This is part of a recurring series examining landmark articles in Emergency Medicine, in the style of ALiEM’s 52 Articles
Emergency Department Bedside Ultrasonographic Measurement of the Caval Index for Noninvasive Determination of Low Central Venous Pressure
- Adults (n=73) that were going to get central lines were enrolled in this prospective, observational study.
- Patients had both the collapsability of their IVC (caval index) and their CVP measured by different people blinded to the results of the other test.
- There was a correlation between IVC collapsability greater than or equal to 50% and CVP < 8 mm Hg.
The holy grail in resuscitation remains how to determine a patient’s volume status and fluid responsiveness. In spite of advances in technology and hemodynamic monitoring, we continue to rely on surrogate markers -- like CVP -- for volume status. Early Goal-Directed Therapy, based on the Surviving Sepsis campaign, has suggested a CVP of < 8 mmHg as an indicator for “aggressive” IVF. This study was performed to see if we could get the same information from ultrasound, instead of needing to place a central line.
Past studies have shown that caval index (the percent the IVC collapses with each respiratory cycle) can be estimated by specialists other than EPs, and that a high percentage of collapse was associated with lower CVP. This is the first study to evaluate EPs’ use of this method of hemodynamic monitoring, and was done right here at Brown!
This was a prospective observational study performed in the critical care rooms at RIH on a convenience sample of patients who were going to have central lines placed for treatment or monitoring, as deemed necessary by the treating physician. All patients were able to have both ultrasound and CVP measured (otherwise they were excluded).
The IVC was measured in supine patients, 2-3 cm from the right atrial border in a subxiphoid view with a curvilinear probe.
4 different ED doctors obtained measurements for the study, and all 4 had training consisting of 5 scans performed with the lead author before enrolling patients. CVP measurement was obtained by nursing staff after IVC ultrasound was obtained, and the EPs were blinded to it. Treating physicians were blinded to the ultrasound results.
Researchers who were blinded to study results noted time from ultrasound completion to CVP measurement, and amount of fluid given in between these two events.
82 were enrolled, 9 were excluded due to inability to measure the IVC. Each 12.5% increase in IVC and caval index was predictive of a 1-mm Hg decrease in CVP, and none of the other extracted variables were related to either.
Limitations include relatively small sample size, convenience sample, lack of standardization of time between ultrasound and CVP measurement, as well as lack of applicability in that 9 out of 82 patients were unable to have the study done.
Looking beyond structural limitations, recent literature has challenged the use of CVP as a means to measure intravascular volume, though in some contexts and settings it is still regularly used. High CVP can be caused by a number of factors, including cardiac valvular or contractile dysfunction, and pulmonary hypertension. The authors cite a recent meta-analysis that challenges the use of CVP before stating that low CVP “may be a good marker the patient will be fluid responsive”, referring to a study that suggests a CVP < 10 mm Hg had the greatest response in cardiac output.
Level of Evidence:
ACEP Clinical Policies Committee Level III evidence
Resident Reviewer: Dr. Anatoly Kazakin
Faculty Reviewer: Dr. Matt Siket
Magder S, Bafaqeeh F. The clinical role of central venous pressure measurements. J Intensive Care Med. 2007;22:44-51. http://www.ncbi.nlm.nih.gov/pubmed/?term=J+Intensive+Care+Med.2007%3B22%3A44-51.
Brennan JM, Ronan A, Goonewardena S, et al. Handcarried ultrasound measurement of the inferior vena cava for assessment of intravascular volume status in the outpatient hemodialysis clinic. Clin J Am Soc Nephrol. 2006;1:749-753. http://www.ncbi.nlm.nih.gov/pubmed/?term=Clin+J+Am+Soc+Nephrol.+2006%3B1%3A749-753.