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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.

To evaluate the effects of acute hypercapnia induced by positive end-expiratory pressure (PEEP) variations at constant plateau pressure (P (plat)) in patients with severe acute respiratory distress syndrome (ARDS) on right ventricular (RV) function.Prospective observational study in two academic intensive care units enrolling 11 adults with severe ARDS (PaO(2)/FiO(2)150 mmHg at PEEP5 cmH(2)O). We compared three ventilatory strategies, each used for 1 h, with P (plat) at 22 (20-25) cmH(2)O: low PEEP (5.4 cmH(2)O) or high PEEP (11.0 cmH(2)O) with compensation of the tidal volume reduction by either a high respiratory rate (high PEEP/high rate) or instrumental dead space decrease (high PEEP/low rate). We assessed RV function (transesophageal echocardiography), alveolar dead space (expired CO(2)), and alveolar recruitment (pressure-volume curves).Compared to low PEEP, PaO(2)/FiO(2) ratio and alveolar recruitment were increased with high PEEP. Alveolar dead space remained unchanged. Both high-PEEP strategies induced higher PaCO(2) levels [71 (60-94) and 75 (53-84), vs. 52 (43-68) mmHg] and lower pH values [7.17 (7.12-7.23) and 7.20 (7.16-7.25) vs. 7.30 (7.24-7.35)], as well as RV dilatation, LV deformation and a significant decrease in cardiac index. The decrease in stroke index tended to be negatively correlated to the increase in alveolar recruitment with high PEEP.Acidosis and hypercapnia induced by tidal volume reduction and increase in PEEP at constant P (plat) were associated with impaired RV function and hemodynamics despite positive effects on oxygenation and alveolar recruitment ( ClinicalTrials.gov #NCT00236262).

The diagnosis of pulmonary embolism (PE) is difficult, despite validated diagnostic models. We sought to determine the value of a portable ultrasound device for triage of patients with suspected PE referred to the emergency department, using simplified echo criteria. We prospectively studied 103 consecutive patients with suspected PE, referred to our emergency department. After D-dimer screening, 76 patients were prospectively enrolled in this ultrasound study and underwent helical chest tomography, transthoracic echocardiography, and venous ultrasonography. Among patients with PE (n = 31), a right ventricular dilation was detected in 17 patients (55%), a direct visualization of clot in the lower limbs was present in 18 patients (58%), and 8 patients (26%) had both right ventricular dilation and deep venous thrombosis. The sensitivity and specificity of a combined ultrasound strategy using echocardiography and venous ultrasonography were respectively 87% (95% confidence interval 74% to 96%), and 69% (95% confidence interval 53% to 82%). The sensitivity of this combined strategy was significantly improved as compared to venous ultrasonography alone (P = 0.01) or echocardiography alone (P = 0.005). In patients with dyspnea or with high clinical probability of PE, this combined strategy was particularly relevant with high sensitivities (respectively 94% and 100%). Echocardiography combined with venous ultrasonography using a portable ultrasound device is a reliable method for screening patients with suspected PE referred to an emergency department, especially in patients with dyspnea or with high clinical probability.

To determine the effects of passive leg raising (PLR) on hemodynamics and on cardiac function according to the preload dependency defined by the superior vena cava collapsibility index (DeltaSVC).Forty patients with shock, sedated and mechanically ventilated, were included. Transesophageal echocardiography was performed. At baseline (T1), two groups were defined according to DeltaSVC. Eighteen patients presenting a DeltaSVC36%, an indicator of preload dependency, formed group 1, whereas 22 patients (group 2) exhibited a DeltaSVC30% (not preload-dependent). Measurements were then performed during PLR (T2), back to baseline (T3), and after volume expansion (T4) in group 1 only. At T1, DeltaSVC was significantly higher in group 1 than in group 2, 50 +/- 9% and 7 +/- 6%, respectively. In group 1, we found a decrease in DeltaSVC at T2 (24 +/- 9%) and T4 (17 +/- 7%), associated with increased systolic, diastolic and arterial pulse pressures. Cardiac index also increased, from 1.92 +/- 0.74 (T1) to 2.35 +/- 0.92 (T2) and 2.85 +/- 1.2 l/min/m(2) (T4) and left ventricular end-diastolic volume from 51 +/- 41 to 61 +/- 51 and 73 +/- 51 ml/m(2). None of these variations was found in group 2. No change in heart rate was observed.Hemodynamic changes related to PLR were only induced by increased cardiac preload.

We investigated implementation and efficacy of mild therapeutic hypothermia in the treatment of out-of-hospital cardiac arrest due to ventricular fibrillation.Two periods were compared, an historical one (36 patients) between 2000 and 2002 where therapeutic hypothermia was never used, and a recent period (32 patients) between 2003 and 2005 where therapeutic hypothermia (32-34 degrees C) was implemented prospectively in our unit. Cooling was obtained by simply using wet cloths and ice packs. Survival in the two groups and factors associated with survival were analysed, together with the neurological prognosis in discharged patients.Survival was significantly higher in the hypothermia group (56% versus 36%), whereas no significant difference was observed in severity between the two periods. Only age, time from return to spontaneous circulation20min, and therapeutic hypothermia were independently associated with survival. Therapeutic hypothermia was well tolerated and was associated with a significant improvement in neurological outcome. Whereas only 23% of patients actually reached the target temperature in 2003, 100% did in 2005.Therapeutic hypothermia is efficient in significantly improving survival and neurological outcome of out-of-hospital cardiac arrest with ventricular fibrillation. By using a simple method, it can be implemented easily and quickly, without side effects.

Despite airway pressure limitation, acute cor pulmonale persists in a minority of ARDS patients. Insufficient airway pressure limitation, hypercapnia, or both may be responsible. Because prone positioning (PP) has been shown to be a safe way to reduce airway pressure and to improve alveolar ventilation, we decided to assess its effect on right ventricular (RV) pressure overload in ARDS patients.Between January 1998 and December 2006, we studied 42 ARDS patients treated by PP to correct severe oxygenation impairment (Pao2/fraction of inspired oxygen ratio,100 mm Hg). RV function was evaluated by bedside transesophageal echocardiography, before and after 18 h of prone-position ventilation. RV enlargement was measured by RV/left ventricular (LV) end-diastolic area ratio in the long axis. Septal dyskinesia was quantified by measuring short-axis systolic eccentricity of the LV.Before PP, 21 patients (50%) had acute cor pulmonale, defined by RV enlargement associated with septal dyskinesia (group 1), whereas 21 patients had a normal RV (group 2). PP was accompanied by a significant decrease in airway pressure and Paco2. In group 1, this produced a significant decrease in mean (+/-SD) RV enlargement (from 0.91+/-0.22 to 0.61+/-0.21) after 18 h of PP (p=0.000) and a significant reduction in mean septal dyskinesia (from 1.5+/-0.2 to 1.1+/-0.1) after 18 h of PP (p=0.000).In the most severe forms of ARDS, PP was an efficient means of controlling RV pressure overload.

Objective Transesophageal echocardiography (TEE) is increasingly used in hemodynamic monitoring in the intensive care unit. This paper describes and validates a scoring system for assessing competence in TEE performed by intensivists for this indication.

Airway pressure limitation is now a largely accepted strategy in adult respiratory distress syndrome (ARDS) patients; however, some debate persists about the exact level of plateau pressure which can be safely used. The objective of the present study was to examine if the echocardiographic evaluation of right ventricular function performed in ARDS may help to answer to this question. For more than 20 years, we have regularly monitored right ventricular function by echocardiography in ARDS patients, during two different periods, a first (1980–1992) where airway pressure was not limited, and a second (1993–2006) where airway pressure was limited. By pooling our data, we can observe the effect of a large range of plateau pressure upon mortality rate and incidence of acute cor pulmonale. In this whole group of 352 ARDS patients, mortality rate and incidence of cor pulmonale were 80 and 56%, respectively, when plateau pressure was > 35 cmH2O; 42 and 32%, respectively, when plateau pressure was between 27 and 35 cmH2O; and 30 and 13%, respectively, when plateau pressure was

Transesophageal echocardiography (TEE) has proven its efficiency in assessing hemodynamics in patients by its ability to evaluate cardiac function and fluid responsiveness. Classically, it requires quantitative measurements, whereas in routine practice TEE is used in our unit especially as a qualitative procedure. We assessed the accuracy of this qualitative central hemodynamic evaluation obtained by TEE at the bedside.Prospective study conducted in a medical ICU between September 2004 and April 2005. All TEE examinations performed in consecutive patients hospitalized for septic shock and mechanically ventilated for an associated acute lung injury were eligible for evaluation. Intensivists trained in echocardiography were asked to classify (a) respiratory changes in the superior vena cava (SVC), (b) left ventricular (LV) systolic function, (c) right ventricular (RV) end-diastolic size, and (d) shape and kinetics of the interventricular septum (IVS). A post-hoc quantitative evaluation was then performed by a trained investigator unaware of the patients' status.We evaluated 83 examinations in 30 patients. Qualitative evaluation was easily able to distinguish patients with significant or nonsignificant SVC respiratory changes, normal, moderately or markedly depressed LV systolic function, and nondilated or dilated right ventricle. Acute cor pulmonale was also well recognized.By its ability accurately to evaluate hemodynamic status qualitative TEE could be useful for intensivists in managing circulatory failure in septic shock, rendering the more time-consuming quantitative evaluation useless.

Meprobamate self-poisoning has been reported as potentially inducing hypotension. We examined the incidence and causes of hypotension induced by this poisoning and its prognosis.Retrospective observational study conducted in a medical ICU between June 1997 and October 2003. Seventy-four patients admitted for meprobamate poisoning and needing mechanical ventilation were included. Demographic, clinical, and laboratory data were compared between patients with and without hypotension. All echocardiograms recorded in patients with hypotension were reviewed, and left ventricular (LV) and right ventricular (RV) functions were assessed.Twenty-nine (40%) patients exhibited hypotension without any significant difference in age, gender, cardiac history, or meprobamate concentration in blood when compared to patients without hypotension. Base excess was significantly lower in patients with hypotension. Echocardiography demonstrated a hypokinetic state, associating decreased LV ejection fraction (45+/-15%) and cardiac index (2+/-0.7 l min(-1) m(-2)), and increased inferior vena cava diameter. Most patients with hypotension received inotropic drugs by infusion, and were ventilated for significantly longer.Meprobamate self-poisoning induces hypotension, notably related to cardiac failure, in about 40% of cases. This has important therapeutic consequences, as frequent inotropic drug infusion. The mechanisms of cardiac toxicity remain largely unknown, and no predictive factor could be isolated.

Background: The diagnosis of pulmonary embolism (PE) remains difficult. Ultrasounds allow for the exploration of the venous system to great extent and for the detection of indirect signs of PE. The aim of this study was to determine the incidence of acute cor pulmonale (ACP) and deep venous thrombosis (DVT) found by ultrasonographic techniques in a population of patients with PE. Methods: One hundred and seventy-three consecutive patients with acute PE (diagnosed either by spiral computed tomography or selective pulmonary angiography) had subsequently both transthoracic echocardiography (TTE) and venous ultrasonography. The diagnostic criterion used for defining ACP by echocardiography was the right to left ventricular end-diastolic area ratio over (or equal to) 0.6 with paradoxical septal wall motion. The diagnosis of DVT rested on vein incompressibility. Results: ACP was found in 56% of our patients while 75% were found to have DVT and 89% of the patients had either ACP or DVT or both. All of the patients with proximal PE had ACP and/or DVT. The presence of ACP using echocardiography was significantly different according to the localization of PE ( P P =0.0001). The incidence of ACP and/or DVT was significantly different according to the localization of PE ( P =0.001). Echocardiography combined with venous ultrasonography had improved the diagnosis value of venous ultrasonography in only 4% of patients with distal PE ( P =0.65). Conclusion: A combined strategy using echocardiography with venous ultrasonography improves significantly the diagnostic value of venous ultrasonography in proximal and lobar PE and fails in distal PE.

To evaluate the extent to which respiratory changes in inferior vena cava (IVC) diameter can be used to predict fluid responsiveness. Prospective clinical study. Hospital intensive care unit. Twenty-three patients with acute circulatory failure related to sepsis and mechanically ventilated because of an acute lung injury. Inferior vena cava diameter (D) at end-expiration (Dmin) and at end-inspiration (Dmax) was measured by echocardiography using a subcostal approach. The distensibility index of the IVC (dIVC) was calculated as the ratio of Dmax − Dmin / Dmin, and expressed as a percentage. The Doppler technique was applied in the pulmonary artery trunk to determine cardiac index (CI). Measurements were performed at baseline and after a 7 ml/kg volume expansion using a plasma expander. Patients were separated into responders (increase in CI ≥15%) and non-responders (increase in CI

Septic shock is associated with important hemodynamic alterations, including absolute or relative decrease in central blood volume (1), systolic alterations of left ventricular (LV) (2, 3) and right ventricular (RV) (4) function, and severe peripheral vasodilatation responsible in part for alterations in regional blood flow distribution and probably linked to outcome (5). Hemodynamic treatment of septic shock requires blood volume expansion, which has proved to enhance survival if not delayed (6), and vasoactive support with catecholamines, according to the hemodynamic status (7). For a long time, assessment of hemodynamic instability in sepsis was based on right heart catheterization at the bedside. Recently, the Task Force of the American College of Critical Care Medicine reiterated the usefulness of right heart catheterization in guiding hemodynamic support in patients requiring more than an initial blood volume expansion (7). Concerns about the data obtained by this technique, and their interpretation in a mechanically ventilated patient, are not new (8). Moreover, this technique has been criticized for its invasiveness and associated specific complications (9). However, large cooperative clinical trials have not demonstrated an increase in mortality carried by right heart catheterization (10, 11). We abandoned right heart catheterization in our unit in 1990 and have replaced it by routine echocardiography. Since then, all patients hospitalized with septic shock have been monitored using echocardiography as a noninvasive bedside procedure. In our daily practice, echocardiography is performed after physical examination in all hemodynamically unstable patients and repeated immediately after each major hemodynamic intervention. For this purpose, the frozen multiplane probe can be kept in the esophagus for the time needed to assess the results of a major hemodynamic intervention (10–20 minutes). This strategy is original, few French teams use it, and no trial has demonstrated the usefulness of echocardiography in severe sepsis. But the quality of the data obtained and the growing demand for training from intensivists have convinced us that this procedure will be widely used in the future. Data from echocardiographic evaluation of a series of 183 patients have been published, emphasizing that a large spectrum of changes in ventricular systolic function can be observed in

When used in patients free of previous cardiorespiratory disease, mechanical ventilation with a normal tidal volume does not have any discernible hemodynamic consequences. Conversely, the presence of a pulmonary disease affecting the bronchial tree, lung parenchyma, or both, may induce extreme conditions for mechanical ventilation. In this setting, an adverse hemodynamic effect may seriously complicate respiratory support.

1. Tulevski II, Groenink M, van Der Wall EE, van Veldhuisen DJ, Boomsma F, Stoker J, Hirsch A, Lemkes JS, Mulder BJM. Increased brain and atrial natriuretic peptides in patients with chronic right ventricular pressure overload: correlation between plasma neurohormones and right ventricular dysfunction. Heart 2001; 86:27–30. 2. Tulevski II, van der Wall EE, Groenink M, Dodge-Khatami A, Hirsch A, Stoker J, Mulder BJM. Usefulness of magnetic resonance imaging dobutamine stress in asymptomatic and minimally symptomatic patients with decreased cardiac reserve from congenital heart disease (complete and corrected transposition of the great arteries and subpulmonic obstruction). Am J Cardiol 2002;89: 1077–1081. 3. Tulevski II, Lee PL, Groenink M, van der Wall EE, Stoker J, Pieper PG, Romkes H, Hirsch A, Mulder BJM. Dobutamine-induced increase of right ventricular contractility without increased stroke volume in adolescent patients with transposition of the great arteries: evaluation with magnetic resonance imaging. Int J Card Imaging 2000;16:471–478. 4. Rebergen SA, Niezen RA, Helbing WA, van der Wall EE, de Roos A. Cine gradient-echo MR imaging and MR velocity mapping in the evaluation of congenital heart disease. Radiographics 1996;3:467–481. 5. Krabill KA, Wang Y, Einzig S, Moller JH. Rest and exercise hemodynamics in pulmonary stenosis: comparison of children and adults. Am J Cardiol 1985; 56:360–365. 6. Nugent EW, Freedom RM, Nora JJ, Ellison RC, Rowe RD, Nadas AS. Clinical course in pulmonary stenosis. Circulation 1977;56:138–147. 7. Helbing WA, Niezen RA, Le Cessie S, van der Geest RJ, Ottenkamp J, de Roos A. Right ventricular diastolic function in children with pulmonary regurgitation after repair of tetralogy of Fallot: volumetric evaluation by magnetic resonance velocity mapping. J Am Coll Cardiol 1996;28:1827–1835. 8. Fogel MA, Rychik J. Right ventricular function in congenital heart disease: pressure and volume overload lesions. Prog Cardiovasc Dis 1998;40:343–356. 9. Therrien J, Siu SC, McLaughlin PR, Liu PP, Williams WG, Webb GD. Pulmonary valve replacement in adults late after repair of tetralogy of Fallot: are we operating too late? J Am Coll Cardiol 2000;36:1670–1675. 10. Vliegen HW, Van Straten A, De Roos A, Roest AAW, Schoof PH, Zwinderman AH, Ottenkamp J, Van der Wall EE, Hazekamp MG. Magnetic resonance imaging to assess the hemodynamic effects of pulmonary valve replacement in adults late after repair of tetralogy of Fallot. Circulation 2002;106:1703–1707.

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.

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.

Study objective: We hypothesized that a dynamic leftventricular (LV) evaluation during a loading challenge might enhancediagnostic capabilities of routine transesophageal echocardiography incritically ill patients and selection of therapeutic options againstcirculatory failure, particularly the choice between volume expansionand vasoactive agent infusion. Design: Prospectiveclinical study in a group of 26 patients requiring hemodynamic supportby vasoactive infusion because of low systemic arterial pressure( Setting: University hospital ICU. Patients: Patients required respiratory support for anepisode of acute respiratory failure of various causes or for anepisode of coma. They were studied by transesophageal echocardiographyduring mechanical ventilation in the controlled mode, before and duringa loading challenge made using the legs compartment of medicalantishock trousers inflated at 80 mm Hg. Measurements: A short-axis view of the left ventricle was obtained by a transgastricapproach, and end-diastolic and end-systolic areas were measured. LVstroke area (LVSA) and LV fractional area contraction (LVFAC) werecalculated. Results: Changes in LVechocardiographic measurements permitted separation of the patientsinto two groups. In nine patients (group 1), LVSA, used as an index ofstroke output, was significantly increased during the challenge, together with a significant increase in LV end-diastolic area, suggesting preload improvement by the challenge. Conversely, in 17patients (group 2), LVSA was significantly reduced by the challenge, together with a significant decrease in LVFAC, suggesting a negativeeffect of increased afterload by the challenge. Conclusion: Study of the changes in LV dimensions duringloading challenge in hemodynamically unstable patients was used toevaluate the balance between the adequacy of preload and the ability ofthe heart to pump against an increased load, and might thus guidehemodynamic support.

Summary Introduction Idiopathic spontaneous pneumothorax is a frequent disorder with a poorly codified treatment. Methods We retrospectively studied 48 patients with an idiopathic pneumothorax hospitalized between 1993 and 1997, and we discuss the location and time of surgical treatment. We compare the outcome of patients treated by chest tube (24 F), and by small caliber catheter (8 F). Results One patient was treated by needle aspiration, five patients were just observed and three underwent surgery. Fifteen patients were treated by chest tube and 24 by small catheter. The duration of hospitalization of the 26 successfully drained patients was 3.1 ± 2 days. The recurrence rate of these patients was 31% after a 27 ± 17 month follow-up. The failure rate was 33% at 3.7 ± 2 days of hospitalization regardless of the drainage method, leading to surgical treatment. The hospital stay of surgically treated patients was 15.8 ± 5 days. None of the 20 patients treated by video-assisted thoracoscopic surgery re lapsed after a 26 ± 17 month period. Conclusion Taking into account a recurrence rate of 30% and a surgical success rate of 95%, we propose an early surgical treatment in case of drainage failure, performed on the third day. This attitude shortens the hospital stay of successfully drained patients to 3.1 ± 2 days. Moreover, small caliber catheter drainage seems to be as efficient as chest tubes to treat spontaneous pneumothorax.

In a context such as acute respiratory distress syndrome, where optimum tidal volume and airway pressure levels are debated, the present study was designed to differentiate the right ventricular (RV) consequences of increasing lung volume from those secondary to increasing airway pressure during tidal ventilation. The study was conducted by combined two-dimensional echocardiographic and Doppler studies in 10 patients requiring mechanical ventilation in the controlled mode because of acute respiratory failure. Continuous monitoring of airway pressure on echocardiographic and Doppler recordings provided accurate timing of each cardiac event during the respiratory cycle, with particular attention being paid to end-expiratory and end-inspiratory atrial diameters, RV dimensions, and pulmonary artery and tricuspid flow estimated by the velocity-time integral (PAVTIand TVTI, respectively). At baseline, lung inflation during the inspiratory phase of mechanical ventilation produced a drop in PAVTIfrom 14.3 ± 2.6 cm at end expiration to 11.3 ± 2.1 cm at end inspiration. This drop occurred without reduction in right atrial diameter or in RV diastolic dimensions. It was not preceded but was followed by a decrease in TVTI, thus confirming an increase in RV outflow impedance. Manipulation of tidal volume without changing airway pressure and manipulation of airway pressure without changing tidal volume demonstrated that tidal volume, but not airway pressure, was the main determinant factor of RV afterloading during mechanical ventilation.

Study objective To investigate the rate of recovery from septic shock in patients with suspected left ventricular (LV) preload deficiency and LV systolic dysfunction. Design A monitoring period was defined by the need for inotropic/vasopressor support, and LV function was assessed daily during this period by bedside two-dimensional echocardiography (2D-ECHO). Setting University hospital ICU. Patients During a 5-year period, 90 patients with an episode of septic shock (60% with gram-positive bacteria as the causative agent) were consecutively enrolled in the study (mean age, 55 ± 18 years). Standard volume resuscitation combined with inotropic/vasopressor support was used to maintain systolic arterial pressure > 90 mm Hg. All patients received mechanical ventilation because of associated respiratory failure. The average duration of hemodynamic support was 4.4 ± 1.6 days. Thirty-four patients were weaned from hemodynamic support during the monitoring period and ultimately recovered (group I). Twenty-eight patients died from refractory circulatory failure during the monitoring period, and 28 died later from ARDS or multiple organ dysfunction syndrome, leading to a 62% overall mortality rate (group II). Methods Daily bedside LV volumes and ejection fraction (LVEF) were recorded using 2D-ECHO. Data obtained at the start (day 1 and day 2) and end of the monitoring period (day n ) were compared. Results LV end-diastolic volume was within the normal range of our laboratory values in all patients, but was initially smaller in group II than in group I, and remained so despite fluid loading. LVEF was significantly depressed in all patients, resulting in severe reduction in LV stroke volume (LVSV), which was initially more marked in group I. In group I patients, LVEF significantly improved during the monitoring period, resulting in an increase in LVSV. Conclusion 2D-ECHO changes during hemodynamic support in 90 septic patients confirmed defective LV preload with a propensity to worsen despite fluid loading in nonsurvivors (62% in the present study). Our results are also in agreement with previous studies reporting depressed LV systolic function at the initial phase of septic shock. Since LV dysfunction was more marked in patients who recovered, we suggest that the exact significance of this finding should be reevaluated.

To compare the hemodynamic effects of medical antishock trousers (MAST) inflation in mechanically ventilated patients with normal and poor left ventricular function.Twelve patients requiring respiratory support were divided into two groups according to baseline transesophageal echocardiography (TEE) measurements: normal left ventricular dimensions and fractional area of contraction (FAC=61 +/- 5%) (n=7) and dilated cardiomyopathy with reduced FAC (21 +/- 1%) (n=5). All patients were studied when two successive levels of load (mild load by inflation of the leg compartment of MAST at 50 cmH2O and high load by adding the abdominal compartment of MAST inflated at 30 cmH2O) were applied. Global left ventricular systolic function was assessed on the TEE transgastric short-axis view. End-systolic wall stress (ESWS) was used as an indicator of left ventricular afterload.Total respiratory, lung and chest wall compliances were reduced by 48%, 51% and 27% respectively at the high load level (P0.05). Whereas no hemodynamic changes occurred at mild load, the high load level produced an increase in left ventricular afterload as evidenced by concomitant increases in diastolic arterial blood pressure (66 +/- 6 to 79 +/- 6 mmHg, P0.05) and ESWS (69 +/- 12 to 74 +/- 12 Kdyn x cm(-2) x m(-2), P0.05). In patients with dilated cardiomyopathy, this increase in afterload impaired the left ventricular systolic function and end-systolic area increased (19.0 +/- 2.5 to 21.4 +/- 2.9 cm2 x m(-2), P0.05) while FAC decreased (22 +/- 2 to 16 +/- 2%, P0.05). Left ventricular end-diastolic area remained unchanged during the study in both groups.MAST inflation impairs respiratory mechanics and global left ventricular systolic function in cardiac patients without changes in left ventricular preload.

Case Report: We report a 35-year-old woman who developed severe acidosis, massive gastrointestinal hemorrhage, acute renal failure, and hepatic injury following ingestion of chromic acid (50 mL) and died 12 hours after ingestion. Postmortem liver biopsy revealed a fatty degeneration with chromium concentration 3.6 μmol/g. The kidney, with chromium concentration 2.6 μmol/g, had extensive necrosis and ischemic lesions. Erythrocyte chromium was 1903 μmol/L at 3 hours declining to 865 μmol/L at 11 hours.

Study objectives Positive end-expiratory pressure (PEEP) has been proposed to improve cardiac output in patients with left ventricular (LV) dysfunction. This study was designed to compare quantitative global and regional LV performance in response to PEEP in patients with normal and poor LV function. Design A prospective clinical trial. Setting Adult medical ICU in a university hospital. Patients Twelve critically ill patients requiring respiratory support and divided into two groups according to baseline transesophageal echocardiographic (TEE) measurements: normal LV dimensions and fractional area of contraction (FAC=61 ±5%) (n=7) and dilated cardiomyopathy with reduced FAC (21±1%) (n=5). Measurements and results All patients were studied when two successive levels of PEEP (best PEEP as the highest value of respiratory compliance and high PEEP as best PEEP+10 cm H 2 O) were applied. Global systolic LV performance and quantitative regional wall motion analysis performed by the centerline method were assessed on the TEE transgastric short-axis view. End-systolic wall stress (ESWS) was used as a reliable indication of LV afterload. PEEP reduced LV dimensions asymmetrically in both groups of patients and septolateral diameter significantly decreased without affecting global LV systolic performance. Additionally, high PEEP produced a significant impairment in septal kinetics as evidenced by the centerline method. High PEEP also decreased ESWS for all patients (—27% in normal group and −23% in cardiac group, p Conclusions PEEP cannot be recommended routinely to improve LV performance in patients with severe dilated cardiomyopathy.

The left (LV) and right ventricles (RV) are enclosed in a stiff envelope, the pericardium. They have similar enddiastolic volumes, and there is no free space for acute ventricular dilatation within a normal pericardial space. Thus, when RV end-diastolic volume increases owing to increased RV loading, it can only occur at the expense of the space devoted to the left ventricle, which is prevented from dilating to as large an end-diastolic volume as it would otherwise given its distending pressure. From a practical point of view this reduced LV end-diastolic volume is accompanied by decreases in LV diastolic compliance, such that for the same LV distending pressure LV end-diastolic volume is less. This point was described in a previous Physiological Note [1]. LV impaired relaxation by RV enlargement is evidenced by Doppler examination of mitral flow velocity (Fig. 1).

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 …

In addition to excluding hydrostatic edema and monitoring the patient with septic shock or trauma, which are the leading causes of acute respiratory distress syndrome (ARDS), echocardiography is useful as it may detect some specific hemodynamic alterations related to the disease or its therapy, and this may have marked influence on ARDS management.

Summary In this study, the case was reported of a 60-year-old male with a chronic respiratory disorder following a poliomyelitic infection. He was treated by a SAMU team (Glasgow score=4) for a comatose state, and no sign of localization of disease or meningitis was found. Given the preliminary diagnostic findings, mechanical ventilation was instigated; and several minutes later generalized seizures were observed which did not respond to 10 mg diazepam, but which continued when the subject was admitted to the emergency ward, The following day, the patient appeared to have regained normal function and consciousness. It was concluded that these seizures were due to a rapid acidemia-alcalemia shift in a person with a preexisting chronic respiratory disorder.

Purpose of review Acute cor pulmonale is a form of acute right heart failure produced by a sudden increase in resistance to blood flow in the pulmonary circulation, which is now rapidly recognized by bedside echocardiography. Recent findings In the clinical setting, acute cor pulmonale is mainly observed as a complication of massive pulmonary embolism or acute respiratory distress syndrome. In acute respiratory distress syndrome, the worsening effect of mechanical ventilation has been recently emphasized. Summary As a general rule, the treatment consists in rapidly reducing resistance to blood flow in the pulmonary circulation, obtained by a specific strategy according to etiology.

To evaluate the actual incidence of global left ventricular hypokinesia in septic shock.All mechanically ventilated patients treated for an episode of septic shock in our unit were studied by transesophageal echocardiography, at least once a day, during the first 3 days of hemodynamic support. In patients who recovered, echocardiography was repeated after weaning from vasoactive agents. Main measurements were obtained from the software of the apparatus. Global left ventricular hypokinesia was defined as a left ventricular ejection fraction of45%.During a 3-yr period (January 2004 through December 2006), 67 patients free from previous cardiac disease, and who survived for48 hrs, were repeatedly studied. Global left ventricular hypokinesia was observed in 26 of these 67 patients at admission (primary hypokinesia) and in 14 after 24 or 48 hrs of hemodynamic support by norepinephrine (secondary hypokinesia), leading to an overall hypokinesia rate of 60%. Left ventricular hypokinesia was partially corrected by dobutamine, added to a reduced dosage of norepinephrine, or by epinephrine. This reversible acute left ventricular dysfunction was not associated with a worse prognosis.Global left ventricular hypokinesia is very frequent in adult septic shock and could be unmasked, in some patients, by norepinephrine treatment. Left ventricular hypokinesia is usually corrected by addition of an inotropic agent to the hemodynamic support.

Acute right heart failure related to pulmonary causes (acute cor pulmonale) is caused mainly by acute pulmonary embolism or acute respiratory distress syndrome (ARDS) requiring mechanical ventilatory support. The echocardiogram is even more useful than right heart catheterization in this situation, because the pulmonary arterial pressure correlates poorly with right ventricular function and cardiac output measurements are often unreliable. The echo also gives information not only on the extent of right ventricular dysfunction and dilation, but also on left ventricular filling and function. Acute cor pulmonale due to massive pulmonary embolism occurs in the majority of pulmonary embolism patients admitted to the ICU and may respond rapidly to thrombolytic therapy. Acute cor pulmonale in patients with ARDS is partly related to positive pressure ventilation and its effect on increasing the impedance of the pulmonary vasculature. Lung-protective ventilatory strategies using limited tidal volumes and plateau pressures can greatly lower the occurrence of acute cor pulmonale in ARDS patients. The therapy for acute cor pulmonale aims at minimizing the pulmonary vascular resistance and optimizing fluid volume. Vasopressor agents should be used in hypotensive patients to maintain coronary perfusion, but inhaled vasodilator agents like inhaled nitric oxide and prostacyclin are seeing increasing use in critical care settings to selectively dilate the pulmonary arterial bed.

Assessing right ventricular (RV) function in acute conditions, such as circulatory and respiratory failure, is of great importance for hemodynamic monitoring and therapeutic adaptation (1, 2). Right ventricular function is responsible for the back-pressure of systemic venous return (3), and for the amount of blood that reaches the pulmonary circulation, which is one of the main determinants of left ventricular (LV) stroke volume (4). Right ventricular failure in septic shock may explain why blood volume expansion is unable to increase cardiac output (5). In certain conditions, such as massive pulmonary embolism (PE) and acute respiratory distress syndrome (ARDS), RV failure may be the main cause of shock, leading to specific therapeutic interventions such as thrombolysis or limitation of airway pressures. Before considering the main causes of RV dysfunction, it is essential to understand the specific features of RV physiology.

Fluid responsiveness is a relatively new concept. It enables the efficacy of volume expansion to be predicted before use, rather than assessed afterwards, thus avoiding inappropriate fluid infusion. Echocardiography is a fantastic noninvasive tool which can directly visualize the heart and assess cardiac function. Its use was long limited by the absence of accurate indices to diagnose hypovolemia and predict the effect of volume expansion. In the last few years, several French teams have used echocardiography to develop new parameters of fluid responsiveness, taking advantage of its ability to monitor cardiac function beat by beat during the respiratory cycle.In mechanically ventilated patients perfectly adapted to the respirator, respiratory variations in superior and inferior vena cava diameters and in left ventricular stroke volume have been validated as parameters of fluid responsiveness. In our opinion, the collapsibility index of the superior vena cava is the most reliable of these parameters, but does require transesophageal echocardiography.Echocardiography has been widely demonstrated to predict fluid responsiveness accurately. This is now a complete and noninvasive tool able to accurately determine hemodynamic status in circulatory failure.

The effect of laparoscopy on cardiac function is controversial. We hypothesized that cardiac dysfunction related to increased afterload could be predominant in patients undergoing elective abdominal aortic repair. To test this hypothesis, we conducted a transesophageal echocardiographic study in 15 patients during laparoscopic aortic surgery. We systematically assessed left ventricular (LV) and right ventricular (RV) functions. Measurements were obtained in the supine position without pneumoperitoneum and with an intraabdominal pressure of 14 mm Hg. Then, patients were turned to the right lateral position without pneumoperitoneum and intraabdominal pressure was increased to 7 mm Hg and to 14 mm Hg. Pneumoperitoneum induced a 25% arterial blood pressure increase and a 38% increase in LV systolic wall stress. A 25% decrease in LV ejection fraction and an 18% decrease in LV stroke volume were observed, associated with an increase in LV end-systolic volume. LV diastolic function impairment was observed without change in LV end-diastolic volume. Respiratory alterations in superior vena cava diameter were never observed, suggesting that volume status remained optimal. Respiratory changes in RV stroke volume were increased according to intraabdominal pressure and body position, reflecting an increase in RV afterload. In conclusion, peritoneal CO2 insufflation in patients scheduled for laparoscopic aortic surgery could impair LV and RV systolic functions as a consequence of increased afterload.

Because the right side of the heart supplies blood to the pulmonary circulation, its integrity is required for both adequate respiratory and circulatory function. By reducing pulmonary perfusion, right-sided heart failure may compromise arterial oxygenation and left ventricular filling, and monitoring of right-sided heart function at the bedside in critically ill patients is fundamental. Two recent clinical commentaries have focused on the invaluable help provided by echocardiography for this purpose.Bedside echocardiography has supplanted invasive procedures as the best tool to evaluate right-sided heart function. Although not recent, this technique, previously reserved for cardiologists, has recently gained a larger acceptance in respiratory intensive care units. Echocardiographic examination detects excessive right ventricular afterload, visualized by septal dyskinesia, and its usual consequence, right ventricular enlargement, which impairs left ventricular filling.Monitoring of right-sided heart function is essential in a clinical setting associated with hemodynamic instability, such as severe sepsis or acute coronary artery obstruction, and also in that it is associated with increased pulmonary vascular resistance, as in massive pulmonary embolism or acute respiratory failure. Moreover, use of mechanical ventilation requires regular evaluation of its effects on the right side of the heart.

Forty-six consecutive patients with pulmonary embolism (PE) who underwent pulmonary angiography, helical computed tomography (CT), and echocardiography in the investigators' emergency department were studied. It was determined that the CT right ventricular (RV)/left ventricular (LV) end-diastolic area ratio was correlated with PE obstruction and echocardiography. A CT RV/LV area ratio >1 had a sensitivity of 88% and a specificity of 88% in diagnosing significant PE. The present study suggests that helical CT may be used as a triage tool in acute PE for selecting high-risk patients, using calculation of the RV/LV area ratio to detect RV dysfunction.

In mechanically ventilated patients inspiratory increase in pleural pressure during lung inflation may produce complete or partial collapse of the superior vena cava. Occurrence of this collapse suggests that at this time external pressure exerted by the thoracic cavity on the superior vena cava is greater than the venous pressure required to maintain the vessel fully open. We tested the hypothesis that measurement of superior vena caval collapsibility would reveal the need for volume expansion in a given septic patient. Prospective data collection for 66 successive patients in septic shock admitted in a medical intensive care unit and mechanically ventilated for an associated acute lung injury. We simultaneously measured superior vena caval collapsibility by echocardiography and cardiac index by the Doppler technique at baseline and after a 10 ml/kg volume expansion by 6% hydroxyethyl starch in 30 min. The threshold superior vena caval collapsibility of 36%, calculated as (maximum diameter on expiration−minimum diameter on inspiration)/maximum diameter on expiration, allowed discrimination between responders (defined by an increase in cardiac index of at least 11% induced by volume expansion) and nonresponders, with a sensitivity of 90% and a specificity of 100%. Superior vena cava measurement should be systematically performed during routine echocardiography in septic shock as it gives an accurate index of fluid responsiveness.

We tested the hypothesis that ventilation in the prone position might improve homogenization of tidal ventilation by reducing time-constant inequalities, and thus improving alveolar ventilation. We have recently reported in ARDS patients that these inequalities are responsible for the presence of a "slow compartment," excluded from tidal ventilation at supportive respiratory rate.In 11 ARDS patients treated by ventilation in the prone position because of a major oxygenation impairment (PaO(2)/FIO(2)/=100 mm Hg) we studied mechanical and blood gas changes produced by a low PEEP (6+/-1 cm H(2)O), ventilation in the prone position, and the two combined.Ventilation in the prone position significantly reduced the expiratory time constant from 1.98+/-0.53 s at baseline with ZEEP to 1.53+/-0.34 s, and significantly decreased PaCO(2) from 55+/-11 mm Hg at baseline with ZEEP to 50+/-7 mm Hg. This improvement in alveolar ventilation was accompanied by a significant improvement in respiratory system mechanics, and in arterial oxygenation, the latter being markedly increased by application of a low PEEP (PaO(2)/FIO(2) increasing from 64+/-19 mm Hg in supine position with ZEEP to 137+/-88 mm Hg in prone with a low PEEP).In severely hypoxemic patients, prone position was able to improve alveolar ventilation significantly by reducing the expiratory time constant.

For a given level of arterial distensibility, the amplitude of the arterial pulse is directly related to the left ventricular (LV) stroke volume. Thus, rapid changes in arterial pulse pressure, the difference between systolic and diastolic pressures, essentially reflect changes in LV stroke volume.

It has long been known that there are cyclic changes in arterial pressure during mechanical ventilation. They are caused by cyclic changes in both the right and left ventricular stroke output, occurring in opposite phases. As a result, arterial pulse pressure is increased during inspiration and decreased during expiration. A cyclic improvement in left ventricular systolic function could thus be expected during mechanical lung inflation. We tested this hypothesis in 31 septic patients who were mechanically ventilated in controlled mode by combining left ventricular measurements by transesophageal echocardiography with invasive arterial pressure recordings and Doppler analysis of pulmonary venous flow and right and left ventricular stroke volume. Lung inflation by tidal ventilation significantly improved left ventricular stroke volume (26 +/- 0.4 cm3/m2 [mean +/- SEM] vs. 22.3 +/- 0.4 cm3/m2 at end deflation). Beat-to-beat analysis of pulmonary venous flow velocity illustrated the boosting effect of lung inflation on pulmonary venous return. The beneficial effect of inspiration thus appeared directly related to a significant increase in left ventricular diastolic volume (60.3 +/- 1.5 cm3/m2 vs. 53.3 +/- 1.4 cm3/m2 at end-expiration) and to a lesser extent to an improved left ventricular ejection fraction. We concluded that the transient beneficial hemodynamic effect of tidal ventilation on the left ventricular pump is essentially mediated by an improved left ventricular filling.