I thank Dr Rodgers for his thoughtful comments. I agree that clinicians should treat calculated variables, be these related to acid-base status or hemodynamics, with a healthy degree of skepticism. However, although heart rate, mean arterial pressure, and cardiac output are the primary hemodynamic variables that should concern the intensivist, systemic vascular resistance (SVR) has a theoretical construct that may be useful. For example, if an intervention increases the cardiac output without a concomitant increase in mean arterial pressure, this is best explained by a fall in SVR. Among the articles cited in my review article,1 Pierrakos et al2 demonstrated a fall in SVR in patients who were volume responders, but it did not fall in the nonresponders. This is best explained by vasodilatation in the fluid responders. Similarly, using esophageal ultrasound, Monnet et al3 measured the cross-sectional area of the aorta before and after a fluid challenge and demonstrated an increase in area after volume expansion in the fluid responders but not in the fluid nonresponders. These clinical studies support the concept that fluid loading may have detrimental effects in both fluid responders and fluid nonresponders. Furthermore, to answer the question, “Should the term ‘systemic vascular resistance’ be banned,” I would say, no!