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Objectives Individualizing a target mean arterial pressure is challenging during the initial resuscitation of patients with septic shock. The Sepsis and Mean Arterial Pressure (SEPSISPAM) trial suggested that targeting high mean arterial pressure might reduce the occurrence of acute kidney injury among those included patients with a past history of chronic hypertension. We investigated whether the class of antihypertensive medications used before the ICU stay in chronic hypertensive patients was associated with the severity of acute kidney injury occurring after inclusion, according to mean arterial pressure target. Design Post hoc analysis of the SEPSISPAM trial. Setting The primary outcome was the occurrence of severe acute kidney injury during the ICU stay defined as kidney disease improving global outcome stage 2 or higher. Secondary outcomes were mortality at day 28 and mortality at day 90. Patients All patients with chronic hypertension included in SEPSISPAM with available antihypertensive medications data in the hospitalization report were included. Measurements and main results We analyzed 297 patients. Severe acute kidney injury occurred in 184 patients, without difference according to pre-ICU exposure to antihypertensive medications. Patients with pre-ICU exposure to angiotensin II receptor blockers had significantly less severe acute kidney injury in the high mean arterial pressure target group (adjusted odd ratio 0.24 with 95% CI [0.09-0.66]; p = 0.006). No statistically significant association was found after adjustment for pre-ICU exposure to antihypertensive medications and survival. Conclusions Our results suggest that patients with septic shock and chronic hypertension treated with angiotensin II receptor blocker may benefit from a high mean arterial pressure target to reduce the risk of acute kidney injury occurrence.

Objectives The association between outcome and kidney injury detected at discharge from the ICU using different biomarkers remains unknown. The objective was to evaluate the association between 1-year survival and kidney injury at ICU discharge. Design Ancillary investigation of a prospective observational study. Setting Twenty-one ICUs with 1-year follow-up. Patients Critically ill patients receiving mechanical ventilation and/or hemodynamic support for at least 24 hours were included. Interventions Serum creatinine, plasma Cystatin C, plasma neutrophil gelatinase-associated lipocalin, urinary neutrophil gelatinase-associated lipocalin, plasma Proenkephalin A 119-159, and estimated glomerular filtration rate (on serum creatinine and plasma Cystatin C) were measured at ICU discharge among ICU survivors. Measurements and main results The association between kidney biomarkers at discharge and mortality was estimated using logistic model with and without adjustment for prognostic factors previously identified in this cohort. Subgroup analyses were performed in patients with discharge serum creatinine less than 1.5-fold baseline at ICU discharge. Among 1,207 ICU survivors included, 231 died during the year following ICU discharge (19.2%). Estimated glomerular filtration rate was significantly lower and kidney injury biomarkers higher at discharge in nonsurvivors. The association between biomarker levels or estimated glomerular filtration rate and mortality remained after adjustment to potential cofounding factors influencing outcome. In patients with low serum creatinine at ICU discharge, 25-47% of patients were classified as subclinical kidney injury depending on the biomarker. The association between kidney biomarkers and mortality remained and mortality was higher than patients without subclinical kidney injury. The majority of patients who developed acute kidney injury during ICU stay had elevated biomarkers of kidney injury at discharge even with apparent recovery based on serum creatinine (i.e., subclinical acute kidney disease). Conclusions Elevated kidney biomarkers measured at ICU discharge are associated with poor 1-year outcome, including in patients with low serum creatinine at ICU discharge.

Purpose of reviewCritical care echocardiography (CCE) has become an important component of general critical care ultrasonography, and a current review of its performance is presented.Recent findingsBasic CCE should be performed as a goal-directed examination to better identify specific signs and to

Purpose of review The right ventricle (RV) plays a pivotal role during respiratory failure because of its high sensitivity to small loading changes during inspiration. Both RVs, preload and afterload, are altered during inspiration, either in spontaneous breathing or during mechanical ventilation. Some clinical situations especially affect RV load during inspiration, for example acute asthma and acute respiratory distress syndrome. The aim of this review is to explain and to summarize the different mechanisms leading to RV failure in these situations. Recent findings Research has recently reemphasized the importance to well known physiology of the venous return which is a contributor of RV preload. Authors recently focused on the mean systemic filling pressure which is one of the determinants of venous return. Venous return may change in opposite direction according to the type of ventilation (spontaneous or assisted). Recent works have also demonstrated the crucial impact of lung inflation and driving pressure on RV afterload, and have confirmed the deleterious effect of severe RV failure, described as acute cor pulmonale. In most situations of RV overload induced by inspiration, significant pulse pressure variations are observed, either called 'pulsus paradoxus' in spontaneously breathing patients or 'reverse pulsus paradoxus' in mechanically ventilated patients. Summary RV is very sensitive to abnormal inspiration, which is always responsible for an increase in its afterload. Pulse pressure variations, central venous pressure and especially echocardiography may monitor RV function in abnormal clinical situations. The pulmonary artery catheter was also proposed although now less used.

Pocket ultrasound devices (PUDs) increase the scope of transthoracic echocardiography. We assessed the ability of emergency physicians (EPs) to obtain and interpret views using PUDs in prehospital emergencies.Nine EPs underwent a 2-day training program focused on acquisition of four views and on evaluation of left ventricular function, right ventricular size, the inferior vena cava, and detection of pericardial effusion. Then, EPs used a PUD to perform transthoracic echocardiography in patients with shock or acute respiratory failure. The quality and interpretation of views were graded by an expert as not obtained/inadequate, adequate, or optimal. Agreement between the expert and the physicians was evaluated using Cohen's κ test.One hundred consecutive exams were evaluated in patients with shock or acute respiratory failure. Parasternal long-axis and short-axis views, and a subcostal view were not obtained or inadequate in 56, 54, and 54 patients, respectively. An apical four-chamber view was not obtained or inadequate in 33 patients. One, two, or three views were graded as adequate or optimal in 86, 65, and 35 patients. Agreement between physicians and experts for left ventricular systolic function, right ventricular size, and pericardial effusion was weak [κ 0.37 (0.17; 0.59), 0.27 (0.023; 0.53), and 0.33 (-0.008; 0.67)]. Agreement for inferior vena cava evaluation was very weak [0.13 (-0.17; 0.43)].After a very short training program, echocardiography using a PUD in prehospital emergencies was feasible in half of patients. Acquisition of technical skills is reasonable, but accurate evaluation of cardiac function may require more extensive training.

Sepsis induces alterations of coagulation suggesting both hypercoagulable or hypocoagulable features. The result of their combination remains unknown, making it difficult to predict whether one prevails over the other. Thrombin generation tests (TGTs) stand as an interesting tool to establish an integrative phenotype of coagulation. It has been reported that septic patients display a hypocoagulable trait using TGT. However, protein C (PC) system response was not evaluated. We aimed at describing the thrombin generation profile in patients with septic shock under conditions that are sensitive to PC system to evaluate the net results of coagulation abnormalities and to determine whether hypercoagulable or hypocoagulable traits coexist within a given individual. Thrombin generation was studied in plasma from patients presenting with septic shock at diagnosis and 6 h after a conventional therapeutic management using calibrated automated thrombography with or without thrombomodulin (TM) addition. Patients exhibit clear alterations of TGT that present as both consumption-related hypocoagulability (evidenced without TM addition) but also hypercoagulability by decreased sensitivity to the PC system evidenced with TM addition. No difference could be demonstrated between survivors and nonsurvivors at Day 28, but patients who do not respond to therapeutics at 6 h seem to be more hypercoagulable. More importantly, if our results evidence heterogeneity between patients, we show that alterations of coagulation result in an equilibrium in the majority of patients, thus suggesting "normocoagulability"; but, in the presence of a biological imbalance between baseline thrombin generation and sensitivity to TM, the global effect mostly tends toward hypercoagulability. Thus, TGT may help identify distinct biological coagulation phenotypes in the complex alterations induced by sepsis.

PURPOSE OF REVIEW To reiterate the necessity of integrating echocardiography in the management of shocked patients and to propose a step-by-step functional evaluation of hemodynamics proven to optimize hemodynamic monitoring and to adapt the treatment. RECENT FINDINGS Echocardiography has become the cornerstone to hemodynamic monitoring. By providing real-time images, echocardiography has the advantage over 'blind' technologies of an excellent diagnostic performance and of quick provision of information about the pathophysiology of circulatory failure. Critical care echocardiography (CCE) has been defined as echocardiography performed and interpreted by intensivists themselves, 7/7 and 24/24, at the bedside. Basic CCE is mainly a diagnostic approach, allowing quick and focused examination of cardiac function. Advanced CCE is the core of functional hemodynamic monitoring. It is based not only on transthoracic echocardiography but also strongly on transesophageal echocardiography, a very useful approach in ventilated patients. However, this monitoring is discontinuous. A single-use 72-h indwelling transesophageal probe was recently tested, allowing functional hemodynamic monitoring more continuously. SUMMARY Echocardiography has become a hemodynamic monitoring technique used worldwide. It allows to make a quick and simple diagnosis of typical hemodynamic situations, by means of basic CCE, and also to achieve real functional hemodynamic monitoring, through advanced CCE.

To compare therapeutic interventions during initial resuscitation derived from echocardiographic assessment of hemodynamics and from the Surviving Sepsis Campaign guidelines in intensive care unit septic patients.Prospective, descriptive study in two intensive care units of teaching hospitals.The number of ventilated patients with septic shock who were studied was 46. Transesophageal echocardiography was first performed (T13 hrs after intensive care unit admission) to adapt therapy according to the following predefined hemodynamic profiles: fluid loading (index of collapsibility of the superior vena cava≥36%), inotropic support (left ventricular fractional area change45% without relevant index of collapsibility of the superior vena cava), or increased vasopressor support (right ventricular systolic dysfunction, unremarkable transesophageal echocardiography study consistent with sustained vasoplegia). Agreement for treatment decision between transesophageal echocardiography and Surviving Sepsis Campaign guidelines was evaluated. A second transesophageal echocardiography assessment (T2) was performed to validate therapeutic interventions.Although transesophageal echocardiography and Surviving Sepsis Campaign approaches were concordant to manage fluid loading in 32 of 46 patients (70%), echocardiography led to the absence of blood volume expansion in the remaining 14 patients who all had a central venous pressure12 mm Hg. Accordingly, the agreement was weak between transesophageal echocardiography and Surviving Sepsis Campaign for the decision of fluid loading (κ: 0.37 [0.16;0.59]). With a cut-off value8 mm Hg for central venous pressure, κ was 0.33 [-0.03;0.69]. Inotropes were prescribed based on transesophageal echocardiography assessment in 14 patients but would have been decided in only four patients according to Surviving Sepsis Campaign guidelines. As a result, the agreement between the two approaches for the decision of inotropic support was weak (κ: 0.23 [-0.04;0.50]). No right ventricular dysfunction was observed. No patient had anemia and only three patients with transesophageal echocardiography documented left ventricular systolic dysfunction had a central venous oxygen saturation70%.A weak agreement was found in the prescription of fluid loading and inotropic support derived from early transesophageal echocardiography assessment of hemodynamics and Surviving Sepsis Campaign guidelines in patients presenting with septic shock.

In critically ill patients, the assessment of neurologic function can be difficult because of the use of sedative agents. It is not known whether neurologic signs observed under sedation can predict short-term outcomes. The objective of this study was to assess whether abnormal brainstem responses within the first 24 hrs of sedation are associated with mortality and altered mental status postsedation.Observational prospective study including an initial single-center and a subsequent multicenter study to develop and then validate the prognostic models.Three mixed and two medical intensive care units.Mechanically ventilated intensive care unit patients sedated with midazolam (± sufentanyl).Neurologic examination including the Glasgow Coma Scale, the Assessment to Intensive Care Environment score, cranial nerve examination, response to noxious stimuli, and the cough reflex was performed.Seventy-two patients were included in the initial group and 72 in a subsequent validation study. Neurologic responses were independent of sedative dose. Twenty-two patients in the development cohort and 21 (29%) in the validation group died within 28 days of inclusion. Adjusted for Simplified Acute Physiology Score II score, absent cough reflex was independently associated with 28-day mortality in the development (adjusted odds ratio [OR], 7.80; 95% confidence interval [CI], 2.00-30.4; p = .003) and validation groups (adjusted OR, 5.44; 95% CI, 1.35-22.0; p = .017). Absent oculocephalic response, adjusted for Simplified Acute Physiology Score II score, was independently associated with altered mental status after the withdrawal of sedation in the development (adjusted OR, 4.54; 95% CI, 1.34-15.4; p = .015) and validation groups (adjusted OR, 6.10; 95% CI, 1.18-25.5; p = .012).Assessment of brainstem responses is feasible in sedated critically ill patients and loss of selected responses is predictive of mortality and altered mental status.

Background— Cardiogenic unilateral pulmonary edema (UPE) is a rare entity, frequently leading to initial misdiagnosis. We sought to assess the prevalence of UPE and to determine its impact on prognosis compared with bilateral pulmonary edema. Methods and Results— We studied the characteristics and outcomes of patients admitted to our institution for cardiogenic pulmonary edema during an 8-year period. The study population included 869 consecutive patients. The prevalence of UPE was 2.1%: 16 right-sided UPE (89%) and 2 left-sided UPE (11%). In patients with UPE, blood pressure was significantly lower ( P ≤0.01), whereas noninvasive or invasive ventilation and catecholamines were used more frequently ( P =0.0004 and P P P P =0.003, respectively). In-hospital mortality was 9%: 39% for UPE versus 8% for bilateral pulmonary edema (odds ratio, 6.9; 95% confidence interval, 2.6 to 18; P P =0.021 for model A; and adjusted odds ratio, 6.8; 95% confidence interval, 1.1 to 41; P =0.037 for model B). Conclusions— Unilateral pulmonary edema represented 2.1% of cardiogenic pulmonary edema in our study, usually appeared as an opacity involving the right lung, and was always associated with severe mitral regurgitation. Unilateral pulmonary edema is related to an independent increased risk of mortality and should be promptly recognized to avoid delays in treatment.

Thoracic bioimpedance cardiography (ICG) has been proposed as a noninvasive, continuous, operator-independent, and cost-effective method for cardiac output monitoring. In the present study, we compared cardiac index (CI) measurements with ICG (Niccomo device) and transthoracic Doppler echocardiography in resting healthy volunteers undergoing hemodynamic load challenge.Twenty-five healthy volunteers (7 men and 18 women, mean age 36 +/- 6 yr, body surface area 1.75 +/- 0.17 m(2)) were investigated during three experimental conditions: baseline, positive end-expiratory pressure + 10 cm H(2)O and lower body positive pressure by means of medical antishock trousers inflated to 30 cm H(2)O in the abdominal compartment.ICG signal quality was89% over all sets of measurements. A weak but significant relationship was observed between CI(TTE) and CI(ICG) (r = 0.36; P = 0.002). Agreement between both techniques was 0.94 L x min(-1) x m(-2) (95% CI: 0.77-1.11), limits of agreement were -0.47 to 2.35 L x min(-1) x m(-2), and percentage error was 53%. No statistically significant relationships were found between percent changes in CI(TTE) and CI(ICG) after applications of positive end-expiratory pressure + 10 cm H(2)O (r = 0.21; P = 0.31) and medical antishock trousers (r = 0.22; P = 0.30).Poor correlation and lack of agreement between absolute values of CI measured by ICG and transthoracic Doppler echocardiography were found in resting healthy volunteers. The Niccomo device was also unreliable for monitoring changes in CI during hemodynamic load challenge.

Even a slight increase in pulmonary vascular resistance can overload a normal right ventricle, which ejects blood through a low-pressure circuit. In a clinical setting, a persistent increase in pulmonary vascular resistance produces acute cor pulmonale. From an echocardiographic point of view, may be defined as the combination of a paradoxical septal motion, reflecting systolic overload, with right ventricular enlargement, reflecting diastolic overload. In patients with acute respiratory distress syndrome, this complication reflects the severity of the pulmonary disease involving the microvasculature but may also be caused or exacerbated by an aggressive ventilatory strategy. In the past, conventional respiratory support used in acute respiratory distress syndrome to obtain normocapnia was associated with a poor prognosis and a high frequency of acute cor pulmonale, suggesting some relation between the two findings. This prognosis has greatly improved with protective ventilation. At the same time, the incidence of acute cor pulmonale has diminished in acute respiratory distress syndrome, and the prognosis of this specific complication has also improved, suggesting that the right ventricle may develop some adaptation against persistent overload. Past lessons, however, have taught us that this potential may be limited and lead us to recommend right ventricular protection during mechanical ventilation.

AT embolism syndrome (FES) is a combination of respiratory, neurologic, cutaneous, and hematologic symptoms associated with physical trauma to fat tissue secondary to bone fracture or to medical or surgical softtissue injury. 1–4 The incidence in patients with bone fractures is usually reported as low (0.5–10%), 4 but can reach more than 30%. 2,5 Diagnosis is based on major or minor criteria historicallydescribedbyGurdandWilson. 6 Wereportthecaseofa 67-yr-old female polytrauma patient who developed FES secondary to unusual bone fractures.

Increasing respiratory rate has recently been proposed to improve CO2 clearance in patients with acute respiratory failure who are receiving mechanical ventilation. However, the efficacy of this strategy may be limited by deadspace ventilation, and it might induce adverse hemodynamic effects related to dynamic hyperinflation.An intensive care unit of a university hospital.We studied 14 patients with acute respiratory failure during the adjustment of ventilator settings on the first day of mechanical ventilation in volume-controlled mode.After determining the positive end-expiratory pressure that suppresses any intrinsic positive end-expiratory pressure at a respiratory rate of 15 breaths/min, we compared blood gas analysis, respiratory measurements, and Doppler evaluation of right ventricular systolic function by using two different respiratory strategies with the same airway pressure limitation (plateau pressure,or =25 cm H2O), a low-rate conventional respiratory strategy with a respiratory rate of 15 breaths/min, and a high-rate strategy with a respiratory rate of 30 breaths/min.Compared with the low-rate strategy, the high-rate strategy neither significantly reduced PaCO2 (47 +/- 8 vs. 51 +/- 7 mm Hg with the low-rate strategy) nor significantly improved PaO2 (99 +/- 40 vs. 95 +/- 35 mm Hg with the low-rate strategy). It significantly increased alveolar deadspace to tidal volume ratio (21% +/- 8%, vs. 14% +/- 6% with the low-rate strategy) and produced dynamic hyperinflation, resulting in a substantial intrinsic positive end-expiratory pressure (6.4 +/- 2.7 cm H2O). Right ventricular outflow impedance was increased, resulting in a significant drop in the cardiac index (2.9 +/- 0.6 vs. 3.3 +/- 0.7 L/min/m with the low-rate strategy).We conclude that a high respiratory rate strategy during mechanical ventilation in patients with acute respiratory failure did not improve CO2 clearance, produced dynamic hyperinflation, and impaired right ventricular ejection.

Background Adequate fluid resuscitation in critically ill patients undergoing mechanical ventilation remains a difficult challenge, and diastolic and systolic right ventricular (RV) changes produced by positive airway pressure are important to consider in an individual patient with inadequate circulatory adaptation during respiratory support. We hypothesized that insufficient thoracic vena cava filling, predisposing to inspiratory collapse (zone 2 condition), may transiently affect RV outflow. Methods We measured beat-to-beat superior vena caval diameter and Doppler RV outflow during a routine transesophageal echocardiographic examination in 22 patients undergoing mechanical ventilation, all of whom required hemodynamic monitoring, and we calculated a collapsibility index for the superior vena cava as maximal expiratory diameter minus minimal inspiratory diameter, divided by maximal expiratory diameter. Results In 15 patients (group 1), the collapsibility index was low (17 +/- 7%) and was associated with a moderate inspiratory decrease in RV outflow (25 +/- 17%). However, in seven patients (group 2), we observed a high collapsibility index (71 +/- 7%), which was associated with a major inspiratory decrease in RV outflow (69 +/- 14%) combined with a reduced pulmonary artery flow period. A rapid volume expansion, only performed on group 2, markedly and significantly reduced both the collapsibility index (15 +/- 12%) and the inspiratory decrease in RV outflow (31 +/- 20%). Conclusion A major inspiratory decrease in RV outflow associated with a reduced pulmonary artery flow period in a patient undergoing mechanical ventilation reflected a high collapsibility index of the thoracic vena cava, suggesting a zone 2 condition, and may be corrected by blood volume expansion.

The incidence of acute cor pulmonale (ACP), a frequent and usually lethal complication of acute respiratory distress syndrome (ARDS) during traditional respiratory support, has never been re-evaluated since protective ventilation gained acceptance.We performed a longitudinal transesophageal echocardiographic (TEE) study to determine whether this incidence, and its severe implications for prognosis, might have changed in our unit as we altered respiratory strategy.Prospective open clinical study.Medical intensive care unit of a university hospital.Seventy-five consecutive ARDS patients given respiratory support with airway pressure limitation (plateau pressureor =30 cm H2O).ACP was defined as a ratio of right ventricular end-diastolic area to left ventricular end-diastolic area in the long axis0.6 associated with septal dyskinesia in the short axis during TEE examination.Normal right ventricular function was present in 56 patients, whereas right ventricular dysfunction was observed in 19 patients after 2 days of respiratory support. ACP was associated with pulmonary artery hypertension, increased heart rate, and decreased stroke index. Significant impairment of left ventricular diastolic function was also seen. All echo-Doppler abnormalities were reversible in patients who recovered, and the mortality rate was the same in both groups (32%). However, ACP patients who recovered required a longer period of respiratory support. A multivariate analysis individualized Paco2 level as the sole factor independently associated with ACP, suggesting that ACP development in ARDS is influenced by the severity of lung damage and/or the respiratory strategy.Evaluation of right ventricular function by TEE in a group of 75 ARDS patients submitted to protective ventilation revealed the persistence of a 25% incidence of ACP, resulting in detrimental hemodynamic consequences associated with tachycardia. However, ACP was reversible in patients who recovered and did not increase mortality.

Background An accepted concept in septic shock is that preload adaptation by acute left ventricular dilatation, when occurring spontaneously or with the aid of volume loading, permits maintenance of an adequate cardiac output, leading to final recovery. From a physiologic point of view, this concept appears debatable because a normal pericardium exerts a restraining action on a normal heart. Methods During a 26-month period, the authors investigated, by transesophageal echocardiography, 40 patients hospitalized in their unit for an episode of septic shock. Transesophageal echocardiography was performed in the first hours after admission, proceeded by correction of any hypovolemia, and stabilization of arterial pressure by vasoactive agent infusion if necessary. Left ventricular dimensions were obtained in long- and short-axis views, permitting calculation of left ventricular ejection fraction (long axis) and fractional area contraction (short axis). Stroke index was simultaneously measured by the Doppler technique. Results Stroke index was strongly correlated with both echocardiographic left ventricle ejection fraction (r = 0.75; P < 0.0001) and left ventricle fractional area contraction (r = 0.76; P < 0.0001), whereas it was independent of echocardiographic left ventricle diastolic dimensions. Conclusions The transesophageal echocardiography study was unable to confirm the reality of the concept of early preload adaptation by left ventricular dilatation in septic shock. Conversely, because left ventricular volume always remained in a normal range after correcting hypovolemia, systolic function was the unique determinant of stroke index in septic shock.

First, we thank Dr Lacout et al for their interest in and comments concerning our report that described the prevalence, characteristics, and outcomes of patients presenting with cardiogenic unilateral pulmonary edema (UPE).1 As detailed in the Methods section, this was not a study that included all patients with acute respiratory failure referred to our hospital, but a retrospective study that included patients with a final diagnosis of acute cardiogenic pulmonary edema. Thus, patients who presented with pulmonary embolism could not be included in our study. We agree with …