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Predicting Fluid Responsiveness in ICU Patients^*

A Critical Analysis of the Evidence

^* From the Medical ICU, CHU de Bicêtre, Assistance Publique-Hôpitaux de Paris, Le Kremlin-Bicêtre, Université Paris XI, France.

Correspondence to: Frédéric Michard, MD, PhD, Service de Réanimation Médicale, CHU de Bicêtre, Université Paris XI, 78, rue du Général Leclerc, 94275 Le Kremlin Bicêtre cedex, France; e-mail: f.michard{at}wanadoo.fr

	Abstract

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Study objective: To identify and critically review the published peer-reviewed, English-language studies investigating predictive factors of fluid responsiveness in ICU patients.

Design: Studies were collected by doing a search in MEDLINE (from 1966) and scanning the reference lists of the articles. Studies were selected according to the following criteria: volume expansion performed in critically ill patients, patients classified in two groups (responders and nonresponders) according to the effects of volume expansion on stroke volume or on cardiac output, and comparison of responder and nonresponder patients’ characteristics before volume expansion.

Results: Twelve studies were analyzed in which the parameters tested were as follows: (1) static indicators of cardiac preload (right atrial pressure [RAP], pulmonary artery occlusion pressure [PAOP], right ventricular end-diastolic volume [RVEDV], and left ventricular end-diastolic area [LVEDA]); and (2) dynamic parameters (inspiratory decrease in RAP [RAP], expiratory decrease in arterial systolic pressure [down], respiratory changes in pulse pressure [PP], and respiratory changes in aortic blood velocity [Vpeak]). Before fluid infusion, RAP, PAOP, RVEDV, and LVEDA were not significantly lower in responders than in nonresponders in three of five studies, in seven of nine studies, in four of six studies, and in one of three studies, respectively. When a significant difference was found, no threshold value could discriminate responders and nonresponders. Before fluid infusion, RAP, down, PP, and Vpeak were significantly higher in responders, and a threshold value predicted fluid responsiveness with high positive (77 to 95%) and negative (81 to 100%) predictive values.

Conclusion: Dynamic parameters should be used preferentially to static parameters to predict fluid responsiveness in ICU patients.

Key Words: arterial pressure • cardiac output • cardiac preload • fluid responsiveness • left ventricular end-diastolic area • pulmonary artery occlusion pressure • right atrial pressure • right ventricular end-diastolic volume • stroke volume • volume expansion

	Introduction

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Volume expansion is frequently used in critically ill patients to improve hemodynamics. Because of the positive relationship between ventricular end-diastolic volume and stroke volume,¹ the expected hemodynamic response to volume expansion is an increase in right ventricular end-diastolic volume (RVEDV), left ventricular end-diastolic volume, stroke volume, and cardiac output. The increase in end-diastolic volume as a result of fluid therapy depends on the partitioning of the fluid into the different cardiovascular compliances organized in series. The increase in stroke volume as a result of end-diastolic volume increase depends on ventricular function since a decrease in ventricular contractility decreases the slope of the relationship between end-diastolic volume and stroke volume.¹ Therefore, only 40 to 72% of critically ill patients have been shown to respond to volume expansion by a significant increase in stroke volume or cardiac output in studies^{2 3 4 5 6 7 8 9 10 11 12 13} designed to examine fluid responsiveness. This finding emphasizes the need for predictive factors of fluid responsiveness in order to select patients who might benefit from volume expansion and to avoid ineffective or even deleterious volume expansion (worsening in gas exchange, hemodilution) in nonresponder patients, in whom inotropic and/or vasopressor support should preferentially be used.

Bedside indicators of ventricular preload have been proposed as predictors of fluid responsiveness.^{2 3 4 6 7 8 9 11 12 13} In this regard, a postal survey in Germany showed that right atrial pressure (RAP) and pulmonary artery occlusion pressure (PAOP) are used by a majority of ICU physicians when deciding to administer fluid,¹⁴ and several recommendations support the use of cardiac filling pressures in order to guide fluid therapy in critically ill patients.^{15 16} Other bedside indicators of ventricular preload, namely RVEDV and left ventricular end-diastolic area (LVEDA), have also been tested as predictors of the hemodynamic effects of volume expansion in critically ill patients.^{2 3 4 6 7 8 9 11 13}

The respiratory changes in RAP, arterial pressure, and aortic blood velocity, assumed to be dynamic indicators of the sensitivity of the heart to changes in preload induced by changes in pleural pressure, have also been proposed to predict fluid responsiveness in critically ill patients.^{5 9 10 12 13} Therefore, the aim of the present study was to analyze the clinical studies investigating predictive factors of fluid responsiveness in critically ill patients in order to assess the value of each parameter tested.

	Materials and Methods

TOP Abstract Introduction Materials and Methods Results Discussion References

 
Selection of Studies To Be Evaluated
We collected studies investigating the predictive factors of fluid responsiveness in critically ill patients by doing a search in MEDLINE (from 1966). Studies were selected according to the following criteria: volume expansion performed in critically ill patients, patients classified in two groups (responders and nonresponders) according to the effects of volume expansion on stroke volume or on cardiac output, and comparison of responder and nonresponder patients characteristics before volume expansion. The reference lists of the selected articles were scanned for additional studies. Of the 12 included studies,^{2 3 4 5 6 7 8 9 10 11 12 13} 11 studies were identified from the electronic database and 1 study was identified from reference tracing.⁵ The main characteristics of these studies are presented in Table 1 .

Five studies have investigated the value of dynamic parameters in predicting fluid responsiveness. These parameters were the inspiratory decrease in RAP (RAP) in two studies,^{5 10} the expiratory decrease in arterial systolic pressure (down) in one study,⁹ the respiratory changes in arterial pulse pressure (PP) in one study,¹² and the respiratory changes in aortic blood velocity (Vpeak) in one study¹³ (Table 1) . The RAP was calculated as the difference between the expiratory and the inspiratory RAP.^{5 10} The down was calculated as the difference between the value of the systolic pressure during an end-expiratory pause and the minimal value of systolic pressure over a single respiratory cycle.⁹ The PP was calculated as the difference between the maximal and the minimal value of pulse pressure over a single respiratory cycle, divided by the mean of the two values, and expressed as a percentage.¹² The Vpeak was calculated as the difference between the maximal and minimal peak velocity of aortic blood flow over a single respiratory cycle, divided by the mean of the two values, and expressed as a percentage.¹³ Aortic blood flow was measured by a pulsed-wave Doppler echocardiographic beam at the level of the aortic valve.¹³

	Results

TOP Abstract Introduction Materials and Methods Results Discussion References

 
There were 406 fluid challenges in 334 patients (Table 1) . Most of the patients were septic (55%) and receiving mechanical ventilation (84%). The decision of volume expansion was based on criteria listed in Table 2 . Fluid administration was performed using colloid solutions (albumin, fresh frozen plasma, or hydroxyethylstarch) in 253 instances, and crystalloid solutions (serum saline solution or Ringer’s lactate) in 153 instances (Table 1) . In nine studies, the volume infused was predetermined and ranged from 250 to 500 mL for colloids and from 300 to 500 mL for crystalloids (Table 1) . In two studies,^{5 10} volume infusion was performed until a rise in RAP 2 mm Hg was obtained; hence, the volume of serum saline solution infused varied from 100 to 950 mL. In another study,⁸ fluid was administered until a rise in PAOP 3 mm Hg was obtained. In this case, the volume infused was 938 ± 480 mL for serum saline solution and 574 ± 187 mL for 5% albumin or fresh frozen plasma. The speeds of fluid infusion are reported in Table 1 . In all studies but one,⁹ hemodynamic measurements were performed just before and immediately at the end of fluid infusion.

RAP
Before volume expansion, RAP was not significantly lower in responders than in nonresponders in three of five studies^{2 4 12} (Fig 1 ). The two remaining studies^{3 8} reported a lower value of baseline RAP in responders than in nonresponders (Fig 1) , and a significant relationship between the baseline RAP (r² = 0.20), and the increase in stroke volume in response to volume expansion was reported by Wagner and Leatherman.⁸ However, the marked overlap of individual RAP values did not allow the identification of a RAP threshold value discriminating responders and nonresponders before fluid was administered.

View larger version (16K): [in this window] [in a new window] [Download PPT slide]   Figure 1.. Mean RAP before volume expansion in responders and nonresponders.

View larger version (21K): [in this window] [in a new window] [Download PPT slide]   Figure 2.. Mean RVEDV index before volume expansion in responders and nonresponders.

RAP

down

PP
In sedated patients receiving mechanical ventilation with acute circulatory failure related to sepsis, one study¹² demonstrated that PP was significantly greater (24 ± 9% vs 7 ± 3%, p < 0.001) in responders than in nonresponders, and that a PP threshold value of 13% allowed discrimination between responder and nonresponder patients with a positive predictive value of 94% and a negative predictive value of 96% (Table 5) . Moreover, in this study,¹² the value of PP before fluid administration was significantly and closely correlated (r² = 0.85, p < 0.001) with the volume expansion-induced changes in cardiac output, such that the higher PP at baseline, the greater was the increase in cardiac output in response to fluid infusion.

Vpeak
In sedated patients receiving mechanical ventilation with septic shock, one study¹³ demonstrated that Vpeak was significantly greater (20 ± 6% vs 10 ± 3%, p < 0.01) in responder patients than in nonresponder patients, and that a Vpeak threshold value of 12% allowed discrimination between responder and nonresponder patients with a positive predictive value of 91% and a negative predictive value of 100% (Table 5) . Moreover, a positive and tight linear correlation (r² = 0.83, p < 0.001) was found between the Vpeak before volume expansion and the volume expansion-induced changes in cardiac output.

	Discussion

TOP Abstract Introduction Materials and Methods Results Discussion References

 
The present analysis emphasizes the minimal clinical value of ventricular preload indicators and the higher value of dynamic parameters (testing the cardiovascular response to respiratory changes in pleural pressure) in predicting fluid responsiveness in critically ill patients. It has been suggested that a beneficial hemodynamic effect of volume expansion cannot be expected in critically ill patients with a RAP > 12 mm Hg¹⁷ and/or a PAOP > 12 mm Hg or > 15 mm Hg.^{15 18} In this regard, RAP and PAOP have been reported to be lower in responders than in nonresponder patients in two studies (Fig 1 , Table 3 ). Moreover, a significant relationship between the increase in stroke volume in response to volume expansion and the baseline RAP (r² = 0.20) or the baseline PAOP (r² = 0.33) was reported by Wagner and Leatherman,⁸ suggesting that the lower RAP or PAOP before volume expansion, the greater the increase in stroke volume in response to fluid infusion. However, although statistically significant, these relationships were weak because a given value of RAP or of PAOP could not be used to discriminate responders and nonresponders before fluid was administered. Moreover, in all other clinical studies (Fig 1 , Table 3 ), no difference between responder and nonresponder patients was observed with regard to the baseline value of RAP and of PAOP, and no relationship was reported between cardiac filling pressures before volume expansion and the hemodynamic response to volume expansion. Finally, it must be noted that fluid infusion has been shown to significantly increase cardiac output in some critically ill patients with central venous pressures > 15 mm Hg.¹⁹

Two studies of Diebel et al^{6 7} reported a lower value of RVEDV index in responder than in nonresponder patients, and suggested that a beneficial hemodynamic effect of volume expansion was likely (rate of response 100% and 64%) when the RVEDV index was below 90 mL/m² and very unlikely (rate of response of 0%) when the RVEDV index was > 138 mL/m². However, when the RVEDV index ranged from 90 to 138 mL/m², no cutoff value could be proposed to discriminate responder and nonresponder patients. Moreover, Wagner and Leatherman⁸ reported positive responses to volume expansion in patients with a RVEDV index > 138 mL/m², and the lack of response in patients with a RVEDV index < 90 mL/m². Finally, in four of six studies investigating whether RVEDV could predict fluid responsiveness, no significant difference was observed between responders and nonresponders with regard to the baseline value of RVEDV index (Fig 2) .

The echocardiographic measurement of LVEDA has been shown to reflect more accurately the left ventricular preload when compared with PAOP,²⁰ and to improve the ability to detect changes in left ventricular function caused by acute blood loss.²¹ In nine anesthetized mongrel dogs, Swenson et al²² reported a significant relationship between baseline LVEDA and changes in cardiac output induced by IV fluid therapy, suggesting that LVEDA could be an indicator of fluid responsiveness. In this regard, LVEDA was found to be significantly lower in responders than in nonresponders in two clinical studies,^{9 11} and a significant relationship between the baseline LVEDA index and the changes in stroke volume induced by volume expansion has also been reported.⁹ However, using receiver operating characteristic curve analysis, Tavernier et al⁹ demonstrated in patients with sepsis-induced hypotension the minimal value of a given LVEDA index value to discriminate responders and nonresponders before fluid was administered. Moreover, in the study of Tousignant et al,¹¹ including medical-surgical ICU patients, considerable overlap of baseline individual values of LVEDA was observed between responders and nonresponders, supporting the interpretation that a specific LVEDA value cannot reliably predict fluid responsiveness in an individual patient. Recently, in patients with septic shock, Feissel et al¹³ did not observe any difference between the mean baseline value of LVEDA index in responders and nonresponders, neither any relationship between the baseline value of LVEDA index and the percentage of change in cardiac index in response to volume expansion.

Therefore, all clinical studies have emphasized the lack of value of ventricular preload indicators as predictors of fluid responsiveness in critically ill patients. Methodologic and physiologic reasons could be advanced to explain these findings. First, RAP, PAOP, RVEDV, and LVEDA are not always accurate indicators of ventricular preload. Indeed, RAP and PAOP have been shown to overestimate transmural pressures in patients with external²³ or intrinsic²⁴ PEEP. The PAOP is highly dependent on left ventricular compliance,²⁵ which is frequently decreased in ICU patients (sepsis, ischemic, or hypertrophic cardiopathy). Because it is the transmural pressures and not intracavitary pressures such as RAP and PAOP that are related to end-diastolic volumes via the chamber compliance, it is not surprising that those surrogates bear little relationship to fluid responsiveness. The evaluation of RVEDV by thermodilution has been shown influenced by tricuspid regurgitation,²⁶ which is frequently encountered in patients with pulmonary hypertension (ARDS, mechanical ventilation with PEEP). The estimation of the LVEDA by echocardiography does not always accurately reflect left ventricular end-diastolic volume²⁷ and hence LV preload. Second, in case of right ventricular dysfunction, a beneficial hemodynamic effect of volume expansion cannot be expected, even in the case of low left ventricular preload.²⁸ Third, knowing the preinfusion end-diastolic volume tells little about the diastolic chamber compliance. In this regard, hypovolemia can be associated with a normal or high LVEDA value in patients with dilated cardiopathy. Finally, two matters must be stressed: (1) the increase in end-diastolic volume as a result of fluid therapy depends on the partitioning of the fluid into the different cardiovascular compliances organized in series, and (2) the rise in stroke volume as a result of end-diastolic volume increase depends on ventricular function since a decrease in ventricular contractility decreases the slope of the relationship between end-diastolic volume and stroke volume.¹ Therefore, a patient can be nonresponder to a fluid challenge because of high venous compliance, low ventricular compliance and/or ventricular dysfunction. In this regard, it is not so surprising that bedside indicators of cardiac chambers dimensions are not accurate predictors of fluid responsiveness in ICU patients in whom venous capacitance, ventricular compliance, and contractility are frequently altered.

Assuming that respiratory changes in pleural pressure induce greater changes in RAP when the right ventricle is highly compliant than when it is poorly compliant, Magder et al investigated whether the inspiratory decrease in RAP could be used to predict fluid responsiveness.^{5 10} Two studies^{5 10} demonstrated that a positive response to volume expansion was very likely in patients with an inspiratory decrease in RAP 1 mm Hg, while it was unlikely if the inspiratory decrease in RAP was < 1 mm Hg. Unfortunately, most of ICU patients with acute circulatory failure are sedated and receiving mechanical ventilation, thus are unable to produce an inspiratory decrease in pleural pressure sufficient to decrease the RAP.¹⁰ In this condition, analysis of the respiratory changes in left ventricular stroke volume has been proposed to predict fluid responsiveness. Indeed, by decreasing the venous return pressure gradient, mechanical insufflation may decrease the right ventricular filling,²⁹ and consequently the right ventricular output if the right ventricle is sensitive to changes in preload. In this condition, the following decrease in left ventricular filling may also induce a significant decrease in left ventricular output if the left ventricle is sensitive to changes in preload. Therefore, the magnitude of the respiratory changes in left ventricular stroke volume, which reflects the sensitivity of the heart to changes in preload induced by mechanical insufflation, has been proposed as a predictor of fluid responsiveness. Because the arterial pulse pressure (systolic minus diastolic pressure) is directly proportional to left ventricular stroke volume,³⁰ the respiratory changes in left ventricular stroke volume have been shown reflected by changes in pulse pressure.³¹ Accordingly, the respiratory changes in pulse pressure have been shown to accurately predict fluid responsiveness in patients receiving mechanical ventilation with acute circulatory failure related to sepsis.¹² The analysis of the respiratory changes in systolic pressure has also been proposed to assess fluid responsiveness. However, the systolic pressure variation induced by mechanical ventilation results not only from changes in aortic transmural pressure (mainly related to changes in left ventricular stroke volume), but also from changes in extramural pressure (ie, from changes in pleural pressure).^{32 33} Therefore, the systolic pressure variation is a less specific indicator of changes in left ventricular stroke volume and hence a less accurate predictor of fluid responsiveness than the pulse pressure variation.¹² In this regard, it has been proposed to discriminate the inspiratory increase in systolic pressure (not necessarily due to a change in left ventricular stroke volume) from the down, which in contrast necessarily reflects a change in left ventricular stroke volume.³⁴ Experimental and clinical studies^{34 35} have emphasized the influence of volume status on down (hemorrhage increases down, while volume expansion decreases down), and Tavernier et al⁹ demonstrated that down is an accurate predictor of fluid responsiveness in septic patients with hypotension.

The analysis of the arterial pressure waveform is not possible in patients with cardiac arrhythmias.³⁶ Indeed, in this condition, the changes in arterial pressure do not reflect the effects of mechanical insufflation on left ventricular stroke volume. It must be emphasized that the evaluation of down and of PP requires invasive arterial pressure catheterization. However, in shock states, estimation of BP using a cuff is commonly inaccurate, and use of an arterial cannula provides a more appropriate and reproducible measurement of arterial pressure.¹⁵ Interestingly, Feissel et al¹³ have recently demonstrated that Doppler echocardiographic imaging of aortic blood velocity could be used to assess noninvasively the respiratory changes in aortic blood velocity and to predict fluid responsiveness in patients with septic shock. It must be noted that down, PP, and Vpeak have been shown to be accurate predictors of fluid responsiveness in sedated patients receiving mechanical ventilation with sepsis. Whether they also predict fluid responsiveness in nonsedated, spontaneously breathing patients without sepsis remains to be determined.

It must be emphasized that various types and volumes of fluid, speeds of fluid infusion, and definitions of responders to volume expansion have been used in the studies analyzed (Table 1) . This may have a significant influence on the results and conclusions of the studies. Indeed, the hemodynamic effects of an hypertonic colloid infusion are expected to be more dramatic than those of an equal volume of isotonic crystalloid infusion. Because of intravascular-extravascular equilibration, the speed of volume infusion should also greatly influence the hemodynamic response, particularly in septic patients with systemic capillary leakness. Moreover, because of different definitions of responders from one study to another, some patients considered as responders in some studies, would have been considered as nonresponders in other studies. Unfortunately, because individual data were not available in all but one study, a comparison of the predictive value of each parameter using the same definition of responders was not possible. Finally, the predictive value of dynamic parameters has been tested by only few studies. Therefore, further studies are required to confirm the high value of dynamic parameters in discriminating responder and nonresponder patients before fluid infusion. However, our analysis emphasizes the minimal value of static ventricular preload parameters as predictors of fluid responsiveness and strongly supports the use of the dynamic parameters in the decision-making process concerning volume expansion in critically ill patients.

	Acknowledgements

 
The authors thank Dr. Denis Chemla for helpful discussion.

	Footnotes

 
Abbreviations: down = expiratory decrease in arterial systolic pressure; LVEDA = left ventricular end-diastolic area; PAOP = pulmonary artery occlusion pressure; PEEP = positive end-expiratory pressure; PP = respiratory changes in arterial pulse pressure; RAP = right atrial pressure; RAP = inspiratory decrease in right atrial pressure; RVEDV = right ventricular end-diastolic volume; Vpeak = respiratory changes in aortic peak velocity

Received for publication June 4, 2001. Accepted for publication December 19, 2001.

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