Volume Management in Critically Ill Patients

US Cardiology, 2007;4(2):47-8

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.

References:
  1. Michard F, Teboul JL, Predicting fluid responsiveness in ICU patients: a critical analysis of the evidence, Chest, 2002;121: 2000–2008.
  2. Berkenstadt H, Margalit N, Hadani M, et al., Stroke volume variation as a predictor of fluid responsiveness in patients undergoing brain surgery, Anesth Analg, 2001;92:984–9.
  3. Reuter DA, Felbinger TW, Schmidt C, et al., Stroke volume variations for assessment of cardiac responsiveness to volume loading in mechanically ventilated patients after cardiac surgery, Intensive Care Med, 2002;28:392–8.
  4. Marx G, Cope T, McCrossan L, et al., Assessing fluid responsiveness by stroke volume variation in mechanically ventilated patients with severe sepsis, Eur J Anaesth, 2004; 21:132–8.
  5. Hofer CK, Muller SM, Furrer L, et al., Stroke volume and pulse pressure variation for prediction of fluid responsiveness in patients undergoing off-pump coronary artery bypass grafting, Chest, 2005;128:848–54.
  6. Michard F, Changes in arterial pressure during mechanical ventilation, Anesthesiology, 2005;103:419–28
  7. Kumar A, Anel R, Bunnell E, et al., Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects, Crit Care Med, 2004;32:691–9.
  8. Osman D, Ridel C, Ray P, et al., Cardiac filling pressures are not appropriate to predict hemodynamic response to volume challenge, Crit Care Med, 2007;35:64–8.
  9. Pinsky M, Vincent JL, De Smet JM, Estimating left ventricular filling pressure during positive end-expiratory pressure in humans, Am Rev Respir Dis, 1991;143:993–4.
  10. Michard F, Volume management using dynamic parameters: the good, the bad, and the ugly, Chest, 2005;128:1902–3.
  11. Monnet X, Rienzo M, Osman D, et al., Passive leg raising predicts fluid responsiveness in the critically ill, Crit Care Med, 2006;34: 1402–7.
  12. Hamzaoui O, Monnet X, Richard C, et al., Effects of changes in vascular tone on the agreement between pulse contour and transpulmonary thermodilution cardiac output measurements within an up to 6-hour calibration-free period, Crit Care Med, 2008;36:434–40.
  13. de Wall EE, Kalkman CJ, Rex S, Buhre WF, Validation of a new arterial pulse contour-based cardiac output device, Crit Care Med, 2007;35:1904–9.
  14. Button D,Weibel L, Reuthebuch O, et al., Clinical evaluation of the FloTrac/VigileoTM system and two established continuous cardiac output monitoring devices in patients undergoing cardiac surgery, Br J Anaesth, 2007;99(3):329–36.
  15. Prasser C, Trabold B, Schwab A, et al., Evaluation of an improved algorithm for arterial pressure-based cardiac output assessment without external calibration, Intensive Care Med, 2007;33:2223–5.
  16. Mayer J, Boldt J,Wolf MW, et al., Cardiac output derived from arterial pressure waveform analysis in patients undergoing cardiac surgery: validity of a second generation device, Anesth Analg, 2008; in press.

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