Fluid resuscitation plays an important role in the resuscitation of critically unwell patients. In particular, early goal directed therapy (or EGDT) aimed at normalizing central venous oxygen saturation and plasma [lactate] has been shown to improve clinical outcome in patients presenting with septic shock  and has consequently been adopted into sepsis management protocols across the world [2,3]. Similarly, the early work in this field by Shoemaker et al. to provide ‘supra-normal oxygen delivery’ to deal with the ‘oxygen dept’ which is latent in critically unwell septic patients who proceed to develop multiple organ failure has also left a lasting impression in the collective memory of the critical care fraternity [4,5]. For these reasons, monitoring adequacy of tissue perfusion- directly or indirectly, is considered desirable and is widely practiced in high-risk patients. The inability or the unreliability of arterial blood pressure to serve as a surrogate marker of global or regional blood flow due to compensatory vasoconstriction, has led to several alternate measures of blood flow to be adopted as end-points in guiding this ‘aggressive’ fluid therapy. In this context, intermittent or more continuous measurements of cardiac output, utilizing one of the several technologies currently available for bedside are widely practiced as standard care in many critical care units. In the United Kingdom the National Institute of Clinical Excellence (NICE), recently came up with recommendations encouraging the use of one of these technologies/devices for measuring cardiac output to optimize fluid therapy even during the peri-operative period (http://www.nice.org.uk/MTG3 – accessed 21st November 2013) . As opposed to a single or continuous measurement of cardiac output, some groups have advocated the concept of ‘fluid responsiveness’ as a more dynamic marker to guide fluid therapy in these patient groups [7,8].
The age-old Frank–Starling curve is frequently used to illustrate the physiological principles that underpin many of the recommendations that currently guide fluid resuscitation in these patient groups. The general premise advocated is that patients who show a > 10% in stroke volume following an ‘external’ or an ‘internal’ fluid challenge' associated with infusion of a fluid bolus or passive leg raising, respectively are deemed to operate on the steep portion of the Frank–Starling curve and classified as being ‘fluid responsive’. Patients classified as being ‘fluid responsive’ is argued, require more fluids, in small or large aliquots, until they are not ‘fluid responsive’ any more  (or the stroke volume does not increase by >10% following a fluid challenge). In other words, the current dogma in the field is that we need to ensure that all our patients are in fact operating on the ‘flat portion’ of the Frank–Starling curve, in order to optimize their cardiac performances . Until this end point is achieved fluids, more fluids and even more fluids should be the mainstay of therapy…or so the argument goes.
The fundamental fallacy inherent in the above argument is that, virtually none of us – leading perfectly normal lives, doing our day-to-day activities, running marathons, playing football etc. in fact operate on the ‘flat portion’ of our Frank–Starling curves. All of us – you and me included, will increase our stroke volumes when challenged with a bolus of fluid administered either as an external infusion or as an auto transfusion by passively raising our legs. Physiological reserve and the ability to increase our cardiac performance during a physiological challenge – through the flight, fright and fight responses, is an evolutionary imperative. We see the existence of such physiological reserves virtually in every organ system in the body. For example it is well known that we all utilize only a tiny proportion of the hepatocytes, cerebral neurons or capacity for oxygen delivery during ordinary healthy living. What then is the rationale in insisting that all our critically unwell and peri-operative patients should be made to lose this physiological reserve in cardiac performance – which has presumably evolved over several millennia, by dragging them up the Frank–Staling curve virtually ‘kicking and screaming’…it does not make physiological sense. No wonder then none of the hemodynamic monitoring strategies, to date, have been shown to be superior or to significantly alter clinical outcome in carefully designed prospective randomized clinical trials [10,11]. If the end-points chosen (fluid administration until patients are moved to the flat portion of the Frank–Starling curve) are physiologically unsound, why would one expect one method (pulmonary artery catheter for example) of achieving this ‘flawed’ end point to be better than another way of doing so?
How then should we determine whether or not our patients require fluid therapy. In my view, the first step in this iteration should always be a clinical/biochemical assessment of the patient in order to determine whether or not the patient is fluid depleted. This could be in the form of the presence or absence of thirst (in conscious patients), capillary filling time, skin turgor, state of the skin and mucous membranes, plasma [lactate], cumulative fluid balance and perhaps venous oxygen saturation. Sorry, there are no automated, algorithm driven shortcuts/alternatives to this old-fashioned bedside assessment by a qualified clinician. Of course none of these are perfect or even suitable in every single patient we come across in the ICU. But, the key point is every effort must be made to make this initial clinical assessment as to whether the patient is fluid depleted or not. It is then and only then should one resort to applying the concept of ‘fluid responsiveness’ to determine the volume of fluid that should be administered. It must always be kept in mind that in such patients, if the volume administered is such that the patients are not ‘fluid responsive’ any more, the chances are that we have over done the task…and that have adverse consequences on patient outcome. The current dogma in this field – that I have heard repeatedly at virtually every critical care conference/meeting I have attended over the past 20 years or so, encourages this ‘flawed’ logic. We must remember at all times that all of us…even those of us who are lining up to start the London Marathon, are by design ‘fluid responsive’.
 Rivers E, Nguyen B, Havstad S, Ressler J, Muzzin A, Knoblich B, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001;345:1368-1377.
 Dellinger RP, Carlet JM, Masur H, Gerlach H, Calandra T, Cohen J, et al. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. Crit Care Med 2004;32:858-873.
 Dellinger RP, Levy MM, Rhodes A, Annane D, Gerlach H, Opal SM, et al. Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012. Crit Care Med 2013;41:580-637.
 Shoemaker WC, Appel PL, Kram HB, Bishop MH, Abraham E. Sequence of physiologic patterns in surgical septic shock. Crit Care Med 1993;21:1876-1889.
 Shoemaker WC, Appel PL, Kram HB, Bishop MH, Abraham E. Temporal hemodynamic and oxygen transport patterns in medical patients. Septic Shock Chest 1993;104:1529-1536.
 Singer M. Oesophageal doppler monitoring: a not-so-NICE editorial. Anaesthesia 2012;67:428-430.
 Monnet X, Rienzo M, Osman D, Anguel N, Richard C, Pinsky MR, et al. Passive leg raising predicts fluid responsiveness in the critically ill. Crit Care Med 2006;34:1402-1407.
 Monnet X, Teboul JL. Volume responsiveness. Curr Opin Crit Care 2007;13:549-553.
 Marik PE, Monnet X, Teboul JL. Hemodynamic parameters to guide fluid therapy. Ann Intensive Care 2011;1:1.
 Harvey S, Harrison DA, Singer M, Ashcroft J, Jones CM, Elbourne D, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in management of patients in intensive care (PAC-Man): a randomised controlled trial. Lancet 2005;366:472-477.
 Sandham JD, Hull RD, Brant RF, Knox L, Pineo GF, Doig CJ, et al. A randomized, controlled trial of the use of pulmonary-artery catheters in high-risk surgical patients. N Engl J Med 2003;348:5-14.