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Correspondence |

Central Venous Pressure as Popular Resuscitation Surrogate: Not Totally Unjustified FREE TO VIEW

Nishith K. Singh, MD; Gaurav Sangwan, MD; Peter White, MD
Author and Funding Information

Southern Illinois University School of Medicine Springfield, IL

Correspondence to: Nishith K. Singh, MD, Department of Internal Medicine, Southern Illinois University School of Medicine, 701 N First St, Springfield, IL 62794-9636


The authors have no conflicts of interest to disclose.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/misc/reprints.shtml).


Chest. 2008;134(6):1352. doi:10.1378/chest.08-2024
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To the Editor:

Marik and colleagues,1 using statistical analysis and data from controlled studies, show that isolated central venous pressure (CVP) measurements are a poor guide to the assessment of volume status and fluid responsiveness. They called attention to a common myth that CVP is a good guide to fluid management. It is an interesting reminder of related misconceptions in classical works of cardiovascular physiology. For instance, the experiments of Guyton and Starling are commonly misunderstood. The pump is commonly seen as the main orchestrator of output. Guyton's experiments demonstrated the role of peripheral vasculature in controlling cardiac output.2 Physicians commonly mistake venous inflow to the atria as the determinant of left ventricular stroke volume. Starling, working on denervated hearts, showed that atrial filling and thus “ventricular wall stretch” was the primary determinant of stroke volume.3 Perhaps these misconceptions are a result of confusion between the cause and the consequence.

CVP is affected by a myriad of intrinsic and extrinsic factors including IV fluids, positioning, intrathoracic pressures, heart rate, contractility, and myocardial and venous compliance, among others. Further confusing the issue is discrepancy between normal physiology and disease state pathology. As an example, sepsis alters total effective vascular compliance.4 Thus while CVP reflects mean right atrial pressure, it is not expected to show an independent correlation with effective circulatory blood volume.

Apparently, it is the intuitive simplicity of CVP that attracts a new learner as compared to the lack of receptiveness encountered with terms such as upstream and downstream resistance, flow limitation, and capacitance. The CVP-centric practice may also be widespread because it comes with convenience and there are no controlled studies that prove definite disadvantage related to the method use for fluid management. The 2008 Surviving Sepsis Campaign guidelines say “… recommend fluid resuscitation initially target a CVP of at least 8 mm Hg.”5 Justification of this statement is mostly based on a single study. The attempt at getting at least one of the determinants (CVP in this case) of cardiac output right, ie, achieving physiologic limits, may be a reasonable approach toward attempting to optimize perfusion in critically ill patients.

To conclude, we feel that the findings reported by Marik and colleagues are not unexpected. CVP remains meaningful along with the other parameters (BP, heart rate, urine output, extra heart sounds, cool extremities, fractional excretion of sodium) that are used by experienced clinicians to assess volume status.

Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness?: a systematic review of the literature and the tale of seven mares. Chest. 2008;134:172-178. [PubMed] [CrossRef]
 
Guyton AC. Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev. 1955;35:123-129. [PubMed]
 
Reddi BA, Carpenter RH. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol. 2005;98:356-364. [PubMed]
 
Stephan F, Novara A, Tournier B, et al. Determination of total effective vascular compliance in patients with sepsis syndrome. Am J Respir Crit Care Med. 1998;157:50-56. [PubMed]
 
Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock; 2008. Intensive Care Med. 2008;34:17-60. [PubMed]
 

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References

Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness?: a systematic review of the literature and the tale of seven mares. Chest. 2008;134:172-178. [PubMed] [CrossRef]
 
Guyton AC. Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev. 1955;35:123-129. [PubMed]
 
Reddi BA, Carpenter RH. Venous excess: a new approach to cardiovascular control and its teaching. J Appl Physiol. 2005;98:356-364. [PubMed]
 
Stephan F, Novara A, Tournier B, et al. Determination of total effective vascular compliance in patients with sepsis syndrome. Am J Respir Crit Care Med. 1998;157:50-56. [PubMed]
 
Dellinger RP, Levy MM, Carlet JM, et al. Surviving Sepsis Campaign: international guidelines for management of severe sepsis and septic shock; 2008. Intensive Care Med. 2008;34:17-60. [PubMed]
 
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