blood-gas analysis had been performed. CONCLUSIONS: Arterial blood gas analysis proved to be helpful in the optimal management of out of hospital cardiac arrest. The incidence of severe acidosis in patients undergoing cardiopulmonary resuscitation was 80%. The probability of developing acidosis was found to increase slightly depending on the time elapsed since the beginning of CPR. The application of a calculated buffering of acidosis with sodium bicarbonate showed a good outcome in selected cases. In emergency patients alternative methods fail to detect severe disturbances of the patients oxygen and/or carbon dioxide status and the acid-base balance. Management of prehospital cardiac arrest could be optimized by the routine use of blood gas analysis.

A comparison of the end-tidal-CO2 documented by capnometry and the arterial pCO2 in emergency patients.

Satisfactory artificial ventilation is defined as sufficient oxygenation and normo- or slight arterial hypocarbia. Monitoring end tidal CO2 values with non-invasive capnometry is a routine procedure in anaesthesia, emergency medicine and intensive care. In anaesthesia the ventilation volume is adjusted to the capnometric end tidal CO2 (ETCO2), taking into account a normal variation from the pACO2 of 3-8 mmHg. We evaluated the usefulness and practicability of using ETCO2 for correctly adjusting ventilation parameters in prehospital emergency care, by comparing arterial pCO2 and ETCO2 of 27 intubated and ventilated patients. We used the side-stream capnometry module of the Defigard 2000 (Bruker, ChemoMedica Austria) and a portable blood gas analyzer (OPTI 1, AVL Graz, Austria). Evaluation of the group of patients as a whole showed that there was no correlation whatsoever between the end expiratory and arterial CO2. Dividing the patients into three subgroups (1, During CPR; II, respiratory disturbances of pulmonary and cardiac origin; III, extrapulmonary respiratory disturbances), we found that only patients without primary cardiorespiratory damage showed a slight, but not statistically significant, correlation. This can be explained by the fact that almost any degree of cardiorespiratory failure causes changes of the ventilation-perfusion ratio, impairing pulmonary CO2 elimination. We conclude, that the ventilation of emergency patients can only be correctly adjusted according to values derived from an arterial blood gas analysis and ETCO2 measurements cannot be absolutely relied upon for accuracy except, perhaps, in patients without primary cardiorespiratory dysfunction.

[Preclinical blood gas analysis. Technical description--initial experiences--indications]. / Präklinische Blutgasanalyse. Gerätebeschreibung--Erste Erfahrungen--Indikationen.

OBJECTIVE: A new portable device for blood gas analyses (BGA) has been examined for prehospital application. METHODS: After a 1 h introduction to the procedure, two physicians used the blood gas analyzer in the emergency medical system in Graz, Austria, for 7 months. The indications for prehospital BGA were prolonged cardiopulmonary resuscitation, mechanical ventilation, hyperventilation for reducing increased intracranial pressure, respiratory failure and metabolic disorders. All patients tested were also checked with pulse oximetry and capnography. TECHNICAL SPECIFICATION: The device measures pO2, pCO2 and pH using the fluorescence method. The innovation of a single-use cassette system makes it unnecessary to do any calibrations or transport any test substances. The storage battery measures eight samples without recharge. The time spent on one measurement is 3-6 min. RESULTS: We took 49 samples from 24 patients and found 16 indications for therapeutical intervention, such as buffering metabolic acidosis and adjusting mechanical ventilation by means of BGA. In all cases the analyzer worked reliably. CONCLUSIONS: One advantage of BGA over the non-invasive methods pulse oximetry and capnography is that it does not interfere with factors like peripheral vasoconstriction or inequality of the pulmonary ventilation/ perfusion ratio. Moreover, it is the only method for controlled buffering of acid-base disturbances. This means more security in diagnostics and therapeutical interventions for the patient in danger of dying. The device has proved to be a useful addition to the monitoring methods for prehospital application.