Cardiopulmonary Effects of Lipid Emulsions in Patients With ARDS Marion Faucher, Fabienne Bregeon, Marc Gainnier, Xavier Thirion, Jean-Pierre Auffray and Laurent Papazian Chest 2003;124;285-291 DOI 10.1378/chest.124.1.285

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CHEST is the official journal of the American College of Chest Physicians. It has been published monthly since 1935. Copyright 2007 by the American College of Chest Physicians, 3300 Dundee Road, Northbrook IL 60062. All rights reserved. No part of this article or PDF may be reproduced or distributed without the prior written permission of the copyright holder (http://www.chestjournal.org/misc/reprints.shtml). ISSN: 0012-3692.

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Cardiopulmonary Effects of Lipid Emulsions in Patients With ARDS* Marion Faucher, MD; Fabienne Bregeon, MD; Marc Gainnier, MD; Xavier Thirion, MD; Jean-Pierre Auffray, MD; and Laurent Papazian, MD

Study objectives: Lipid emulsions have been suspected of inducing certain modifications in gas exchange and pulmonary hemodynamics. The aim of this prospective study was to evaluate the hemodynamic and pulmonary effects of two lipid emulsions. Design: Prospective, randomized, double-blind, crossover study. Setting: Medical and surgical ICU in a French university hospital. Patients: Eighteen patients presenting ARDS. Interventions: Each patient received a 6-h infusion of a 20% fat emulsion containing 100% long-chain triglycerides (LCTs) and a 6-h infusion of 50% LCTs/50% medium-chain triglycerides (MCTs) 20% lipid emulsion at the rate of 1.0 mL/kg/h. An 18-h period with no lipids separated the two periods. An additional 18-h period after the end of the second lipid emulsion administration was observed prior to the final measurements. Measurements and results: The MCT/LCT emulsion increased the PaO2/fraction of inspired oxygen (FIO2) ratio (p ⴝ 0.005) compared with LCT emulsion alone. The mean (ⴞ SD) PaO2/FIO2 ratio increased from 165 ⴞ 55 to 191 ⴞ 64 mm Hg after 1 h of LCT/MCT administration (p < 0.03), and to 175 ⴞ 46 mm Hg after 6 h. Moreover, there was an increase in oxygen delivery after 6 h of LCT/MCT administration (p < 0.001 vs baseline). While a time-related increase in mean pulmonary artery pressure (p ⴝ 0.012) during lipid administration was found, no effect of the kind of lipid emulsion was observed. The time-related increase in cardiac index (p ⴝ 0.002) was more marked when the patients received the LCT/MCT emulsion (p ⴝ 0.002). Pulmonary vascular resistances were not affected by the kind of lipid emulsion. Conclusions: The present work showed that while the LCT emulsion induced no deleterious effects on oxygenation in ARDS patients, the LCT/MCT emulsion improved the PaO2/FIO2 ratio and had a further beneficial effect on oxygen delivery. (CHEST 2003; 124:285–291) Key words: ARDS; emulsion; hemodynamic; lipid; oxygenation Abbreviations: ANOVA ⫽ analysis of variance; CI ⫽ cardiac index; Do2I ⫽ oxygen delivery index; Fio2 ⫽ fraction of inspired oxygen; LCT ⫽ long-chain triglyceride; MCT ⫽ medium-chain triglyceride; MPAP ⫽ mean pulmonary arterial pressure; PAOP ⫽ pulmonary artery occluded pressure; PEEP ⫽ positive end-expiratory pressure; PVRI ⫽ pulmonary vascular resistances indexed; QVA/QT ⫽ venous admixture

lipid emulsions are routinely used as a A lthough caloric source for critically ill patients, these emulsions have been suspected of inducing certain modifications in gas exchange and pulmonary hemodynamics. However, there are conflicting data in the literature about the effects of lipid emulsions on pulmonary diffusion capacity and arterial oxygen tension (Table 1).1–10 The composition in fatty acids *From the Service de Re´animation Polyvalente (Drs. Faucher and Auffray), Hoˆpitaux Sud, Marseille, France; Laboratoire de Physiopathologie Respiratoire (Dr. Bregeon), UPRES EA 2201, Faculte´ de Me´decine de Marseille, Marseille, France; Service de Re´animation Me´dicale (Drs. Gainnier and Papazian), Hoˆpitaux Sud, Marseille, France; and Service d’Information Me´dicale (Dr. Thirion), Hoˆpitaux Sud, Marseille, France. This research was supported by the l’Association Re´gionale d’Assistance Respiratoire a` Domicile; La Penne sur Huveaune, France.

of the available lipid emulsions is considered to be the main factor responsible for the cardiopulmonary effects of such lipids. Long-chain polyunsaturated fatty acids are precursors of substances such as prostaglandins, leukotrienes, and thromboxanes. These substances are able to modify the ventilation/ perfusion ratio, causing hypoxemia and the modification of pulmonary arterial pressure. Currently available commercial lipid emulsions are derived Manuscript received May 17, 2001; revision accepted December 5, 2002. Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (e-mail: [email protected]). Correspondence to: Laurent Papazian, MD, Re´animation Me´dicale, Hoˆpital Sainte-Marguerite, 13274 Marseille Cedex 9, France; e-mail: [email protected]

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Table 1—Lipid Emulsions in ICU Patients Study

Design

Radermacher et al1 Masclans et al2

Noncomparative Comparative

Smirniotis et al3

Comparative

Hwang et al4

Comparative

Fiaccadori et al5 Mathru et al6

Noncomparative Comparative

Venus et al7 Chassard et al8

Noncomparative Comparative

Ball and White9 Venus et al10

Noncomparative Noncomparative

Lipid

Patients, No.

Patients

LCT/MCT, 0.15 g/kg/h for 4 h LCT, 2 mg/kg/min for 12 h LCT/MCT, 2 mg/kg/min for 12 h Control subjects LCT, 12 g/h for 8 h LCT/MCT, 12 g/h for 8 h LCT, 6 mg/kg/min for 4 h LCT, 3 mg/kg/min for 8 h LCT/MCT, 3.3 mg/kg/min for 2 h LCT, 5 g/h for 10 h LCT, 10 g/h for 5 h LCT 5 g/h for 10 h LCT, 3 mg/kg/min for 8 h LCT/MCT, 3 mg/kg/min for 8 h

Sepsis ARDS

ICU Sepsis

10 11 5 5 12 8 7 20 6

LCT/MCT, 3.5 mg/kg/min for 3.5 h LCT, 3 mg/kg/min for 8 h

Trauma or surgery ARDS

17 19

from soybeans and/or safflower oils, and they contain long-chain ⍀-6 and ⍀-3 polyunsaturated fatty acids that have been esterified with glycerol to form long-chain triglycerides (LCTs). A new lipid emulsion was characterized by the partial replacement of LCT by medium-chain triglycerides (MCTs). MCTs are oxidized faster than LCTs without acting as precursors of prostanoids.9 Therefore, while MCTs do not interfere with eicosanoid synthesis, it has been hypothesized that the use of LCT/MCT emulsions could be associated with fewer pulmonary effects. Nutritional support could influence the prognosis of patients presenting with ARDS. Moreover, the impairment in oxygenation and the modifications of pulmonary hemodynamics found during ARDS could be altered by agents that are supposed to interfere with inflammatory mediators. Therefore, the effects of lipids on gas exchange were studied in patients presenting with acute respiratory failure. However, the results have been contradictory. The aim of this prospective study therefore was to evaluate the hemodynamic and pulmonary effects of two lipid emulsions (ie, one LCT emulsion, and one LCT/MCT emulsion) in patients presenting with ARDS. Materials and Methods Study Population During a 12-month period, we performed a prospective, randomized, double-blind, crossover study that included 18 patients (15 men and 3 women; mean [⫾ SD] age, 52 ⫾ 14 years; simplified acute physiology II score on hospital admission,

9 7 7

Surgical septic ARDS ARDS Open-heart surgery Septic ARDS

Change in Oxygenation No No No Decrease No Decrease Decrease No No No Decrease No No No No Decrease

36 ⫾ 10) who had been admitted to the medical and surgical ICUs of Sainte-Marguerite University Hospital in Marseille, France. These patients were prospectively investigated 3 ⫾ 2 days after the onset of ARDS. They were included after written informed consent was obtained from each patient’s next of kin. When the study was started, no patient had evidence of dyslipemia, diabetes mellitus, or renal, cardiovascular, or hepatic dysfunction. No anti-inflammatory drugs were administered during the week prior to the beginning of the study or during the study. The study was approved by our ethics committee (Comite´ Consultatif de Protection des Personnes dans la Recherche Biome´ dicale de Marseille) and was supported by l’Association Re´ gionale d’Assistance Respiratoire a` Domicile. ARDS was defined according to the recommendations of the AmericanEuropean Consensus Conference.11 Among the 18 patients enrolled in the study, 9 had been admitted to the hospital for an acute medical illness, 4 had been admitted for postoperative complications following major surgery, and 5 had been admitted to the ICU after experiencing multiple trauma. ARDS was related to pulmonary causes in 72% of the patients (infectious pneumonia, six patients; lung contusion, one patient; aspiration pneumonia, six patients), and to extrapulmonary causes in 28% of the patients (extrapulmonary sepsis, four patients; acute pancreatitis, one patient). Instrumentation and Measurements Blood Gas Analyses: Systemic and pulmonary arterial blood samples were simultaneously withdrawn within 3 min before the measurement of cardiac output. Arterial pH, Po2, mixed venous partial pressure of oxygen, and Paco2 were measured using a blood gas analyzer (model 278-blood gas system; Ciba Corning; Medfield, MA). Hemoglobin concentration, arterial oxygen saturation, and mixed venous oxygen saturation were measured using a calibrated hemoximeter (model 270-CO-oxymeter; Ciba Corning). Determination of Blood Concentration of Lipids: In order to verify that baseline conditions were identical before each lipid emulsion infusion, blood samples were drawn before the beginning of each lipid emulsion infusion period and 18 h after the end

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of the second emulsion infusion period. They were analyzed for triglycerides, nonesterified fatty acids, and cholesterol (measured by enzymatic methods). Hemodynamic Parameters: All of the patients had a radial artery catheter (Seldicath; Plastimed; Saint Leu la Foreˆ t, France) and a pulmonary artery catheter (model 93 A-434H-7.5F; Baxter Healthcare Corporation; Irvine, CA), which were inserted percutaneously through the right jugular or the left axillary vein and were positioned so that the distal port was in the pulmonary artery and the proximal port was in the right atrium, just above the tricuspid valve. Systolic arterial pressure, diastolic arterial pressure, systolic pulmonary arterial pressure, diastolic pulmonary arterial pressure, pulmonary artery occluded pressure (PAOP), and right atrial pressure were measured at end-expiration. Cardiac index (CI), oxygen delivery index (Do2I), oxygen consumption index, and venous admixture (QVA/QT) were calculated using standard formulas. Pulmonary vascular resistances indexed (PVRI) were calculated using the following standard formula: PVRI ⫽ (mean pulmonary arterial pressure [MPAP] ⫺ PAOP) ⫻ 79.9/CI.

performed in patients whose only caloric source was a 5% glucose infusion (infusion rate, 1.5 mg/kg/min). Measurements were obtained before starting the first lipid emulsion infusion, after 1 h of administration, at the end of the 6-h period of administration, and, finally, 18 h after the end of the administration of each lipid emulsion. Statistical Analysis The data were expressed as the mean ⫾ SD. Statistical calculations were performed using a statistical software package (SPSS, version 8.0; SPSS Inc; Chicago, IL). Statistically significant differences were analyzed by parametric or nonparametric tests when required. The effects of the two lipid emulsions were compared by using a two-way, repeated-measures analysis of variance (ANOVA) [factors considered were time and type of lipid emulsion]. When appropriate, a post hoc analysis was performed using a pairwise multicomparison procedure (ie, Tukey test). A p value of ⬍ 0.05 indicated significance.

Procedure

Results

The study was performed after the optimization of the treatment of hypoxemia in order to obtain at least 12 h of stability of Po2/fraction of inspired oxygen (Fio2) without any change in ventilator settings (fluctuation, ⬍ 20%). Selection of the appropriate level of positive end-expiratory pressure (PEEP) was performed by increasing PEEP in steps of 2 cm H2O. A blood gas analysis was performed when pulse oximetric saturation was stable during a 30-min period after PEEP level adjustment. Finally, the lower level of PEEP giving the greater improvement in oxygenation was chosen. When no improvement was found while increasing PEEP, the level was set at 8 cm H2O. Nitric oxide and almitrine bismesylate were used when the Pao2/Fio2 ratio remained at ⬍ 150 mm Hg despite PEEP adjustment. For the purpose of the study, prone position was not permitted until completion of the protocol. For each patient, tidal volume and PEEP levels were kept constant throughout the study period. No patient received lipid emulsion prior to inclusion in the study. On days 1 and 2, each patient received, in random order, a 6-h infusion of a 20% fat emulsion containing LCTs (Endolipide [20%]; B. Braun Medical; Boulogne, France) or an infusion of 50% LCT/50% MCTs (Medialipide [20%]; B. Braun Medical) at the rate of 1.0 mL/kg/h. An 18-h period without lipid administration separated the two periods. An additional 18-h period after the end of the second lipid emulsion administration was observed prior to the final measurements (control 2) [Fig 1]. Both lipid emulsions contained LCTs derived from soybean oil. The LCT emulsion contained 200 g soybean oil per liter, while the LCT/MCT emulsions contained 100 g soybean oil. Soybean oil provides 54% of linoleic acid and 8% of ␣-linoleic acid. The LCT/MCT emulsion also contained 100 g MCTs (caprilic acid, 54%; capric acid, 40%; lauric acid, 4%; and caproic acid, 2%). One liter of the 20% LCT emulsion and 1 L LCT/MCT emulsion contained 25 g glycerol and 12 g lecithin. The study was

Characteristics of the Study Population The duration of mechanical ventilation preceding the study was 4.4 ⫾ 2.8 days. All of the patients were sedated with a continuous infusion of sufentanil and midazolam, and lungs were ventilated using conventional volume-controlled mechanical ventilation (7200 series; Mallinckrodt Puritan Bennett; Carlsbad, CA). On the day of the study, the mean lung injury score was 2.7 ⫾ 0.2. On inclusion in the study, the mean respiratory parameters were as follows: tidal volume, 7.1 ⫾ 1.6 mL/kg; Fio2, 0.63 ⫾ 0.11; PEEP, 10.0 ⫾ 2.5 cm H2O. Only four patients received inhaled nitric oxide and/or a continuous infusion of almitrine bismesylate during the study period. There was no modification in core temperature between the two groups (data not shown). Effects of Lipid Administration on Oxygenation The LCT emulsion had no effect on oxygenation, whereas the MCT/LCT emulsion improved the Pao2/Fio2 ratio (p ⫽ 0.04 [by one-way, repeatedmeasures ANOVA]). When the two lipid emulsions were compared, two-way, repeated-measures ANOVA showed that the MCT/LCT emulsion improved the Pao2/Fio2 ratio (p ⫽ 0.005) compared with the LCT emulsion (Fig 2). The order of lipid emulsions did

Figure 1. Study design. www.chestjournal.org

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Figure 2. Evolution of the Pao2/Fio2 ratio before, 1 h after, and 6 h after the beginning of the administration of both lipid emulsions. Values are given as the mean ⫾ SEM. * ⫽ p ⬍ 0.03 vs before administration of LCT/MCT.

not influence their effects (ANOVA, not significant), and the baseline value after the first period was equivalent to the initial baseline value for each patient group (ANOVA, not significant). A pairwise multicomparison procedure (ie, Tukey test) showed that the 16% increase in the Pao2/Fio2 ratio 1 h after the beginning of the MCT/LCT emulsion infusion was significant (p ⫽ 0.03), while the Pao2/Fio2 ratio at the end of the 6-h infusion was not different from the baseline value (Fig 2 and Table 2). Using ANOVA, we verified that inhaled nitric oxide and almitrine bismesylate did not influence the effects of these lipid emulsions.

Effects of Lipid Administration on Gas Exchange and Respiratory Parameters No modification in Paco2 was observed during the study period. We did not observe any modification in respiratory parameters related to lipid administration. Effects of Lipid Administration on Hemodynamics We did not observe a significant effect of the kind of lipid emulsion on MPAP (Table 2). However, a time-related increase in MPAP during the administration of lipid emulsion (p ⫽ 0.012 [by ANOVA])

Table 2—Respiratory and Hemodynamic Parameters* LCT Emulsion Variables Pao2/Fio2, mm Hg Paco2, mm Hg MPAP, mm Hg HR, beats/min CI, L/min/m2 PVRI, dyne䡠s䡠cm⫺5/m2 QVA/QT, % Do2I, mL/min/m2 Vo2I, mL/min/m2

LCT/MCT Emulsion

Control 1

Before

1h

6h

Before

1h

6h

Control 2

164 ⫾ 45 44 ⫾ 8 24 ⫾ 6 87 ⫾ 14 4.6 ⫾ 1.3 236 ⫾ 128 37 ⫾ 8 564 ⫾ 145 119 ⫾ 42

156 ⫾ 44 45 ⫾ 9 24 ⫾ 7 90 ⫾ 11 4.8 ⫾ 1.3 225 ⫾ 123 40 ⫾ 8 597 ⫾ 161 114 ⫾ 38

161 ⫾ 43 44 ⫾ 8 25 ⫾ 7 86 ⫾ 11 4.4 ⫾ 1.2 263 ⫾ 127 37 ⫾ 8 547 ⫾ 153 116 ⫾ 33

156 ⫾ 42 45 ⫾ 9 26 ⫾ 7 95 ⫾ 17 4.9 ⫾ 1.5 251 ⫾ 117 37 ⫾ 9 608 ⫾ 197 133 ⫾ 37

165 ⫾ 55 43 ⫾ 8 23 ⫾ 6 88 ⫾ 14 4.3 ⫾ 1.0 231 ⫾ 99 37 ⫾ 10 532 ⫾ 131 116 ⫾ 40

191 ⫾ 64† 43 ⫾ 7 24 ⫾ 7 86 ⫾ 12 4.4 ⫾ 1.0 244 ⫾ 109 35 ⫾ 8 551 ⫾ 133 123 ⫾ 34

175 ⫾ 46 44 ⫾ 7 25 ⫾ 6 99 ⫾ 19‡ 5.4 ⫾ 1.6§ 206 ⫾ 105 38 ⫾ 11 672 ⫾ 181§㛳 136 ⫾ 53

177 ⫾ 65 43 ⫾ 7 25 ⫾ 5 90 ⫾ 15 4.7 ⫾ 0.9 213 ⫾ 68 33 ⫾ 6 573 ⫾ 116 142 ⫾ 39

*Values given as mean ⫾ SD. HR ⫽ heart rate; V˙o2I ⫽ oxygen consumption index. †p ⬍ 0.03 vs before LCT/MCT administration. ‡p ⬍ 0.02 vs before and 1 h after LCT/MCT administration. §p ⬍ 0.001 vs before and 1 h after LCT/MCT administration. 㛳p ⬍ 0.01 vs 6 h after LCT administration. 288

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was observed as well as a time-related increase in heart rate and CI (p ⫽ 0.002 by ANOVA). An interaction effect on CI also was noted between the kind of lipid emulsion and the duration of its administration (p ⫽ 0.002 [by ANOVA]), indicating that the increase in cardiac output during lipid infusion was more marked when the patients received the LCT/ MCT emulsion. For example, a 27% increase in CI was noted at the sixth hour of administration of the LCT/MCT emulsion (p ⫽ 0.001 vs before and at 1 h) [Fig 3], while no significant change in CI was related to LCT emulsion administration (Fig 3). A timerelated increase in oxygen delivery (p ⫽ 0.003 [by ANOVA]) and in oxygen consumption (p ⫽ 0.029 [by ANOVA]) was observed during lipid emulsion administration. An interaction effect on oxygen delivery also was found between the duration of lipid administration and the kind of lipid emulsion (p ⫽ 0.002 [by ANOVA]) [Table 2]. The increase in oxygen delivery related to LCT/MCT emulsion, which reached 4% after 1 h of infusion and 26% after 6 h of infusion, illustrates this action (Fig 4). Pulmonary vascular resistances were not affected by the kind of lipid emulsion (p ⫽ 0.067). No statistically significant alterations in mean arterial pressure, right atrial pressure, or PAOP were noted during the entire period of investigation. No significant change in the rate of fluid administration was observed for a given patient throughout the study period.

Effect of Lipid Emulsion Administration on Plasma Levels of Triglycerides, Cholesterol, and Nonesterified Fatty Acids As shown in Table 3, triglycerides, cholesterol, and nonesterified fatty acid levels were not different before and 18 h after the administration of both lipid emulsions. Discussion The results of the present study suggested that neither lipid emulsion (ie, LCT or LCT/MCT lipid emulsion) decreased Pao2. Moreover, no deleterious effects on pulmonary hemodynamics were noted. In the literature, lipid emulsions have been associated with changes in oxygenation and pulmonary hemodynamics. Increased oxygen consumption and increased CO2 production have been reported after MCT administration.12,13 A review of the literature to date showed no clear evidence that major clinical changes in oxygenation occurred with lipid administration in ARDS patients. Discrepancies between studies may be a consequence of alterations in lipid metabolite concentrations due to differences either in metabolic clearance or lipid administration rates and durations.5,7,14,15 For example, Hunt et al16 reported that slow infusion rates of lipid emulsion resulted in a relative predominance of vasodilating prostaglandins, while rapid

Figure 3. Evolution of the CI before, 1 h after, and 6 h after the beginning of the administration of both lipid emulsions. Values are given as the mean ⫾ SEM. *p ⫽ 0.001 vs before and 1 h after the beginning of MCT/LCT emulsion administration. www.chestjournal.org

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Figure 4. Evolution of Do2I before, 1 h after, and 6 h after the beginning of the administration of both lipid emulsions. Values are given as the mean ⫾ SD. * ⫽ p ⬍ 0.001 vs before and 1 h after the beginning of LCT/MCT emulsion, and p ⬍ 0.01 vs 6 h after the beginning of LCT administration.

infusion induced the predominance of vasoconstricting prostaglandins. It has been hypothesized that rapid infusion could increase the production of vasoconstrictive eicosanoids.17–19 In the present work, we found a time-related increase in MPAP only during lipid administration, with no significant difference between the two kinds of lipid emulsions. This increase in MPAP could be related to the concomitantly observed increase in CI. Preexisting lung status with the degree of lung injury also could explain certain discrepancies between studies.4,6 Indeed, it was demonstrated in an animal study19 that while lipid emulsion administration has a negligible effect on healthy lungs, it induced hypoxemia in animals with injured lungs. In a rabbit model,15 there were no significant blood gas or prostaglandins changes in the saline solution control groups or in the normal lung groups that were infused with an LCT emulsion. However, in the lung-damaged groups (ie, by oleic acid), there was a small but significant decrease in Pao2, which

reached 12 mm Hg.15 There was also a significant increase in arterial vasodilating prostaglandin levels.15 A vasodilatory response to prostaglandins precursors was noted in the presence of an increased pulmonary vascular tone.19 Finally, controversy remains as to whether and which prostaglandins are involved in these sometimes-observed manifestations. The mechanisms by which fat emulsions could influence oxygenation and pulmonary hemodynamics are poorly understood. The prevention of the decrease in Pao2 by indomethacin has suggested that these changes are at least in part mediated by prostaglandins.19,20 Nevertheless, one can argue that the beginning of a rapid lipid emulsion infusion (as during the first hour in the present work) could provoke an increase in vasoconstrictive products. These substances could enhance selective regional hypoxic pulmonary vasoconstriction in lung areas with low ventilation/perfusion ratio, resulting in a decrease in blood flow in such areas. However, Planas et al21 have shown that the administration of

Table 3—Plasma Levels of Triglycerides, Cholesterol, and Nonesterified Fatty Acids* LCT/MCT Emulsion

LCT/MCT Emulsion

Variables

Control 1

Before Infusion

18 h Postinfusion

Before Infusion

18 h Postinfusion

Control 2

Triglycerides, mmol/L Cholesterol, mmol/L Nonesterified fatty acids, mmol/L

1.7 ⫾ 1.2 2.7 ⫾ 0.8 0.5 ⫾ 0.3

1.6 ⫾ 1.2 2.7 ⫾ 0.8 0.4 ⫾ 0.2

1.5 ⫾ 0.8 2.7 ⫾ 1.1 0.3 ⫾ 0.1

1.8 ⫾ 1.3 2.7 ⫾ 1.1 0.4 ⫾ 0.3

1.8 ⫾ 1.3 2.7 ⫾ 1.0 0.3 ⫾ 0.2

1.6 ⫾ 0.9 2.7 ⫾ 1.1 0.2 ⫾ 0.1

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lipid emulsion (LCT or LCT/MCT emulsion) in ARDS patients did not alter the plasma levels of prostanoids compared with those who did not receive infusion of a lipid emulsion. Smirniotis et al3 found that LCT infusion induced an elevation of MPAP and QVA/QT while the Pao2/Fio2 ratio declined, whereas LCT/MCT emulsion infusion induced no significant changes either in oxygenation or in pulmonary hemodynamics. However, when changes in oxygenation and pulmonary hemodynamics have been reported, they have generally not been clinically significant. As in the present work, Masclans et al2 found that LCT administration did not modify oxygenation. Furthermore, they also reported increased cardiac output and increased oxygen delivery to peripheral tissues. Radermacher et al1 found that pulmonary hemodynamics and gas exchange were not modified by LCT/MCT administration. Moreover, no modification of low ventilation/perfusion ratio in the lung regions was observed after LCT/MCT administration.1 In 19 patients presenting with moderate respiratory failure (ie, Pao2/ Fio2 ratio, 241 ⫾ 50 mm Hg), Venus et al10 reported that LCT administration induced a 24% decrease in Pao2/Fio2 ratio that was associated with a significant increase in MPAP and QVA/QT. The same group also reported an increase in MPAP related to LCT administration in non-ARDS patients.7 However, patient baseline physiologic data are difficult to estimate in a great number of these studies. In the present study, we chose to give the highest amount of fat emulsion recommended per day at the maximal infusion rate, as recommended by the manufacturer. Indeed, a dose-dependent effect of the fat infusion rate has been shown in patients presenting with septic respiratory failure.6 Conclusions The present work showed that lipid emulsion infusion induced no deleterious effects on oxygenation and hemodynamics. However, it should be noted that the composition of LCT emulsions varies from formulation to formulation. Finally, the unexpected transient increase in the Pao2/Fio2 ratio 1 h after the beginning of the MCT/LCT lipid emulsion requires further investigations, for example, by measuring the plasma concentrations of the lipid components. References 1 Radermacher P, Santak B, Strobach H, et al. Fat emulsions containing medium chain triglycerides in patients with sepsis syndrome: effects on pulmonary hemodynamics and gas

exchange. Intensive Care Med 1992; 18:231–234 2 Masclans JR, Iglesia R, Bermejo B, et al. Gas exchange and pulmonary haemodynamic responses to fat emulsions in acute respiratory distress syndrome. Intensive Care Med 1998; 24:918 –923 3 Smirniotis V, Kostopanagiotou G, Vassiliou J, et al. Long chain versus medium chain lipids in patients with ARDS: effects on pulmonary haemodynamics and gas exchange. Intensive Care Med 1998; 24:1029 –1033 4 Hwang TL, Huang SL, Chen MF. Effects of intravenous fat emulsion on respiratory failure. Chest 1990; 97:934 –938 5 Fiaccadori E, Tortorella G, Gonzi G, et al. Hemodynamic, respiratory, and metabolic effects of medium-chain triglyceride-enriched lipid emulsions following valvular heart surgery. Chest 1994; 106:1660 –1667 6 Mathru M, Dries DJ, Zecca A, et al. Effect of fast vs slow intralipid infusion on gas exchange, pulmonary hemodynamics, and prostaglandin metabolism. Chest 1991; 99:426 – 429 7 Venus B, Prager R, Patel CB, et al. Cardiopulmonary effects of intralipid infusion in critically ill patients. Crit Care Med 1988; 16:587–590 8 Chassard D, Guiraud M, Gauthier M, et al. Effects of intravenous medium-chain triglycerides on pulmonary gas exchanges in mechanically ventilated patients. Crit Care Med 1994; 22:248 –251 9 Ball MJ, White K. Comparison of medium and long chain triglyceride metabolism in intensive care patients on parenteral nutrition. Intensive Care Med 1989; 15:250 –254 10 Venus B, Smith RA, Patel C, et al. Hemodynamic and gas exchange alterations during intralipid infusion in patients with adult respiratory distress syndrome. Chest 1989; 95:1278 – 1281 11 Bernard GR, Artigas A, Brigham KL, et al. The AmericanEuropean consensus conference on ARDS. Am J Respir Crit Care Med 1994; 149:818 – 824 12 Mascioli EA, Randall S, Porter KA, et al. Thermogenesis from intravenous medium-chain triglycerides. JPEN J Parenter Enteral Nutr 1991; 15:27–31 13 Seaton TB, Welle SL, Warenko MK, et al. Thermic effect of medium-chain and long-chain triglycerides in man. Am J Clin Nutr 1986; 44:630 – 634 14 Kinsella JE. Lipids, membrane receptors, and enzymes: effects of dietary fatty acids. JPEN J Parenter Enteral Nutr 1990; 14:200S–217S 15 Hageman JR, McCulloch K, Gora P, et al. Intralipid alterations in pulmonary prostaglandin metabolism and gas exchange. Crit Care Med 1983; 11:794 –798 16 Hunt CE, Pachman LM, Hageman JR, et al. Liposyn infusion increases plasma prostaglandin concentrations. Pediatr Pulmonol 1986; 2:154 –158 17 Skeie B, Askanazi J, Rothkopf MM, et al. Intravenous fat emulsions and lung function: a review. Crit Care Med 1988; 16:183–194 18 Hageman JR, Hunt CE. Fat emulsions and lung function. Clin Chest Med 1986; 7:69 –77 19 McKeen CR, Brigham KL, Bowers RE, et al. Pulmonary vascular effects of fat emulsion infusion in unanesthetized sheep: prevention by indomethacin. J Clin Invest 1978; 61:1291–1297 20 Kadowitz PJ, Spannhake EW, Levin JL, et al. Differential actions of the prostaglandins on the pulmonary vascular bed. Adv Prostaglandin Thromboxane Res 1980; 7:731–743 21 Planas M, Masclans JR, Iglesia R, et al. Eicosanoids and fat emulsions in acute respiratory distress syndrome patients. Nutrition 1997; 13:202–205

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Cardiopulmonary Effects of Lipid Emulsions in Patients With ARDS Marion Faucher, Fabienne Bregeon, Marc Gainnier, Xavier Thirion, Jean-Pierre Auffray and Laurent Papazian Chest 2003;124;285-291 DOI 10.1378/chest.124.1.285 This information is current as of January 25, 2008 Updated Information & Services

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