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.

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.

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.

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.

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.

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.

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.

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.

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.

Rapid and beneficial hemodynamic effects of activated protein C in septic shock patients.

OBJECTIVE: Because recombinant human activated protein C (rhAPC) reduces NO production during sepsis, it could improve the vascular tone. We tested whether rhAPC reduces the dose of norepinephrine required to maintain mean arterial pressure (MAP) in septic shock patients. DESIGN AND SETTING: Retrospective study in intensive care unit of two university hospitals. PATIENTS: Twenty-two septic shock patients with at least two organ failures were retrospectively investigated for MAP and the required dose of norepinephrine before and 24 h after rhAPC administration. A control group of 22 septic shock patients with at least two organ failures who did not receive rhAPC was matched on age, SAPS II, MAP, and norepinephrine dose at the time of the theoretical start of rhAPC. MEASUREMENTS AND RESULTS: The MAP remained stable and similar in the two groups (86+/-16 vs. 89+/-9 mmHg at 24 h). The required dose of norepinephrine increased in the control group (+38%, from -41% to +38%) but decreased in the treated group (-33%, from -74% to +11%). CONCLUSIONS: rhAPC rapidly improved the vascular tone in septic shock patients as assessed by a decrease in the norepinephrine dose required to maintain arterial pressure.

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.

Global energetic failure in brain-dead patients.

The objective of this prospective, clinical study of consecutive patients was to test the hypothesis of a global energetic failure in brain-dead patients by analyzing indices of peripheral oxygenation during brain-dead resuscitation. Subjects comprised 24 subjects with brain death criteria from a multidisciplinary intensive care unit. The causes of brain death were multiple: severe traumatic head injury, cerebrovascular event, cerebral anoxia, primary brain tumor, and gunshot wound to the head. Interventions used were radial and pulmonary artery catheterization. Hemodynamic and gasometric parameters and blood lactate levels were measured immediately after the diagnosis of brain death (T0) and 4 hr later (T4), while patients were receiving a therapeutic protocol (fluids, vasopressive drugs) adjusted to reach a mean arterial pressure of 75 mmHg. In 18 of our 24 patients, a blood lactate level > or = 2 mmol/L (mean +/- SD: 4 +/- 2 mmol/L) associated with an increased mean lactate to pyruvate ratio (14.4 +/- 3.2) was observed at T0, while oxygen delivery (DO2) was high (533 +/- 208 ml/min/m2) and mean arterial pressure was 76 +/- 21 mmHg. Patients were subdivided into two groups according to changes in DO2 from T0 to T4: group D comprised 14 patients (10 with hyperlactatemia and 4 with normal lactate) in whom DO2 and oxygen consumption (VO2) simultaneously decreased from T0 to T4 without significant change in lactate level; group I comprised 10 patients (8 with hyperlactatemia and 2 with normal lactate) in whom DO2 and VO2 simultaneously increased, while the blood lactate level decreased significantly from 3.5 +/- 2.5 mmol/L at T0 to 2.1 +/- 1.0 mmol/L at T4 (P < 0.05). Our results indicate that the brain-dead state was frequently associated with a global energetic failure probably due to a cellular oxygen deficit, despite blood pressure within the normal range. This energetic failure, because it is associated with high levels of DO2, could result from a defect in peripheral oxygen extraction. Aggressive therapy, achieved by producing a further increase in DO2, may reduce this global tissue oxygen deficit.

Cardiorespiratory effects of pressure-controlled ventilation with and without inverse ratio in the adult respiratory distress syndrome.

To assess the cardiorespiratory effects of pressure-controlled ventilation (PCV) and pressure-controlled inverse ratio ventilation (PC-IRV), we compared pressure-controlled ventilation with an inspiratory-to-expiratory time ratio (I/E) of 1/2 (PCV) and of 2/1 (PC-IRV) to volume-controlled ventilation (VCV) with an I/E of 1/2 in 10 patients suffering from the adult respiratory distress syndrome. In all modes, the inspiratory oxygen fraction, tidal volume, respiratory rate, and total positive end-expiratory pressure (PEEPt = applied PEEP + intrinsic PEEP) were kept constant. Each ventilatory mode was applied for 1 h in a randomized order. No significant differences in PaO2 were observed among the three modes. The PaCO2 was lower (p < 0.05) in PC-IRV (39 +/- 4 mm Hg) than in PCV (43 +/- 5 mm Hg) and in VCV (45 +/- 5 mm Hg). The peak airway pressure was significantly lower in PC-IRV than in PCV (p < 0.05) and in PCV than in VCV (p < 0.05), but plateau pressure was not different in the 3 modes. The mean airway pressure (mPaw) was significantly higher (p < 0.05) in PC-IRV (21.4 +/- 0.7 cm H2O) than in PCV (17.1 +/- 0.7 cm H2O) and VCV (16.4 +/- 0.5 cm H2O). As a consequence of this increased mPaw, PC-IRV induced a decrease in cardiac index (CI) (3.3 +/- 0.2 vs 3.7 +/- 0.2 L/min/m2 in VCV; p < 0.05) and hence in oxygen delivery (DO2) (424 +/- 28 vs 469 +/- 38 ml/min/m2 in VCV; p < 0.05). Our results suggest that neither PCV nor PC-IRV bring any benefit over VCV in terms of arterial oxygenation. Moreover, the increase in mPaw induced by PC-IRV may be deleterious to the CI and DO2.

Spontaneous pneumothorax. Comparison of thoracic drainage vs immediate or delayed needle aspiration.

In the first part of this study, 61 patients admitted for the first episode or the first recurrence of a spontaneous pneumothorax (SP) were randomly treated with thoracic drainage (TD; 28 patients) or with simple needle aspiration (NA; 33 patients). Success rate of therapy was significantly higher with TD than with NA (93%, CI 84 to 100 vs 67%, CI 51 to 83; p = 0.01). Hospital stay was similar between the two groups (7 +/- 4.6 vs 7 +/- 5.6 days), mainly because NA was delayed by 72 h in 26 patients. Recurrence rates at 3 months were 29% (CI 11 to 47%) after TD, and 14% (CI 0 to 29%) after NA (p > 0.20, NS). In the second part of the study, an additional population of 35 patients was treated by immediate NA, with a success rate of 68.5% (CI 53.5 to 83.5%), and a recurrence rate at 3 months of 30% (CI 10 to 50%). Taken together, our results indicate that NA may be proposed as a first-line treatment of SP, with a successful result in two thirds of patients and recurrence in one fifth of patients. In patients who do not heal with NA, a combined risk of TD failure and short-term recurrence of 50% may be an incentive for undelayed surgical procedures.

Cardiac index vs oxygen-derived parameters for rational use of dobutamine in patients with congestive heart failure.

In patients with congestive heart failure (CHF), catecholaminergic agents may exert thermogenic effects that limit their beneficial effects in terms of global tissue oxygenation. Oxygen extraction ratio (O2ER) or mixed venous blood saturation (SvO2) might take into account better than cardiac index (CI) the resultant effect of such agents on peripheral oxygenation. We tested this hypothesis in a series of 20 patients with severe CHF and normal blood lactate levels undergoing pulmonary artery catheterization and receiving incremental doses of dobutamine: 0 (Do), 5 (D5), 10 (D10), and 15 micrograms/kg/min (D15). A significant dose-effect relationship (p < 0.01) was found between dose of dobutamine and CI (CI = 0.06 dose + 1.82). By contrast, no dose-effect relationship was observed between dobutamine dose and either O2ER or SvO2. Indeed, a biphasic profile was observed for O2ER and SvO2. From D0 to D10, O2ER decreased (from 45 +/- 6 to 35 +/- 7 percent) and SvO2 increased (from 52 +/- 7 to 62 +/- 7 percent). From D10 to D15, no further change was observed for both parameters. This latter finding was related to a significant increase in VO2 at D15 (p < 0.01). In these normolactatemic patients with unchanged VO2 from D0 to D10 while DO2 linearly increased (from D0 to D15), the increase in VO2 at D15 was probably due to an increase in oxygen demand induced by the drug. Our results suggest that dobutamine at a dose of 15 micrograms/kg/min can induce an increase in O2 demand that might offset the improvement in CI. Thus, in patients with CHF, oxygen-derived parameters such as O2ER and SvO2 should be more appropriate than CI to assess the efficacy of dobutamine.

Effects of cardiovascular drugs on oxygen consumption/oxygen delivery relationship in patients with congestive heart failure.

The oxygen consumption (VO2)/oxygen delivery (DO2) relationship was analyzed in ten patients with severe congestive heart failure (CHF) and normal blood lactate levels. First dobutamine and then enoximone, after a washout period, were administered to each patient to increase cardiac output by at least 15 percent. Similar increases in DO2 were obtained with both drugs: from 285 +/- 46 to 393 +/- 87 ml/min/m2 for dobutamine, and from 285 +/- 54 to 392 +/- 99 ml/min/m2 for enoximone. However, while VO2 did not change (132 +/- 24 vs 132 +/- 21 ml/min/m2) (VO2/DO2 independency) with a dobutamine infusion (mean dose of 10 +/- 2 micrograms/kg/min), a significant increase in VO2 from 134 +/- 22 to 157 +/- 21 ml/min/m2 was observed with a bolus infusion of enoximone (mean dose of 1.7 +/- 0.5 mg/kg). These results, observed in patients with CHF without patent oxygen debt, suggest that an artefactual VO2/DO2 dependency might be induced by the cardiovascular drug used to elevate DO2, probably because of a drug-induced oxygen demand increase.