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Paul E. Marik, MD
Author and Funding Information

From the Division of Pulmonary and Critical Care Medicine, Eastern Virginia Medical School.

CORRESPONDENCE TO: Paul E. Marik, MD, Virginia Medical School, 825 Fairfax Ave, Ste 410, Norfolk, VA 23507; e-mail: marikpe@evms.edu


FINANCIAL/NONFINANCIAL DISCLOSURES: The author has reported to CHEST the following conflicts of interest: In the last three years Dr Marik has received an honorarium from Pulsion Medical, manufacturer of the PiCCO hemodynamic device, for a lecture delivered at an International Critical Care Symposium and an honorarium from Cheetah Medical, manufacturer of the NiCOM hemodynamic device, for a lecture delivered at medical grand rounds.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2014;146(4):e143-e144. doi:10.1378/chest.14-1460
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To the Editor:

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!

References

Marik PE. Early management of severe sepsis: concepts and controversies. Chest. 2014;145(6):1407-1418. [CrossRef] [PubMed]
 
Pierrakos 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(3):422-428. [CrossRef] [PubMed]
 
Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med. 2007;35(2):477-482. [CrossRef] [PubMed]
 

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Tables

References

Marik PE. Early management of severe sepsis: concepts and controversies. Chest. 2014;145(6):1407-1418. [CrossRef] [PubMed]
 
Pierrakos 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(3):422-428. [CrossRef] [PubMed]
 
Monnet X, Chemla D, Osman D, et al. Measuring aortic diameter improves accuracy of esophageal Doppler in assessing fluid responsiveness. Crit Care Med. 2007;35(2):477-482. [CrossRef] [PubMed]
 
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