Xavier Monnet

Esophageal Doppler monitoring predicts fluid responsiveness in critically ill ventilated patients

ObjectiveTo 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 settingProspective study in a 24-bed medical intensive care unit of a university hospital.Patients38 mechanically ventilated patients with sinus rhythm and without spontaneous breathing activity in whom volume expansion was planned.InterventionsThe aortic blood flow was measured using an esophageal Doppler monitoring device before and after fluid infusion (500xa0ml NaCl 0.9% over 10xa0min). 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 resultsAortic 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 277xa0ms 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.ConclusionsThe respiratory variation in aortic blood flow reliably predicts fluid responsiveness in patients with sinus rhythm and without breathing activity.

Incidence and prognostic value of right ventricular failure in acute respiratory distress syndrome

ObjectiveTo analyse the incidence and the impact on outcome of right ventricular failure (RVF) in patients with acute respiratory distress syndrome (ARDS).Patients and methodsA 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)xa0>xa025xa0mmHg, (2) a central venous pressure (CVP) higher than pulmonary artery occlusion pressure (PAOP) and (3) a stroke volume indexxa0<xa030xa0mLxa0m−2.ResultsRight 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, PaO2/FiO2 and PaCO2 were similar in both groups. Tidal volume and I/E ratio were significantly higher in RVF+ (9.7xa0±xa02.8 vs. 8.6xa0±xa01.8xa0mlxa0m−2 and 0.7xa0±xa00.5 vs. 0.5xa0±xa00.2). Plateau pressure tended to be higher in RVF+ (28xa0±xa06 vs. 25xa0±xa06 cmH2O, NS). In multivariate analysis, PaO2/FiO2, mean arterial pressure, arterial pH, SvO2, MPAP and presence of CVPxa0>xa0PAOP, but not RVF, were independently associated with day-90 mortality.ConclusionIn 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 CVPxa0>xa0PAOP, RVF at this early stage did not appear as an independent factor of mortality.

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

ObjectiveBecause 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 settingRetrospective study in intensive care unit of two university hospitals.PatientsTwenty-two septic shock patients with at least two organ failures were retrospectively investigated for MAP and the required dose of norepinephrine before and 24xa0h 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, SAPSxa0II, MAP, and norepinephrine dose at the time of the theoretical start of rhAPC.Measurements and resultsThe MAP remained stable and similar in the two groups (86±16 vs. 89±9xa0mmHg at 24xa0h). 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%).ConclusionsrhAPC rapidly improved the vascular tone in septic shock patients as assessed by a decrease in the norepinephrine dose required to maintain arterial pressure.

Heart rate reduction by inhibition of If or by β-blockade has different effects on postsystolic wall thickening

Postsystolic wall thickening (PSWT) is part of thickening that occurs after end‐systole and represents wasted effort as it does not contribute to ejection. The effects of antianginal drugs on PSWT remain to be established. We compared the effects on PSWT of two agents that reduce heart rate, the β‐blocker atenolol and the selective inhibitor of If current, ivabradine.

Regional and temporal heterogeneity of postsystolic wall thickening is associated with left ventricular asynchrony in normal and experimental stunned myocardium.

AimsPostsystolic wall thickening (PSWT) occurs after aortic valve closure. We investigated the influence of ischemia location and wall interactions on PSWT in normal and stunned myocardium.Methods and resultsTwenty-two dogs were studied. Seven chronically instrumented dogs (sonomicrometry) underwent 10-min coronary artery occlusion (CAO) of left circumflex artery (“LCX stunning”) and seven other dogs underwent 10-min CAO of the anterior descending artery (“LAD stunning”) followed by reperfusion. At baseline, there was no PSWT in the anterior wall whereas posterior wall started and finished to thicken after the anterior wall, demonstrating PSWT. With LCX stunning, PSWT was observed in the posterior wall without affecting the remote anterior wall. With LAD stunning, PSWT in the anterior wall was transient and of lower magnitude Vs. posterior wall; in the remote posterior wall, PSWT previously observed at baseline, almost vanished. Postsystolic to systolic wall thickening ratio identified (ROC analysis) normal, ischemic and stunned myocardium with different amplitudes between walls. Tissue Doppler Imaging demonstrated similar pattern in basal, mid and apical segments (additional n = 4 for both LCX and LAD stunning).ConclusionThe present study demonstrates that location of ischemia and wall interactions produce discrepancies in PSWT between anterior and posterior walls in stunned myocardium.