Basic concepts of fluid responsiveness
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- Cherpanath, T.G.V., Geerts, B.F., Lagrand, W.K. et al. Neth Heart J (2013) 21: 530. doi:10.1007/s12471-013-0487-7
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Predicting fluid responsiveness, the response of stroke volume to fluid loading, is a relatively novel concept that aims to optimise circulation, and as such organ perfusion, while avoiding futile and potentially deleterious fluid administrations in critically ill patients. Dynamic parameters have shown to be superior in predicting the response to fluid loading compared with static cardiac filling pressures. However, in routine clinical practice the conditions necessary for dynamic parameters to predict fluid responsiveness are frequently not met. Passive leg raising as a means to alter biventricular preload in combination with subsequent measurement of the change in stroke volume can provide a fast and accurate way to guide fluid management in a broad population of critically ill patients.
KeywordsFluid responsivenessVenous returnCardiac functionPulse contour analysisPassive leg raising
The cornerstone of resuscitation of haemodynamically unstable critically ill patients is often considered to be fluid loading. However, only roughly half of haemodynamically unstable patients respond to a fluid challenge, defined as an increase in stroke volume or cardiac output upon fluid loading [1, 2]. Although rapid optimisation of volume status has shown to improve outcome, extended fluid loading is associated with increased morbidity and mortality [3–6]. Little evidence is available for the type and exact dosing of fluid administration. Establishing volume status is complex, making accurate prediction of an increase in stroke volume upon fluid loading, so-called fluid responsiveness, difficult.
Static cardiac filling pressures such as central venous pressure have shown to be incapable of predicting fluid responsiveness accurately. Dynamic parameters on the other hand, using mechanical ventilation-induced changes in preload to track subsequent changes in stroke volume, have shown promise and have been the subject of extensive research in critically ill patients. New methods have been conceived that can easily be used at the bedside in a large variety of patients.
In this review we discuss the basic concepts of fluid responsiveness with a special focus on applications and limitations on use in clinical practice.
Cardiac function and venous return
Means to lower RAP are limited, since the critical pressure (Pcrit) at which the great veins at the thoracic inlet start to collapse causes a subsequent increase in Rv, thereby preventing a further increase in venous return. In the absence of collapsing veins, thus above Pcrit, Guyton confirmed, in extensive experimental models, that venous return changes linearly .
Decreasing Rv may be achieved by venodilation. However, by simultaneously increasing venous compliance, MSFP will decrease due to an increase of unstressed volume at the expense of stressed volume. The net effect on venous return is therefore uncertain depending on the relative changes of Rv and MSFP.
Increasing MSFP can be achieved by venoconstriction, but venous return can be limited by an increase in Rv. MSFP can also be increased by enlarging the stressed volume more than RAP by means of fluid loading. Since MSFP is equal to RAP in the absence of circulation, MSFP can be depicted at the horizontal intercept of the venous return curve. Upon fluid loading a right and upward shift is seen with no increase in venous resistance (Fig. 2).
Before one aims to increase cardiac output to prevent or treat organ hypoperfusion, it is imperative to first find out whether signs of inadequate tissue perfusion are present. Signs of tissue hypoperfusion for instance are decreased venous oxygen saturation or increased lactate levels, necessitating cardiac output augmentation. Note that subclinical signs of hypoperfusion can easily be missed. When tissue hypoperfusion is likely, it is key to find out a patient’s position on the combined venous return/cardiac function curve to predict whether an increase in cardiac output is to be expected from fluid loading or cardiac function augmentation (Fig. 3). This is especially important since achieving supra-physiological cardiac outputs through inotropics has shown to be detrimental . On the other hand, when decreased cardiac performance with a subsequent rise in RAP and reduced cardiac output is overcome by fluid loading to restore cardiac output, RAP will increase even further. On the ‘flat’ part of the cardiac function curve a rise in MSFP upon fluid loading is accompanied by a similar increase in RAP negating an increase in venous return and cardiac output indicating fluid unresponsiveness (Fig. 3, point I→II). Fluid administration in a non-fluid responsive patient will accelerate a rise in cardiac filling pressures and thus hydrostatic pressures causing pulmonary and general oedema. In that light it is of little surprise that a positive fluid balance has been associated with a worse outcome . Determining volume status is challenging but important since insufficient resuscitation on the other hand has been associated with organ hypoperfusion and ischaemia . The need for predictors of fluid responsiveness is high to select patients who might benefit from fluid loading, and thereby avoiding ineffective and potentially deleterious fluid administration where inotropics may better be used.
Static and dynamic predictors of fluid responsiveness
Central venous pressure as the classic static cardiac filling pressure is still the most often used parameter to guide fluid loading in Dutch critically ill patients . However, endless studies have shown that static cardiac filling pressures are poor predictors of fluid responsiveness [14, 15]. This can largely be explained by three mechanisms. First, cardiac filling pressures are intramural pressures not taking into account extramural pressures and thereby not fully reflecting transmural pressures, which represents preload. This can misguide clinical decision-making when solely using intramurally obtained cardiac filling pressures, especially in mechanically ventilated patients . Furthermore, the combination of cardiac filling pressures with ventricular end-diastolic radius determines preload, which is dependent on ventricular compliance varying largely between patients and within patients when critically ill. Finally, even low cardiac filling pressures do not imply that a patient is fluid responsive (Fig. 3, point I→II). So despite the fact that central venous pressure is a sufficient reflection of RAP as a determinant of right ventricular filling, it is unable to function as a reliable indicator, neither of preload nor of fluid responsiveness. Even right and left ventricular end-diastolic area or volume cannot establish the patient’s position on the combined venous return/cardiac function curve as a decline in cardiac performance decreases the slope of the relationship between end-diastolic volume and stroke volume . Right and left ventricular end-diastolic area and volume can therefore not accurately predict an increase in stroke volume upon fluid loading either .
To test fluid responsiveness, a change in preload must be provoked while monitoring the subsequent change in stroke volume or its derivatives such as pulse pressure. In recent years dynamic parameters of fluid responsiveness have been described using mechanical ventilation-induced changes in preload resulting in variation of stroke volume or pulse pressure, so-called stroke volume variation (SVV) and pulse pressure variation (PPV) respectively. Positive pressure mechanical ventilation induces a reduction in left ventricular preload mainly through a decrease in venous return . So when the patient’s position is on the steep portion of the cardiac function curve, mechanical ventilation will induce a larger decrease in stroke volume than when positioned on the flat part of the curve. In other words, SVV induced by mechanical ventilation will be higher when the patient operates on the steep portion of the cardiac function curve predicting an increase in stroke volume upon fluid loading.
Static haemodynamic parameters are inferior to dynamic parameters in predicting fluid responsiveness
However, several limitations in the use of dynamic parameters exist. First, controlled mechanical ventilation must be present to induce the required changes in preload. SVV was found to be inaccurate in patients with spontaneous breathing activity . Furthermore, tidal volumes have to be large enough to facilitate significant changes in preload. SVV is unreliable as a predictor of fluid responsiveness in case of tidal volumes <8 ml/kg [28, 29]. Moreover, a regular heart rhythm has to be present as determination of SVV and PPV becomes highly variable and inaccurate with arrhythmias such as atrial fibrillation. Finally, mechanical ventilation can also induce a decrease in left ventricular preload, primarily through increased RV afterload instead of decreased venous return, especially in view of pulmonary hypertension or RV failure [30, 31]. In that instance a raised SVV does not predict fluid responsiveness and should actually be avoided. This underlines the fact that both the left and right ventricle must function on the ascending portion of the cardiac function curve in order to be fluid responsive. Although it is not possible to monitor continuously, echocardiographic assessment of inferior and superior vena cava distensibility and collapsibility, respectively, have shown to accurately predict fluid responsiveness [32, 33]. Various other methods have been developed, such as the end-expiratory occlusion test, upper arm occlusion pressure and PEEP–induced increase in central venous pressure, to predict fluid responsiveness while avoiding many of the caveats existing for SVV and PPV [34–36].
Clinical use of fluid responsiveness
However, continuous tracking of stroke volume at the bedside is preferable in clinical practice as it allows evaluation of fluid responsiveness at any time with or without subsequent fluid administrations. With the emergence of several pulse contour analysis methods using the arterial pressure waveforms, stroke volume can be measured continuously without the need for invasive pulmonary artery catheterisation [45–47]. This stroke volume calculation is primarily determined by the pressure decay profile and magnitude of the arterial pressure for a given arterial input impedance. However, very rapid changes in stroke volume occurring during a single breath may not be accurately detected. This can be explained by the possible change in arterial input impedance used to calculate stroke volume . Nevertheless, pulse contour analysis has shown the ability to track the less rapid changes in stroke volume induced by PLR with accurate prediction of fluid responsiveness in patients with spontaneous breathing activity . PLR–induced changes in pulse pressure, as a surrogate for stroke volume, has shown to predict the response to fluid loading as well . Nonetheless, changes in cardiac output upon PLR have been demonstrated to have a better predictive value compared with changes in pulse pressure . This difference can probably be explained by the fact that pulse pressure is not only a direct measure of stroke volume, but also depends on arterial compliance. In other words, the response of arterial pressure upon fluid loading is dependent on arterial tone in contrast to the response of stroke volume. This is important because the aim of haemodynamic resuscitation is not only maintaining adequate organ perfusion by optimising cardiac output, but providing sufficient organ perfusion pressure as well. The arterial pressure response upon fluid loading can be predicted using the PPV to SVV ratio as measure of arterial tone . Since pulse contour analysis has the ability to measure PPV as well as SVV, it is possible to predict ‘blood pressure responsiveness’ besides fluid responsiveness.
Surprisingly, no consensus exists on the exact amount and type of fluid loading nor the timing and cut-off value for cardiac output defining fluid responders. Even the recommended technique of stroke volume measurements or its derivatives such as pulse pressure and cardiac output have not been agreed upon. Although non-invasive measurement would be ideally suited for patients on the ward or for critically ill patients on initial presentation, plethysmographic waveform analysis has shown to be a weak predictor of fluid responsiveness upon PLR in patients with spontaneous breathing activity probably due to acute changes in vasomotor tone . In that respect the emergence of non-invasive bioreactance cardiac output measurements is promising, requiring only four electrodes attached to the body with the ability to predict fluid responsiveness upon PLR .
Fluid responsiveness assessment in daily medical practice is feasible when combining an induced change in cardiac preload while measuring the subsequent change in stroke volume or its derivatives such as pulse pressure on the other hand. In this way, one can dynamically elucidate the position of the patient on the combined venous return/cardiac function curve (Fig. 3) and predict the response to fluid loading. It is important to note that a rise in the delivery of oxygen to the tissues to prevent or treat organ hypoperfusion can be obtained through optimisation of the concentration and saturation of haemoglobin besides an increase in cardiac output. Even in the presence of increased delivery of oxygen, impaired oxygen extraction and consumption can be predominant, especially during sepsis. Furthermore, cardiac output is not only determined by preload and contractility, but in particular by afterload and heart rate as well, making the increase in cardiac output by fluid loading just part of the solution. Echocardiography remains advocated in unexplained haemodynamic instability to provide important information regarding contractility and loading conditions of the heart. Finally, trials outside the operating theatre with hard clinical endpoints on morbidity and mortality are needed to validate and stimulate the assessment of fluid responsiveness in critically ill patients.
‘To fill or not to fill’, that is the question frequently faced by physicians caring for haemodynamically unstable critically ill patients. To successfully predict fluid responsiveness, the response of stroke volume to fluid loading, two requirements must be met: on one hand a change in preload must be generated as well as measuring the subsequent changes in stroke volume or its derivatives such as pulse pressure on the other hand. Static markers of cardiac preload are therefore unable to predict fluid responsiveness with dynamic markers being superior. However, a regular heart rhythm and mechanical ventilation without spontaneous breathing activity with larger than currently recommended tidal volumes are necessary for dynamic parameters to predict fluid responsiveness limiting its clinical application. Passive leg raising is an easy alternative tool that can be applied at the bedside to effectively change preload temporarily. Increases in cardiac output by passive leg raising predict fluid responsiveness despite spontaneous breathing activity or cardiac arrhythmias. When used in combination with a direct measure of continuously tracking stroke volume and/or its derivatives, physicians are enabled to prevent and treat organ hypoperfusion at any time, while avoiding unnecessary and potentially harmful fluid loading and inotropics. Understanding the basic concepts of the connection between venous return and cardiac function is pivotal to accomplish tailor-made fluid titration in the treatment of haemodynamically unstable critically ill patients.
We would like to thank Carolien Paes for her assistance with the figure preparations.
No conflicts of interest, financial or otherwise, are declared by the authors.
Conflict of interests
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