This chapter is barely relevant to Section G4(iii) of the 2017 CICM Primary Syllabus, which asks the exam candidate to "explain the factors that determine systemic blood pressures and their regulation". Because the college used the word pressures, and because their written records are without reproach, this syllabus item can be extended to encompass central venous pressure. After all, that's blood in there, it's got a measurable pressure, and it is a part of the range systemic circulation pressures (as opposed to pulmonary). The candidates have been asked to comment on this topic on at least two occasions:
In the carboniferous pre-dawn of the JFICM geological period, this topic had also appeared in the Second Part exam (Question 14 from the first paper of 2001). One might have expected it to migrate into the First Part entirely, but it was asked again in Question 8 from the first paper of 2014. Even though it would be sensible to never expect it to appear in that exam again, the vestigial bud of a primitive summary has been left in the Procedures and Equipment section in case the examiners try to recycle it.
- 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
- The main factors which influence the measured CVP are:
- Central venous blood volume, determined by:
- Cardiac output and venous return
- Total blood volume
- Vascular resistance, including external compression (eg. intraabdominal pressure)
- Central venous compliance, determined by:
- Right atrial, ventricular and pericardial compliance
- Intrathoracic pressure
- Trucspid valve competence
- Cardiac rhythm, i.e atrial contractility and AV synchrony
- Measurement technique
- transducer position and timing of measurement with the cardiac and respiratory cycle
Definition of central venous pressure
For most ICU trainees, the term "central venous pressure" would usually mean "the pressure you transduce from the central line", and in the vast majority of situations that would be sufficient. Thus, the usual pragmatic definition would have to be something like this:
"The venous pressure of the right atrium of the heart, obtained by inserting a catheter into a vein (such as the subclavian vein) and advancing it to the right atrium through the superior vena cava".
"Central venous pressure is the intravascular pressure in the great thoracic veins, measured relative to atmospheric pressure."
Practically speaking, that's the pressure you would use at the bedside, depending on what your views on that are. However, for exam purposes, we must transcend the vulgar notions of usefulness and practicality. For the CICM exams, you'd probably be expected to discuss it in Guytonian terms. Thus:
"Central venous pressure (CVP) is defined by the relationship between the right ventricular function... and venous return curves."
In other words, in this clockwork universe, the CVP is defined by the intersection of three main variables: cardiac contractility, vascular resistance and the mean systemic filling pressure. At any given set of those three values, there can only be One True CVP.
Factors which influence the measured central venous pressure
From the college comments to Question 6 from the second paper of 2019, "it was expected that answers include central venous blood volume, central venous vascular compliance, intrathoracic pressure and tricuspid valvular function". Some effort will be made to remix and recombine the Guytonian definition of the CVP to meet this expectation. At the same time, it would be wonderful if at least some of the ensuing discussion could remain attached to reality. Thus, in the discussion of the determinant factors, some attempt will be made to discuss the factors that affect the measured CVP, rather than just the abstract physiological variables.
The classification system for this list of factors is borrowed from Smith, Grounds & Rhodes (2005). These authors created a particularly popular in their chapter for Functional Haemodynamic Monitoring (p101), and many other authors have also reproduced it, which makes it very likely that the college examiners came across it in the course of Googling up their written answer marking rubrics.
Central venous blood volume
Central venous blood volume is usually listed as one of the determinants of CVP. This, in turn, depends on several factors, which can be interpreted using the cardiac and vascular function curve model of the circulatory system, after Arthur Guyton:
- Cardiac output determines venous return, and therefore should influence the venous blood volume. As cardiac contractility decreases and the venous return falls, the right atrial pressure increases:
- Mean systemic filling pressure: The determinants of this factor are discussed in detail elsewhere. In short, it is the pressure that would be measured at all points in the entire circulatory system if the heart were stopped suddenly and the blood were redistributed instantaneously in such a manner that all pressures were equal. As MSFP increases, so does the right atrial pressure, all other things remaining equal:
MSFP is in turn determined by the vascular tone of the systemic circulation and by the total blood volume.
- Vascular tone plays a role by changing the relationship between mean systemic filling pressure. As peripheral vascular resistance increases, it acts as an impediment for blood flow into the venous circulation, and the central venous pressure decreases:
For example, intraabdominal pressure may decrease the CVP, by increasing the resistance for venous return from the lower body.
- Total blood volume factors into the CVP by increasing the mean systemic filling pressure. Beyond a certain volume (the "unstressed" volume), the contribution of total blood volume becomes negligible; i.e. it appears that only about 15% of the total blood volume normally contributes to CVP (whereas the rest apparently exerts no pressure). This relationship between volume and pressure (i.e. the change in pressure per change in volume) is elastance or the reciprocal of compliance (change in volume per change in pressure). Which is a handy segue into:
Elastance of the right atrium and greater vessels
The relationship of the pressure and volume in the central venous compartment is usually referred to as "central venous vascular compliance", even though elastance is probably a better term if one is specifically interested in looking at the change in pressure. This relationship is mainly affected by:
- Vascular tone of the central venous walls (greatly affected by noradrenaline, for example)
- External pressure on the central venous walls:
- Intrathoracic pressure is transmitted to the central venous compartment, as well as to the right atrium and ventricle.
- Thus, an increase in PEEP will be interpreted as an increase in CVP
- A tension pneumothorax will also increase CVP by increasing intrathoracic pressure
- 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
Properties of the tricuspid valve
- Tricuspid stenosis will increase the mean central venous pressure by offering resistance to right ventricular inflow
- Tricuspid regurgitation will increase the central venous pressure transiently, by allowing the retrograde transmission of right ventricular systolic pressure
- The influence of tricuspid disease on the interpretation of central venous pressure waveforms is discussed elsewhere
- 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.
- 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)