Estimating the rapid haemodynamic effects of passive leg raising in critically ill patients using bioreactance.

BACKGROUND: Rapid detection of changes in cardiac index (CI) in real time using minimally invasive monitors may be of clinical benefit. We tested whether the Starling-SV bioreactance device, which averages CI over a short 8 s period, could assess the effects of passive leg raising (PLR), a clinical test that is recommended to assess fluid responsiveness during septic shock. METHODS: In 32 critically ill patients, we measured CI by transpulmonary thermodilution (PiCCO2, CItd), pulse contour analysis (PiCCO2, CIPulse), and the Starling-SV device (CIStarling) at baseline. CIPulse and CIStarling were measured again at the end of a PLR test. In the 13 patients with a positive PLR test, CItd, CIPulse, and CIStarling were measured before and after a 500 ml saline infusion. The primary outcome was relative changes from baseline measurements in CItd, CIPulse, and CIStarling. Secondary outcomes compared absolute values measured by each method. RESULTS: Relative changes in CIPulse and CItd were significantly correlated (r=0.82; n=45; P<0.001), with an 89% concordance rate (n=45 paired measurements). Relative changes in CIStarling and CItd were also significantly correlated (r=0.59; n=45; P<0.001) with a 78% concordance rate. For absolute measures of CI (n=77 paired measurements), the bias between CIPulse and CItd was 0.01 L min-1 m-2 (limits of agreement, -0.49 and 0.51 L min-1 m-2; 15% percentage error). Bias between CIStarling and CItd was 0.03 L min-1 m-2 (limits of agreement, -1.61 and 1.67 L min-1 m-2; 48% percentage error). CONCLUSIONS: In critically ill patients, a non-invasive bioreactance device with a shorter averaging period assessed a passive leg raising test with reasonable accuracy.

Norepinephrine exerts an inotropic effect during the early phase of human septic shock.

BACKGROUND: We conducted this study to investigate whether norepinephrine increases cardiac contractility when administered during the early phase of septic shock. METHODS: We studied 38 patients with septic shock who had been resuscitated for <3 h and whose mean arterial pressure (MAP) remained <65 mm Hg. Echocardiographic variables were obtained before (T0) and after either initiation or an increase in the dose of a norepinephrine infusion to increase MAP to ≥ 65 mm Hg (T1). We collected left ventricular ejection fraction (LVEF), velocity-time integral of the left ventricular outflow tract (VTI), tissue Doppler imaging of mean systolic velocity of the lateral tricuspid annulus (Sa) and of the lateral mitral annulus (Sm), and tricuspid annular plane systolic excursion (TAPSE). RESULTS: There were significant (P<0.05) increases from T0 to T1 in MAP [mean (sd): from 56 (7) to 80 (9) mm Hg], LVEF [from 49 (13) to 56 (13)%], VTI [from 18 (5) to 20 (6) cm], Sm [from 10.8 (5.1) to 12.1 (5.0) cm s-1], TAPSE [from 1.8 (0.5) to 2.0 (0.5) cm], and Sa [from 13.0 (5.6) to 15.1 (6.4) cm s-1]. In the subgroup of 15 patients with LVEF ≤45%, significant increases in VTI [from 16 (8) to 18 (7) cm] and in LVEF [from 36 (7) to 44 (10)%] were observed. CONCLUSIONS: Norepinephrine administration during early resuscitation in patients with septic shock increased the cardiac systolic function despite the presumed increase in left ventricular afterload secondary to the increased arterial pressure. Whether such an effect persists over time remains to be evaluated. CLINICAL TRIAL REGISTRATION: NCT02750683.

Comparison of different techniques of central venous pressure measurement in mechanically ventilated critically ill patients.

BACKGROUND: Several techniques exist for measuring central venous pressure (CVP) but little information is available about the accuracy of each method. The aim of this study was to compare different methods of CVP measurements in mechanically ventilated patients. METHODS: CVP was measured in mechanically ventilated patients without spontaneous breathing using four different techniques: 1) end expiratory CVP measurement at the base of the" c" wave (CVPMEASURED), chosen as the reference method; 2) CVP measurement from the monitor averaging CVP over the cardiac and respiratory cycles (CVPMONITOR); 3) CVP measurement after a transient withdrawing of mechanical ventilation (CVPNADIR); 4) CVP measurement corrected for the transmitted respiratory pressure induced by intrinsic PEEP (calculated CVP: CVPCALCULATED). Bias, precision, limits of agreement, and proportions of outliers (difference > 2 mm Hg) were determined. RESULTS: Among 61 included patients, 103 CVP assessments were performed. CVPMONITOR bias [-0.87 (1.06) mm Hg] was significantly different from those of CVPCALCULATED [1.42 (1.07), P < 0.001 and CVPNADIR (1.04 (1.29), P < 0.001]. The limits of agreement of CVPMONITOR [-2.96 to 1.21 mm Hg] were not significantly different to those of CVPNADIR (-1.49 to 3.57 mm Hg, P = 0.39) and CVPCALCULATED (-0.68 to 3.53 mm Hg, P = 0.31). The proportion of outliers was not significantly different between CVPMONITOR (n = 5, 5%) and CVPNADIR (n = 9, 9%, P = 0.27) but was greater with CVPCALCULATED (n = 16, 15%, P = 0.01). CONCLUSIONS: In mechanically ventilated patients, CVPMONITOR is a reliable method for assessing CVPMEASURED Taking into account transmitted respiratory pressures, CVPCALCULATED had a higher proportion of outliers and precision than CVPNADIR.

Experts' opinion on management of hemodynamics in ARDS patients: focus on the effects of mechanical ventilation.

RATIONALE: Acute respiratory distress syndrome (ARDS) is frequently associated with hemodynamic instability which appears as the main factor associated with mortality. Shock is driven by pulmonary hypertension, deleterious effects of mechanical ventilation (MV) on right ventricular (RV) function, and associated-sepsis. Hemodynamic effects of ventilation are due to changes in pleural pressure (Ppl) and changes in transpulmonary pressure (TP). TP affects RV afterload, whereas changes in Ppl affect venous return. Tidal forces and positive end-expiratory pressure (PEEP) increase pulmonary vascular resistance (PVR) in direct proportion to their effects on mean airway pressure (mPaw). The acutely injured lung has a reduced capacity to accommodate flowing blood and increases of blood flow accentuate fluid filtration. The dynamics of vascular pressure may contribute to ventilator-induced injury (VILI). In order to optimize perfusion, improve gas exchange, and minimize VILI risk, monitoring hemodynamics is important. RESULTS: During passive ventilation pulse pressure variations are a predictor of fluid responsiveness when conditions to ensure its validity are observed, but may also reflect afterload effects of MV. Central venous pressure can be helpful to monitor the response of RV function to treatment. Echocardiography is suitable to visualize the RV and to detect acute cor pulmonale (ACP), which occurs in 20-25 % of cases. Inserting a pulmonary artery catheter may be useful to measure/calculate pulmonary artery pressure, pulmonary and systemic vascular resistance, and cardiac output. These last two indexes may be misleading, however, in cases of West zones 2 or 1 and tricuspid regurgitation associated with RV dilatation. Transpulmonary thermodilution may be useful to evaluate extravascular lung water and the pulmonary vascular permeability index. To ensure adequate intravascular volume is the first goal of hemodynamic support in patients with shock. The benefit and risk balance of fluid expansion has to be carefully evaluated since it may improve systemic perfusion but also may decrease ventilator-free days, increase pulmonary edema, and promote RV failure. ACP can be prevented or treated by applying RV protective MV (low driving pressure, limited hypercapnia, PEEP adapted to lung recruitability) and by prone positioning. In cases of shock that do not respond to intravascular fluid administration, norepinephrine infusion and vasodilators inhalation may improve RV function. Extracorporeal membrane oxygenation (ECMO) has the potential to be the cause of, as well as a remedy for, hemodynamic problems. Continuous thermodilution-based and pulse contour analysis-based cardiac output monitoring are not recommended in patients treated with ECMO, since the results are frequently inaccurate. Extracorporeal CO2 removal, which could have the capability to reduce hypercapnia/acidosis-induced ACP, cannot currently be recommended because of the lack of sufficient data.

Comparison of pulse contour analysis by Pulsioflex and Vigileo to measure and track changes of cardiac output in critically ill patients.

BACKGROUND: We compared the new Pulsioflex and the Vigileo devices to measure cardiac index (CI) in critically ill patients. Both devices measure CI by pulse-contour analysis. The Pulsioflex device also allows an auto-calibration (not based on thermodilution). METHODS: Patients were included if we administered fluids (20 patients), reduced (20 patients), or increased (20 patients) the dose of norepinephrine. Before and after interventions, we measured CI provided by the Vigileo (CIVig) and Pulsioflex (CIPfx) devices before and after its auto-calibration. CI measured by transpulmonary thermodilution (CIthermo) was used as the reference. RESULTS: Considering absolute values of CI (n=120), the percentage error was 59% for CIVig vs CIthermo and 40% for CIthermo vs CIPfx. Auto-calibrating CIPfx after interventions did not improve the percentage error between CIPfx and CIthermo (39%). Considering the fluid-induced changes in CI, the coefficient of correlation with changes in CIthermo was 0.50 for CIVig, and 0.73 for CIPfx (P=0.27). It was not significantly improved if CIPfx was auto-calibrated (r=0.64). Considering the norepinephrine-induced changes in CI, the coefficient of correlation with changes in CIthermo was 0.41 for CIVig. It tended to be better for CIPfx (r=0.71, P=0.07). It was not significantly improved by auto-calibration (r=0.53). CONCLUSIONS: The Pulsioflex did not reliably estimate the absolute values of CI. For tracking fluid-induced changes in CI, the Pulsioflex was reliable, and also the Vigileo. For tracking norepinephrine-induced changes in CI, it was also reliable and tended to be better than the Vigileo. Auto-calibration allowed by the system did not improve its reliability.

The role of beta-blockers in septic patients.

ß-blockers are widely used to treat cardiovascular diseases and in the peri-operative period in selected patients. The main benefit in terms of morbidity and/or mortality of their use is believed to be linked to specific effects on myocardial oxygen supply/demand balance, to anti-arrhythmic effects and anti-inflammatory effects. Use of ß-blockers in severe sepsis is still under debate and if any, their appropriate indications remain unclear. In this article, we analyze the recent literature addressing the metabolic, immuno-modulatory and hemodynamic effects of non cardio-selective and of cardio-selective ß-blockers in experimental and human sepsis in order to help clarifying the potential place of these drugs in patients with severe sepsis. From this analysis, it appears that ß-adrenoceptor blocking agents may represent a therapeutic approach in patients with severe sepsis, in whom catecholaminergic hyperactivity including excessive tachycardia is supposed to play an aggravating role. However, many questions about effectiveness, safety and cardio-selectivity of the drugs and about the appropriate target population remain partially unanswered. Recently, esmolol, a short-time acting ß1-adrenoceptor blocker titrated to decrease heart rate below 95 beats/min was shown to exert beneficial effects in a monocentric randomized clinical trial including selected septic patients. Further large multicenter randomized trials are required to confirm the potential benefit of such a therapy in patients with severe sepsis.

Bioreactance is not reliable for estimating cardiac output and the effects of passive leg raising in critically ill patients.

BACKGROUND: Bioreactance estimates cardiac output in a non-invasive way. We evaluated the ability of a bioreactance device (NICOM®) to estimate cardiac index (CI) and to track relative changes induced by volume expansion. METHODS: In 48 critically ill patients, we measured CI estimated by the NICOM® device (CINicom) and by transpulmonary thermodilution (CItd, PiCCO2™ device) before and after a 500 ml saline infusion. Before volume expansion, we performed a passive leg raising (PLR) test and measured the changes it induced in CINicom and in pulse contour analysis-derived CI. RESULTS: Considering the values recorded before PLR and before and after volume expansion (n=144), the bias (lower and upper limits of agreement) between CItd and CINicom was 0.9 (-2.2 to 4.1) litre min(-1) m(-2). The percentage error was 82%. There was no significant correlation between the changes in CItd and CINicom induced by volume expansion (P=0.24). An increase in CI estimated by pulse contour analysis >9% during the PLR test predicted fluid responsiveness with a sensitivity of 84% (95% confidence interval 60-97%) and a specificity of 97% (95% confidence interval 82-100%). The area under the receiver operating characteristic curve constructed to test the ability of the PLR-induced changes in CINicom in predicting fluid responsiveness did not differ significantly from 0.5 (P=0.77). CONCLUSIONS: The NICOM® device cannot accurately estimate the cardiac output in critically ill patients. Moreover, it could not predict fluid responsiveness through the PLR test.

Assessment of changes in left ventricular systolic function with oesophageal Doppler.

BACKGROUND: We tested the ability of mean acceleration (Acc) and peak velocity (V peak) of the aortic velocity signal measured by oesophageal Doppler to reflect left ventricular (LV) systolic performance. METHODS: We included critically ill patients in whom a fluid challenge (n=25) or the introduction of dobutamine, 5 µg kg(-1) min(-1) (n=25), was planned by the attending physician. Before and after therapeutic interventions, we measured Acc and V peak (CardioQ device) and LV ejection fraction (LVEF) using echocardiography. RESULTS: For all pairs of measurements, the absolute values of Acc and V peak correlated with LVEF (r=0.36 and 0.57, respectively). The correlation was significantly higher for V peak than for Acc. Volume expansion did not significantly change LVEF and Acc, but significantly increased V peak by 7 (8)%. Dobutamine increased LVEF by 30 (15)%, Acc by 33 (25)%, and V peak by 20 (10)%. Considering the pooled effects of volume expansion and dobutamine, changes in Acc and V peak and those of LVEF were correlated (r=0.53 and 0.67, respectively). When excluding changes <18% (i.e. the least significant change for LVEF), the concordance rate was 96% for Acc and 100% for V peak. CONCLUSIONS: V peak and, to a lesser extent, Acc measured by oesophageal Doppler behaved as markers of LV systolic performance as they were almost insensitive to fluid administration and changed to a much larger extent with dobutamine. These indices could be used to estimate LV systolic performance and to assess the effects of inotropic therapy.

Pulse pressure variation and ARDS.

Fluid management is a crucial issue in patients with acute respiratory distress syndrome (ARDS). Assessment of preload responsiveness should help to define the best fluid strategy. Arterial pulse pressure variation (PPV), which represents the amplitude of the respiratory changes in arterial pulse pressure, is considered as a marker of preload responsiveness in patients mechanically ventilated and fully adapted to their ventilator. The good ability of PPV to predict fluid responsiveness has been confirmed in various clinical situations (sepsis, operative and post-operative periods). However, there are a number of limits of using PPV (e.g., spontaneous breathing activity, cardiac arrhythmias, low tidal volume ventilation, low lung compliance), which are particularly important in ARDS. Clinical studies have confirmed the poor reliability of PPV in predicting fluid responsiveness in patients with ARDS, ventilated according to the currently recommended lung protective strategy. Although a PPV >10-12% still keeps its good predictive value, a lower PPV (<10%) is far to guarantee fluid unresponsiveness since many false-negative cases can be encountered in this setting. Thus, performance of alternative preload responsiveness tests such as passive leg raising or end-expiratory occlusion tests, is necessary when low PPV values are measured. This review addresses the meaning of PPV, its conditions of use and its limits in ARDS patients.

Pleth variability index is a weak predictor of fluid responsiveness in patients receiving norepinephrine.

BACKGROUND: In patients receiving an infusion of norepinephrine, the relationship between the amplitude of the oximeter plethysmographic waveform and stroke volume may be variable and quality of the waveform might be reduced, compared with patients not receiving norepinephrine. We assessed the reliability of the pleth variability index (PVI), an automatic measurement of the respiratory variation of the plethysmographic waveform, for predicting fluid responsiveness in patients receiving norepinephrine infusions. METHODS: We measured the response of cardiac index (transpulmonary thermodilution) to i.v. fluid administration in 42 critically ill patients receiving norepinephrine. Patients with arrhythmias, spontaneous breathing, tidal volume <8 ml kg(-1), and respiratory system compliance <30 ml cm H(2)O(-1) were excluded. Before fluid administration, we recorded the arterial pulse pressure variation (PPV) and pulse contour analysis-derived stroke volume variation (SVV, PiCCO2) and PVI (Masimo Radical-7). RESULTS: In seven patients, the plethysmographic signal could not be obtained. Among the 35 remaining patients [mean SAPS II score=77 (sd=17)], i.v. fluid increased cardiac index ≥15% in 15 'responders'. A baseline PVI ≥16% predicted fluid responsiveness with a sensitivity of 47 (inter-quartile range=21-73)% and a specificity of 90 (68-99)%. The area under the receiver operating characteristic curve was significantly lower for PVI [0.68 (0.09)] than for PPV and SVV [0.93 (0.06) and 0.89 (0.07), respectively]. Considering all pairs of measurements, PVI was correlated with PPV (r(2)=0.27). The fluid-induced changes in PVI and PPV were not significantly correlated. CONCLUSIONS: PVI was less reliable than PPV and SVV for predicting fluid responsiveness in critically ill patients receiving norepinephrine. In addition, PVI could not be measured in a significant proportion of patients. This suggests that PVI is not useful in patients receiving norepinephrine.

Prediction of fluid responsiveness by a continuous non-invasive assessment of arterial pressure in critically ill patients: comparison with four other dynamic indices.

BACKGROUND: We evaluated the ability of an infrared photoplethysmography arterial waveform (continuous non-invasive arterial pressure, CNAP) to estimate arterial pulse pressure variation (PPV). We compared the ability of non-invasive PPV to predict fluid responsiveness with invasive PPV, respiratory variation of pulse contour-derived stroke volume, and changes in cardiac index induced by passive leg raising (PLR) and end-expiratory occlusion (EEO) tests. METHODS: We measured the responses of cardiac index (PiCCO) to 500 ml of saline in 47 critically ill patients with haemodynamic failure. Before fluid administration, we recorded non-invasive and invasive PPVs, stroke volume variation, and changes in cardiac index induced by PLR and by 15 s EEO. Logistic regressions were performed to investigate the advantage of combining invasive PPV, stroke volume variation, PLR, and EEO when predicting fluid responsiveness. RESULTS: In eight patients, CNAP could not record arterial pressure. In the 39 remaining patients, fluid increased cardiac index by ≥15% in 17 'responders'. Considering the 195 pairs of measurements, the bias (sd) between invasive and non-invasive PPVs was -0.6 (2.3)%. The areas under the receiver operating characteristic (ROC) curves for predicting fluid responsiveness were 0.89 (95% confidence interval, 0.78-1.01) for non-invasive PPV compared with 0.89 (0.77-1.01), 0.84 (0.70-0.96), 0.95 (0.88-1.03), and 0.97 (0.91-1.03) for invasive pulse pressure, stroke volume variations, PLR, and EEO tests (no significant difference). Combining multiple tests did not significantly improve the area under the ROC curves. CONCLUSIONS: Non-invasive assessment of PPV seems valuable in predicting fluid responsiveness.

Third-generation FloTrac/Vigileo does not reliably track changes in cardiac output induced by norepinephrine in critically ill patients.

BACKGROUND: The ability of the third-generation FloTrac/Vigileo software to track changes in cardiac index (CI) induced by volume expansion and norepinephrine in critically ill patients is unknown. METHODS: In subjects with circulatory failure, we administered volume expansion (20 subjects) and increased (20 subjects) or decreased (20 subjects) the dose of norepinephrine. We measured arterial pressure waveform-derived CI provided by the third-generation FloTrac/Vigileo device (CI(pw)) and transpulmonary thermodilution CI (CI(td)) before and after therapeutic interventions. RESULTS: Considering the pairs of measurements performed before and after all therapeutic interventions (n=60), a bias between the absolute values of CI(pw) and CI(td) was 0.26 (0.94) litre min(-1) m(-2) and the percentage error was 54%. Changes in CI(pw) tracked changes in CI(td) induced by volume expansion with moderate accuracy [n=20, bias=-0.11 (0.54) litre min(-1) m(-2), r(2)=0.26, P=0.02]. When changes in CI(td) were induced by norepinephrine (n=40), a bias between CI(pw) and CI(td) was 0.01 (0.41) litre min(-1) m(-2) (r(2)=0.11, P=0.04). The concordance rates between changes in CI(pw) and CI(td) induced by volume expansion and norepinephrine were 73% and 60%, respectively. The bias between changes in CI(pw) and CI(td) significantly correlated with changes in total systemic vascular resistance (r(2)=0.41, P<0.0001). CONCLUSIONS: The third-generation FloTrac/Vigileo device was moderately reliable for tracking changes in CI induced by volume expansion and poorly reliable for tracking changes in CI induced by norepinephrine.

Complications related to less-invasive haemodynamic monitoring.

BACKGROUND: The aim of this study was to evaluate the type and incidence of complications during insertion, maintenance, and withdrawal of central arterial catheters used for transpulmonary thermodilution haemodynamic monitoring (PiCCO™). METHODS: We conducted a prospective, observational, multicentre study in 14 European intensive care units (six countries). A total of 514 consecutive patients in whom haemodynamic monitoring by PiCCO™ was indicated were studied. RESULTS: Five hundred and fourteen PiCCO catheters (475 in femoral, 26 in radial, nine in axillary, and four in brachial arteries) were inserted. Arterial access was obtained on the first attempt in 86.4% of the patients. Minor problems such as oozing after insertion (3.3%) or removal of the catheter (3.5%) were observed, but no episodes of serious bleeding (more than 50 ml) were recorded. Small local haematomas were observed after insertion (4.5%) and after removal (1.2%) of the catheter. These complications were not more frequent in patients with coagulation abnormalities. The incidence of site inflammation and catheter-related infection was 2% and 0.78%, respectively. Other complications such as ischaemia (0.4%), pulse loss (0.4%), or femoral artery thrombosis (0.2%) were rare, transient, and all resolved with catheter removal or embolectomy, respectively. CONCLUSIONS: In this series of patients, central arterial catheters used for PiCCO™ monitoring were demonstrated to be a safe alternative for advanced haemodynamic monitoring.

Interpretation of blood pressure signal: physiological bases, clinical relevance, and objectives during shock states.

Achievement of a mean blood pressure (MBP) target is one of the hemodynamic goals to ensure an adequate blood perfusion pressure in critically ill patients. Arterial catheter allows for a continuous and precise monitoring of arterial pressure signal. In addition to giving a precise MBP monitoring, analysis of the blood pressure wave provides information that may help the clinician to interpret hemodynamic status. The interpretation of BP wave requires the understanding of simple principles. In this review, we first discuss the physiological mechanism responsible for arterial pressure generation. We then emphasize the interpretation of the static indexes and the dynamic indexes generated by heart-lung interactions derived from arterial pressure wave. Finally, we focus on MBP value as a therapeutic target in critically ill patients. We discuss the recommended target MBP value by reviewing available data from experimental and clinical studies.

Could B-type Natriuretic Peptide (BNP) plasma concentration be useful to predict fluid responsiveness [corrected] in critically ill patients with acute circulatory failure?

BACKGROUND AND OBJECTIVES: As B-type Natriuretic Peptide (BNP) is a marker of ventricular wall stress, the present study was aimed at determining whether plasma BNP concentration could predict fluid responsiveness in critically ill patients with acute circulatory failure. METHODS: This prospective and non randomized interventional study included 33 sedated, mechanically ventilated patients, with acute circulatory failure requiring cardiac output measurement and fluid challenge. Plasma BNP concentration was measured before and after fluid challenge (250 to 500 ml with infusion rate=999 ml/h). An increase in stroke index (SI) greater than or equal to 15% allowed separation of responders from nonresponders. Receiver operating characteristic (ROC) curves were generated for BNP and compared to that of central venous pressure (CVP) that is routinely considered as a marker of cardiac preload. RESULTS: Among 33 patients, there were 24 responders. At baseline, BNP plasma values were less in responders (328 [35-1190] pg/ml versus 535 [223-5000] pg/ml, p<0.03). The area under the ROC curves was 0.74+/-0.11, that was similar to the area under the ROC curve for CVP (0.77+/-0.10). The best cut-off value of plasma BNP level for predicting fluid responsiveness was 193 pg/ml (sensitivity: 38%, specificity: 100%, positive predictive value: 100%, negative predictive value: 38%, accuracy: 55%). Fluid challenge did not increase plasma BNP concentrations in responders and nonresponders. CONCLUSION: In critically ill patients with acute circulatory failure, BNP does not accurately predict fluid responsiveness.

[Field 6. Safety practices for haemodynamic procedures (administration of vasoactive drugs, vascular and cardiac catheterization). French-speaking Society of Intensive Care. French Society of Anesthesia and Resuscitation]. / Champ 6. Sécurisation des procédures "circulatoires" (administration des substances vasoactives, utilisation des cathéters artériels, veineux centraux et artériels pulmonaires). SRLF. SFAR.

Arterial and central venous catheterizations and their use for continuous infusion of vasoactive drugs could lead to serious adverses events that could be life threatening. The incidence of human errors related patient adverses events could be decreased by the uses of algorithms and procedures. Concerning the continuous infusion of vasoactive drugs, the name of drug and its concentration should be clearly notified. The use of modern pump and noncompliant pipe could reduce the frequency bolus infusion and their related haemodynamic alterations. Reasonable procedure could reduce the arterial and central venous catheters related complications. Subclavian and radial sites should be preferred for central venous and arterial catheter insertion, respectively. The use of real time echographic guidance could facilitate the catheter insertion. These catheters should be removed when they are not indicated. Concerning the pulmonary artery catheter, the balloon tip should be inflated with visual control of the pulmonary artery pressure. Its removal is recommended within the first five days.

B-type natriuretic peptide to assess haemodynamic status after cardiac surgery.

BACKGROUND: B-type natriuretic peptide (BNP) is the most powerful hormonal marker of left ventricular dysfunction and could be considered as an indicator of ventricular preload. The aim of this prospective study was to compare the respective value of BNP and cardiac filling pressures to assess the response to volume load after cardiac surgery. METHODS: Thirty-seven mechanically ventilated patients suffering from acute circulatory failure immediately after cardiac surgery, and equipped with a pulmonary-artery catheter were included. All haemodynamic measurements were taken before and after volume expansion using 500 ml of 4% modified fluid gelatin. RESULTS: Fifteen patients were volume responders (CI increase>or=15%) and 22 were non-responders. Right atrial pressure, pulmonary-artery occlusion pressure and BNP before volume loading were not significantly different between the responders and non-responders. BNP concentration before volume infusion significantly correlated to preoperative left ventricular ejection fraction, aortic cross-clamping time, serum creatinine, mean pulmonary arterial pressure and intensive care unit duration whereas no correlation was found with pulmonary-artery occlusion pressure or cardiac index. CONCLUSION: BNP level after cardiac surgery was influenced by many perioperative variables, limiting its usefulness as an indicator of cardiac preload or a predictor of volume responsiveness in this population.