clinical

INVASIVE H A E M O D Y N A A A I C M O N I T O R I N G :
THE ROLE O F E M E R G E N C Y NURSES I N
ELPING T O PROVIDE CRITICAL CARE
Emergency nurses can increase their knowledge and develop their skills by evaluating the
haemodynamic function of critically ill patients by invasive monitoring, says HEATHER JA R M A N
Heather Jarman
RCN, MSc Dist
BSc(Hons), is
consultant nurse
in emergency
care, St George's
Healthcare NHS
Trust, London
This article has been
subjected to double
blind peer review
A
ccurate monitoring of critically ill patients in
emergency departments (EDs) is crucial to pro-
viding the information needed to optimise patient
outcome.
Advances in the use of technology and early
intervention in patient management have led to
a need for greater knowledge and skills among
nurses who care for such patients in EDs,
By evaluating critically ill patients' haemodynamic
functions, information about their circulatory
systems and their ability to perfuse tissues and
remove metabolic waste, can be discerned.
M onitoring haemodynamic function also acts as a
guide to a patient's response to treatment.
This article describes the faaors involved in tissue
perfusion and three different invasive methods of
assessing haemodynamic function in the ED. It also
aims to help nurses provide safe and effective care
for critically ill patients.
TISSUE PERFUSION
Nurses who care for critically ill patients must
understand tissue perfusion and the factors involved
in this that are measured by haemodynamic
monitoring.
A dequate tissue perfusion requires adequate
blood pressure, which is determined by cardiac
output and systemic vascular resistance (SVR).
The pressure exerted as the left ventricle ejects blood
into the aorta is termed systolic pressure. Pressure in
the aorta falls after the left ventricle contracts, and the
lowest point, just before the left ventricle ejects blood
again, is known as the diastolic pressure.
Pressure varies widely throughout the cardiac
cycle, and the mean arterial pressure (MAP), rather
than systolic and diastolic values, most directly
reflects tissue perfusion. Mean arterial pressure is
determined by CO, SVR and centra! venous pressure
(CVP)(Box 1).
But the MAP is not a true average of the systolic
and diastolic pressures, and the often cited
formula, MAP = diastolic + 1/3 (systolic + diastolic).
H aemodynamic equations
M ean arterial _ Cardiac output x
pressure Systemic vascular resistance
Cardiac _ S troke volume x
output H eart rate
Blood _ H eart rate X
pressure S troke volume x
Systemic vascular resistance
is accurate only if the diastole length is two thirds of
that of the total cardiac cycle (Darovic 2002).
This makes the values displayed on blood pressure
monitors usually more accurate than paper
calculations (Woodrow 2006).
A MAP of between 70 and lOOmmHg is usually
regarded as normal, although the aim should be
to produce adequate renal perfusion, which is
indicated by a urine output of between 0.5 and
I ml/kg/hr (Ball 2000).
Cardiac output
Cardiac output is determined by stroke volume
(SV) and heart rate. Stroke volume is the quantity
of blood ejected forward from the left ventricle
with each contraction. It is around 70ml at rest
(Woodrow 2006).
Preload
Preload is determined by the amount of blood
returning to the heart, which is known as the
venous return. It is the degree to which cardiac
fibres stretch at the end of the diastole as the heart
fills. The amount of stretch affects the strength
of the next cardiac contraction and the SV, This is
known as Starling's Law.
Preload is influenced by intravascular volume and
venous tone (Adams 2004). It can be manipulated
most easily by administering fluid but also by
administering vasopressors-
20 emergency nurse voi 15 no 1 april 2007
clinical
Normal arterial line trace
Normal
(Andrews and Nolan 2006)
'Dampened' arterial line trace
Dampened
(Andrews and Nolan 2006)
Afterload
Afterload is the resistance the aorta and the
systemic vascular system apply to the blood ejected
from the left ventricle (Ball 2000).
Systemic vascular resistance is determined by the
resistance of the peripheral vessels to blood flow,
which is decreased by vasodilatation and increased
by vasoconstnction,
Vasodilatation therefore causes a decrease in
afterload and so reduces the amount of effort
required by the left ventricle. This in turn decreases
myocardial oxygeri consumption.
Vasoconstnction, which can be caused by a
response to hypovolaemia or the use of positive
inotropes or vasopressors, increases SVR and
therefore afterload.
An increase in SVR increases blood pressure,
provided there is no change in the other factors.
ARTERIAL BLOOD PRESSURE MONITORING
Arterial blood pressure monitoring is an invasive
technique that is becoming increasingly common in
EDs as a way of evaluating haemodynamic status.
It can provi de di rect and cont i nuous
measurement of the blood pressure of critically
Time
ill patients who require frequent blood pressure
recordings. It is especially useful when cuff inflation
is uncomfortable or when compromise of the
circulatory system makes conventional recording
difficult (Sargent 2006).
Such monitoring is also more accurate than
non-invasive measurement, which is affected by
the tissues between the arteries and skin, and
gives readings that are between 5 and 20mmHg
more accurate than those obtained from a cuff
(Woodrow2006).
Measuring arterial blood pressure requires
a cannula and a transducer tubing system.
The cannula is usually inserted in the radial artery
because this is an accessible and visible site, but
brachial, femoral or dorsalis paedis arteries can also
be used {Andrews and Nolan 2006).
Transducer systems differ depending on what
equipment is available locally, but they all consist of
a transducer cable and tubing connected to a bag
of fluid, usually saline.
The fluid is kept under a pressure of 300mmHg to
prevent backflow to the transducer tubing (Jevon
and Ewens (2002), which occurs when arterial
pressure is greater than the pressure exerted by
the fluid. This can cause occlusion of the tubing
and lead to inaccurate arterial blood pressure
readings.
The transducer cable senses the pressure of
blood flow past the cannula tip and converts
this information into arterial pressure waveforms
(Figs. 1 and 2) and numerical data visible on the
monitor.
Calibrating, or 'zeroing', transducers
There are minor variations between
different monitoring systems but in
principle:
Turn the three-way tap off t o the
patient and open to air. This registers
atmospheric pressure
Press the 'zero' button and wait for the
machine to display '0'. There may be an
audible tone when this is achieved
Turn the three-way tap off t o air and
open t o the patient
Ensure that there is return of a trace
and that the values shown are, in your
clinical judgement, of a reasonable
value.
(Adapted from Jevon and Ewens 2002)
15 2007 emergency nurse
21
clinical
A trace of central venous pressure
Dampened
Time
a: point of right atrial contraction
c: tricuspid valve closure
v: right atrial pressure during ventricular contraction
The transducer has a 'zero' reference point, which
should be placed m line with the middle of the
patient's underarm. Incorrea 'zeroing' procedures,
the patient's position and long transducer tubing
can all affect the accuracy of arterial blood pressure
monitoring (Box 2).
Placing the transducer below the middle of
the underarm gives artificially high pressures;
conversely, placing it too high records falsely low
blood pressures.
The general principles in the use of transducers
are summarised in Box 3.
ARTERIAL PRESSURE WAVEFORM
As shown in Fig. 1, a normal arterial trace should
have a rapid upstroke, known as the anacrotic
rise, indicating the force of ventricular contraction.
The trace then slopes downwards as arteriai
pressure decreases. This is followed by a small
second upstroke, called the diacrotic notch, as the
aortic valve closes,
A 'dampened' trace, an example of which is
shown in Fig, 2, looks abnormal or flattened.
It usually occurs because of a blocked cannula or
tubing, or because the pressure bag has deflated so
that its pressure is less than 300mmHg.
A significant complication with arterial lines is
displacement, which can lead to bleeding orartenal
occlusion.
The risk of bleeding can be reduced by ensuring
that the line is secured and covered with a
transparent dressing, and that the site of line
insertion is exposed to allow for observation.
Arterial occlusion interrupts blood flow and causes
blanching to the hand and possibly ischaemia. The
line should be removed immediately if occlusion
occurs.
CENTRAL VENOUS PRESSURE MONITORING
Central venous pressure monitoring is used to
assess patients' intravascular volume. It measures
the pressure in the vena cava and right atrial
filling.
There is a wide variation in normal CVP, from
6 to 20mmHg (Andrews and Nolan 2006),
because it depends on venous tone, intrathoracic
pressure and patient position, as well as
intravascuiar volume. A value of between 0 and
8mmHg is considered normal (Woodrow 2006) for
monitoring purposes.
Central venous pressure does not directly
measure blood volume so should be interpreted
alongside other values such as blood pressure and
urine output. For a fuller picture, it is important to
take serial measurements, rather than single values,
to monitor response to treatment.
Low CVP values indicate reduced preload, usually
because of inadequate circulating volume; high
CVP values can be a sign of overfilling, right heart
failure or a rise in intrathoracic pressure caused by
pulmonary embolus or mechanical ventilation.
It is important to note that high CVP values
related to disease states do not necessarily
indicate volume overload and patients may still be
underfilled (Elgart 2004).
Causes of an elevated CVP include increased
intrathoracic pressure, for example in cases of non-
invasive ventilation, cardiac failure or an occluded
lumen (Woodrow 2006)
Central venous pressure measurements can be
taken using a manometer or, as is increasingly
popular, a monitor connected to a transducer
system similar to that used for invasive blood
pressure recording.
Transducer recording of CVP produces a trace
that mirrors right atrial pressure changes during the
cardiac cycle (Fig. 3).
General principles in the use of transducers
Ensure that the transducer is level wi th
the 'zero' reference point, usually the
middle of the underarm
Reduce and limit the use of extension
sets and three-way taps
If there is a flat trace, check the patient's
condition for loss of output, check for
breaks in the transducer circuit, and
check that the pressure bag is inflated
Maintain a pressure bag pressure of
300mmHg
22
emergency nurse
april 2007
clinical
CENTRAL VENOUS OXYGEN SATURATION
MONITORING
Central venous oxygen saturation ^
monitoring is increasingly used in EDs during
early goal directed therapy to manage sepsis
(Rivers ef a/2001).
Blood sampling from pulmonary artery catheters
(PACs) enables evaluation in critical care areas of
the oxygen saturation of mixed venous blood (SvO^)
from the inferior and superior vena cava.
The degree of saturation gives an indication of
the balance between oxygen supply and demand
on the tissues. Consumption of oxygen from
oxygenated haemoglobin is normally 25 per cent,
which leaves an SvO^ level of 75 per cent; an SvO^
of less than this indicates inadequate oxygen
delivery or excessive oxygen demand.
This is an important part of haemodynamic
monitoring in critically ill patients because low
SvO, values are associated with cardiac failure and
poorer patient outcome in sepsis (Andrews and
Nolan 2006).
Inserting a PAC is not appropriate in EDs, but it is
possible to measure ScvO, levels by taking a sample
using a central venous catheter and analysing it
with a gas machine.
There is close correlation between pulmonary
artery blood oxygen saturation and ScvO, values
in critically ill patients (Andrews and Nolan 2006).
It IS possible to transduce an ScvO, with an
appropriate monitoring device placed in the port of
central line, but these are rarely used in EDs because
they are expensive and can be used only in patients
being transferred to intensive care units,
CONCLUSION
Invasive blood pressure, CVP and ScvO^ monitoring
are crucial components of assessing critically ill
patients in emergency departments.
The dependency and complexity of this patient
group mean it is necessary for emergency nursing
staff to know about haemodynamic monitoring
to ensure safe, effective care and to influence and
improve patient outcomes.
References
Adams KL (2004) Hemodynamic assessment:
Ihe physiologic basis for turning data into clinical
information AACN Clinical Issues. 15, 4. 534-546.
Andrews F, Nolan J (2006) Cnlical care in the
emergency department monitoring the critically (II
patient. Emergency MedicalJournal 23, 7, 561-564
Ball C120001 Optimizing oxygen delivery
haemodynamic workshop. Part2. Intensiveand
Critical Care Nursing 16, 1, 33-44
Darovic GO (2002) Hemodynamic Monitoring:
Invasive and non-invasive clinical application.
Third edition. WB Saunders, Philadelphia PA
Elgart H (2004) Assessment of fluids and
electrolytes. Advanced Practice in Acute and
Critical Care Clinicallssues 15, 4, 607-621
Jevon R Ewens B (20021 Mon/tonng the
Critically III Patient. Slackwell Science,
Oxford,
Rivera E, Nguyen B, Havstad S et al (2001)
Early goal-directed therapy in the treatment of
severe sepsis New England Journal of Medicine
345. 19, 1368-1377.
Sargent A (2006) Arterial blood pressure
monitoring. Bhtisf] Journal of Cardiac Nursing.
1,2,69-72,
Woodrow P t2Q06} Intensive Care Nursing.
Second edition Routledge, New York NY.
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