This is relevant to Question 14 from the first paper of 2001, "What are the determinants of central venous pressure? How may its measurement guide patient management?" A very similar question (Question 8) was again repeated in the first paper of 2014. An excellent overview of this topic exists in this book chapter by Smith, Grounds and Rhodes; their Table 1 was used as the basis of the following list. At a basic level, the determinants of CVP can be divided into six broad groups. These groups are measurement technique, central venous blood volume, central venous vascular compliance, tricuspid valve competence, cardiac rhythm, and the compartment pressures in the thorax and abdomen.
Factors which determine CVP:
- 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
- Cardiac output (which determines venous return)
- Volume of blood in the central capacitance vessels
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
- 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.
CVP is vaguely equivalent to right atrial pressure.