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 cm(3)/m(2)[mean +/- SEM] vs. 22.3 +/- 0.4 cm(3)/m(2) 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 cm(3)/m(2) vs. 53.3 +/- 1.4 cm(3)/m(2) 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.

The presence of an initial segment with a low compliance on the static pressure-volume (PV) curve in patients with acute respiratory distress syndrome (ARDS) indicates that some lung compartments do not initially receive insufflated gas. We tested the hypothesis that an uneven distribution of time constants, producing a "slow compartment," was in part responsible for the change in compliance between the initial and the intermediate segment of the PV curve. In 16 patients with ARDS submitted to mechanical ventilation in volume-controlled mode with a supportive respiratory rate of 15 breaths/minute, we constructed the static PV curve on the first day of respiratory support and determined the intrinsic positive end-expiratory pressure (PEEPi4) during a prolonged end-expiratory pause (4 seconds). We also measured the volume of a "slow compartment" during a prolonged expiration (> 6 seconds), and determined an external PEEP (PEEPe) suppressing PEEPi4. Among the 16 patients studied, 11 exhibited a low inflection point, associated with a "slow compartment" of 172 +/- 83 ml, responsible for a PEEPi4 of 3 +/- 2 cm H2O. Conversely, the five remaining patients had a linear PV curve, associated with a minimal "slow compartment" of 28 +/- 10 ml, responsible for a negligible PEEPi4. We observed that individual slopes of the initial segment of the PV curve were inversely and significantly correlated with the proportion of the "slow compartment" (r = -0.85). We concluded that the shape of the inspiratory PV curve in ARDS might be dependent on the presence of a "slow compartment," and demonstrated that a low external PEEP appeared sufficient to achieve a substantial mechanical improvement in clinical practice.

Background 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. Setting An intensive care unit of a university hospital. Patients 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. Measurements 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, ≤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. Results 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). Conclusion 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.

. Objective : The indications for the use of thrombolytic agents in massive pulmonary embolism (MPE) remain controversial and it has been suggested that transthoracic echocardiographic (TTE) examination, which is able to detect an associated right ventricular dysfunction, may cast light on this question. The goal of this study was to examine the incidence of acute cor pulmonale (ACP) in MPE, diagnosed on the basis of TTE criteria, its clinical implications and its resolution rate. Design : Ten-year retrospective clinical study. Setting : A medical and a coronary intensive care unit, university hospital. Patients : One hundred sixty-one patients with proven MPE. Interventions : Acute cor pulmonale was defined as right ventricular end-diastolic area / left ventricular end-diastolic area (RVEDA/LVEDA) ratio in the long axis greater than 0.6 associated with septal dyskinesia in the short axis. ACP patients were divided into three groups according to circulatory status: 32 patients without circulatory failure constituted group 1, 32 patients with circulatory failure requiring inotropic support, but free of metabolic acidosis, constituted group 2 and 34 patients in whom circulatory failure was associated with metabolic acidosis (defined by a base deficit >5 mEq/l) constituted group 3. Results : Acute cor pulmonale was present in 61% of patients with MPE and carried a 23% mortality, but this mortality was very different in stable patients (groups 1 and 2, 64 patients, 3% mortality) and in unstable patients (group 3, 34 patients, 59% mortality). A multivariate logistic regression analysis showed that the TTE results were not predictive of the risk of death. Conversely, the same analysis showed that the presence of metabolic acidosis was a powerful predictor of death. Conclusion : Because none of the TTE measurements in ACP could be used to stratify the severity of MPE, TTE was of no help in deciding on medical thrombolysis. However, depending on its severity, metabolic acidosis could justify a large cooperative study to assess the impact of thrombolytic therapy on mortality rate in this specific group.

Objective Positive end-expiratory pressure (PEEP) titration in acute respiratory distress syndrome patients remains debatable. We used two mechanical approaches, calculation of the compliance of the respiratory system and determination of the lower inflexion point of the pressure-volume curve of the respiratory system, to identify specific PEEPs (PEEPS and PEEPA) whose impact on right ventricular (RV) outflow was compared with Doppler analysis of pulmonary artery flow velocity. Design Prospective, open, clinical study. Setting Medical intensive care unit of a university hospital. Patients Sixteen consecutive ventilator-dependent acute respiratory distress syndrome patients. Interventions Two PEEPs were determined: PEEPS was the highest PEEP associated with the highest value of respiratory compliance, and PEEPA was the coordinate of the lower inflexion point of the inspiratory pressure-volume curve on the pressure axis plus 2 cm H2O. Measurements and Main Results We observed a large difference between the two PEEPs, with PEEPA (13 + 4 cm H2O) > PEEPS (6 + 3 cm H2O). Changes in RV outflow impedance produced by tidal ventilation with zero end-expiratory pressure (ZEEP) and after application of these two PEEPs were assessed by Doppler study of pulmonary artery flow velocity obtained by a transesophageal approach, with particular reference to the end-expiratory and end-inspiratory pulmonary artery velocity-time integral, as reflecting RV stroke output, and mean acceleration as reflecting RV outflow impedance during an unchanged flow period. A significant inspiratory reduction in pulmonary artery velocity-time integral (from 11.8 + 0.3 to 10.0 + 0.3 cm) and mean acceleration (from 11.9 + 0.9 to 8.0 + 0.9 m/sec2) was observed with ZEEP, showing a reduction in RV stroke index (from 29.0 + 0.9 to 26.0 + 0.6 cm3/m2) by a sudden increase in outflow impedance during tidal ventilation. Application of PEEPA, which improved Pao2 (102 + 40 vs. 65 + 18 torr with ZEEP), worsened the inspiratory drop in RV stroke index (21.6 + 0.8 cm3/m2), resulting in a significant reduction in cardiac index compared with ZEEP (from 3.0 + 1.0 to 2.7 + 1.1). Application of PEEPS, which also significantly improved Pao2 (81 + 21 torr), was associated with a lesser impact on RV outflow impedance (inspiratory mean acceleration: 9.5 + 1 m/sec2) and cardiac index (3.2 + 1.0) than PEEPA. Conclusion RV outflow impedance evaluated by the Doppler technique appeared sensitive to PEEP titration. Application of PEEPA worsened RV systolic function impairment produced by tidal ventilation. Conversely, application of PEEPS reduced RV systolic function impairment, suggesting an association with a lower pulmonary vascular resistance.