In an article published in a recent issue of CHEST (June 2014), Marik1 mentioned, “In patients with septic shock who are fluid responders (an increase in cardiac output with fluid boluses), vasodilatation with a fall in systematic vascular resistance has been observed….Hence, although the cardiac output increases, vasodilatation occurs.” I believe that this statement is erroneous because there is no way to measure vasodilatation quantitatively. The decrease in systemic vascular resistance (SVR) is simply due to mathematical coupling: SVR = (mean arterial pressure − central venous pressure)/cardiac output. According to this equation, SVR must decrease if the cardiac output increases, but in the patient, this does not have to be the case and could lead to dangerous errors in patient management. This error in thinking is made time and again in publications and clinical practice. I believe that SVR is meaningless in clinical practice because it simply does not indicate whether the patient is vasodilated. It is a term derived from Ohm’s law on electrical circuits and has no place in the treatment of patients.