Central venous pressure
Central venous pressure (CVP) (also known as: right atrial pressure; RAP) describes the pressure of blood in the thoracic vena cava, near the right atrium of the heart. CVP reflects the amount of blood returning to the heart and the ability of the heart to pump the blood into the arterial system.
It is a good approximation of right atrial pressure, which is a major determinant of right ventricular end diastolic volume. CVP has been, and often still is, used as a surrogate for preload, and changes in CVP in response to infusions of intravenous fluid have been used to predict volume-responsiveness (i.e. whether more fluid will improve cardiac output). However, there is increasing evidence that CVP, whether as an absolute value or in terms of changes in response to fluid, does not correlate with ventricular volume (i.e. preload) or volume-responsiveness, and so should not be used to guide intravenous fluid therapy. Nevertheless, CVP monitoring is a useful tool to guide hemodynamic therapy. The cardiopulmonary baroreflex responds to an increase in CVP by decreasing total peripheral resistance while increasing HR and ventricular contractility in dogs.
|Central venous pressure||3–8|
|Right ventricular pressure||systolic||15–30|
|Pulmonary artery pressure||systolic||15–30|
|Left ventricular pressure||systolic||100–140|
Normal CVP can be measured from two points of reference:
CVP can be measured by connecting the patient's central venous catheter to a special infusion set which is connected to a small diameter water column. If the water column is calibrated properly the height of the column indicates the CVP.
In most intensive care units, facilities are available to measure CVP continuously.
Normal values are 5-10 cmH20 
Factors affecting CVP
Factors that increase CVP include:
- forced exhalation
- Tension pneumothorax
- Heart failure
- Pleural effusion
- Decreased cardiac output
- Cardiac tamponade
- Mechanical ventilation and the application of positive end-expiratory pressure (PEEP)
- Pulmonary Hypertension
- Pulmonary Embolism
Factors that decrease CVP include:
- "Central Venous Catheter Physiology". Retrieved 2009-02-27.
- Kumar A, Anel R, Bunnell E, Habet K, Zanotti S, Marshall S et al. (2004). "Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects". Crit Care Med 32 (3).
- Marik P, Baram M, Vahid B (July 2008). "Does Central Venous Pressure Predict Fluid Responsiveness?". Chest 134 (1). doi:10.1378/chest.08-1846.
- Sala-Mercado JA, Moslehpour M, Hammond RL, Ichinose M, Chen X, Evan S, O'Leary DS, Mukkamala R (June 2014). "Stimulation of the Cardiopulmonary Baroreflex Enhances Ventricular Contractility in Awake Dogs: A Mathematical Analysis Study". American Journal of Physiology - Regulatory, Integrative and Comparative Physiology 307 (4): R455–R464. doi:10.1152/ajpregu.00510.2013.
- Table 30-1 in: Trudie A Goers; Washington University School of Medicine Department of Surgery; Klingensmith, Mary E; Li Ern Chen; Sean C Glasgow (2008). The Washington manual of surgery. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. ISBN 0-7817-7447-0.
- Egan's Fundamentals of Respiratory Care 9th ed, p. 1140
- Venous function and central venous pressure: a physiologic story - a technical discussion of the more modern understanding of central venous pressure; this may well conflict with the sources below.
- Central Venous Pressure Monitoring
- Cardiovascular Physiology Concepts
- Central Venous Pressure and Pulmonary Capillary Wedge Monitoring
- Cardiovascular Physiology
- Central Venous Pressure at the US National Library of Medicine Medical Subject Headings (MeSH)