Healthcare and Medicine Reference
In-Depth Information
Box 19.2 Causes of high and low CVPs
Box 19.3 Factors affecting CVP
Raised CVP >15 cm H 2 O
Hypervolaemia
Central venous blood volume
Venous return/cardiac output
Heart failure
Total blood volume
Right ventricular infarction
Regional vascular tone
Cor pulmonale/right ventricular failure
Compliance of central compartment
Vascular tone
Constrictive pericarditis/restrictive cardiomyopathy
Pulmonary embolus
Right ventricular compliance
SVC obstruction
Myocardial disease
{
Intermittent positive pressure ventilation
Pericardial disease
{
Tricuspid incompetence
Tamponade
{
Lowered CVP <3 cm H 2 O
Acute hypovolaemia e.g. haemorrhage
Tricuspid valve disease
Stenosis
High-output cardiac failure e.g. sepsis, thyrotoxicosis
Regurgitation
Decreased sympathetic tone e.g. anaphylaxis, spinal anaesthesia,
spinal shock
Drugs, e.g. vasodilators (GTN, sodium nitroprusside)
Cardiac rhythm
Junctional rhythm
AF
A-V dissociation
correlates with right ventricular end-diastolic pressure, i.e. a mea-
sure of preload.
Reference level of transducer
Positioning of patient
Factors affecting central venous pressure
There are various factors that affect the measurement of CVP. These
include the intravascular volume and venous return as well as the
vascular tone of the venous system. Any increase in vascular tone
will result in a pressure rise within the venous capacitance system
and lead to a rise in CVP.
The CVP is subject to swings because of the transmission of
pressure from the lungs to the SVC during respiration. During the
inspiratory phase the pressure within the thoracic cavity decreases to
facilitate gas fl ow into the lungs and this in turn causes a drop in CVP.
These changes may frequently be reversed in critically ill patients ven-
tilated on intensive care because of the positive pressure used during
the inspiratory phase of mechanical ventilation. These patients may
have positive end-expiratory pressure (PEEP) applied as part of their
respiratory support which also increases the measured CVP.
Additionally, abnormalities of the tricuspid valve, cardiac rhythm
and myocardial pathology may lead to erroneous CVP measure-
ment and waveforms (Box 19.2).
Intrathoracic pressure
Respiration
Intermittent positive pressure ventilation (IPPV)
Positive end-expiratory pressure (PEEP)
Tension pneumothorax
When fl uid is administered it is important to note the trend of
the change in the CVP and also to see if any increase in the CVP is
sustained over time.
Transient rise in CVP with fl uid bolus —Indicates that the right
ventricle is operating on the ascending part of the Starling curve and
therefore more fl uid will be needed to optimise cardiac preload.
Sustained rise in CVP with fl uid bolus —The plateau part of the
Starling curve has been reached. If a patient's cardiac function is
still inadequate after a sustained increase in the CVP then inotropes
may be needed to improve myocardial contractility further .
Marked rise in CVP with clinical deterioration —The heart is begin-
ning to fail due to excessive preload and overstretching of the muscle
fi bres. Cardiac output is decreasing and is likely to require support
with inotropes and possibly vasodilators and diuretics.
Interpretation of the CVP
When interpreting the CVP, the actual value is less important than
the trend that emerges with response to therapy. There are a variety
of patient factors that contribute to variations in CVP, for example
the stiffness of the ventricular wall, the position of the catheter, the
position of the patient, the intrapulmonary pressures, etc. In prac-
tice, the measured CVP value is often not used as a direct measure
of preload but as a guide to the likelihood of a patient responding
to fl uid therapy.
A low CVP can be indicative of acute hypovolaemic states, high-
output cardiac failure states, decreased sympathetic tone or the
use of vasodilatory drugs. A raised CVP can be as a result of fl uid
therapy (see below) or can have various pathological causes (see
Box 19.3).
Mixed venous oxygen saturation
Oxygen delivery to the tissues is dependent on a combination of the
following: cardiac output, the amount of oxygen in the blood and
haemoglobin concentration.
Critical illness can cause a decrease in oxygen delivery due
to a reduction in each of these factors. When oxygen delivery is
decreased so that it does not meet demand, tissues compensate
by increasing their percentage oxygen extraction from each mL of
blood passing through the tissue and as a consequence the venous
 
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