, BOTH INVOLVING SPONTANEOUSLY BREATHING PATIENTS, HAVE SHOWN THAT...

24], both involving spontaneously breathing patients, have shown that an inspira-

tory fall in CVP by ≥ 1 mmHg is highly predictive of a fluid responsive cardiac

index (positive predictive value 77%/84% and negative predictive value

81%/93%).

Although the CVP in the supine patient is a poor index of circulating volume

postural changes in CVP may be a more reliable indicator of intravascular volume

status [4]. Measurement of postural changes in CVP seems, however, unlikely to

106 T. Smith, R. M. Grounds, and A. Rhodes

become a widely adopted clinical tool within the context of the acutely or critically

ill patient in the ICU.

Utility of CVP as a Measure of Circulatory Filling

Central venous pressure can without doubt be affected by the intravascular vol-

ume. Approximately two thirds of the intravascular volume is contained in the

venous system and the total intravascular volume will affect the mean venous

pressure. Only a proportion of the total intravascular volume exerts any distend-

ing force on the vasculature [25] thereby causing a positive pressure within the

vasculature; this volume cannot be measured in the intact human and will vary

with the vascular tone which is therefore also an important determinant of the

CVP. The volume of blood in the central veins will also be affected by the distribu-

tion of the venous blood volume through the venous system: peripheral venocon-

striction and the effects of the muscle pump will redistribute volume from the

peripheral veins to the central veins and so increase CVP whereas peripheral

vasodilatation and upright posture will redistribute volume to the peripheral

venous compartment and decrease the CVP. Furthermore, the CVP depends not

only on the volume of blood in the central venous system but on the compliance of

that system. With so many factors other than intravascular volume affecting the

CVP one might expect that CVP would be a relatively inexact measure of intravas-

cular volume particularly in the intact organism where feedback mechanisms will

compensate for a decreased intravascular volume by stimulating vasoconstric-

tion. This expectation is borne out in clinical studies where not only has CVP been

shown to correlate poorly with blood volumes measured by indicator dilution but

the change in CVP after fluid resuscitation of shocked patients also correlated

poorly with the measured change in blood volume [26, 27]. CVP has also been

found to correlate poorly with the volume of fluid administered during ENT

surgery in spite of a progressive decrease in hematocrit during surgery suggesting

intravascular volume expansion [28].

Clinical Outcomes and CVP monitoring

Considering the paucity of data to support CVP as a useful physiological monitor

one would not expect CVP monitoring to have a significant positive effect on

outcome. There are relatively few studies that examine this issue particularly in

the critically ill, presumably because CVP monitoring has become an almost

routine part of ICU care.

Fluid administration targeted by CVP monitoring during hip surgery shortened

the time before patients were medically fit for discharge [29]. However, similar

results were obtained using Doppler flow monitoring to guide fluid administration

and it might be suggested that similar results in both groups could have been

achieved by simply giving larger volumes of fluid without additional monitoring.

In another study, fluid administration aiming to keep the CVP greater than 5

mmHg during renal transplant surgery resulted in a greater frequency of graft

Central Venous Pressure: Uses and Limitations 107

function within the first three postoperative days than in a control group without

CVP monitoring [30]. Whilst these studies probably demonstrate an important use

of CVP monitoring in detecting low circulating volumes in surgical patients which

when detected can be appropriately managed and thus lead to improved outcome

it is doubtful what bearing they have in critically ill patients where more usually

the CVP is relatively high and the question is whether fluid or vasoactive drugs

should be the next intervention.

In some circumstances CVP monitoring may provide prognostic information.

A CVP of > 15 mmHg after cardiac surgery is a significant predictor of poor

outcome [31].

Of more relevance to ICU medicine, the decrease in cardiac output in response

to an increase in PEEP (from 0 to 30 mmHg) correlates with the initial level of CVP

and patients with an initial CVP of ≤ 10 mmHg experience a greater fall in cardiac

index than patients with CVP >10 mmHg (–30% +/– 9 vs. –8% +/– 7) [32].

Maintaining a CVP of >10 mmHg may therefore be desirable in the ventilated

patient. Surprisingly the inspiratory decrease in CVP appears unable to predict the

cardiovascular response to PEEP in a similar way [33].

When considering the utility of CVP monitoring it is appropriate to make the

analysis in the context of other possible modalities of monitoring available to

measure similar physiological variables. The most common alternative to CVP

monitoring as an index of cardiac preload and volume status is pulmonary artery

pressure monitoring using a pulmonary artery catheter (PAC). The use of PACs

has been associated with greater morbidity and cost than the use of central venous

catheters and a number of studies have suggested that in many cases they do not

offer any advantages over CVP monitoring, particularly in low risk surgical patients

[34] and may in fact worsen outcome increasing both the complication rate and

time spent intubated after cardiac surgery [35]. An examination of the utility of

PACs as an alternative to central venous catheters is outside the scope of this

chapter but it is to be hoped that a clear answer to this question will be given by the

large multicenter study currently underway.

Perhaps the most powerful studies indicating the usefulness of CVP monitoring,

or lack thereof, in critical care are those involving goal directed therapy. One such

study in septic patients showed no difference in outcome between patients with

CVP or PAC monitoring where therapy was directed towards achieving normal

values of measured variables; however, in those patients where therapy was di-

rected to achieving supraphysiological values for cardiac index and oxygen delivery

an improved outcome was seen [36]. Clearly such goal directed therapy requires

monitoring other than simple CVP monitoring. Similarly, early goal directed

therapy of septic patients in the emergency department resulted in significantly

improved outcomes when therapy was directed at improving mixed venous satu-

rations rather than at normalizing the CVP, mean arterial pressure (MAP) and

urine output [37].

108 T. Smith, R. M. Grounds, and A. Rhodes

Conclusion

The two clinical studies on surgical patients [29, 30] confirm the potential utility

of CVP monitoring in some patient groups. As a decrease in CVP is a relatively late

sign of intravascular volume depletion in a patient with intact vasoconstrictor

reflexes it is possible that in the patient groups in these two studies there is a

significant risk of severe hypovolemia which would, if not detected by CVP moni-

toring, remain untreated causing increased morbidity. It may, however, be argued

that CVP may be a better measure of volume status in anesthetized patients whose

vasoconstrictor reflexes are pharmacologically impaired by the anesthetic drugs.

There is no convincing evidence that CVP monitoring improves outcome in the

critically ill patient, particularly when other variables are being assessed. Addition-

ally, it is clear from studies examining goal directed therapy that targeting fluid

therapy to normalizing the CVP in a critically ill patient is not an optimal treatment

strategy.

There is no doubt that there is a significant morbidity and possibly even

mortality associated with obtaining central venous access; central cannulation

having a complication rate of up to 6% even when performed by experienced staff

[38]. This risk may outweigh the risk of giving large volumes of fluid without central

pressure monitoring in the general surgical population. However, the majority of

critically ill patients require central venous access for the administration of drugs

or potassium and there appears to be some potential advantage in measuring

central venous oxygen saturation at least during the early stages of treatment for

which central access is also required. If central venous access is to be obtained then

it would seem appropriate to monitor the CVP. As long as this variable is consid-

ered in the context of the whole clinical picture and other monitored and laboratory

variables and the underlying pathophysiology taken into account then it is unlikely

that CVP monitoring will lead to a worsened outcome and there are some situations

such as a large occult blood loss or extreme vasodilatation where a change in CVP

may provide an early warning of the problem.

The role for CVP as a monitor for use in the cardiovascular optimization of

critically ill patients remains important largely because most critically ill patients

will require central venous access for other reasons and so monitoring the CVP

becomes essentially a risk free procedure as the risks are associated with obtaining

access rather than the monitoring process itself. However, as a monitor it has

significant weaknesses and with the increasing availability of other less invasive

and apparently better measures of preload and circulatory filling the importance

of CVP monitoring is likely to decline in this context, at least within the critical care

setting, although it may be some time before other preload monitors are available

on general wards in our hospitals.

References