Background In patients with the acute respiratory distress syndrome, massive alveolar collapse and cyclic lung reopening and overdistention during mechanical ventilation may perpetuate alveolar injury. We determined whether a ventilatory strategy designed to minimize such lung injuries could reduce not only pulmonary complications but also mortality at 28 days in patients with the acute respiratory distress syndrome. Methods We randomly assigned 53 patients with early acute respiratory distress syndrome (including 28 described previously), all of whom were receiving identical hemodynamic and general support, to conventional or protective mechanical ventilation. Conventional ventilation was based on the strategy of maintaining the lowest positive end-expiratory pressure (PEEP) for acceptable oxygenation, with a tidal volume of 12 ml per kilogram of body weight and normal arterial carbon dioxide levels (35 to 38 mm Hg). Protective ventilation involved end-expiratory pressures above the lower inflection poin...

https://www.nejm.org/doi/pdf/10.1056/NEJM199802053380602

Effect of a Protective-Ventilation Strategy on Mortality in the Acute Respiratory Distress Syndrome

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

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Relation between respiratory changes in arterial pulse pressure and fluid responsiveness in septic patients with acute circulatory failure.

Objective:Values of central venous pressure of 8–12 mm Hg and of pulmonary artery occlusion pressure of 12–15 mm Hg have been proposed as volume resuscitation targets in recent international guidelines on management of severe sepsis. By analyzing a large number of volume challenges, our aim was to t

Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge

Respiratory Changes in Aortic Blood Velocity as an Indicator of Fluid Responsiveness in Ventilated Patients With Septic Shock

BackgroundMonitoring left ventricular preload is critical to achieve adequate fluid resuscitation in patients with hypotension and sepsis. This prospective study tested the correlation of the pulmonary artery occlusion pressure, the left ventricular end-diastolic area index measured by transesophage

Systolic Pressure Variation as a Guide to Fluid Therapy in Patients with Sepsis-induced Hypotension

A bedside index assessing the reliability of pulmonary artery occlusion pressure measurements during mechanical ventilation with positive end-expiratory pressure

OBJECTIVE To assess the effects of various catecholaminergic agents on pulmonary venous tone. DESIGN Prospective, randomized, controlled, experimental study. SETTING Physiology laboratory of a university hospital. SUBJECTS Thirty anesthetized, mechanically ventilated adult sheep. INTERVENTIONS Four groups of six animals received 1-hr infusions of norepinephrine (0.5 microg/kg/min), epinephrine (0.5 microg/kg/ min), dopamine (10 microg/kg/min), or dobutamine (10 microg/kg/min). MEASUREMENTS AND MAIN RESULTS A 7-Fr pulmonary artery catheter was placed in a proximal location to measure cardiac output and pressure in a large pulmonary vein (Ppw) after balloon inflation. Another catheter wedged in a small pulmonary artery measured pressure in a small pulmonary vein (Pdw). A third catheter measured left atrial pressure (PLA ). This method was able to detect the pulmonary venoconstrictive effects of histamine in a separate group of six animals. Pdw-PLA increased from a mean of 2.0+/-1.7 to 3.0+/-1.5 (SD) cm H2O (p < .01), 2.3+/-1.6 to 4.4+/-1.3 cm H2O (p < .01), and 1.7+/-1.0 to 3.5+/-2.2 cm H2O (p < .05) with norepinephrine, epinephrine, and dopamine, respectively. All of these drugs increased Pdw-Ppw, but only norepinephrine and epinephrine increased Ppw-PLA . No change in either pressure difference was observed with dobutamine. Elevation of cardiac output alone could not account for these findings since the increase in cardiac output induced by fluid infusion did not change the pressure differences. CONCLUSION Norepinephrine, epinephrine, and dopamine at doses commonly used in humans increase pulmonary venous tone in sheep.

Effects of catecholamines on the pulmonary venous bed in sheep.

This study describes a non-invasive method for assessment of the lung transit time distribution of a tracer, using first-pass technetium-99m albumin angiocardiography and a model-free method of deconvolution. Ten patients received a first injection of 1 MBq kg−1 in the external jugular vein to position a gamma camera in the left anterior oblique position and two additional injections (5 MBq kg−1 to record first-pass angiocardiographic data. Right and left ventricular time-activity curves were derived from regions of interest every 0.5 s over a 1-min period. The left ventricular curve was deconvoluted by the right ventricular curve to obtain the lung transport function. The deconvolution procedure was based on a modified version of the Kalman filtering technique. The procedure was repeated at an interval of 30 min in eight patients. Two patients were re-examined up to 2 years later. Skewness, kurtosis and relative dispersion of the distributions did not change over time. We also found that the distribution, once normalized by its first moment, was independent of isolated changes in heart rate or cardiac output. Comparison of curve shapes at an interval of 30 min by point by point analysis demonstrated the reproducibility of the technique. We conclude that computation of the pulmonary transit time distribution of99mTc-albumin from a standard angiocardiography procedure by model-free deconvolution is reliable and reproducible over time. We suggest that it may be a valuable toot for the non-invasive follow-up of the pulmonary circulation.

Dominique Douguet

Papers

A bedside index assessing the reliability of pulmonary artery occlusion pressure measurements during mechanical ventilation with positive end-expiratory pressure

Effects of catecholamines on the pulmonary venous bed in sheep.

Non-invasive assessment of technetium-99m albumin transit time distribution in the pulmonary circulation by first-pass angiocardiography

Usefulness of dopamine in the maintenance of hemodynamic parameters in brain-dead dogs.