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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.

Objective: Few outcome data are available about posterior reversible encephalopathy syndrome (PRES). We studied 90-day functional outcomes and their determinants in patients with severe PRES., Design: 70 patients with severe PRES admitted to 24 ICUs in 2001-2010 were included in a retrospective cohort study. The main outcome measure was a Glasgow Outcome Scale (GOS) of 5 (good recovery) on day 90., Main Results: Consciousness impairment was the most common clinical sign, occurring in 66 (94%) patients. Clinical seizures occurred in 57 (81%) patients. Median mean arterial pressure was 122 (105-143) mmHg on scene. Cerebral imaging abnormalities were bilateral (93%) and predominated in the parietal (93%) and occipital (86%) white matter. Median number of brain areas involved was 4 (3-5). Imaging abnormalities resolved in 43 (88%) patients. Ischaemic and/or haemorrhagic complications occurred in 7 (14%) patients. The most common causes were drug toxicity (44%) and hypertensive encephalopathy (41%). On day 90, 11 (16%) patients had died, 26 (37%) had marked functional impairments (GOS, 2 to 4), and 33 (56%) had a good recovery (GOS, 5). Factors independently associated with GOS<5 were highest glycaemia on day 1 (OR, 1.22; 95%CI, 1.02-1.45, p = 0.03) and time to causative-factor control (OR, 3.3; 95%CI, 1.04-10.46, p = 0.04), whereas GOS = 5 was associated with toxaemia of pregnancy (preeclampsia/eclampsia) (OR, 0.06; 95%CI, 0.01-0.38, p = 0.003)., Conclusions: By day 90 after admission for severe PRES, 44% of survivors had severe functional impairments. Highest glycaemia on day 1 and time to causative-factor control were strong early predictors of outcomes, suggesting areas for improvement.

Objective: To evaluate to which extent the systemic arterial pulse pressure could be used as a surrogate of cardiac output for assessing the effects of a fluid challenge and of norepinephrine., Design: Observational study., Setting: Medical intensive care unit., Patients: Patients with an acute circulatory failure who received a fluid challenge (228 patients, group 1) or in whom norepinephrine was introduced or increased (145 patients, group 2)., Interventions: We measured the systolic, diastolic, and mean arterial pressure, pulse pressure, and the transpulmonary thermodilution cardiac output before and after the therapeutic interventions., Main Results: In group 1, the fluid challenge significantly increased cardiac output by 24% ± 25%. It significantly increased cardiac output by ≥15% (+35% ± 27%) in 142 patients ("responders"). The fluid-induced changes in cardiac output were correlated with the changes in pulse pressure (r = .56, p < .0001), systolic arterial pressure (r = .55, p < .0001), diastolic arterial pressure (r = .37, p < .0001), and mean arterial pressure (r = .52, p < .0001). At multivariate analysis, changes in pulse pressure were significantly related to changes in stroke volume (multiple r = .52) and to age (r = .12). A fluid-induced increase in pulse pressure of ≥17% allowed detecting a fluid-induced increase in cardiac output of ≥15% with a sensitivity of 65[56-72]% and a specificity of 85[76-92]%. The area under the receiver operating characteristic curves for the fluid-induced changes in mean arterial pressure and in diastolic arterial pressure was significantly lower than for pulse pressure. In group 2, the introduction/increase of norepinephrine significantly increased cardiac output by 14% ± 18%. The changes in cardiac output induced by the introduction/increase in the dose of norepinephrine were correlated with the changes in pulse pressure and systolic arterial pressure (r = .21 and .29, respectively, p = .001) but to a significantly lesser extent than in group 1., Conclusions: Pulse pressure and systolic arterial pressure could be used for detecting the fluid-induced changes in cardiac output, in spite of a significant proportion of false-negative cases. By contrast, the changes in pulse pressure and systolic arterial pressure were unable to detect the changes in cardiac output induced by norepinephrine.

Introduction: We compared the ability of two devices estimating cardiac output from arterial pressure-curve analysis to track the changes in cardiac output measured with transpulmonary thermodilution induced by volume expansion and norepinephrine in sepsis patients., Methods: In 80 patients with septic circulatory failure, we administered volume expansion (40 patients) or introduced/increased norepinephrine (40 patients). We measured the pulse contour-derived cardiac index (CI) provided by the PiCCO device (CIpc), the arterial pressure waveform-derived CI provided by the Vigileo device (CIpw), and the transpulmonary thermodilution CI (CItd) before and after therapeutic interventions., Results: The changes in CIpc accurately tracked the changes in CItd induced by volume expansion (bias, -0.20 +/- 0.63 L/min/m2) as well as by norepinephrine (bias, -0.05 +/- 0.74 L/min/m2). The changes in CIpc accurately detected an increase in CItd >or= 15% induced by volume expansion and norepinephrine introduction/increase (area under ROC curves, 0.878 (0.736 to 0.960) and 0.924 (0.795 to 0.983), respectively; P < 0.05 versus 0.500 for both). The changes in CIpw were less reliable for tracking the volume-induced changes in CItd (bias, -0.23 +/- 0.95 L/min/m2) and norepinephrine-induced changes in CItd (bias, -0.01 +/- 1.75 L/min/m2). The changes in CIpw were unable to detect an increase in CItd >or= 15% induced by volume expansion and norepinephrine introduction/increase (area under ROC curves, 0.564 (0.398 to 0.720) and 0.541 (0.377 to 0.700, respectively, both not significantly different from versus 0.500)., Conclusions: The CIpc was reliable and accurate for assessing the CI changes induced by volume expansion and norepinephrine. By contrast, the CIpw poorly tracked the trends in CI induced by those therapeutic interventions.

Background: Critically ill patients often require emergency intubation. The use of etomidate as the sedative agent in this context has been challenged because it might cause a reversible adrenal insufficiency, potentially associated with increased in-hospital morbidity. We compared early and 28-day morbidity after a single dose of etomidate or ketamine used for emergency endotracheal intubation of critically ill patients., Methods: In this randomised, controlled, single-blind trial, 655 patients who needed sedation for emergency intubation were prospectively enrolled from 12 emergency medical services or emergency departments and 65 intensive care units in France. Patients were randomly assigned by a computerised random-number generator list to receive 0.3 mg/kg of etomidate (n=328) or 2 mg/kg of ketamine (n=327) for intubation. Only the emergency physician enrolling patients was aware of group assignment. The primary endpoint was the maximum score of the sequential organ failure assessment during the first 3 days in the intensive care unit. We excluded from the analysis patients who died before reaching the hospital or those discharged from the intensive care unit before 3 days (modified intention to treat). This trial is registered with ClinicalTrials.gov, number NCT00440102., Findings: 234 patients were analysed in the etomidate group and 235 in the ketamine group. The mean maximum SOFA score between the two groups did not differ significantly (10.3 [SD 3.7] for etomidate vs 9.6 [3.9] for ketamine; mean difference 0.7 [95% CI 0.0-1.4], p=0.056). Intubation conditions did not differ significantly between the two groups (median intubation difficulty score 1 [IQR 0-3] in both groups; p=0.70). The percentage of patients with adrenal insufficiency was significantly higher in the etomidate group than in the ketamine group (OR 6.7, 3.5-12.7). We recorded no serious adverse events with either study drug., Interpretation: Our results show that ketamine is a safe and valuable alternative to etomidate for endotracheal intubation in critically ill patients, and should be considered in those with sepsis., Funding: French Ministry of Health.

The CTX-M-15 extended spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae isolates were identified in 36 patients hospitalized from December 2006 to September 2007 in the medical intensive care unit (ICU) of the Bicêtre hospital, South Paris, France. The incidence of colonization and/or infection was 4.8%. Eighty-nine percent of the ESBL-producing K. pneumoniae isolates were acquired in the ICU, and only 8.3% of the patients were infected. Pulsed field gel electrophoresis (PFGE) analysis of the isolates showed that 32 isolates were clonally related and contained a 160-kb plasmid carrying the bla(CTX-M-15), bla(OXA-1), bla(TEM-1), and aac6'-Ib-cr genes. CTX-M-15-producing Escherichia coli isolates collected in the ward during the same period of time contained distinct plasmids and were not clonally related. This study highlights the possible occurrence of outbreaks due to CTX-M-producing K. pneumoniae within hospital settings, whereas CTX-Ms are mostly reported in E. coli in community-acquired infections.

Objective: To analyse the incidence and the impact on outcome of right ventricular failure (RVF) in patients with acute respiratory distress syndrome (ARDS)., Patients and Methods: A total of 145 ARDS patients included in the previously published French Pulmonary Artery Catheter (PAC) study were randomly assigned to receive a PAC. All patients were ventilated according to a strategy aimed at limiting plateau pressure. The RVF was defined by the concomitant presence of: (1) a mean pulmonary artery pressure (MPAP) > 25 mmHg, (2) a central venous pressure (CVP) higher than pulmonary artery occlusion pressure (PAOP) and (3) a stroke volume index < 30 mL m(-2)., Results: Right ventricular failure was present in 9.6% of patients. Mortality was 68% at day-90 with no difference between patients with RVF (RVF+) and without RVF (71 vs. 67%, respectively). SAPS II, PaO(2)/FiO(2) and PaCO(2) were similar in both groups. Tidal volume and I/E ratio were significantly higher in RVF+ (9.7 +/- 2.8 vs. 8.6 +/- 1.8 ml m(-2) and 0.7 +/- 0.5 vs. 0.5 +/- 0.2). Plateau pressure tended to be higher in RVF+ (28 +/- 6 vs. 25 +/- 6 cmH(2)O, NS). In multivariate analysis, PaO(2)/FiO(2), mean arterial pressure, arterial pH, SvO(2), MPAP and presence of CVP > PAOP, but not RVF, were independently associated with day-90 mortality., Conclusion: In this group of patients investigated early in the course of ARDS and ventilated according to a strategy aimed at limiting plateau pressure, the presence of RVF was about 10%. Unlike MPAP and the presence of CVP > PAOP, RVF at this early stage did not appear as an independent factor of mortality.

Objective: Weaning-induced cardiogenic pulmonary oedema is a cause of weaning failure that is classically diagnosed by an increase in pulmonary artery occlusion pressure during a spontaneous breathing trial. During cardiogenic pulmonary oedema, a hypo-oncotic fluid is filtered toward the interstitial space. Thus, we tested whether the changes in plasma protein concentration during a weaning trial could diagnose weaning-induced pulmonary oedema., Design: Prospective study., Setting: The 24-bed medical intensive care unit of a university hospital., Patients: Forty-six patients who had failed two weaning trials., Intervention: Weaning-induced pulmonary oedema was diagnosed if a respiratory failure associated with an increase in pulmonary artery occlusion pressure above 18 mmHg occurred during a third weaning trial on a T-tube. The plasma protein concentration was measured before and at the end of the spontaneous breathing trial., Measurements and Results: During the weaning trial, pulmonary oedema was observed in 24 patients. In these patients, the plasma protein concentration increased by 11% (3-25%). The plasma protein concentration did not change significantly in patients who did not experience weaning-induced pulmonary oedema. An increase in the plasma protein concentration greater than 6% from baseline to the end of the weaning trial allowed detecting a weaning-induced pulmonary oedema with a sensitivity of 87% and a specificity of 95%., Conclusion: The acute changes in plasma protein concentration during a weaning trial represent an alternative method to right heart catheterisation for assessing weaning-induced pulmonary oedema.

Objective: Several studies have reported a close relationship between an increased dose of dialysis and survival in patients treated for acute renal failure. Unfortunately, the quantification of dialysis in critically ill patients based on the urea nitrogen formula Kt/V is not applicable. Ionic dialysance is a new parameter calculated in real time from the dialysate conductivity and correlated with the effective urea clearance in chronic hemodialysis patients. The aim of our study was to evaluate ionic dialysance in the quantification of dialysis in critically ill patients with acute renal failure., Design: Prospective open-label study., Setting: An 18-bed medical intensive care unit., Patients: Thirty-one patients with multiple organ dysfunction syndrome and acute renal failure requiring intermittent hemodialysis were included., Measurements: Using the first dialysis session of each patient, we compared the delivered dose of dialysis based on ionic dialysance measurement (Kt(ID)) with the well-accepted gold standard method based on fractional dialysate sampling (Kt(dialysate)). The data were analyzed using linear regression and Bland-Altman analysis., Results: Thirty-one intermittent hemodialysis sessions were performed in 31 critically ill patients (mean age 58+/-12 years, SAPS II score 56+/-10). We found a close correlation between Kt(dialysate) and Kt(ID) (Kt(dialysate) = 36.3+/-11.4 l; Kt(ID)=38.4+/-11.8; r=0.96) with excellent limits of agreement (-2.2 l; 6.4 l)., Conclusion: The feasibility of dialysis quantification based on ionic dialysance in the critically ill patient is good. This method is a simple and accurate tool for the determination of dialysis dose in critically ill patients.

Objective: To test whether assessing pulmonary permeability by transpulmonary thermodilution enables to differentiate increased permeability pulmonary edema (ALI/ARDS) from hydrostatic pulmonary edema., Design: Retrospective review of cases., Setting: A 24-bed medical intensive care unit of a university hospital., Patients: Forty-eight critically ill patients ventilated for acute respiratory failure with bilateral infiltrates on chest radiograph, a PaO(2)/FiO(2) ratio < 300 mmHg and extravascular lung water indexed for body weight >/= 12 ml/kg., Intervention: We assessed pulmonary permeability by two indexes obtained from transpulmonary thermodilution: extravascular lung water/pulmonary blood volume (PVPI) and the ratio of extravascular lung water index over global end-diastolic volume index. The cause of pulmonary edema was determined a posteriori by three experts, taking into account medical history, clinical features, echocardiographic left ventricular function, chest radiography findings, B-type natriuretic peptide serum concentration and the time-course of these findings with therapy. Experts were blind for pulmonary permeability indexes and for global end-diastolic volume., Measurements and Results: ALI/ARDS was diagnosed in 36 cases. The PVPI was 4.7+/-1.8 and 2.1+/-0.5 in patients with ALI/ARDS and hydrostatic pulmonary edema, respectively (p<0.05). The extravascular lung water index/global end-diastolic volume index ratio was 3.0 x 10(-2)+/-1.2 x 10(-2) and 1.4 x 10(-2)+/-0.4 x 10(-2) in patients with ALI/ARDS and with hydrostatic pulmonary edema, respectively (p<0.05). A PVPI >/= 3 and an extravascular lung water index/global end-diastolic index ratio >/= 1.8 x 10(-2) allowed the diagnosis of ALI/ARDS with a sensitivity of 85% and specificity of 100%., Conclusion: These results suggest that indexes of pulmonary permeability provided by transpulmonary thermodilution may be useful for determining the mechanism of pulmonary edema in the critically ill.

Objective: Fluid responsiveness requires the accurate measurement of cardiac output that can be approached by aortic blood flow (ABF) as measured by esophageal Doppler monitoring (EDM). EDM devices may either include an echo-determination of aortic diameter or estimate aortic diameter from nomograms and thus consider it as constant. However, it is unclear if measuring aortic diameter increases the accuracy of EDM to identify fluid responsiveness. Aortic diameter varies with arterial pressure such that its measure could be essential for assessing the changes in ABF during acute circulatory failure. We attempted to demonstrate that measuring aortic diameter improved the accuracy of EDM to assess fluid responsiveness., Design: Prospective study., Setting: University hospital intensive care unit., Patients: Seventy-six patients with acute circulatory failure in whom a fluid challenge was given., Interventions: Rapid volume expansion (500 mL of NaCl 0.9%)., Measurements and Main Results: We measured aortic velocity and area by EDM before and after fluid loading and evaluated the effects of fluid challenge on ABF, either measured after fluid infusion (measured ABFafter) or estimated assuming an unchanging aortic area (estimated ABFafter). If measured ABFafter was used for assessing fluid response, it was increased above 15% compared with ABF at baseline in 41 patients (responders). Conversely, estimated ABFafter increased above 15% from ABF at baseline in 27 patients only; that is, the effects of the challenge were underestimated in 14 patients. In these 14 patients, the relative change in mean arterial pressure during volume expansion was of greater magnitude than in patients who were classified as nonresponders by considering measured ABFafter., Conclusions: Monitoring the changes in aortic diameter improves the accuracy of EDM in assessing the hemodynamic effects of a fluid challenge, especially if it induces a large increase in arterial pressure. Estimating rather than measuring the aortic diameter may lead to underestimation of fluid responsiveness.

Objective: Values of central venous pressure of 8-12 mm Hg and of pulmonary artery occlusion pressure of 12-15 mm Hg have been proposed as volume resuscitation targets in recent international guidelines on management of severe sepsis. By analyzing a large number of volume challenges, our aim was to test the significance of the recommended target values in terms of prediction of volume responsiveness., Design: Retrospective study., Setting: A 24-bed medical intensive care unit., Patients: All consecutive septic patients monitored with a pulmonary artery catheter who underwent a volume challenge between 2001 and 2004., Intervention: None., Measurements and Main Results: A total of 150 volume challenges in 96 patients were reviewed. In 65 instances, the volume challenge resulted in an increase in cardiac index of > or =15% (responders). The pre-infusion central venous pressure was similar in responders and nonresponders (8 +/- 4 vs. 9 +/- 4 mm Hg). The pre-infusion pulmonary artery occlusion pressure was slightly lower in responders (10 +/- 4 vs. 11 +/- 4 mm Hg, p < .05). However, the significance of pulmonary artery occlusion pressure to predict fluid responsiveness was poor and similar to that of central venous pressure, as indicated by low values of areas under the receiver operating characteristic curves (0.58 and 0.63, respectively). A central venous pressure of <8 mm Hg and a pulmonary artery occlusion pressure of <12 mm Hg predicted volume responsiveness with a positive predictive value of only 47% and 54%, respectively. With the knowledge of a low stroke volume index (<30 mL.m), their positive predictive values were still unsatisfactory: 61% and 69%, respectively. When the combination of central venous pressure and pulmonary artery occlusion pressure was considered instead of either pressure alone, the degree of prediction of volume responsiveness was not improved., Conclusion: Our study demonstrates that cardiac filling pressures are poor predictors of fluid responsiveness in septic patients. Therefore, their use as targets for volume resuscitation must be discouraged, at least after the early phase of sepsis has concluded.

Objective: Passive leg raising (PLR) represents a "self-volume challenge" that could predict fluid response and might be useful when the respiratory variation of stroke volume cannot be used for that purpose. We hypothesized that the hemodynamic response to PLR predicts fluid responsiveness in mechanically ventilated patients., Design: Prospective study., Setting: Medical intensive care unit of a university hospital., Patients: We investigated 71 mechanically ventilated patients considered for volume expansion. Thirty-one patients had spontaneous breathing activity and/or arrhythmias., Interventions: We assessed hemodynamic status at baseline, after PLR, and after volume expansion (500 mL NaCl 0.9% infusion over 10 mins)., Measurements and Main Results: We recorded aortic blood flow using esophageal Doppler and arterial pulse pressure. We calculated the respiratory variation of pulse pressure in patients without arrhythmias. In 37 patients (responders), aortic blood flow increased by > or =15% after fluid infusion. A PLR increase of aortic blood flow > or =10% predicted fluid responsiveness with a sensitivity of 97% and a specificity of 94%. A PLR increase of pulse pressure > or =12% predicted volume responsiveness with significantly lower sensitivity (60%) and specificity (85%). In 30 patients without arrhythmias or spontaneous breathing, a respiratory variation in pulse pressure > or =12% was of similar predictive value as was PLR increases in aortic blood flow (sensitivity of 88% and specificity of 93%). In patients with spontaneous breathing activity, the specificity of respiratory variations in pulse pressure was poor (46%)., Conclusions: The changes in aortic blood flow induced by PLR predict preload responsiveness in ventilated patients, whereas with arrhythmias and spontaneous breathing activity, respiratory variations of arterial pulse pressure poorly predict preload responsiveness.

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.

Objective: To test whether fluid responsiveness can be predicted by the respiratory variation in aortic blood flow and/or the flow time corrected for heart rate monitored with esophageal Doppler., Design and Setting: Prospective study in a 24-bed medical intensive care unit of a university hospital., Patients: 38 mechanically ventilated patients with sinus rhythm and without spontaneous breathing activity in whom volume expansion was planned., Interventions: The aortic blood flow was measured using an esophageal Doppler monitoring device before and after fluid infusion (500 ml NaCl 0.9% over 10 min). The variation in aortic blood flow over a respiratory cycle between its minimal and maximal values was calculated. The flow time was also measured., Measurements and Results: Aortic blood flow increased by at least 15% after volume expansion in 20 patients (defined as responders). Before fluid infusion the respiratory variation in aortic flow was higher in responders than in nonresponders (28+/-12% vs. 12+/-5%). It significantly decreased after volume expansion (18+/-11%) in responders only. A respiratory variation in aortic flow before volume expansion of at least 18% predicted fluid responsiveness with a sensitivity of 90% and a specificity of 94%. Flow time increased with fluid infusion in responders and nonresponders. A flow time corrected for heart rate below 277 ms predicted fluid responsiveness with a sensitivity of 55% and a specificity of 94%. The area under the ROC curve generated for variation in aortic blood flow ABF was greater than that generated for flow time., Conclusions: The respiratory variation in aortic blood flow reliably predicts fluid responsiveness in patients with sinus rhythm and without breathing activity.

Context: Many physicians believe that the pulmonary artery catheter (PAC) is useful for the diagnosis and treatment of cardiopulmonary disturbances; however, observational studies suggest that its use may be harmful., Objective: To determine the effects on outcome of the early use of a PAC in patients with shock mainly of septic origin, acute respiratory distress syndrome (ARDS), or both., Design, Setting, and Patients: A multicenter randomized controlled study of 676 patients aged 18 years or older who fulfilled the standard criteria for shock, ARDS, or both conducted in 36 intensive care units in France from January 30, 1999, to June 29, 2001., Intervention: Patients were randomly assigned to either receive a PAC (n = 335) or not (n = 341). The treatment was left to the discretion of each individual physician., Main Outcome Measures: The primary end point was mortality at 28 days. The principal secondary end points were day 14 and 90 mortality; day 14 organ system, renal support, and vasoactive agents-free days; hospital, intensive care unit, and mechanical ventilation-free days at day 28., Results: The 2 groups were similar at baseline. There were no significant differences in mortality with or without the PAC at day 14: 49.9% vs 51.3% (mortality relative risk [RR], 0.97; 95% confidence interval [CI], 0.84-1.13; P =.70); day 28: 59.4% vs 61.0% (RR, 0.97; 95% CI, 0.86-1.10; P =.67); or day 90: 70.7% vs 72.0% (RR, 0.98; 95% CI, 0.89-1.08; P =.71). At day 14, the mean (SD) number of days free of organ system failures with or without the PAC (2.3 [3.6] vs 2.4 [3.5]), renal support (7.4 [6.0] vs 7.5 [5.9]), and vasoactive agents (3.8 [4.8] vs 3.9 [4.9]) did not differ. At day 28, mean (SD) days in hospital with or without the PAC (0.9 [3.6] vs 0.9 [3.3]), in the intensive care unit (3.4 [6.8] vs 3.3 [6.9]), or mechanical ventilation use (5.2 [8.5] vs 5.0 [8.5]) did not differ., Conclusion: Clinical management involving the early use of a PAC in patients with shock, ARDS, or both did not significantly affect mortality and morbidity.

Objective: Under conditions of tissue hypoxia total CO2 production (VCO2) should be less reduced than O2 consumption (VO2) since an anaerobic CO2 production should occur. Thus the VCO(2)/VO(2) ratio, and hence the venoarterial CO2 tension difference/arteriovenous O2 content difference ratio (DeltaPCO2/C(a-v)O2), should increase. We tested the value of the DeltaPCO2/C(a-v)O2 ratio in detecting the presence of global anaerobic metabolism as defined by an increase in arterial lactate level above 2 mmol/l (Lac+)., Design and Setting: Retrospective study over a 17-month period in medical intensive care unit of a university hospital., Patients: We obtained 148 sets of measurements in 89 critically ill patients monitored by a pulmonary artery catheter., Results: The DeltaPCO2/C(a-v)O2 ratio was higher in those with increased ( n=73) than in the normolactatemic group (2.0+/-0.9 vs. 1.1+/-0.6, p<0.0001). Among all the O2- and CO2-derived parameters the DeltaPCO2/C(a-v)O2 ratio had the highest correlation with the arterial lactate level ( r=0.57). Moreover, for a threshold value of 1.4 the DeltaPCO2/C(a-v)O2 ratio predicted significantly better than the other parameters (receiver operating characteristic curves) the presence of hyperlactatemia (positive and negative predictive values of 86% and 80%, respectively). The overall survival estimate at 1 month was greater when the DeltaPCO2/C(a-v)O2 ratio was less than 1.4 on the first set of measurements (38+/-10% vs. 20+/-8%, p<0.01)., Conclusion: The DeltaPCO2/C(a-v)O2 ratio seems a reliable marker of global anaerobic metabolism. Its calculation would be helpful for a better interpretation of pulmonary artery catheter data.

Objective: This study was conducted with the aim of testing the effects of a reduction in tidal volume (V(T)) on gastric mucosal perfusion using laser-Doppler flowmetry in patients with acute respiratory distress syndrome (ARDS)., Design: It was designed as a prospective study., Patients: Seventeen patients with ARDS were enrolled in the study. All patients were mechanically ventilated in volume-controlled mode. Before the start of the protocol, V(T) was set at 9 ml/kg body weight., Intervention: V(T) was reduced to 6 ml/kg body weight., Measurements and Results: Measurements of systemic hemodynamic parameters and gastric mucosal blood flow (GMBF) were obtained before and after reduction of V(T). Cardiac index, heaart rate and pulmonary arterial pressure increased significantly after V(T) reduction. The increase in cardiac output was observed in all patients. However, despite a mean 25% increase in cardiac output after V(T) reduction, no significant increase in mean GMBF was observed, and individual GMBF responses were heterogeneous., Conclusion: V(T) reduction in patients with ARDS, despite resulting in an increase in cardiac output, did not change gastric mucosal perfusion. The heterogeneity in the individual response of GMBF to V(T) reduction could be due to opposite direct (i.e., local vasodilatory effect) and indirect (i.e., global sympathetic stimulation) effects of hypercapnia on gut vessels.

Objective: To assess the short-term effects of extending inspiratory time by lengthening end-inspiratory pause (EIP) without inducing a clinically significant increase in intrinsic positive end-expiratory pressure (PEEPi) in patients with acute respiratory distress syndrome (ARDS)., Design: Controlled, randomized, crossover study., Setting: Two medical intensive care units of university hospitals., Patients: Sixteen patients with early (< or =48 hrs) ARDS., Intervention: We applied two durations of EIP (0.2 secs and extended) each for 1 hr while keeping all the following ventilatory parameters constant: FIO2, total PEEP (PEEPtot = applied PEEP + PEEPi), tidal volume, inspiratory flow, and respiratory rate. The duration of extended EIP was titrated to avoid an increase of PEEPi of > or =1 cm H2O., Measurements and Main Results: Despite an increase in mean airway pressure (20.6 +/- 2.3 vs. 17.6 +/- 2.1 cm H2O, p < .01), extended EIP did not significantly improve PaO2 (93 +/- 21 vs. 86 +/-16 torr [12.40 +/- 2.80 vs. 11.46 +/- 2.13 kPa] with 0.2 secs EIP, NS). However, although the difference in PaO2 between the two EIP durations was <20 torr (<2.66 kPa) in 14 patients, two patients exhibited a >40 torr (>5.33 kPa) increase in PaO2 with extended EIP. Extended EIP decreased PaCO2 (62 +/- 13 vs. 67 +/- 13 torr [8.26 +/- 1.73 vs. 8.93 +/- 1.73 kPa] with 0.2 secs EIP, p < .01), which resulted in a higher pH (7.22 +/- 0.10 vs. 7.19 +/- 0.09 with 0.2 secs EIP, p < .01) and contributed to a slight increase in arterial hemoglobin saturation (94 +/- 3 vs. 93 +/- 3% with 0.2 EIP, p < .01). No significant difference in hemodynamics was observed., Conclusion: In patients with ARDS, extending EIP without inducing a clinically significant increase in PEEPi does not consistently improve arterial oxygenation but enhances CO2 elimination.

Objective: When positive end-expiratory pressure (PEEP) is applied, the intracavitary left ventricular end-diastolic pressure (LVEDP) exceeds the LV filling pressure because pericardial pressure exceeds 0 at end-expiration. Under those conditions, the LV filling pressure is itself better reflected by the transmural LVEDP (tLVEDP) (LVEDP minus pericardial pressure). By extension, end-expiratory pulmonary artery occlusion pressure (eePAOP), as an estimate of end-expiratory LVEDP, overestimates LV filling pressure when pericardial pressure is >0, because it occurs when PEEP is present. We hypothesized that LV filling pressure could be measured from eePAOP by also knowing the proportional transmission of alveolar pressure to pulmonary vessels calculated as index of transmission = (end-inspiratory PAOP--eePAOP)/(plateau pressure--total PEEP). We calculated transmural pulmonary artery occlusion pressure (tPAOP) with this equation: tPAOP = eePAOP--(index of transmission x total PEEP). We compared tPAOP with airway disconnection nadir PAOP measured during rapid airway disconnection in subjects undergoing PEEP with and without evidence of dynamic pulmonary hyperinflation., Design: Prospective study., Setting: Medical intensive care unit of a university hospital., Patients: We studied 107 patients mechanically ventilated with PEEP for acute respiratory failure. Patients without dynamic pulmonary hyperinflation (group A; n = 58) were analyzed separately from patients with dynamic pulmonary hyperinflation (group B; n = 49)., Intervention: Transient airway disconnection., Measurements and Main Results: In group A, tPAOP (8.5+/-6.0 mm Hg) and nadir PAOP (8.6+/-6.0 mm Hg) did not differ from each other but were lower than eePAOP (12.4+/-5.6 mm Hg; p < .05). The agreement between tPAOP and nadir PAOP was good (bias, 0.15 mm Hg; limits of agreement, -1.5-1.8 mm Hg). In group B, tPAOP (9.7+/-5.4 mm Hg) was lower than both nadir PAOP and eePAOP (12.1+/-5.4 and 13.9+/-5.2 mm Hg, respectively; p < .05 for both comparisons). The agreement between tPAOP and nadir PAOP was poor (bias, 2.3 mm Hg; limits of agreement, -0.2-4.8 mm Hg)., Conclusions: Indexing the transmission of proportional alveolar pressure to PAOP in the estimation of LV filling pressure is equivalent to the nadir method in patients without dynamic pulmonary hyperinflation and may be more reliable than the nadir PAOP method in patients with dynamic pulmonary hyperinflation.

In mechanically ventilated patients with acute circulatory failure related to sepsis, we investigated whether the respiratory changes in arterial pressure could be related to the effects of volume expansion (VE) on cardiac index (CI). Forty patients instrumented with indwelling systemic and pulmonary artery catheters were studied before and after VE. Maximal and minimal values of pulse pressure (Pp(max) and Pp(min)) and systolic pressure (Ps(max) and Ps(min)) were determined over one respiratory cycle. The respiratory changes in pulse pressure (DeltaPp) were calculated as the difference between Pp(max) and Pp(min) divided by the mean of the two values and were expressed as a percentage. The respiratory changes in systolic pressure (DeltaPs) were calculated using a similar formula. The VE-induced increase in CI was >/= 15% in 16 patients (responders) and < 15% in 24 patients (nonresponders). Before VE, DeltaPp (24 +/- 9 versus 7 +/- 3%, p < 0.001) and DeltaPs (15 +/- 5 versus 6 +/- 3%, p < 0.001) were higher in responders than in nonresponders. Receiver operating characteristic (ROC) curves analysis showed that DeltaPp was a more accurate indicator of fluid responsiveness than DeltaPs. Before VE, a DeltaPp value of 13% allowed discrimination between responders and nonresponders with a sensitivity of 94% and a specificity of 96%. VE-induced changes in CI closely correlated with DeltaPp before volume expansion (r(2) = 0. 85, p < 0.001). VE decreased DeltaPp from 14 +/- 10 to 7 +/- 5% (p < 0.001) and VE-induced changes in DeltaPp correlated with VE-induced changes in CI (r(2) = 0.72, p < 0.001). It was concluded that in mechanically ventilated patients with acute circulatory failure related to sepsis, analysis of DeltaPp is a simple method for predicting and assessing the hemodynamic effects of VE, and that DeltaPp is a more reliable indicator of fluid responsiveness than DeltaPs.

Objectives: To compare in the same patient with septic shock, respective effects of epinephrine, norepinephrine, and the combination of norepinephrine and dobutamine (5 microg/kg/min) on systemic hemodynamic parameters and gastric mucosal perfusion using gastric tonometry and laser-Doppler flowmetry techniques., Design: Prospective, controlled, randomized, crossover study., Setting: University hospital intensive care unit., Patients: Twelve patients with septic shock., Interventions: Each patient received in a random succession epinephrine, norepinephrine, and norepinephrine plus dobutamine. Dosages of epinephrine and norepinephrine were adjusted to achieve a mean arterial pressure between 70 and 80 mm Hg. A laser-Doppler probe and a tonometer were introduced into the gastric lumen., Measurements and Main Results: The increase in gastric mucosal perfusion detected by laser-Doppler flowmetry was higher with epinephrine and the combination of norepinephrine and dobutamine than with norepinephrine alone (p < .05). In addition, the ratio of gastric mucosal perfusion (local oxygen delivery) to systemic oxygen delivery was increased after norepinephrine plus dobutamine as compared with norepinephrine alone and epinephrine (p< .05). Although values of intramucosal pH and gastroarterial PCO2 tended to be higher with norepinephrine plus dobutamine compared with those obtained with norepinephrine and epinephrine, differences were not statistically significant., Conclusions: For the same mean arterial pressure in patients with septic shock, our study showed that administration of epinephrine increased gastric mucosal perfusion more than norepinephrine administration alone. Addition of dobutamine (5 microg/kg/ min) to norepinephrine improved gastric mucosal perfusion. This result could be explained by a vasodilating effect of dobutamine on gastric mucosal microcirculation.

To assess the cardiorespiratory effects of a prolonged application of inverse ratio ventilation (IRV), we compared IRV (I/E = 2) with conventional ventilation (CV) (I/E = 0.5), applied for 6 h each in a randomized order, with constant tidal volume (VT) and total positive end-expiratory pressure (PEEP(tot)) in eight patients with acute respiratory distress syndrome (ARDS). After 1 h, IRV resulted in a lower peak inspiratory pressure (PIP) (28.2 +/- 1.5 versus 35.6 +/- 1.7 cm H2O, p < 0.05), an unchanged plateau pressure, and a higher mean airway pressure (MAP) (17.8 +/- 0.8 versus 15.6 +/- 0.5 cm H2O, p < 0.05) than CV. No significant difference in Pa(O2) and shunt fraction (QS/QT) was observed (83 +/- 7 mm Hg and 40 +/- 4% in CV versus 92 +/- 14 mm Hg and 35 +/- 3% in IRV, respectively). The Pa(CO2) was lower in IRV (48 +/- 3 versus 55 +/- 5 mm Hg, p < 0.05). Cardiac index (CI) and oxygen delivery (D(O2)) were lower in IRV (3.7 +/- 0.4 L/min/m2 and 500 +/- 61 ml/min/m2 versus 4.6 +/- 0.5 L/min/m2 and 617 +/- 80 ml/min/m2, respectively, p = 0.05 for both). Regardless of the considered parameter, no significant difference was observed between results after 1, 2, 4, and 6 h in each mode. We conclude that IRV at a ratio that results in a significant intrinsic PEEP does not improve Pa(O2), enhances CO2 elimination, decreases cardiac output (CO), and does not exert any time-dependent effect.