CVP Measurement

Reviewed and revised 14 March 2023


Central venous pressure (CVP) is the pressure recorded from the right atrium or superior vena cava and is representative of the filling pressure of the right side of the heart

  • CVP monitoring in the critically ill is established practice but the traditional belief that CVP reflects ventricular preload and predicts fluid responsiveness has been challenged by a large body of evidence
  • CVP represents the driving force for filling the right atrium and ventricle
  • normal is 0-6mmHg in a spontaneously breathing non-ventilated patient


  • recorded at the end of expiration
  • measured by transducing the waveform of a central venous line
  • electronic transducer placed & zeroed at the level of the RA (the “phlebostatic axis” – usually the 4th intercostal space in the mid-axillary line is used)


a = atrial contraction
c = closing and bulging of the tricuspid valve
x = atrial relaxation, with downward movement of the tricuspid valve during ventricular contraction
v = passive filling of atrium (tricuspid valve still closed)
y = ventricular filling with opening of the tricuspid valve

CVP waveform, alongside ECG, showing the key components and their timing related to systole and diastole. Image from: Bootsma et al, 2022 (Figure 1).(Click image for source)


CVP approx = RAP

VR = MSFP – RAP / Resistance to venous return

ΔCVP = ΔV / Cv

  • ΔCVP-> change in CVP
  • ΔV -> change in venous blood volume
  • Cv -> venous compliance

Determinants include:

  • right atrial pressure
  • intravascular fluid volume
  • venous capacitance/ tone
  • mean systemic filling pressure
  • right and left ventricular function and compliance
  • pulmonary vascular resistance
  • intrathoracic/pleural pressure
  • intrabdominal pressure


Value and waveform assists with diagnosis of:

  • right ventricular infarction
  • right heart failure and cor pulmonale
  • tamponade
  • Tricuspid regurgitation or stenosis
  • Complete heart block
  • Constrictive pericarditis


  • mechanical atrial capture with AV pacing
  • presence of P waves in cases of SVT
  • differential diagnosis of shock state
  • correct central line placement

Do not use CVP in isolation to assess fluid responsiveness

  • very poor relationship between CVP and blood volume and CVP/DeltaCVP is a poor predictor of the hemodynamic response to a fluid challenge
  • interpretation of CVP should be in association with information relating to other haemodynamic variables


  • Right ventricular failure
  • Tricuspid stenosis or regurgitation
  • Pericardial effusion or constrictive pericarditis
  • Superior vena caval obstruction
  • Fluid overload
  • Hyperdynamic circulation
  • High PEEP settings


Waveform abnormalities may indicate specific pathologies:

  • Dominant a wave – pulmonary hypertension, tricuspid stenosis, pulmonary stenosis
  • Cannon a wave – complete heart block, ventricular tachycardia with atrio-ventricular dissociation
  • Dominant v wave – tricuspid regurgitation
  • Absent x descent – atrial fibrillation
  • Exaggerated x descent – pericardial tamponade, constrictive pericarditis
  • Sharp y descent – severe tricuspid regurgitation, constrictive pericarditis
  • Slow y descent – tricuspid stenosis, atrial myxoma
  • Prominent x and y descent – right ventricular infarction
Figure 2. Important cardiac pathologies and their CVP waveforms. Image from: Bootsma et al, 2022. (Figure 2) (Click image for source).


CVP measurement should be performed at end-expiration, without fluids running

  • Placement of device tip (RA, RV, SVC, SCV, femoral vein)
  • Leveling – the position on the patient that you want to be zero (usually level of RA, the “phlebostatic axis”))
  • Zeroing – zero means atmospheric pressure
  • Calibration – comparing zero and a level above to a gold standard (mercury sphygmomanometer)
  • Damping – assess by a fast flush test, preferred co-efficient around 0.7
  • Frequency response of the system (intrinsic + additional tubing) -> may significantly alter damping (preferred shorter stiffer tubing)
  • Running averages rather than single spontaneous readings
  • PEEP — PEEP of 10 cmH20 usually results in increase of CVP by ~3 cmH20 (depends on lung compliance)


  • minimal difference between SVC and femoral CVP measurements in the supine patient (in the absence of intra-abdominal hypertension)
  • CVP cannot be measured if fluid is running through the same lumen, but if flow rates are slow CVP is minimally affected by infusions through other lumens of the same CVC

Journal articles

  • Bootsma, I.T., Boerma, E.C., de Lange, F. et al. The contemporary pulmonary artery catheter. Part 1: placement and waveform analysis. J Clin Monit Comput 36, 5–15 (2022). https://doi.org/10.1007/s10877-021-00662-8 [article]
  • 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 Jul;134(1):172-8. doi: 10.1378/chest.07-2331. PMID: 18628220.
  • Patrick SP, Tijunelis MA, Johnson S, Herbert ME. Supraclavicular subclavian vein catheterization: the forgotten central line. West J Emerg Med. 2009 May;10(2):110-4. PMC2691520.

FOAM and web resources

  • DerangedPhysiology.com — The CVC

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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