Anaesthesia vol26 no 2 April I971

REVIEW

Interpretation of CVP measurements

G. R. Kelman

Physicians have for many years used the natural manometer provided by
the column of blood contained in the great veins entering the right atrium
to estimate pressures in the right side of the heart. More recently, it has
become increasingly common practice to measure right atrial pressure
(RAP) directly, by measuring the pressure in large intrathoracic (‘central’)
veins via a percutaneously-introduced catheter. Such measurements of
‘central venous pressure’ (CVP) are easy to make, but often difficult to
interpret; it is with these problems of interpretation that this review is
chiefly concerned.

M E A S U R E M E N T OF C V P

The technical aspects of CVP measurement have been well described by

Sykesl, by Huberty and his colleagues2 and by Hardaways. When a
clinician measures a patient’s CVP he is, in fact, estimating the pressure in
that patient’s right atrium. This is so even when the tip of the measuring
catheter lies at some distance from the atrium itself; the intrathoracic veins
are so large that the pressure drop along them is negligible, even over
distances of several centimetres.
It is, of course, necessary to ensure that the zero reference level of the
manometer is on a level with the right atrium, otherwise measured pres-
sures will be incorrect by reason of the hydrostatic pressure difference
between the manometer and the heart, although changes of pressures will
be indicated accurately even when this condition is not obeyed.
Because of uncertainty about the exact position of the right atrium in the
chest, measurements of CVP are usually referred to some well-defined
anatomical landmark, such as the sternal angle or the mid-axillary line.
When a patient of average build lies horizontally, his sternal angle is
roughly lOcm above his mid-axiUary line. A manometer with its scale
zero on a level with the mid-axillary line would therefore indicate a CVP
lOcm HzO (strictly saline) greater than a manometer with its zero at the
level of the sternal angle. The usual zero reference level in a patient who is
sitting up is a line drawn horizontally backwards from the fourth right
interspace near the sternum to cut the mid-axillary line4.
G. R. Kelman, MB, ChB, PhD, MSc, DIC, Professor of Human Physiology, University of
Aberdeen and Honorary Physiologist to North Easiern Regional Hospiial Board.
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It is not that one zero reference level is ‘better’ than another, rather that
the individual clinician should become familiar with CVP measurements
referred to one or other anatomical landmark and then always use that
landmark.
The range of normal pressures quoted in the literature is fairly wide;
typical values, referred to the mid-axiliary line, are 6-12cm H 2 0 3 and
2-1Ocm H20 5. Referred to the sternal angle of the horizontal patient, the
normal range is appropriately reduced e.g. -1 to -7cm H20 6.
The commonly used saline manometer only gives a mean value of RAP;
fortunately, however, it is this mean pressure which is of main interest to
the anaesthetist and surgeon. To obtain the various peaks and troughs
which concern the cardiologist it is necessary to use a more sophisticated
and somewhat expensive electrical manometer.

PHYSIOLOGY
Starling’s Law of the Heart7 may be paraphrased to state that, the more
the myocardial muscle fibres are stretched during diastole, the more
forcibly will the heart contract during its subsequent systole and, therefore,
the more blood will it expel as it contracts. The force which stretches the
heart during diastole is the pressure in the right atrium (or strictly, the
difference between the right atrial pressure and the intrathoracic pressure).
Therefore, other things being equal, the higher the RAP, the greater will be
the right ventricular stroke volume.
But, of course, the clinician is interested, not so much in right ventricular
output, as in lest ventricular output-cardiac output. Fortunately, it
appears that, when the pericardium is intact, an increase of right ventric-
ular output is usually accompanied by an increase in the amount of blood
contained in the pulmonary veins, and therefore by increases of both left
atrial pressure (LAP) and of cardiac output. As a result, an increase of RAP
is usually accompanied by an increase of cardiac output; and, for a given
state of myocardial contractility (ability of the myocardial muscle fibres
to shorten), there is a well-defined experimental relationship between RAP
and cardiac output (figure 1).
The normal situation (curve A) is represented by point x; an increase of
RAP causes an increase of cardiac output (point x’), a decrease of RAP
causes a decreased cardiac output (point x”). What happens when the
functional ability of the heart is increased as by sympathetic stimulation,
or decreased as by parasympathetic stimulation or myocardial ischaemia ?
Under these circumstances the cardiac function curve is shifted upwards
and to the left (increased cardiac efficiency - curve B), or downwards and
to the right (decreased cardiac efficiency - curve C). With increased cardiac
efficiency a given cardiac output can be achieved with a subnormal RAP,
or, what amounts to the same thing, a normal RAP will result in a greater
than normal cardiac output. With a poorly functioning heart the converse
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RAP
FIGURE 1

obtains - to maintain a normal (or even subnormal) output requires a

greater than normal cardiac filling pressure.
However, the central question still to be answered is, what determines
RAP? For, as seen above, it is the value of this parameter and the state of
myocardial contractility which determine cardiac output, and therefore
total body perfusion.
The pressure in the peripheral venous system depends on the relationship
between the volume of the system and the amount of blood which it
contains, i.e. on the appropriateness of the blood volume to the capacity
of the venous system. The greater the actual blood volume or the smaller
the capacity of the system, the greater is the peripheral venous pressure. To
a large extent this peripheral pressure determines RAP, because, although
there is a pressure drop between the periphery and the right atrium, this
pressure drop is relatively constant, with the result that an increase of
peripheral venous pressure is accompanied by an increase of RAP.
Underfilling of the peripheral circulation therefore leads to a reduction
of RAP,with a consequent reduction of cardiac output; its deleterious effects
may however be partially masked by increased sympathetic activity which
increases the efficiency of the cardiac pump and permits a lower than
normal filling pressure to produce an adequate cardiac output (figure 1 -
curve B). Overfilling of the circulation causes an increase of RAP and an
increase of cardiac output. A decrease of cardiac efficiency (figure 1-
curve C) causes a rise of RAP even in the presence of a normal blood
volume, because blood is dammed back in the venous reservoir to maintain
the higher than normal filling pressure which the heart requires to produce
an adequate output * .
*This account is, of course, greatly simplified. For a full account of the factors affecting
RAP and of the way in which this pressure represents a balance between central andperi-
pheral factors, see e.g. Guyton 8 or KelmanQ.
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APPLIED PHYSIOLOGY

It would therefore seem that there are three common clinical situations to
be considered.
Peripheral circulation underfilled, cardiac pump normal. This should lead
to a low cvp and low cardiac output-the condition which, when it
becomes extreme, is known as hypovolaemic shock.
Peripheral circulation overfilled, cardiac pump normal. This should lead
to a high CVP,a raised cardiac output, and a danger of pulmonary oedema
from over-filling of the pulmonary circulation.
Normal peripheral circulation, eficiency of cardiac pump decreased. This
should lead to a high CVP,a low cardiac output, and again a danger of
pulmonary oedema- the condition of cardiogenic shock, as seen for
example after an acute myocardial infarction.
The danger to the patient in cases (b) and (c) arises not from the increase
of RAP per se, but from the likelihood of pulmonary oedema; this danger
is related more to the height of the /eft atrial pressure than to the height of
the RAP. RAP often, but not always, reflects LAP (see later).

CLINICAL PRACTICE

Let us now see how these extrapolations from elementary physiology are
borne out in practice.
Low central venous pressure
Physiology suggests that a low cvp indicates that the patient’s blood
volume is too low for the capacity of his vascular system, particularly that
of the venous reservoir which normally contains at least 50% of the total
blood volume10. This situation usually occurs when the patient’s actual
blood volume is reduced, but it may also occur when the capacity of his
venous system is increased e.g. by spinal anaesthesia.
There is, in fact, ample evidence that changes in blood volume may be
reflected in changes of C V P ~and ~ , that fluid replacement based on CVP
measurement may be the best way to treat acute hypovolaemia12.13.14.
However, there is also evidence that substantial fluctuations of blood
volume sometimes occur without accompanying changes of cv~15*16,17.
The reason for this discrepancy between physiological prediction and
clinical practice is, I believe, partly the inherently large compliance of the
venous reservoir and partly the action of cardiovascular reflexes which
adjust venous tone in response to changes of cardiac output, arterial blood
pressure, etc. Gauer and his colleagues1 1 estimated that the addition of
looml of blood should raise the pressure in the venous reservoir by only
0.5mg Hg.
AS a result, severe hypovolaemia may occur with a CVP which is only at
the lower limit of normal e.g. 6cm H20when referred to the mid-axillary
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line 3. The lesson would seem to be that all patients in whom there is the
possibility of relative or absolute hypovolaemia should be transfused with
the appropriate fluid until their CVP is at the upper limit of normal-
perhaps 12cm H 2 0 293. If this manoeuvre is accompanied by a normal
cardiac output as suggested by an adequate urine flow, a normal arterial
blood pressure and normal peripheral perfusion as indicated by pink,
warm extremities 1 8, the patient’s cardiovascular state is probably satis-
factory. If it is accompanied by signs of inadequate tissue perfusion, with
increasing non-respiratory (lactic) acidosis, the patient’s primary defect
probably lies in poor functioning of his cardiac pump. In this case further
treatment should be directed towards improving cardiac function by
relief of hypoxia, administration of digitalis, correction of acidosis, etc.
High central venous pressure
Physiology suggests that a high CVP indicates either hypervolaemia or
failure of the cardiac pump, and it is well recognised that increased jugular
venous pressure is an important sign of cardiac failure. In both hyper-
volaemia and cardiac failure there is a danger of pulmonary oedema, while
in cardiac failure there is also a danger of acidosis from anaerobic meta-
bolism in underperfused peripheral tissues.
The effects of inadequate cardiac function on CVP are well illustrated by
the action of general anaesthetic agents on this parameter, although con-
fusion may arise from the fact that some general anaesthetics, such as
ether and cyclopropane, cause an increase of sympathetic activity which
*
opposes their direct depressant action on the heart 9. A rise of CVP should
accompany myocardial depression and venoconstriction; and, indeed,
such an increase of CVP has been demonstrated during anaesthesia with
diethyl ether20. with cyclopropane21 and with halothane22. Conversely,
the effects on CVP of improving cardiac function are well shown by the
decrease of venous pressure which accompanies the administration of
digitalis to patients with post-operative heart failure23.
Despite the usefulness of measurements of CVP in clinical practice the
dangers of relying entirely on this parameter for the prevention of pul-
monary oedema must be stressed. With an intact pericardium, RAP
usually closely parallels LAP, because dilatation of the left ventricle inter-
feres mechanically with filling of the right heart, so increasing RAP^^. If
the pericardium is absent or open after operation, however, a marked rise
of LAP, sufficient to cause pulmonary oedema, may occur but with little
rise of RAPIS. (The converse situation is probably less important but may
occur with a purely right sided lesion, such as pulmonary hypertension or
pulmonary stenosis. In this case an increase of RAP may occur with little
or no tendency to the occurrence of pulmonary oedema).
The danger of pulmonary oedema is particularly severe when attempts
are made to correct acute hypovolaemia by transfusion of fluids, such as
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Ringer lactate solution, which do not contain colloids. Such fluids dis-
tribute themselves throughout the entire extracellular compartment, the
extravascular division of which is considerably larger than its intravascular
division. Measurement of CVP assesses only the size of the intravascular
compartment, and therefore considerable accumulation of fluid may occur
around the capillaries with but little rise of CVP. Under these circumstances
the danger of pulmonary oedema is great, especially if the left heart has
been damaged by hypoxia, acidosis, etc.

SUMMARY A N D CONCLUSIONS

A knowledge of elementary physiology is a great help in the interpretation

of measurements of CVP. Two rules may be adumbrated: (1) A low CVP
in the presence of underperfusion of peripheral tissues indicates relative
or absolute hypovolaemia and should be treated by transfusion with the
appropriate fluid until CVP lies at the upper limit of normal (say 12cm
H20 above the mid-axillary line).
(2) A high CVP indicates that the blood volume is too great for the pump-
ing capacity of the heart. Jn the presence of normal tissue perfusion it
indicates relative or absolute hypervolaemia, which probably does not
require active treatment unless pulmonary oedema supervenes; in the
presence of poor peripheral perfusion it indicates heart failure, probably,
but not necessarily (tamponade, etc), due to poor myocardial function and
should therefore be treated by measures designed to improve the efficiency
of the cardiac pump.
As with all ‘rules’ in clinical medicine exceptions abound and CVP
measurements should be interpreted with care in individual cases.
Physiological dogmatism can never replace clinical acumen: nor can
clinical experience compensate for lack of physiological knowledge.

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