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CRITICAL CARE AND TRAUMA

The Influence of Tidal Volume on the Dynamic Variables of Fluid Responsiveness in Critically Ill Patients

Service d’Anesthésie-Réanimation et Unité Propre de Recherche de l’Enseignement Supérieur-Equipe d’Accueil (UPRES-EA 3540); Laboratoire de Biochimie Générale; Laboratoire d’Explorations Fonctionnelles Cardiorespiratoires; Université de Paris Sud, Hôpital de Bicêtre (APHP), Le Kremlin Bicêtre, France

Address correspondence and reprint requests to Alain R. Edouard, MD, PhD, Service d’Anesthésie-Réanimation, Hôpital de Bicêtre, 94275 Le Kremlin Bicêtre, France. Address e-mail to alain.edouard{at}bct.ap-hop-paris.fr.

	Abstract

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Respiratory-related variabilities in stroke volume and arterial pulse pressure (%Pp) are proposed to predict fluid responsiveness. We investigated the influence of tidal volume (Vt) and adrenergic tone on these variables in mechanically ventilated patients. Cyclic changes in aortic velocity–time integrals (%VTI_Ao, echocardiography) and %Pp (catheter) were measured simultaneously before and after intravascular volume expansion, and Vt was randomly varied below and above its basal value. Intravascular volume expansion was performed by hydroxyethyl starch (100 mL, 60 s). Receiver operating characteristic curves were generated for %VTI_Ao, %Pp and left ventricle cross-sectional end-diastolic area (echocardiography), considering the change in stroke volume after intravascular volume expansion (15%) as the response criterion. Covariance analysis was used to test the influence of Vt on %VTI_Ao and %Pp. Twenty-one patients were prospectively included; 9 patients (43%) were responders to intravascular volume expansion. %VTI_Ao and %Pp were higher in responders compared with nonresponders. Predictive values of %VTI_Ao and %Pp were similar (threshold: 20.4% and 10.0%, respectively) and higher than that of left ventricle cross-sectional end-diastolic area at the appropriate level of Vt. %Pp was slightly correlated with norepinephrine dosage. %Pp increased with the increase in the level of Vt both before and after intravascular volume expansion, contrasting with an unexpected stability of %VTI_Ao. In conclusion, %VTI_Ao and %Pp are good predictors of intravascular fluid responsiveness but the divergent evolution of these two variables when Vt was increased needs further explanation.

	Introduction

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Intravascular volume expansion is often used in mechanically ventilated patients with acute circulatory failure (1). However, inadequate or excessive intravascular fluid administration may worsen the associated respiratory failure (2). Predictive factors of volume expansion efficacy are therefore needed to select patients who could benefit from fluid infusion through an increase in left ventricular (LV) stroke volume. Preload dependency is concomitant with an enhancement of cyclic variations of LV stroke volume in ventilated patients. Stroke volume variability is basically generated by the cyclic changes in intrathoracic and transpulmonary pressures. The magnitude of the respiratory changes in LV stroke volume may be assessed by invasive and noninvasive methods in humans (3,4), providing a real-time, accurate prediction of fluid responsiveness (1). Because arterial pulse pressure is usually correlated with LV stroke volume, respiratory changes in pulse pressure (%Pp) are currently used as simple and accurate dynamic indicators of preload dependency in humans (5). However, these dynamic variables of fluid responsiveness, i.e., cyclic changes in stroke volume and %Pp, are influenced by the magnitude of mechanical insufflation (2,6). In this respect, respiratory changes in arterial blood pressure or arterial pulse contour may better reflect the changes in airway and pleural pressure than the changes in intravascular volume status (7,8). We investigated the influence of the level of tidal volume (V_T) and the dosage of norepinephrine infusion on two dynamic variables of fluid responsiveness—aortic velocity-time integrals (%VTI_Ao) as a surrogate for LV stroke volume and %Pp—measured simultaneously with separate techniques in mechanically ventilated patients with acute circulatory failure and receiving vasopressor therapy. Fluid challenge was performed using the rapid infusion of a small volume of hydroxyethyl starch.

	Methods

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Over a 6-mo period, all mechanically ventilated patients admitted to the unit and exhibiting hemodynamic instability were included in the study (n = 21). Instability was defined as a persistent need for norepinephrine infusion and/or intravascular fluid administration to maintain systolic arterial blood pressure 90 mm Hg. The local Ethical Committee approved the protocol; informed consent was obtained from the patients’ closest relatives. Inclusion criteria were as follows: i) age 18 yr, ii) absence of a contraindication for transesophageal echocardiography, iii) absence of acute coronary syndrome, and iv) absence of ventricular arrhythmias impeding the analysis of the arterial blood pressure variations and of the echocardiographic results. All patients were sedated with midazolam and sufentanil, and 16 patients were paralyzed with atracurium besylate during the study. No spontaneous breaths were observed in the remaining five patients during the study period. Patients’ lungs were ventilated in the control mode with a Vt between 6 and 10 mL/kg, a respiratory rate between 14 and 20 breaths/min, an inspiratory:expiratory ratio of 1:2, and an end-inspiratory pause of 0.2 s. All patients were monitored with a pulse oximeter and had an arterial saturation of more than 95%, which was not modified throughout the study.

Arterial blood pressure and heart rate were recorded from a radial or femoral catheter (Summit®; Baxter, Maurepas, France) and displayed together with the end-tidal CO₂ pressure on the monitor (Merlin 1006A®; Hewlett Packard, Les Ulis, France). Pulse pressure (Pp) was calculated as systolic arterial pressure minus diastolic arterial pressure. %Pp was calculated as the difference between the maximal and the minimal value of Pp over a single respiratory cycle, divided by the mean of the two values and expressed as a percentage (5).

Echo Doppler studies were performed with an HP Sonos 5500® (Hewlett Packard) equipped with a multiplane 5 MHz transesophageal echocardiographic transducer. Using the signal from the respirator (Puritan Bennett 7200®; Nellcor Puritan Bennett, Courtaboeuf, France), airway pressure was displayed on the screen, accurately timing cardiac events during the respiratory cycle. A short axis, cross-sectional view of the LV was obtained by a transgastric approach, permitting measurements of LV cross-sectional areas by planimetry at the end of the expiratory period. LV fractional area shortening was calculated as (LV end-diastolic area [LVEDA] – LV end-systolic area)/LVEDA, and was used as an index of LV ejection fraction. Doppler aortic velocity–time integrals (VTI_Ao) were recorded at the level of the LV outflow tract together with aortic diameter, permitting calculation of the LV stroke volume. Cardiac output was calculated as LV stroke volume times heart rate. Measurements of LVEDA, stroke volume, and cardiac output were indexed to body surface area (LVEDA_i, stroke index, and cardiac index, respectively). Maximal and minimal values of VTI_Ao were determined over a single respiratory cycle. %VTI_Ao was calculated as the difference between the maximal and the minimal value of VTI_Ao, divided by the mean of the two values and expressed as a percentage (9). %Pp and %VTI_Ao were measured in triplicate over 3 consecutive respiratory cycles and averaged. In 4 patients, 2 sets of measurements were recorded to analyze the intraobserver reproducibility: 6% for LVEDA and 4% for VTI_Ao.

Blood volume (BV) was measured using an in vivo validated method based on the dilution of hydroxyethyl starch (10). EDTA blood samples were drawn before and 5 min after the injection of 100 mL hydroxyethyl starch (vol_HES, Voluven®; Freysenius, Saint-Cloud, France) over 60 s. After plasma separation, hydroxyethyl starch was completely hydrolyzed (100°C, hydrochloric acid, 15 min), and the resulting glucose concentration was measured by spectrophotometry (CX3®; Beckman-Coulter, Roissy, France). Using the difference in plasma glucose before and after injection (_glucose), which was proportional to the hydroxyethyl starch concentration in the plasma, and the hematocrit of the sample (Hct), BV was calculated within 60 min: BV = k(vol_HES/(_glucose(1 – Hct)). The coefficients of variation for measurement reproducibility were between 1.2% and 2.1%. BV was expressed in mL/kg of body weight.

The hydroxyethyl starch infusion was preceded by a "control" period and followed by a "fluid challenge" period. During each period, static (arterial blood pressure, heart rate, LVEDA_i, stroke volume) and dynamic (%Pp and %VTI_Ao) variables were measured in 3 circumstances: a 15-min period with basal ventilatory settings (basal values) and 2 15-min periods during which Vt was fixed at 6 and 10 mL/kg in a random order without change in respiratory rate.

The number of subjects required for the study was calculated considering an error of 5% and a ß error of 10%, using the results of a previous study reporting a 50% decrease in respiratory changes in LV stroke volume variation in patients demonstrating a substantial (>15%) increase in cardiac index after a rapid large-volume challenge (oxypolygelatin: 370–790 mL, 10 min) (11). Considering that a positive response to intravascular volume expansion was observed in 40% to 60% of ventilated patients (1), we determined that 20 patients were needed.

Comparisons of basal values during the two study periods were performed using Student’s t-test after checking for normality with a Shapiro-Wilk test. Next, patients were divided into two subgroups according to the change of stroke volume in response to hydroxyethyl starch infusion (1). Patients with an increase in stroke volume 15% and <15% were classified as "responders" and "non-responders," respectively. Basal values of hemodynamic variables and evolution of the dynamic variables (%Pp and %VTI_Ao) were compared between the two groups using Student’s t-test for unpaired data. Correlations between variables were performed using linear regressions. A value of P < 0.05 was considered as the minimum level of statistical significance. Data are expressed as mean ± sd.

Receiver operating characteristic (ROC) curves were generated for %Pp, %VTI_Ao, LVEDA_I, and BV, considering the change in stroke volume after fluid challenge as the response criterion. The median area under the ROC curve and its 95% confidence interval, calculated by 1000 bootstrap replications, as well as the Youden index (maximum vertical distance between the ROC curve and the diagonal) are reported.

A covariance analysis was used to test the influence of Vt on %Pp and %VTI_Ao. The whole data set was fitted using mixed effect linear regression (procedure lme for S-PLUS). The structure of the data set was nested with group (responders or nonresponders) as the outer grouping factor and sequence (before/after hydroxyethyl starch infusion) as the inner factor. Indicator values were assigned to the 3 Vt (basal, 6 mL/kg, and 10 mL/kg) to account for the mixed nature of their values. Significance was tested using the Restricted Likelihood Ratio Test and the conditional Student’s t-test.

	Results

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Twenty-one patients were included in the study (Table 1) (15 men, 6 women; 46 ± 20 yr). Eighteen patients (86%) received norepinephrine (0.45 ± 0.25 µg · kg^–1 · min^–1). During the control period, the hemodynamic profile was as follows: mean arterial blood pressure: 85 ± 24 mm Hg, cardiac index: 2.94 ± 1.24 L · min^–1 · m^–2, LVEDA_i: 11.3 ± 1.9 cm²/m², fractional area shortening: 46.7 ± 8.7%. Lactate was more than 2 mmol/L in 13 patients. BV was 68.9 ± 14.8 mL/kg. Twelve patients had an acute lung injury (Table 1). The average gradient between arterial and end-tidal CO₂ pressures ranged from 3 to 21 mm Hg.

For the whole group, mean arterial blood pressure, cardiac index, and LVEDAi remained unchanged after hydroxyethyl starch infusion, but heart rate decreased (97 ± 17 versus 101 ± 21 bpm; P = 0.0078) and stroke index increased (32.1 ± 11.1 versus 29.4 ± 10.2 mL/m²; P = 0.0128). Nine patients (43%) were responders and 12 patients were nonresponders. During the control period, basal values of LVEDA_i (10.3 ± 1.4 versus 12.2 ± 1.9 cm²/m²; P = 0.0212), VTI_Ao (14.8 ± 5.1 versus 20.0 ± 5.5 cm; P = 0.0395), and stroke index (23.9 ± 9.6 versus 33.5 ± 9.0 mL/m²; P = 0.0452) were lower in responders. Basal values of %VTI_Ao and %Pp were higher in responders (Fig. 1). Basal values of %VTI_Ao and Pp in responders decreased after hydroxyethyl starch infusion (Fig. 1), despite the absence of change in LVEDA_i (10.3 ± 1.1 versus 10.3 ± 1.4 cm²/m²). Threshold and predictive values derived from the ROC curves are reported in Table 2 and Figure 2. The Youden index was 0.722 for %Pp, 0.694 for %VTI_Ao, and only 0.472 for LVEDA_i. BV had no significant predictive value and was not correlated with any static or dynamic variables. There was no correlation between %Pp and %VTI_Ao. Finally, a weak relationship was found between %Pp and norepinephrine dosage at the time of the study (Fig. 3). There was no correlation between the change in LV stroke index after fluid infusion and norepinephrine dosage, suggesting that the patients receiving the larger dose of vasopressor were not the more volume depleted.

View larger version (18K): [in this window] [in a new window]   Figure 1. Evolution of the dynamic variables (%Pp and %VTIAo) after fluid challenge, in responders (black bars) and nonresponders (white bars). Basal values during the control period are indicated near the corresponding bars. The superior P value refers to the intergroup difference in basal values, and the inferior P value refers to the intergroup difference in the evolution of the variable. %VTIAo and %Pp, cyclic variations of the aortic velocity–time integral, and the pulse pressure, respectively.

View this table: [in this window] [in a new window]   Table 2. Predictive Values of Dynamic (%VTIAo and %Pp) and Static (LVEDAi and BV) Variables

View larger version (29K): [in this window] [in a new window]   Figure 2. ROC curves comparing the ability of %Pp, %VTIAo, LVEDAi, and BV to discriminate responders (stroke volume increase 15%) and nonresponders to intravascular volume expansion. BV, blood volume; %VTIAo and %Pp, cyclic variations of the aortic velocity–time integral and the pulse pressure, respectively; LVEDAi, left ventricular end-diastolic cross-sectional area.

View larger version (20K): [in this window] [in a new window]   Figure 3. Scattergram of the basal values of cyclic variations of the pulse pressure (%Pp) plotted against the norepinephrine dosage at the time of the study.

Covariance analysis revealed that basal Vt was similar in responders and nonresponders (approximately 8 mL/kg; Fig. 4). %VTI_Ao was lower during the fluid challenge period as compared with the control period in responders, regardless of Vt (P = 0.0190). %VTI_Ao demonstrated a parallel evolution in responders and nonresponders during the 2 periods and was not significantly modified by the level of Vt changes (P = 0.4275). %Pp was lower during the fluid challenge period as compared with the control period in responders, regardless of Vt (P < 0.0001). %Pp increased with the increase in Vt during the 2 periods, with a parallel evolution of %Pp as a function of Vt in responders and nonresponders (P < 0.0001). The number of patients whose %Pp was more than 10% (threshold calculated at the basal value of Vt) increased with the increase in Vt: 5 at 6 mL/kg, 10 at basal values, and 13 at 10 mL/kg.

View larger version (30K): [in this window] [in a new window]   Figure 4. Schematic representation of the influence of tidal volume on %Pp and %VTIAo, before (control) and after (fluid challenge) hydroxyethyl starch infusion, in responders (black circles) and nonresponders (white circles). The dashed line indicates the threshold value for the variable in the basal conditions (mid-value of tidal volume) during the control period. %VTIAo and %Pp, cyclic variations of the aortic velocity–time integral and the pulse pressure, respectively.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
By inducing cyclic changes in intrathoracic and transpulmonary pressures, mechanical ventilation induces cyclic changes in the preload and the afterload of both ventricles. The resulting changes in stroke volume are reflected by pulse pressure variation over the respiratory cycle. These changes are important in the case of cardiac preload reserve and volume responsiveness (12). This study i) proposes the rapid injection of a small volume of hydroxyethyl starch as a fluid challenge, ii) demonstrates the equivalent predictive value of %VTI_Ao and of %Pp measured simultaneously by two separate techniques, and iii) suggests a discrepancy between these two variables as a function of tidal volume.

The first question to ask is whether this colloid infusion is really a fluid challenge in the absence of change in LVEDA_i. The present results confirmed those of Axler et al. (13), who did not detect a change in LVEDA_i after an equivalent fluid challenge (normal saline: 500 mL, 5 to 10 min). A small pixel error in drawing the border on the screen results in an undetectable increase in the cross-sectional area of the LV (14). An 8% increase in LV end-diastolic volume was exclusively detected by radionuclide cineangiography and not by echocardiography after crystalloid infusion (3000 mL, 180 min) in healthy subjects (15). However, the sensitivity of echocardiography compared with thermodilution may explain the difference with other previous studies in which the infusion of the same volume of colloid had no hemodynamic effect (16). The reported increase in stroke volume infusion could be preload-independent. In fact, a decrease in LV afterload may be discarded because a reflex vasodilation in norepinephrine-treated patients as well as a decrease in blood viscosity after a 100-mL infusion of colloid seemed unlikely. In the same way, an increase in LV contractility through a human Bainbridge reflex or a sodium-induced myocardial stimulation hardly explained the increase in stroke index in the absence of concomitant tachycardia or considering the small amount of sodium infused (20 mmol). Finally, a similar incidence of positive responses and of proportional decreases in dynamic variables was observed in previous studies using a slower infusion of larger volumes of fluid (2,17,18). A peak of intravascular volume expansion after colloid infusion similar to the present fluid challenge was observed 5 to 10 min after the end of infusion (19) and supports a preload-dependent increase in stroke volume in the responders.

In basal conditions the present respiratory changes in stroke index and arterial blood pressure had the same predictive value for fluid responsiveness. Concerning %VTI_Ao, the present results using a direct measurement of stroke volume through the velocity profile of aortic flow confirm those obtained with the peak value of velocity (3) or derived from the arterial pulse contour (11). This value of %VTI_Ao and %Pp was better than that of the classical static variable, LVEDA_i. Responders to fluid challenge had lower LVEDA_i when compared with nonresponders, but, as reported by Tousignant et al. (20), there was a considerable overlapping in basal values from the two groups and it was not possible to identify a clinically relevant threshold value below which most patients demonstrated a volume-recruitable increase in LV ejection.

Despite the absence of direct measurement, it can be reasonably assumed that the rather large changes in Vt resulted in significant changes in thoracic and transpulmonary pressures despite subnormal compliance of our patients (21). The vascular effects of changes in arterial CO₂ tensions related to the changes in minute ventilation were probably negligible in these patients under vasopressor therapy. Conversely, because arterial blood pressure variability is frequency dependent in humans, the differences in respiratory rates among our patients must be considered.

An increase in the respiratory component of arterial blood pressure variability was observed as spontaneous respiration slowed to 0.07–0.09 Hz in healthy subjects (22). The present data were obtained with higher values (0.23–0.33 Hz), and the difference in respiratory rates among patients probably had no influence on the results. %Pp increased when Vt increased before and after fluid challenge. The analysis of the up/down components of systolic arterial blood pressure variations might have been useful to separate the preload and afterload components of %Pp (23). A significant increase in up resulting from an emptying of pulmonary capacitance vessels might have contributed to the Vt-related increase in %Pp, even in patients with an apparently normal LV function (12). However, an increase in down was probably the main explanation and may be attributed to the influence of intrathoracic pressures on the central BV and ultimately on the LV ejection.

Even if the design of the present study did not include a manipulation of the norepinephrine dosage, the peripheral adrenergic tone may have contributed to the increase in %Pp. Indeed, norepinephrine infusion in young patients with normal arteries increases the aortic impedance and reduces the arterial compliance (24). Such a change in arterial properties may amplify the static value of Pp and ultimately Pp variability, despite a limited cyclic variation of stroke volume, as suggested by the slight relationship between %Pp and norepinephrine dosage.

An unexpected result of this study was the absence of significant changes in %VTI_Ao as a function of Vt. Despite the fact that aortic flow velocity was measured with a multiplane probe, one cannot exclude a slight discrepancy between the respective axis of ultrasound beam and blood flow that would be related to the influence of lung volume on cardiac position. This technical problem may also explain the absence of a significant relationship between %Pp and %VTI_Ao in the present results. Such a relationship was reported between systolic blood pressure variations and LV stroke volume variations obtained by real-time continuous arterial pulse contour analysis (11). In contrast with the present separate techniques, a mathematical coupling between the two values extrapolated from the same measurement may be evoked in this relationship.

Finally, the present study confirms that the measurement of BV may be rapidly obtained in critically ill patients. But normal values of BV do not preclude preload dependency of these patients because an abnormal distribution of BV, including peripheral blood pooling, is usual in patients exhibiting a severe inflammatory syndrome (25).

In conclusion, because fluid challenge was not given at the different experimental Vt levels, we can conclude that the predictive value of %Pp was affected by the depth of lung inflation (6). Conversely, the increase in systolic blood pressure variation during incremental pressure-controlled breaths was recently proposed as a standardized bedside maneuver to guide fluid therapy (26). The present results would support another test using the cyclic changes in pulse pressure and incremental volume-controlled breaths. %Pp remains the easiest and most efficient predictor of fluid responsiveness in mechanically ventilated patients, considering the basal value of Vt and of adrenergic tone.

The authors gratefully acknowledge the assistance of Jean-Louis Teboul, MD, PhD (Service de Réanimation Médicale, Hôpital de Bicêtre (APHP), 94275 Le Kremlin Bicêtre, France) to the revised version of the manuscript.

	Footnotes

 
Accepted for publication January 19, 2006.

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Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999