Volume expansion is one of the most common therapeutic procedures in intensive care units (ICUs). There is no doubt that in some cases (e.g. hemorrhage or severe diarrhea) care-givers can reasonably rely on clinical examination to identify patients who will benefit from fluid loading. However, in more complex—but not uncommon—situations (e.g. septic shock), both clinical examination and indicators of cardiac pre-load have been shown to be of minimal value in answering the question: “Can we improve cardiac output and hence hemodynamics by administering fluid?”1
Over the last decade, many clinical studies have demonstrated the value of stroke volume variation (SVV) induced by mechanical ventilation to predict fluid responsiveness, i.e. an increase in cardiac output as a result of fluid infusion.2–6 SVV is now automatically calculated and displayed on minimally invasive cardiac output monitors. This should greatly facilitate the volume management of critically ill patients.
In the following interview, Frédéric Michard, MD, PhD, discusses some of the important matters relating to the volume management of critically ill patients using SVV and new cardiac output monitoring technologies.
Q. Fluid therapy is often used to increase cardiac pre-load and improve the hemodynamic status of patients with circulatory shock. However, cardiac output increases after a fluid challenge in only approximately 50% of such patients. What is the clinical significance of this observation?
A: Only 50% of patients with shock experience a significant increase in cardiac output in response to fluid administration when the decision to give fluid is based on the clinical examination or on the measurement of cardiac filling pressures.1 This observation means that, until recently, clinicians were unable to accurately identify patients who could benefit from fluid expansion—in other words, fluid-responsive patients.
Over the last few years, the concept of fluid responsiveness has become popular in Europe and South America, likely because it is a pragmatic approach to fluid therapy. Indeed, we have a clear idea of the normal total blood volume (800–1,000ml/m2), and of normal right and left ventricular end-diastolic volumes (90–110ml/m2 and 60–80ml/m2, respectively) in healthy subjects.
However, it is much more difficult to determine which level of pre-load is optimal in an ‘abnormal’ situation, e.g. vasodilation induced by sepsis. Therefore, a practical approach to determine fluid therapy consists of detecting patients who will be able to turn fluid loading into a significant increase in SV and cardiac output. Of course, clinical end-points of fluid therapy are usually different, e.g. increasing blood pressure or urine output, but will be achieved only if the physiological effect (an increase in SV and cardiac output according to the Frank-Starling mechanism) occurs first. If not, fluid administration is useless or even potentially harmful, e.g. leading to a worsening in pulmonary edema.
How useful are standard pre-load indices such as central venous pressure and pulmonary capillary wedge pressure in predicting cardiac response to fluid therapy?
Many clinical studies have demonstrated that central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) are not always useful for predicting cardiac response to fluid therapy.7,8 For example, some patients can respond positively to fluid administration while the CVP and PCWP are elevated. Indeed, CVP and PCWP are often overestimated in patients whose lungs are being mechanically ventilated with positive end-expiratory pressure (PEEP).9 CVP and PCWP are also overestimated in patients with dynamic hyperinflation; that is, in patients with auto-PEEP, e.g. in patients with chronic obstructive pulmonary disease (COPD).
Overestimation of CVP and PCWP can also occur in patients with abdominal hypertension. In fact, all of these situations are quite common in critically ill patients, and that is one of the reasons why cardiac filling pressures are not always accurate in predicting cardiac response to fluid therapy.
We also must keep in mind that the physiological relationship between ventricular end-diastolic pressure and volume is not linear but curvilinear, and highly dependent on cardiac compliance. This means that a given CVP or PCWP value can be associated with a different cardiac filling volume in two patients in whom ventricular compliance is different.
Assessment of stroke volume variation has been proposed to guide fluid therapy in patients receiving mechanical ventilation. Could you comment on the rationale for using stroke volume variation?
By increasing pleural pressure, mechanical inspiration induces cyclic variations in cardiac pre-load that may be turned into cyclic changes in left ventricular SV.6 SVV is neither an indicator of volume status nor a marker of cardiac pre-load, but rather is an indicator of the position on the Frank-Starling curve. In brief, in patients operating on the flat portion of the Frank-Starling curve, SVV is low (<12%) and volume loading does not result in a significant increase in SV. Conversely, in patients operating on the steep portion of the pre-load–SV relationship (and who are thus sensitive to cyclic changes in pre-load induced by mechanical ventilation), SVV is high (>12%) and volume loading leads to a significant increase in SV.
It is important to understand that fluid responsiveness (SVV >12%) does not mean that fluid is needed.10 Most healthy subjects are fluid-responsive. Fortunately, it does not mean that they need volume expansion. Before using SVV, the first question must be: “Does my patient need an increase in SV or in cardiac output?” SVV will not definitively answer this question. To answer this, both clinical examination—e.g. hypotension, mottling, and oliguria—and biological tests—e.g. renal failure and lactate concentration— are of value, but they lack sensitivity and specificity to identify patients in whom cardiac output is insufficient. Venous oxygen saturation is the gold standard for defining global adequacy between oxygen transport and oxygen demand, and can be used as a trigger for deciding to increase cardiac output.
Are there limitations to the use of stroke volume variation?
First, in patients with cardiac arrhythmia the beat-to-beat variation in SV may no longer reflect the effects of mechanical ventilation.10 This is a limitation only in patients with atrial fibrillation or frequent extrasystoles. Indeed, most SVV calculation software is now able to detect and exclude few (and far between) premature heart beats, and hence provide an accurate estimation of SVV even in this context.
Second, if pleural pressure changes are small over a single respiratory cycle, cardiac pre-load changes will be small and inspiration will not induce any significant change in SV, even in fluid-responsive patients.10 Small variations in pleural pressure may be observed in spontaneously breathing patients, in patients receiving mechanical ventilation with small tidal volumes, e.g. 6ml/kg, or in patients with increased chest compliance, e.g. open chest. In this context, caution should be exercised before concluding that a patient will not respond to a fluid challenge because SVV is low (false-negative). However, a high SVV is usually indicative that the patient will be fluid-responsive.
In terms of predicting fluid responsiveness in such patients, how would you overcome the limitations in the use of stroke volume variation?
In situations where it is not possible to use SVV, it can be useful to mimic the effects of fluid loading by a passive leg raising (PLR) maneuver, and to check the efficacy of such a maneuver on SV and cardiac output online. PLR at 45º can effectively translocate the venous blood in the legs to the intrathoracic compartment. In patients who are pre-load-responsive, this creates a transient increase in cardiac output. Clinical studies have confirmed that if a patient is responding to PLR, he or she will be responsive to fluid administration.11 The PLR test is reversible. Therefore, it is particularly useful in patients at risk for fluid-loading-related complications, e.g. patients with severe hypoxemia. In other patients, the continuous monitoring of SV and cardiac output during a fluid challenge, e.g. 250ml of fluid over a short period of time, can be used to check online the efficacy of fluid therapy.
The continuous monitoring of cardiac output is now possible using minimally invasive technologies. Most of them are based on the analysis of the arterial pressure tracing and require frequent manual recalibrations by an independent technique of cardiac output measurement.12 A method that does not require intermittent manual calibration does exist on the market, and has the great advantage of being easy to set up. Importantly, it automatically adjusts to changes in vascular tone every minute, and has been shown to be as accurate as other methods.13–16