Critical Analysis, Critical Care: Central Venous Pressure Monitoring: What's the Evidence?
CVP isn't a reliable guide in making decisions about the use of fluid therapy to optimize perfusion.
Editor's note: This is the first in a series of quarterly columns from nurses at the University of Washington that will examine in depth the research underlying critical care practices.
consider the following hypothetical clinical situation : dications of hypoperfusion ,with low blood pressure and minimal urine output. The patient is central venous pressure CVP is 6 mmHg. How would you treat this patient? Would a fluid bolus improve the patient is blood pressure and perfusion status, or would the administration of a vasopressor be a more appropriate therapy? And what evidence should you use to guide your decision making?
CVP, a hemodynamic parameter commonly used in critical care, is measured from a central venous or pulmonary artery catheter and is an indirect indicator of right ventricular preload.(See Hemodynamic Definitions and Principles for an explanation of many of the terms used in this article.) Preload is the amount of myocardial fiber stretch at the end of diastole: according to the Frank-Starling law of the heart, Within limits, the greater the preload, the force of contraction and stroke volume. Normal CVP values range from 2 to 6 mmHg. One factor that affects preload is intravascular volume; thus, CVP has traditionally been used to estimate intravascular volume. The assumption is that a low CVP value indicates an intravascular volume deficit. If there are indications that a patient has poor perfusion and also has low CVP , fluids may be administered to improve preload and stroke volume. In contrast, a high CVP value suggests intravascular volume overload ,in which case therapy may include diuretics or the administration of medications to strengthen myocardial contraction (inotropes) or alter vascular tone (vasodilators).
A 2008 systematic review of the literature by Marik and colleagues concluded that CVP is not an acurate indicator of intravascular volume, nor is it an accurate predictor of fluid responsiveness that is whether a patient will respond to a fluid bolus with an increase in stroke volume. Further, the authors suggested that the routine use of CVP monitoring should be abandoned until supporting data are published, because CVP values can misguide providers and lead to serious clinical errors. Given that a 2008 update to the international guidelines promulgated by the Surviving Sepsis Campaign specify a range of CVP values as a primary end point of goal-directed therapy, the findings and recommendations of Marik and colleagues become all the more compelling. Also, because studies did not find better outcomes in patients who had pulmonary artery catheters placed , use of these has declined over the past decade and clinicians have increasingly relied on assessment of CVP to guide decisions about fluid management.
To support discussion among critical care clinicians about the role of CVP monitoring in making decisions about fluid therapy, we review the evidence behind the assumptions supporting the use of CVP in critically ill patients. The specific questions addressed here include:(1) Is there a relationship between intravascular volume and CVP? (2)Can the absolute CVP value be used to predict whether a patient will or will not respond to a fluid bolus with an increase in stroke volume?(3) Is there a CVP value below which patients are likely to respond to a fluid bolus?
The answer to all of these questions is"No," which means that the assumptions we hold regarding CVP monitoring to guide fluid therapy are not supported by evidence. We also provide a primer on the statistics commonly used in studies evaluating the utility of CVP. The statistics are presented to enhance the reader is ability to be a "smart consumer" to evidence.