F. Sztark

Continuous non-invasive arterial pressure measurement: Evaluation of CNAP™ device during vascular surgery

OBJECTIVEnStandard non-invasive blood pressure (BP) monitoring is an intermittent, discontinuous procedure. Beat-to-beat BP monitoring requires invasive measurement via an arterial catheter and may be associated with serious complications. The Infinity CNAP SmartPod (Dräger Medical AG & Co. KG, Lübeck, Germany) has recently been proposed for non-invasive continuous beat-to-beat BP measurements. The present study was designed to compare BP obtained with the CNAP and with an invasive method in the operating room.nnnSTUDY DESIGNnProspective study.nnnPATIENTS AND METHODSnTwenty-five patients undergoing major vascular surgery were included. Systolic, mean and diastolic BP were monitored invasively (SAP, MAP and DAP respectively) and not invasively using the CNAP (CNAP-S, CNAP-M and CNAP-D respectively). Measurements were performed intraoperatively every minute during 1 hour.nnnRESULTSnOne thousand and five hundred pairs of simultaneous CNAP and invasive BP measurements were obtained and 148 were eliminated. The range of BP measurements was 63-205 mmHg for SAP and 57-187 mmHg for CNAP-S, 38-143 mmHg for MAP and 43-142 mmHg for CNAP-M, 29-126 mmHg for DAP and 33-121 mmHg for CNAP-D. Bias and 95% limit of agreement between CNAP and invasive BP measurements were respectively 7.2 and -17.7 to 32.2 mmHg for SAP, -1.8 and -22.0 to 18.3 mmHg for MAP, and -7.5 and -27.3 to 12.4 mmHg for DAP. The percentage of CNAP measurements with a bias <10% with the arterial line was 69%, 86% and 91% for systolic, diastolic and mean pressures, respectively.nnnCONCLUSIONnDespite low accuracy for SAP and DAP measurements, CNAP system seems more accurate for MAP measurement in patients undergoing vascular surgery.

Risk factors for bleeding and transfusion during orthotopic liver transplantation

OBJECTIVEnWhile orthotopic liver transplantation (OLT) can be associated with haemorrhage, the risk factors for bleeding and transfusion remain difficult to predict. Perioperative transfusion has potentially deleterious side effects and impairs graft and patient survival. Preoperative identification of patients at high risk of bleeding is of clinical interest to manage perioperative transfusion and blood product storage.nnnSTUDY DESIGNnRetrospective study.nnnPATIENTS AND METHODSnAll OLT conducted between 2004 and 2008 in the University Hospital of Bordeaux were studied. Risk factors for bleeding greater than one blood volume and for massive red blood cell (RBC) transfusion were determined using univariate and multivariate analysis. Thresholds were determined with ROC curve analysis.nnnRESULTSnOne hundred and forty-eight transplantations were studied. Preoperative haemoglobin and Child class A were independent protective risk factors for bleeding greater than one blood volume (OR 0.81 [0.67-0.98] and 0.27 [0.10-0.72], respectively). Preoperative Hb was a protective risk factor (OR 0.71 [0.58-0.88]) whereas history of oesophageal varicose bleeding was a risk factor (OR 4.67 [1.45-15.05]) for transfusion of more than eight RBC.nnnCONCLUSIONnRisk factors for bleeding and transfusion during OLT identified in this study were of little clinical usefulness so blood products should always be available during the procedure.

Time course of mitochondrial metabolism alterations to repeated injections of bupivacaine in rat muscle

PurposeBupivacaine-induced myotoxicity is associated with mitochondrial bioenergetic alterations. The impact of the duration of bupivacaine treatment on mitochondrial energy production remains undetermined. Here, we assessed, in vivo, the alteration of mitochondrial metabolism following different durations of bupivacaine exposure (40, 56, or 112xa0hr) that correspond to 5, 7, or 14 repeated injections of 0.25% bupivacaine, respectively.MethodsRats were divided randomly into seven different groups: one control group (no catheter); three groups with normal saline injections (1xa0mL·kg−1) every eight hours via a femoral nerve catheter for 40, 56, and 112xa0hr, respectively; and three groups with 0.25% bupivacaine injections (1xa0mL·kg−1) every eight hours via a femoral nerve catheter for 40, 56, and 112xa0hr. Psoas and gracilis muscle samples located within the bupivacaine infusion-diffusion space were investigated. To estimate mitochondrial respiratory capacity, the protein content of the mitochondrial respiratory chain apparatus was evaluated by measuring citrate synthase activity. To measure mitochondrial respiratory function, adenosine diphosphate-stimulated oxygen consumption was measured by polarography in saponin-skinned muscle fibres using glutamate-malate or succinate as energy substrates.ResultsIn psoas and gracilis muscles, saline solution had no effect on the two mitochondrial parameters. Bupivacaine induced a significant decrease in the citrate synthase activity in psoas (r2xa0=xa00.74; Pxa0<xa00.001) and gracilis muscle (r2xa0=xa00.52; Pxa0<xa00.001), and there was a significant decrease in the adenosine diphosphate-stimulated oxygen consumption using glutamate or succinate as substrates in both muscles (Pxa0<xa00.001).ConclusionsThe severity of bupivacaine-induced myotoxicity is closely linked to the duration of bupivacaine exposure in the muscle fibres located close to the catheter tip.RésuméObjectifLa myotoxicité induite par bupivacaïne est associée à des altérations du métabolisme énergétique mitochondrial. Nous ne connaissons pas l’impact de la durée d’un traitement de bupivacaïne sur la production énergétique mitochondriale. Dans cette étude, nous avons évalué in vivo l’altération du métabolisme mitochondrial à la suite de différentes durées d’exposition à la bupivacaïne (40, 56 ou 112 h), ce qui correspond respectivement à cinq, sept ou 14 injections répétées de bupivacaïne à 0,25xa0%.MéthodeLes rats ont été randomisés en sept groupes différents: un groupe témoin (pas de cathéter); trois groupes avec des injections de sérum physiologique (1xa0mL·kg−1) toutes les huit heures via un cathéter au niveau du nerf fémoral pendant 40, 56 et 112xa0h, respectivement; et trois groupes recevant des injections de bupivacaïne à 0,25xa0% (1xa0mL·kg−1) toutes les huit heures via un cathéter au niveau du nerf fémoral pendant 40, 56 et 112xa0h. Des échantillons du muscle psoas et du muscle gracilis situés dans l’espace de diffusion de la bupivacaïne ont été examinés. Le contenu protéinique de la chaîne respiratoire mitochondriale a été évalué en mesurant l’activité de la citrate-synthase pour estimer les capacités oxydatives de la chaine respiratoire. Une analyse polarographique réalisée sur les fibres musculaires perméablilisées à la saponine en présence de glutamate-malate ou de succinate comme substrats respiratoires a permis de mesurer la consommation d’oxygène stimulée par l’adénosine diphosphate.RésultatsDans les muscles psoas et gracilis, le sérum physiologique n’a pas eu d’effet sur les deux paramètres mitochondriaux. La bupivacaïne a provoqué une réduction significative de l’activité de la citrate-synthase dans les muscles psoas (r2xa0=xa00,74; Pxa0<xa00,001) et gracilis (r2xa0=xa00,52; Pxa0<xa00,001), et une réduction significative de la consommation d’oxygène stimulée par l’adénosine diphosphate en présence de glutamate ou de succinate comme substrat respiratoire a été observée dans les deux muscles (Pxa0<xa00,001).ConclusionLa gravité de la myotoxicité induite par bupivacaïne est étroitement liée à la durée d’exposition à la bupivacaïne dans les fibres musculaires situées à proximité de la pointe du cathéter.

Automated, continuous and non-invasive assessment of pulse pressure variations using CNAP(®) system.

Non-invasive respiratory variations in arterial pulse pressure using infrared-plethysmography (PPVCNAP) are able to predict fluid responsiveness in mechanically ventilated patients. However, they cannot be continuously monitored. The present study evaluated a new algorithm allowing continuous measurements of PPVCNAP (PPVCNAPauto) (CNSystem, Graz, Austria). Thirty-five patients undergoing vascular surgery were studied after induction of general anaesthesia. Stroke volume was measured using the VigileoTM/FloTracTM. Invasive pulse pressure variations were manually calculated using an arterial line (PPVART) and PPVCNAPauto was continuously displayed. PPVART and PPVCNAPauto were simultaneously recorded before and after volume expansion (500xa0ml hydroxyethylstarch). Subjects were defined as responders if stroke volume increased by ≥15xa0%. Twenty-one patients were responders. Before volume expansion, PPVART and PPVCNAPauto exhibited a bias of 0.1xa0% and limits of agreement from −7.9xa0% to 7.9xa0%. After volume expansion, PPVART and PPVCNAPauto exhibited a bias of −0.4xa0% and limits of agreement from −5.3xa0% to 4.5xa0%. A 14xa0% baseline PPVART threshold discriminated responders with a sensitivity of 86xa0% (95xa0% CI 64–97xa0%) and a specificity of 100xa0% (95xa0% CI 77–100xa0%). Area under the receiver operating characteristic (ROC) curve for PPVART was 0.93 (95xa0% CI 0.79–0.99). A 15xa0% baseline PPVCNAPauto threshold discriminated responders with a sensitivity of 76% (95xa0% CI 53–92xa0%) and a specificity of 93xa0% (95xa0% CI 66–99xa0%). Area under the ROC curves for PPVCNAPauto was 0.91 (95xa0% CI 0.76–0.98), which was not different from that for PPVART. When compared with PPVART, PPVCNAPauto performs satisfactorily in assessing fluid responsiveness in hemodynamically stable surgical patients.