Response

Abstract

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,1Marik PE Early management of severe sepsis: concepts and controversies.Chest. 2014; 145: 1407-1418Abstract Full Text Full Text PDF PubMed Scopus (70) Google Scholar Pierrakos et al2Pierrakos C Velissaris D Scolletta S Heenen S De Backer D Vincent JL Can changes in arterial pressure be used to detect changes in cardiac index during fluid challenge in patients with septic shock?.Intensive Care Med. 2012; 38: 422-428Crossref PubMed Scopus (110) Google Scholar 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 al3Monnet X Chemla D Osman D et al.Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness.Crit Care Med. 2007; 35: 477-482Crossref PubMed Scopus (69) Google Scholar 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! Systemic Vascular Resistance Should Be BannedCHESTVol. 146Issue 4PreviewIn 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. Full-Text PDF