Question 6

College Answer

It was expected that answers include central venous blood volume, central venous vascular compliance, intrathoracic pressure and tricuspid valvular function. Good answers outlined how each of these factors determine CVP and whether it was increased or decreased. Many candidates incorrectly described the effect of venous return.

Discussion

• Central venous pressire (CVP) is the venous blood pressure measured at or near the right atrium.
  • It is measured using a pressure transducer connected to a central line via incompressible tubing, with the transducer zeroed to atmoospheric pressure and levelled at the height of the right atrium.
  • The measurement is performed at end-expiration
• Physiologically, it is defined as the intersection of the vascular function curve and the cardiac output curve

Factors which determine CVP:

• Measurement technique:
  • Transducer position
  • Timing of measurement with the cardiac cycle: measurement should occur relative to the appropriate waveform position (eg. right atrial pressure which correlates best with right ventricular filling pressure is actually the pressure at the onset of the c-wave, rather than the "average" which is calculated by the monitoring software)
  • Timing of measurement with the respiratory cycle (ideally, the end-expiratory CVP is the only 'true" CVP)
• Central venous blood volume
  • Venous return and cardiac output (which determines venous return)
    • As cardiac contractility decreases, the CVP increases
  • Mean systemic filling pressure
    • Total blood volume
    • Vascular resistance 
    • As MSFP increases, so the CVP increases
• Central venous vascular compliance
  • Vascular tone of the central venous walls (greatly affected by noradrenaline, for example)
  • Right atrial and right ventricular compliance
    • Pericardial compliance (i.e. presence of fibrotic restrictive disease, or conversely presence of a pericardial window, pericardectomy, or something even more bizarre like an open mediastinum)
    • Myocardial compliance (eg. presence of stiff ischaemic scarring, or a the boggy oedematous wall of myocarditis)
    • Incompressible fluid in the pericardium, eg. tamponade
  • Pulmonary arterial compliance
    • Right ventricular outflow tract obstruction, for instance a big pulmonary embolus or pulmonary valve disease
    • Pulmonary hypertension
• Tricuspid valve competence
  • Tricuspid stenosis will increase the mean central venous pressure by offering a resistance to right vantricular inflow
  • Tricuspid regurgitation will increase the central venous pressure transiently, by allowing the retrograde transmission of right ventricular systolic pressure
• Cardiac rhythm
  • Atrial contraction influences central venous pressure
  • The absence of atrial contraction decreases the CVP (eg. in atrial fibrillation or in some sort of junctional rhythm)
  • Asynchronous atrial contraction (eg. during ventricular pacing) increases the central venous pressure, because the atrium contracts against a closed tricuspid valve 
• Compartment pressures in the thorax and abdomen.
  • Intrathoracic pressure is transmitted to the central venous compartment, as well as to the right atrium and ventricle.
  • Thus, increase in PEEP will be interpreted as an increase in CVP
  • A tension pneumothorax will also increase CVP by increasing intrathoracic pressure
  • Intrabdominal pressure may increase OR decrease the CVP, by influencing the extent of venous return from the lower body,  and by influencing thoracic compliance.

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Alzeer A et al. Central venous pressure from common iliac vein reflects right atrial pressure. Can J Anaesth 1998 Aug 45 798-801.

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