Download acccns critical care nursing chapter 7

Section 2
Principles and
Practice of
Critical Care
CHAPTER 7
Assessment, Monitoring and
Diagnostics
Bridie Kent
Bruce Dowd
Learning objectives
■
After reading this chapter, you should be able to:
explore the nursing roles in relation to evidence-based
practice and monitoring.
■
describe the reasons for the assessment and monitoring
of critically ill patients
Key words
■
identify the key principles underpinning assessment and
monitoring
oxygen delivery
■
explore reasons for haemodynamic monitoring
neurological assessment
■
understand the physiological bases for different types of
monitoring
diagnostic imaging
haemodynamic monitoring
oxygen consumption
ventilation monitoring
INTRODUCTION
The critical care environment is one that is ‘specifically staffed
and equipped for the continuous monitoring, observation and
care of individuals with a critical illness’.1 The physiological
response of critically ill patients to disease or other stressors
such as trauma will in most cases determine the outcome
of that episode of illness. Monitoring of physiological data
provides baseline details from which future assessments can
be made, and facilitates the response to various medical and
nursing interventions. A vast amount of data is generated by an
unstable patient in an intensive care unit each day—estimated
to be as great as 2000 items in 1987, and presumably much
higher in today’s technological environment.2 It is vital
therefore that nurses understand the principles related to
assessment, monitoring, and diagnostic information obtained
from various sources, as correct interpretation of the data
generated is important in providing timely and effective
interventions while minimising any potential errors.
When considering the data generated from monitoring
and diagnostic devices, it is important that trends be carefully
assessed, rather than relying on one-off results. Trends reveal
patterns among individual and grouped variables and should
therefore be regularly reviewed to reveal the response to
therapy. Although the focus of this chapter is on physiological
data, the importance of the assessment and monitoring of
subjective responses of patients and other psychosocial issues
is acknowledged (see Chapter 8).
Critical care nursing includes assessment and monitoring
of all relevant systems—respiratory, cardiovascular,
gastrointestinal, neuromuscular and urinary. Consequently,
nurses require an in-depth understanding of anatomy,
physiology, pathophysiology and pharmacology to undertake
the ongoing assessment and to achieve early recognition of
complications and the related interventions. Underpinning
all of these are the principles of delivery of optimal and
culturally competent care, relief of distress, compassion and
support, dignity, information, and the care and support of
relatives and caregivers.3
The monitoring and diagnostics specifically addressed
in this chapter include those related to the haemodynamic,
respiratory and neurological systems of the body.
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Principles and practice of critical care
RELATED PHYSIOLOGY
The wellbeing of a patient is dependent on the normal supply
of oxygen and nutrients to the tissues and vital organs. The
monitoring of normal anatomy and physiology in order to
understand the pathophysiology related to patients’ problems
is therefore an essential part of critical care nursing. The
interrelated nature of the body’s systems must be appreciated,
as dysfunction in one system will result in anomalies or
alterations in others. Take, for example, the delivery of
oxygen to the tissues. The cardiovascular and respiratory
systems work harmoniously to ensure that the tissues receive
oxygen to maintain homeostasis. However, other systems also
have vital parts to play in this process: the brain and other
aspects of respiratory control, the kidneys for the production
of buffers, the metabolic systems for production and removal
of other elements, all interact to ensure that normal functions
are maintained. The following section will revisit essential
physiology; if further detail is required, please refer to a
comprehensive anatomy and physiology text.4
Principles of oxygen delivery and oxygen
consumption
The delivery of oxygen (DO2) to the tissue and vital organs
is governed by three important components:
1. cardiac output (stroke volume × heart rate)
2. haemoglobin
3. oxygen saturation.
A balance between DO2 and oxygen consumption (VO2) is
required. The amount of oxygen that tissues need or demand
is determined by the level of metabolic activity of the tissues,
which varies throughout the body. If VO2 exceeds DO2,
deficits occur and a physiological effect will be observed.
The tissues generally extract oxygen in direct proportion to
blood flow. However, at a certain level of oxygen delivery,
a plateau of oxygen consumption is achieved; it is therefore
important that for patients who have sepsis, for example,
there is enhanced blood flow, as supply dependency is more
likely in these patients.5
Oxygen extraction is the percentage of oxygen that is
extracted and utilised by the tissues. At rest, normally just
25% of the total oxygen delivered to the tissue is extracted,
although this amount does vary throughout the body,
with some tissue beds taking more and others taking less.
Venous oxygen content is the amount of oxygen contained
in the venous blood as it returns to the lungs (CvO2). It is
determined by the haemoglobin concentration and the oxygen
saturation of the haemoglobin in venous blood (SvO2). SvO2 is
determined by the amount of oxygen delivered to the tissues in
the arterial blood, as well as the amount of oxygen extracted
and utilised by the tissues. Normally, the oxygen saturation of
venous blood is 60%–75%, with values below this indicating
that more oxygen than normal is being extracted by the
tissues. This can be due to a reduction in oxygen delivery
to the tissues, or to an increase in the tissues’ consumption
of oxygen. Common causes of decreased oxygen delivery
are decreased cardiac output, low haemoglobin levels, and
hypoxia. Tissue oxygen demands can be increased by the
increased effort of breathing, pyrexia, sepsis, shivering,
agitation/restlessness, and increased physical activity.6
Oxygen transport
Assessment of the lungs’ ability to adequately oxygenate
arterial blood is a vital part of critical care. Respiratory
monitoring ensures that oxygenation and all other aspects
of the respiratory system are assessed either continuously
or intermittently. Assessment of oxygenation is performed
by examining arterial oxygen saturation (SaO2) and arterial
oxygen tension (PaO2), usually via arterial blood gas analysis,
which will be described later in this chapter. Caples and
Hubmayr provide an informative summary of the respiratory
monitoring tools used in ICUs.7
Oxygen and carbon dioxide use the process of diffusion
to move around the body. This enables molecules to move
from areas of high concentration to those where the
concentration of molecules is much lower, and is reliant on
the amount of driving pressure, or the pressure gradient.
Where the driving pressure is high, more diffusion of gases
takes place. Oxygen and carbon dioxide concentration
differences in the lungs and surrounding blood vessels
drive the gases across the alveolar membrane; in the alveoli,
oxygen is highly concentrated and the pressure generated
pushes oxygen molecules into the pulmonary capillaries.
Conversely, the same process pushes carbon dioxide from
the highly concentrated pulmonary capillaries into the
alveoli, where concentrations are low. Other determinants
of the rate of diffusion include the thickness of the alveolar
membrane, the amount of surface area of the membrane
available for gas transfer, and the inherent solubility of the
gas.6 Further information on respiratory pathophysiology
is contained in Chapter 11. Oxygen is transported around
the body in two ways: in plasma (3%), and attached to
haemoglobin (97%). There are a number of determinants
of tissue oxygen supply, including haemoglobin level;
oxygen saturation of haemoglobin; oxygen dissociation;
and perfusion pressure.6
HAEMOGLOBIN
Haemoglobin (Hb) contains iron (haem) and polypeptide
proteins called globin. The molecules are relative large
when compared with other blood cells, and consequently,
haemoglobin is not normally found in interstitial fluid
or urine. There are approximately 900 g of circulating
haemoglobin, carried in the red bllod cells, in a 70 kg adult,
and new red blood cells are constantly synthesised while
others are destroyed; the erythrocyte (red blood cell) has a
life of approximately 120 days. Old cells are metabolised by
macrophages and this process releases iron, which is used
for further haemoglobin synthesis in the liver, while waste
products are excreted in bile.6
One gram of haemoglobin can carry 1.34 mL oxygen,
and the level of saturation within the total circulating
haemoglobin can be measured clinically, commonly by pulse
oximetry. As noted previously, a large reserve of oxygen is
available if required, without the need for any increase in
respiratory or cardiac workload. The amount of oxygen
CHAPTER 7
bound to haemoglobin in comparison with the amount of
oxygen the haemoglobin can carry is commonly reported
as SaO2. If the SaO2 is 90%, this means that 90% of the
haemoglobin attachments for oxygen have oxygen bound
to them.
OXYGEN–HAEMOGLOBIN DISSOCIATION CURVE
The affinity of haemoglobin for oxygen can be portrayed
by the oxygen–haemoglobin dissociation curve (see Figure
7.1). The transfer of oxygen across the capillary membranes
is determined by pressure differences on either side of the
membranes. In the upper part of the curve, relatively large
changes in the PaO2 cause only small changes in haemoglobin
saturation. Therefore, if the PaO2 drops from 100 to 60
mmHg (8–14 kPa), the saturation of haemoglobin changes
only 7% (from the normal 97% to 90%). The lower portion
of the oxygen–haemoglobin dissociation curve, however,
indicates that as haemoglobin is further desaturated, larger
amounts of oxygen are released for tissue use to ensure that an
adequate oxygen supply to peripheral tissues is maintained,
even when oxygen delivery is reduced.6
The affinity of haemoglobin for oxygen varies in certain
circumstances and so a number of factors cause shifts to occur
in the oxygen–haemoglobin dissociation curve, resulting in
changes to the affinity between oxygen and haemoglobin.
■
Assessment, monitoring and diagnostics
CARBON DIOXIDE TRANSPORT
Carbon dioxide (CO2) is also carried in the blood and
plays a vital part in maintenance of normal respiratory and
haemostatic functioning. CO2 is produced at a rate of 200
mL/min by metabolism and with only minor differentials
in the normal concentrations of CO2 in arterial (48 mL/dL)
and venous (52 mL/dL) blood. The greater solubility of
CO2 when compared with oxygen results in rapid diffusion
across the capillary membranes, and therefore the gas
can be easily removed for excretion. CO2, a byproduct
of cellular respiration, is carried in the blood in three
ways: plasma (approx 1%); haemoglobin (approx 25%);
and as bicarbonate (approx 74%). When dissolved, CO2
forms bicarbonate ion (HCO3-), carbonic acid (H2CO3) and
carbonate ion (CO32-), concentrations of which affect the
acid–base balance in the body.8 In common with other acids,
carbonic acid partially dissociates when in solution, to form
CO2 and water or bicarbonate and hydrogen ion:
CO2 + H2O ↔ H2CO3 ↔ HCO3 + H+
The strength of the dissociation is defined by the HendersonHasselbach equation which describes the relationship between
bicarbonate, CO2 and pH, and helps to explain why an
increase in dissolved CO2 causes an increase in the acidity
of the plasma, while an increase in bicarbonate causes the
pH to rise (i.e. the acidity falls):
Common factors shifting curve to the left
1. ↑ pH
2. ↓ PCO2
3. ↓ Temperature
4. ↓ 2, 3-DPG (hypothyroidism, bank blood)
5. Carboxyhaemoglobin
100
90
80
Left
Oxygen saturation, percent
Right
70
A
B
C
Common factors shifting curve to the right
1. ↓ pH
2. ↑ PCO2
3. ↑ Temperature
4. ↑ 2, 3-DPG (hyperthyroidism,
anaemia, chronic hypoxaemia)
60
50
P50
40
30
20
10
0
10
20
30
40
111
50
60
70
PaO2, mmHg
FIGURE 7.1 Oxygen–haemoglobin dissociation curve29 (published with permission)
80
90
100
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Principles and practice of critical care
pH = 6.1 + log (HCO3)
(CO2)
(6.1 = the dissociation constant in plasma)6
Determinants of cardiac output
Cardiac performance is altered by numerous homeostatic
mechanisms. Cardiac output is regulated in response to
stress or disease, and changes in any of the factors that
determine cardiac output will result in changes to cardiac
output (see Figure 7.2). Cardiac output is the product of
heart rate and stoke volume; alteration in either of these
will increase or decrease cardiac output, as will alteration in
preload, afterload or contractility. In the healthy individual,
the most immediate change in cardiac output is seen when
heart rate rises. However, in the critically ill, the ability to
raise the heart rate in response to changing circumstances is
limited, and a rising heart rate may have negative effects on
homeostasis, due to decreased diastolic filling and increased
myocardial oxygen demand.
Preload is the load imposed by the initial fibre length of the
cardiac muscle before contraction (i.e. at the end of diastole).9
The primary determinant of preload is the amount of blood
filling the ventricle during diastole, and as indicated in Figure
7.2, it is important in determining stroke volume. Preload
influences the contractility of the ventricles (the strength of
contraction) because of the relationship between myocardial
fibre length and stretch (the Frank-Starling rule—the greater
the volume, the more stretch and force in the contraction; see
Figure 10.8, Chapter 10). However, a threshold is reached
when fibres become overstretched, and force of contraction
and resultant stroke volume will fall.
Preload reduces as a result of large-volume loss (e.g.
haemorrhage), venous dilation (e.g. due to hyperthermia
or drugs), tachycardias (e.g. rapid atrial fibrillation or
supraventricular tachycardias), raised intrathoracic pressures
(a complication of IPPV), and raised intracardiac pressures
(e.g. cardiac tamponade). Some drugs such as vasodilators
can cause a decrease in venous tone and a resulting decrease
in preload. 10,11 Preload increases with fluid overload,
hypothermia or other causes of venous constriction, and
ventricular failure. Body position will affect preload, through
its effect on venous return.
The volume of blood filling the ventricles is also affected
by atrial contraction: a reduction in atrial contraction
ability, as can occur during atrial fibrillation, will result in
Ventricular chamber
pressure
Preload
Contractility
Afterload
Ventricular chamber
dimension/wall thickness
Stroke volume
Heart rate
Systemic vascular
resistance
Arterial
oxygen
content
Oxygen
delivery (D02)
Cardiac output
Mean arterial
pressure
Oxygen
utilisation
(oxygen
consumption, VO2)
Deoxygenated
venous return
FIGURE 7.2 Determinants of cardiac function and oxygen delivery183 (published with permission)
CHAPTER 7
Assessment, monitoring and diagnostics
50
Exhaustion
40
30
20
Compensation
10
0
Volume
Intracranial physiology
Neurological compromise affects many critically ill patients.
Problems such as raised intracranial pressure complicate a
113
variety of conditions, such as meningitis, hepatic failure and
pre-eclampsia, while other patients may experience transient
neurological impairment arising from the treatments given
during the care episode, such as sensory derangement, and
deep sedation. Consequently, knowledge of the related
physiology will assist with the assessment and monitoring
of these patients.
The brain can be divided into three anatomical areas: the
cerebrum, the brainstem, and the cerebellum. Intracranial
volume is 1.7 L in total, consisting of blood (150 mL),
cerebrospinal fluid (150 mL) and brain tissue (1400 mL).
This is encased by the rigid structure of the skull. The brain
contains four ventricles that are filled with cerebrospinal
fluid, and are connected to each other and to the central
canal of the spinal cord. The two lateral ventricles are large,
c-shaped chambers located deep in each cerebral hemisphere,
and are separated anteriorly by a thin membrane, the septum
pellucidum.15 Each of these ventricles connects to the smaller,
narrow third ventricle via the intraventricular foramen.
The third ventricle connects with the fourth ventricle via
the cerebral aqueduct, which runs through the midbrain.
This fourth ventricle forms the connection with the spinal
cord, and has three openings in its walls: the paired lateral
apertures in the side walls, and the median aperture in
the roof. These apertures connect the ventricles with the
subarachnoid space.15
Intracranial contents are non-compressible, so if one
part increases in volume, it will negatively affect the others.
Pressure exerted by the contents is normally 0–15 mmHg,
but this pressure is not constant throughout the intracranial
area. There is limited capacity for compensation if there is an
increase in the intracranial volume; blood or cerebrospinal
fluid may be temporarily displaced into the spinal cord
space (this may occur naturally during sneezing, coughing
or straining), but if this exceeds the compliance threshold,
then intracranial pressure will rise (see Figure 7.3).16,17
Tissue injury occurs if pressures of 20–30 mmHg are
sustained, and cerebral autoregulation ceases when ICP
rises above 40 mmHg. Sustained pressure over 60 mmHg is
usually fatal, as it results in ischaemic damage to the brain
tissue, a vicious cycle of intracranial hypertension and further
tissue damage (see Figure 7.4). Further discussion of related
physiology and clinical neurological states is provided in
Chapter 12.
Pressure (mmHg)
a reduction in ventricular volume, and a corresponding fall
in stroke volume and cardiac output.
Preload of the left side of the heart, assessed at the end of
filling of the left ventricle from the left atrium using the PCWP,
is assumed for clinical purposes to reflect left ventricular enddiastolic volume (LVEDV). Due to the non-linear relationship
between volume and pressure,12,13 caution must, however,
be taken when interpreting these values, as rises in left
ventricular end-diastolic pressure (LVEDP) may indicate
pathology other than increased preload, such as ischaemia.9
Preload of the right side of the heart is indirectly assessed at
the end of filling of the right ventricle from the right atrium
through central venous pressure (CVP) monitoring.
Afterload is the load imposed on the muscle during
contraction, and translates to systolic myocardial wall
tension. It is measured during systole, and is inversely related
to stroke volume and therefore cardiac output, but it is not
synonymous with systemic vascular resistance (SVR), as
this is just one factor determining left ventricular afterload.
Factors that increase afterload include:
• increased ventricular radius;14
• raised intracavity pressure;
• increased aortic impedance;
• negative intrathoracic pressure; and
• increased SVR.
As afterload rises, the speed of muscle fibre shortening and
external work performed falls, which can cause a decrease
in cardiac output in critically ill patients. Afterload of the
right side of the heart is assessed during the ejection of
blood from the right ventricle into the pulmonary artery.
This volume is indirectly assessed by calculating pulmonary
vascular resistance. Ventricular afterload can be altered to
clinically affect cardiac performance. Reducing afterload will
increase the stroke volume and cardiac output, while also
reducing myocardial oxygen demand. However, reductions in
afterload are associated with lower blood pressure, and this
limits the extent to which afterload can be manipulated.
Contractility is the force of ventricular ejection, or the
inherent ability of the ventricle to perform external work,
independent of afterload or preload. It is difficult to measure
clinically. It is increased by catecholamines, calcium, relief of
ischaemia, and digoxin. It is decreased by hypoxia, ischaemia,
and certain drugs such as thiopentone, β-adrenergic blockers,
calcium channel blockers or sedatives. Such changes affect
cardiac performance, with increases in contractility causing
increased stroke volume and cardiac output. Increasing
contractility will increase myocardial oxygen demand, which
could have a detrimental effect on patients with limited
myocardial perfusion.
Stroke volume is the amount of blood ejected from each
ventricle with each heartbeat. For an adult, the volume is
normally 50–100 mL/beat, and equal amounts are ejected
from the right and left ventricle. Further discussion of related
cardiovascular physiology and pathophysiological states is
provided in Chapters 10 and 19.
■
FIGURE 7.3 Intracranial pressure–volume curve185 (published
with permission)
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Principles and practice of critical care
Raised
intercranial
pressure
Capillary
vasodilation
Reduced cerebral Plasma
blood flow
extravasation
Hypercapnia
Metabolic
acidosis
Tissue
hypoxia
Intracellular
oedema
Increased vascular
permeability
Cell membrane
(Na+/K+ pump)
damage
FIGURE 7.4 Intracranial hypertension/tissue damage cycle185
(published with permission)
PHYSICAL ASSESSMENT
Advanced clinical assessment skills are essential for critical
care nurses, as it is important that data are collected that
can be used to identify the immediate and future needs of
the patient and their family members, thereby facilitating the
development of a comprehensive plan of care. Assessment
should use a systematic approach. Initial assessment will
include the history, functional capability of the patient, and
current physiological status to provide a baseline against
which to compare subsequent assessments. For the critically
ill patient, assessments need to occur continuously to evaluate
the response to interventions and to determine the extent
to which goals have been achieved. There are two levels of
assessment: the brief initial assessment, when the patient
arrives in the critical care unit (the primary survey); and a
secondary comprehensive assessment, which generates more
detailed information and will take more time to complete.
There are four main assessment techniques used in
undertaking the primary and secondary surveys. These
are inspection (also referred to as observation), palpation,
percussion, and auscultation:18
• Inspection is a visual examination of body regions
that is much more than just looking. It needs to be
undertaken in a systematic, deliberate and focused
manner, comparing what is seen with what is already
known.
• Palpation is examination of the body using touch,
rather than eyesight. It should be both light and
deep to reveal information about tenderness, painful
areas, areas of rigidity and muscular spasm, swellings,
masses, pulsations, as well as areas of moisture,
temperature differentials and crepitus.
• Percussion is a technique that uses finger tapping to
elicit different sounds that will reveal details about the
underlying area. Direct percussion is the direct tapping
of the body with one or two fingers to obtain sound.
More commonly, however, percussion is performed
indirectly; the middle finger of the non-dominant hand
is placed against the patient’s body and the tip of the
middle finger of the dominant hand strikes against the
distal phalanx to elicit sound. Percussion is commonly
used to assess lung fields or the abdomen.
• Auscultation is listening to sounds, usually via a
stethoscope to block out surrounding sounds. The
diaphragm of the stethoscope is sensitive to highpitched sounds, while the bell is better for detecting
low-pitched sounds. Auscultation is used to evaluate
sounds emanating from the heart, lungs, abdomen and
vascular systems.
Wherever possible, no parts of the body should be left out of
the primary or secondary survey, but inevitably the condition
of critically ill patients will determine the appropriateness
of the assessment, and some parts may have to be delayed
until the patient’s condition has stabilised.
Primary survey
In essence, assessment begins when a nurse first learns of an
impending admission. A pre-arrival assessment is often based
on limited information obtained from the clinician caring
for the patient in locations such as the ward, emergency
department or operating theatre. Sufficient detail must be
provided to ensure that the receiving nurse can prepare
the bed area with the necessary equipment, monitoring
and supplies. Many critical care units have their own preadmission checks, and nurses should refer to these for local
guidance.
As soon as the patient arrives in the critical care unit,
a rapid primary survey to elicit evidence of any airway
obstruction, respiratory failure, circulatory failure or
neurological dysfunction is conducted, using the ABCDE
guide:19
• Airway assessment—any evidence of obstruction;
failure of airway patency/protection; and check
position of artificial airway (if present).
• Breathing assessment—check whether the breathing
is artificial or spontaneous; any evidence of increased
respiratory effort (check rate and pattern of
respirations); any evidence of abnormal breath sounds
indicative of pneumothorax, asthma, heart failure?
• Circulation assessment—ECG rhythm, rate; blood
pressure; peripheral pulses and refill; presence of
bleeding.
• Disability assessment—altered level of consciousness;
evidence of fitting; hypoglycaemia; any localising signs
in pupils, limbs or cranial nerves?
• Environment/exposure assessment—evidence of rash;
abnormal temperature.
It may also be useful to include the following:20
• Presenting problem—primary affected body system;
associated symptoms.
• Drugs and diagnostic tests—drugs administered prior
to admission; current medications; review of available
diagnostic results.
• Equipment—patency of drainage systems and
vascular devices (IV infusions/cannulae); appropriate
CHAPTER 7
•
functioning and labelling of infusion devices, and other
equipment connected to the patient.
Allergies—note whether any are known.
Assessment, monitoring and diagnostics
Heart rate and rhythm are determined by a conduction system
that is highly specialised. Stimulation of cardiac nerve fibres
produces an action potential that is responsible for initiating
depolarisation of cardiac muscle fibres, which have a resting
membrane potential of -80 mV. Individual fibres are separated
by membranes but depolarisation spreads rapidly because
of the presence of gap junctions. There are five key phases
to the cardiac action potential:21
0. depolarisation
1. early rapid repolarisation
2. plateau phase
3. final rapid repolarisation
4. resting membrane phase.
The contractile response begins just after the start of
depolarisation and lasts about 1.5 times as long as the
depolarisation and repolarisation (see Figure 7.5).
The action potential is created by ion exchange triggered
by an intracellular and extracellular fluid transmembrane
imbalance. There are three ions involved: sodium, potassium,
and calcium. Normally, extracellular fluid contains
approximately 140 mmol/L sodium and 4.0 mmol/L
potassium. In intracellular fluid these concentrations are
reversed. At rest, cell membranes are more permeable to
potassium and consequently, potassium moves slowly and
passively from intracellular to extracellular fluid. However,
when the cell is excited, rapid ion movement caused by
sodium flowing into the cell alters the charge from -90 mV
to +30 mV. There follows a brief influx of calcium via the
fast channel and then more via the slower channel to create
a plateau, the time of which determines stroke volume due
to its influence on the contractile strength of muscle fibres.
The third phase occurs when the potassium channel opens,
allowing potassium to leave the cell, to restore the negative
Once the initial checks have been completed, the secondary,
comprehensive assessment to provide a complete picture
of the patient’s condition is undertaken. Details should
be elicited from family members if the patient is unable
to provide them. In addition, each body system should
be assessed using a top-to-toe approach, to ensure that
nothing is missed. Collaboration with other members of
the healthcare team is important in this process, as the
relevant information should be obtained without subjecting
the patient to unnecessary examinations. The nervous,
cardiovascular, respiratory, renal, gastrointestinal, endocrine,
haematological, immune and integumentary systems all
require examination to determine whether there are any
existing problems, or whether problems identified are new.
Information about past health history, social history, family
history, psychosocial issues and spirituality must also be
obtained.
Assessment is an ongoing process, and therefore all
subsequent assessments will be used to establish trends,
determine response to treatments and identify new problems
that may arise. In general, the stability of the patient will
determine the frequency of these ongoing assessments, which
will range from every few minutes for the extremely unstable
patient to every couple of hours for those patients who are
stable and requiring less intensive care. It is important that
the patient be reassessed whenever new nurses take over
the patient’s care, at shift change for example; before and
after new therapy or interventions; before and after any
movements out of or within the unit; and whenever any
deterioration in physical or mental status is observed. Chuley
et al provide a useful template for ongoing assessment (see
further reading).20
Phase 1
Phase 2
Mechanical
Phase 3
contraction
Phase 0
ACTION
POTENTIAL
⫺90 mV
QRS
Phase 4
T
ECG
Depolarisation
FIGURE 7.5 Action potential29 (published with permission)
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HEART RATE AND RHYTHM
MONITORING
Comprehensive assessment
⫹20 mV
■
Repolarisation
⫺90 mV
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Principles and practice of critical care
charge, causing rapid repolarisation. The final resting phase
occurs when slow potassium leakage allows the cell to
increase its negative charge to ensure that it is more negative
than surrounding fluid, before the next depolarisation occurs
and the cycle repeats.22
Cardiac muscle is generally slow to respond to stimuli and
has relatively low ATPase activity. Its fibres are dependent
on oxidative metabolism and require a continuous supply of
oxygen. The length of fibres and the strength of contraction
are determined by the degree of diastolic filling in the heart.
The force of contraction is enhanced by catecholamines.23
The electrical activity of the heart can be detected on the
body surface because body fluids are good conductors; the
fluctuations in potential that represent the algebraic sum of
the action potential of myocardial fibres can be recorded on
an electrocardiogram. In the case of the critically ill patient,
there are two main forms of cardiac monitoring, both of
which are used to generate essential data: continuous cardiac
monitoring, and the 12-lead ECG.
Continuous cardiac monitoring
Internationally, a minimum standard for an ICU is availability
of facilities for cardiovascular monitoring.24 Continuous
cardiac monitoring allows for rapid assessment and
constant evaluation with, when required, the instantaneous
production of paper recordings for more detailed assessment
or documentation into patient records. In addition, practice
standards for electrocardiographic monitoring in hospital
settings have been established.25
It is now common practice for five leads to be used for
continuous cardiac monitoring,26 as this allows a choice of
seven views. The five electrodes are placed as follows:27
• right and left arm electrodes—placed on each
shoulder;
• right and left leg electrodes—placed on the hips or
level with the lowest ribs on the chest;
• V-lead views can be monitored—for V1 place the
electrode at the 4th intercostal space, right of
the sternum; for V6 place the electrode at the 5th
intercostal space, left midaxillary line.
The monitoring lead of choice is determined by the patient’s
clinical situation.27 Generally, two views are better than
one; therefore, one of the channels on the bedside monitor
should display a V lead, preferably V1, and the other display
leads II or III for optimal detection of dysrhythmias. When
the primary purpose of monitoring is to detect ischaemic
changes leads III and V 3 usually present the optimal
combination.25
The skin must be carefully prepared before electrodes
are attached, as contact is required with the body surface
and poor contact will lead to inaccurate or unreadable
recordings, causing interference or noise. Patients who are
sweaty need particular attention, and it may be necessary
to shave the areas where the electrodes are to be placed in
very hairy people.
Heart rate can be obtained from other sources, such as
a pulse oximeter or a defibrillator, which will also display
rhythm.
12-Lead ECG
The Dutch physiologist Einthoven was one of the first
to represent heart electrical conduction as two charged
electrodes, one positive and one negative.28 The body can be
likened to a triangle, with the heart at its centre, and this has
been called Einthoven’s triangle. Cardiac electrical activity
can be captured by placing electrodes on both arms and
on the left leg. When these electrodes are connected to a
common terminal with an indifferent electrode that stays
near zero, an electrical potential is obtained. Depolarisation
moving towards an active electrode produces positive
deflection.
The 12-lead ECG consists of six limb leads and six chest
leads. The limb leads examine electrical activity along a
vertical plane. The standard bipolar limb leads (I, II, III)
record differences in potential between two limbs (see
Figure 7.6):29
I = right arm–left arm (positive);
II = right arm–left leg (positive);
III = left arm–left leg (positive).
The three augmented unipolar limb leads (aVR, aVL, aVF)
record activity between one limb and the other two limbs
to increase the size of the potentials.
The six unipolar chest leads (praecordial leads) are
designated V1–6 and examine electrical activity along
a horizontal plane from the right ventricle, septum, left
ventricle and the left atrium. They are positioned in the
following way (see Figure 7.7):
⫹
⫹ LA
⫺
I
RA ⫺
⫺ ⫹
aV
aV
R
L
⫺
II
III
aVF
⫹
⫹
⫹
LL
Practice tip
Monitors are not substitutes for the observation of patients, but
they do provide information that should be evaluated in context
with other data and the whole person.
FIGURE 7.6 Einthoven triangle formed by standard limb leads29
(published with permission)
CHAPTER 7
V1 = 4th intercostal space, to the right of the patient’s
sternum;
V2 = 4th intercostal space, to the left of the patient’s
sternum;
V3 = equidistant between V2 and V4;
V4 = 5th intercostal space on the midclavicular line;
V5 = 5th intercostal space, anterior axillary line;
V6 = 5th intercostal space on the midaxilla line.
Anterior
view
Angle of Louis
V1
V2
V3
V V
V4 5 6
■
Assessment, monitoring and diagnostics
117
Depolarisation is initiated in the sino-atrial (SA) node
and spreads rapidly through the atria, then converges on the
atrio-ventricular (AV) node; atrial depolarisation normally
takes 0.1 second.
There is a short delay at the AV node (0.1 sec) before
excitation spreads to the ventricles. This delay is shortened
by sympathetic activity and lengthened by vagal stimulation.
Ventricular depolarisation takes 0.08–0.1 sec, and the last
parts of the heart to be depolarised are the posteriobasal
portion of the left ventricle, the pulmonary conus and the
upper septum.21
Amplitude (voltage) in the ECG is measured by a series
of horizontal lines on the ECG (see Figure 7.8a). Each line
is 1 mm apart and represents 0.1 mV. Amplitude reflects
the wave’s electrical force and has no relation to the muscle
strength of ventricular contraction.21
Duration of activity within the ECG is measured by a
series of vertical lines also 1 mm apart (see Figure 7.8a). The
time interval between each line is 0.04 sec. Every 5th line
is printed in bold, producing large squares. Each represents
0.5 mV (vertically) and 0.2 sec (horizontally).
KEY COMPONENTS OF THE ECG
R
L
FIGURE 7.7 Position of chest leads29 (published with permission)
Key components of the cardiac electrical activity are termed
PQRST (see Figure 7.8b):
• The P wave represents electrical activity caused by
spread of impulses from the SA node across the atria
and appears upright in lead II. Inverted P waves
indicate atrial depolarisation from a site other than the
SA node. P wave = 0.08 sec.
• The P-R interval reflects the total time taken for the
3 sec
0.20 sec
10 mm
0.04 sec
5 mm
1 mm
0.20 sec
FIGURE 7.8a ECG graph paper29 (published with permission)
118
SECTION 2
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Principles and practice of critical care
Atrial
depolarisation
Ventricular
depolarisation
Ventricular
depolarisation
R
Atrial
systole
Ventricular
systole
T
P
Q
PR
interval
S
QRS
ST
segment
QT interval
FIGURE 7.8b Normal ECG29 (published with permission)
•
•
•
•
•
atrial impulse to travel through the atria and AV node.
It is measured from the start of the P wave to the
beginning of the QRS complex, but is lengthened by
AV block or some drugs. P-R interval = 0.12–0.2 sec.
The QRS complex is measured from the start of the
Q wave to the end of the S wave and represents the
time taken for ventricular depolarisation. Anything
longer than 0.12 sec is abnormal and may indicate
conduction disorders such as bundle branch block.
The deflections seen in relation to this complex will
vary in size, depending on the lead being viewed.
However, small QRS complexes occur when the heart
is insulated, as in the presence of a pericardial effusion.
Conversely, an exaggerated QRS complex is suggestive
of ventricular hypertrophy. A ‘pathological’ Q wave
(>0.04 sec plus >25% of R wave height) indicates a
previous myocardial infarction.
The Q-T interval is the time taken from ventricular
stimulation to recovery. It is measured from the
beginning of the QRS to the end of the T wave.
Normally, this ranges from 0.35 to 0.45 sec, but
shortens as heart rate increases. It should be less than
50% of the preceding cycle length.
The T wave reflects repolarisation of the ventricles. A
peaked T wave indicates hyperkalaemia, myocardial
infarction (MI) or ischaemia, while a flattened T wave
usually indicates hypokalaemia. An inverted T wave
occurs following an MI, or ventricular hypertrophy. T
wave = 0.16 sec.
The ST segment is measured from the J point (junction
of the S wave and ST segment) to the start of the T
wave. It is usually isoelectric in nature, and elevation
or depression indicates some abnormality in the onset
of recovery of the ventricular muscle, usually due to
myocardial injury.
The U wave is a small positive wave sometimes seen
following the T wave. Its cause is still unknown but
it is exaggerated in hyperkalaemia. Inverted U waves
may be seen and often associated with coronary heart
disease (CHD), and these may appear transiently
during exercise testing.30
ECG INTERPRETATION
Interpretation of a 12-lead ECG is an experiential skill,
requiring consistent exposure and practice. Some steps to
aid interpretation are noted below.
• Heart rate:
— This can be calculated from the ECG. Count the
R waves on a 6 sec strip and multiply by 10 to
calculate the rate (the top of the ECG paper is
usually marked at 3 sec intervals).
— Use an ECG ruler if one is available.
• Rhythm (regularity):
— To assess regularity, mark the R waves on a plain
piece of paper, and if you move the paper either
way, the marks should not be interrupted.
— The R-R interval should not differ by more than
0.12 sec.
• Atrial activity:
— Observe for the presence or absence of P waves.
— Check regularity and shape.
— Is the P wave positive?
— Do P waves precede every QRS complex?
— What is the duration of the P wave?
• AV node activity:
— What is the duration of the P-R interval?
• Ventricular activity:
— Measure the QRS interval.
— Q wave (if present) = less than 0.04 sec.
• General notable aspects of ECG:
— Observe whether the isoelectric line is present
between the S and T waves.
— Examine the T wave to see whether it is positive,
and less than 0.16 sec.
CHAPTER 7
— Examine the duration of the Q-T interval.
— Observe for any extra complexes and note their
rate and shape, and whether they have the same or
different morphology.
HAEMODYNAMIC
MONITORING
Haemodynamic monitoring is performed to provide the
clinician with a greater understanding of the pathophysiology
of the problem being treated than would be possible with
clinical assessment alone. Knowledge of the evidence that
underpins the technology and the processes for interpretation
is therefore essential to facilitate optimal usage and evidencebased decisions.31
This section explores the principles related to
haemodynamic monitoring and the different types of
monitoring available, and introduces the most recent and
appropriate evidence related to haemodynamic monitoring.
The reasons for haemodynamic monitoring are generally
threefold:
1. to establish a precise health-related diagnosis;
2. to determine appropriate therapy; and
3. to monitor the response to that therapy.
Haemodynamic monitoring can be non-invasive or invasive,
and may be required on a continuous or intermittent basis
depending on the needs of the patient.32 In both cases, signals
are processed from a variety of physiological variables, and
these are then clinically interpreted within the individual
patient’s context.
Non-invasive monitoring does not require any device
to be inserted into the body and therefore does not breach
the skin. Directly measured non-invasive variables include
body temperature, heart rate, blood pressure, respiratory
rate and urine output, while other processed forms can
be generated by the ECG, arterial and venous Dopplers,
transcutaneous pulse oximetry (using an external probe on
a digit such as the finger or on the ear), and expired carbon
monoxide monitors.
Invasive monitoring requires the vascular system to
be cannulated and pressure or flow within the circulation
interpreted. Invasive haemodynamic monitoring technology
includes:
• systemic arterial pressure monitoring;
• central venous pressure;
• pulmonary artery pressure; and
• cardiac output (thermodilution).
Invasive monitoring has also facilitated greater use of blood
component analyses, such as arterial and venous blood
gases.
The invasive nature of this monitoring allows the
transducing of pressures that are sensed at the distal ends
of the catheters, and the continuous display and monitoring
of the corresponding waveforms. The extent of monitoring
should reflect how much information is required to optimise
the patient’s condition, and how precisely the data are to be
recorded. As Pinsky argues, a great deal of information is
■
Assessment, monitoring and diagnostics
119
generated by this form of monitoring, and yet little of this
is actually used clinically.33 Consequently, monitors are not
substitutes for careful examination and do not replace the
clinician. The accuracy of the values obtained and a nurse’s
ability to interpret the data and choose an appropriate
intervention directly affect the patient’s condition and
outcome.34
Principles of haemodynamic monitoring
A number of key principles need to be understood in relation
to invasive haemodynamic monitoring of critically ill patients.
These include haemodynamic accuracy, the ability to trend
data, and the maintenance of minimum standards. These
are reviewed below.
HAEMODYNAMIC ACCURACY
Accuracy of the value obtained from haemodynamic
monitoring is essential, as it directly affects the patient’s
condition.35,36 Electronic equipment for this purpose has
four components (see Figure 7.9):
1. an invasive catheter attached to high-pressure tubing;
2. a transducer to detect physiological activity;
3. a flush system; and
4. a recording device, incorporating an amplifier to
increase the size of the signal, to display information.
High-pressure (non-distensible) tubing reduces distortion of
the signal produced between the intravascular device and
the transducer; the pressure is then converted into electrical
energy (a waveform). Fluid (0.9% sodium chloride) is
routinely used to maintain line patency using a continuous
pressure system; the pressure of the flush system fluid bag
should be maintained at 300 mmHg, which delivers a
continual flow of 3 mL/h.37
Accuracy is dependent on levelling the transducer to the
appropriate level (and altering this level with changes in
patient position as appropriate), then zeroing the transducer
in the pressure monitoring system to atmospheric pressure
as well as evaluating the response of the system by fast-flush
wave testing. The transducer must be levelled to the reference
point of the phlebostatic axis, at the intersection of the 4th
intercostal space and the midthoracic anterior-posterior
diameter (not the midaxillary line).36 Error in measurement
can occur if the transducer is placed above or below the
phlebostatic axis.35,36 Measurements taken when the patient is
in the lateral position are not considered as accurate as those
taken when the patient is lying supine or semirecumbent up
to an angle of approximately 45°.38–40
Zeroing the transducing system to atmospheric pressure
is achieved by turning the 3-way stopcock nearest to the
transducer open to the air, and closing it to the patient
and the flush system. The monitor should display zero (0
Practice tip
The transducer must be relevelled when the patient’s position
has been changed, and the height checked prior to data
recording. Too high, and an erroneously low reading will be
given; too low, and a falsely high reading will be produced.
120
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Principles and practice of critical care
Bedside monitor
Normal saline and
pressure bag
Macrodrip
chamber
Electrical
cable
Highpressure
tubing
45°
Fluidfilled
tubing
for flush
Invasive
catheter
Roller
clamp
30°
Electrical
connection
Disposable
transducer
Phlebostatic
axis
3-way
stopcock
(air reference)
Manual
flush
0°
Patient with invasive catheter
FIGURE 7.9 Haemodynamic monitoring system29 (published with permission)
mmHg), as this equates to current atmospheric pressure
(760 mmHg at sea level). With the improved quality of
transducers, repeated zeroing is not necessary, as once zeroed,
the drift from the baseline is minimal.41 Some critical care
units, however, continue to recalibrate transducer(s) at the
beginning of each clinical shift.
Fast-flush square wave testing, or dynamic response
measurement,41 is a way of checking the dynamic response
of the monitor to signals from the blood vessel. It is also
a check on the accuracy of the subsequent haemodynamic
pressure values. The fast-flush device within the system,
when triggered and released, exposes the transducer to the
amount of pressure in the flush solution bag (usually 300
mmHg). The pressure waveform on the monitor will show
a rapid rise in pressure, which then squares off before the
pressure drops back to the baseline (see Figure 7.10a).
Interpretation of the square wave testing is essential; the
clinician must observe the speed with which the wave returns
to the baseline as well as the pattern produced. One to three
rapid oscillations should occur immediately after the square
wave, before the monitored waveform resumes. The distance
between these rapid oscillations should not exceed 1 mm or
CHAPTER 7
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Assessment, monitoring and diagnostics
121
Blood pressure monitoring
Indirect and direct means of monitoring blood pressure
are widely used in critical care units. These are outlined in
more detail below.
NON-INVASIVE BLOOD PRESSURE MONITORING
FIGURE 7.10a Normal dynamic response test
FIGURE 7.10b Over-damped dynamic response test
0.04 sec.41 Absence, or a reduction, of these rapid oscillations,
or a ‘square wave’ with rounded corners, indicates that the
pressure monitoring system is overdamped, in other words
its responsiveness to monitored pressures and waveforms
is reduced (see Figure 7.10b). An underdamped monitoring
system will produce more rapid oscillations after the square
wave than usual.
DATA TRENDS
The ability to trend data via a monitor or a clinical information
system (as discussed in Chapter 3) is essential for critical care
practice. Current monitoring systems used in Australia and
New Zealand can retain data for a period of time, produce
trend graphs, and link to other devices to allow review of
data from locations other than the immediate bedside.
HAEMODYNAMIC MONITORING STANDARDS
There are stated minimum standards for critical care units
in Australia and New Zealand.24,42 The standards require
that patient monitoring include circulation, respiration
and oxygenation, with the following essential equipment
available for every patient: an ECG that facilitates continual
cardiac monitoring; a mechanical ventilator, pulse oxymeter;
and other equipment available where necessary to measure
intra-arterial and pulmonary pressures, cardiac output,
inspiratory pressure and airway flow, intracranial pressures
and expired carbon dioxide.24
Non-invasive blood pressure (NIBP) monitoring requires the
use of a manual or electronic sphygmomanometer. Oscillation
in the pressure generated by alterations in arterial flow is
captured either through auscultation or automatic sensing.
On auscultation, a number of Korotkoff sounds can be heard
as the cuff pressure is released:43
• a sharp thud that is heard when the patient’s systolic
pressure is reached;
• a soft tapping, intermittent in nature;
• a loud tapping, intermittent in nature;
• a low, muffled noise that is continuous in nature and
is heard when the diastolic pressure is reached; as the
cuff pressure diminishes further, the sound disappears.
For critically ill patients, this method of blood pressure
monitoring has limitations but is better than nothing
when invasive methods cannot be utilised.44 It is a less
accurate alternative, as results vary with the size of cuff
used, equipment malfunction, and incorrect placement
of the sphygmomanometer (this must be placed at heart
level). In addition, the pressures generated by the inflating
cuff, particularly those generated by automatic machines,
can be high and become uncomfortable. It is therefore
important that skin integrity be checked regularly to prevent
ischaemia and that the frequency of automated inflations
be minimised.44
Invasive intra-arterial pressure monitoring
Arterial pressure recording is indicated when precise and
continuous monitoring is required, such as in periods of
instability of cardiac output and blood pressure.45 A cannula
is commonally placed in the radial artery, although other
sites can be accessed, including the brachial, femoral, dorsalis
pedis and axillary arteries. Arterial cannulation is performed
aseptically, and it is important that collateral circulation,
patient comfort and risk of infection be assessed before
cannulation is attempted. The radial artery is the most
common site, as the ulnar artery provides additional supply
to extremities if the radial artery becomes compromised.
Complications of arterial pressure monitoring include:
• infection;
• arterial thrombosis;
• distal ischaemia;
• air embolism;
• accidental disconnection (the sites cannulated should
be visible); and
• accidental drug administration through the cannula;
all arterial lines and connections should be clearly
identified as such (e.g. marked with red stickers or
have red bungs).
Pressure in blood vessels has three components: dynamic
blood pressure, hydrostatic pressure, and static pressure. The
blood pressure is the same at all sites along a vertical level
SECTION 2
Pressure (mmHg)
122
120
110
■
Principles and practice of critical care
PRELOAD
Systole
Dicrotic notch
100
90
Diastole
80
Time
FIGURE 7.11 Arterial pressure waveform184 (published with
permission)
but when the vertical level is varied, pressure will change.
Consequently, referencing is required to correct for changes
in hydrostatic pressure in vessels above and below the heart;
if not, the blood pressure will appear to rise when this is not
really the case. It is important to zero the monitoring system
at the left atrial level (phlebostatic axis, see above).36
Arterial waveform. A steep upstroke (corresponding to
ventricular systole) is followed by brief, sustained pressure
(anacrotic shoulder). At the end of systole, pressure falls in the
aorta and left ventricle, causing a downward deflection (see
Figure 7.11). The systolic pressure corresponds to the peak
of the waveform. The arterial pressure waveform changes
its contours when recorded at different sites, becoming more
sharp in distal locations.
Disease has an effect on waveforms: for example,
atherosclerosis causes an increase in systolic waveform, as
well as a decrease in the size of the diastolic wave and dicrotic
notch due to changes in elasticity. Cardiomyopathy causes
reduced stroke volume and mean arterial pressure, and there
is a late secondary systolic peak seen on the waveform.
Direct pressure versus cuff pressure. At times the accuracy
of the direct arterial pressure reading may be checked by
comparing the reading against that generated by a noninvasive device using an inflating cuff. However, there is no
basis for comparing these values, because direct values are
a measure of the actual pressure within the artery whereas
those from the cuff depend on flow-induced oscillations in the
arterial wall.46 Pressure does not equal flow, as resistance does
not remain constant. In addition, radial arterial pressure is
normally higher than that obtained by brachial non-invasive
pressure monitoring because the smaller vessel size exerts
greater resistance to flow, and therefore generates a high
pressure reading.36,46
Invasive cardiovascular monitoring
For many critically ill patients, haemodynamic instability is a
potentially life-threatening condition that necessitates urgent
action. Accurate assessment of the patient’s intracardiac
status is therefore essential. A number of values can be
calculated, and Tables 7.1 and 7.2 list the measurements
commonly made.
As noted earlier, preload is the filling pressure in the ventricles
at the end of diastole. Preload in the right ventricle is generally
measured as CVP, although this may be an unreliable predictor
because CVP is affected by intrathoracic pressure, vascular
tone and obstruction.47,48 Left ventricular preload can be
measured as the pulmonary capillary wedge pressure (PCWP),
but again, due to unreliability, this parameter provides an
estimate rather than a true reflection of volume.48,49 In view of
this, other modalities are now being explored, including right
ventricular end-diastolic volume evaluation via fast-response
pulmonary artery catheters, left ventricular end-diastolic
area measured by echocardiography, and intrathoracic blood
volume measured by transpulmonary thermodilution.50
Central venous pressure (CVP) monitoring. Central venous
catheters are inserted to facilitate the monitoring of central
venous pressure, as well as facilitating the administration
of large amounts of IV fluid or blood; providing long-term
access for fluids, drugs, specimen collection; and/or parenteral
feeding. Monitoring CVP has been used for many years to
evaluate circulating blood volume, albeit with little scientific
support.51 However, it is a common monitoring practice and
continues to be used; consequently, clinicians need to be
aware of possible limitations to this form of measurement
and interpret the data accordingly.33,47,52 CVP monitoring can
produce erroneous results: a low CVP does not always mean
low volume and it may reflect other pathology, including
peripheral dilation due to sepsis. Hypovolaemic patients
may have normal CVP due to sympathetic nervous system
activity increasing vascular tone.
Practice tip
CVP measures should be taken at the end of the expiratory
phase. Don't forget that this point on the waveform will differ
according to the type of ventilation the patient is receiving.
Failure to be consistent with this measurement may lead to
significant fluid status errors. Always have the waveform on
appropriate scales and freeze the waveform, using the cursor to
identify and obtain the end-expiratory reading.
TABLE 7.1 Haemodynamic pressures
Parameter
Resting values
Central venous pressure
0 to +8 mmHg (mean)
Right ventricular pressure
+15 to +30 mmHg systolic
0 to +8 mmHg diastolic
Pulmonary artery wedge
pressure
+5 to +15 mmHg (mean)
Left atrial pressure
+4 to +12 mmHg (mean)
Left ventricular pressure
90 to 140 mmHg systolic
+4 to +12 mmHg diastolic
Aortic pressure
90 to 140 mmHg systolic
60 to 90 mmHg diastolic
70 to 105 mmHg (mean)
CHAPTER 7
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Assessment, monitoring and diagnostics
123
TABLE 7.2 Normal haemodynamic values13,159
Parameter
Description
Normal values
Stroke volume (SV)
Volume of blood ejected from left ventricle/beat
SV = CO/HR
50–100 mL/beat
Stroke volume index (SVI)
Volume of blood ejected/beat indexed to BSA
25–45 mL/beat
Cardiac output (CO)
Volume of blood ejected from left ventricle/min
CO = HR × SV
4–8 L/min
Cardiac index (CI)
A derived value reflecting the volume of blood ejected
from left ventricle/min indexed to BSA
CI = CO/BSA
2.5–4.2 L/min/m2 (normal
assumes an average
weight of 70 kg)
Flow time corrected (FTc)
Systolic flow time corrected for heart rate
330–360 msec
Systemic vascular resistance
(SVR)
Resistance left heart pumps against
SVR = [(MAP – RAP) × 79.9]/CO
900–1300 dynes/sec/cm-5
Systemic vascular resistance
index (SVRI)
Resistance left heart pumps against indexed to body
surface area
SVRI = [(MAP – RAP) × 79.9]/CI
1700–2400 dynes/sec/cm5/
m2
Pulmonary vascular
resistance (PVR)
Resistance right heart pumps against
PVR = [(mPAP – LVEDP) × 79.9]/CO
20–120 dynes/sec/cm-5
Pulmonary vascular
resistance index (PVRI)
Resistance right heart pumps against indexed to body
surface area
PVRI = [(mPAP – LVEDP) × 79.9]/CI
255–285 dynes/sec/cm5/m2
Mixed venous saturation
(SvO2)
Shows the balance between arterial O2 supply and oxygen
demand at the tissue level
70%
Left ventricular stroke work
index (LVSWI)
Amount of work performed by LV with each heartbeat
(MAP – LVEDP) × SVI × 0.0136
50–62 g-m/m2
Right ventricular stroke
work index (RVSWI)
Amount of work performed by RV with each heartbeat
(mPAP – RAP) × SVI × 0.0136
7.9–9.7 g-m/m2
Right ventricular end-systolic The volume of blood remaining in the ventricle at the end
volume (RVESV)
of the ejection phase of the heartbeat
50–100 mL/beat
Right ventricular end-systolic
volume index (RVESVI)
30–60 mL/m2
Right ventricular enddiastolic volume (RVEDV)
The amount of blood in the ventricle immediately before a 100–160 mL/beat
cardiac contraction begins
Right ventricular enddiastolic volume index
(RVEDVI)
60–100 mL/m2
BSA = Body surface area
Central venous catheters used for haemodynamic
monitoring are classed as short-term percutaneous (nontunnelled) devices. Short-term percutaneous catheters are
inserted through the skin, directly into a central vein, and
usually remain in situ for only a few days or for a maximum
of 2–3 weeks.47,52 They are easily removed and changed,
and are manufactured as single- or multi-lumen types.
However, they can be easily dislodged, are thrombogenic
due to their material, and are associated with a high risk
of infection.47,53
A number of locations can be used for central venous
access; the two commonest sites in critically ill patients are the
subclavian and the internal jugular vein approaches. Other
less common sites are the antecubital fossa (generally avoided
but may be used when the patient cannot be positioned
supine), the femoral vein (associated with high infection risk),
and the external jugular vein (although the high incidence of
anomalous anatomy and the severe angle with the subclavian
vein make this an unpopular choice).53
Internal jugular cannulation has a high success rate for
insertion; however, complications related to insertion via this
route include carotid artery puncture and laceration of local
neck structures arising from needle probing.53,54 There are a
number of key structures adjacent to the vein, including the
124
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Principles and practice of critical care
vagus nerve (located posteriorly to the internal jugular vein);
the sympathetic trunk (located behind the vagus nerve); and
the phrenic nerve (located laterally to the internal jugular).55
Damage can also occur to the sympathetic chain, which
leads to Horner’s syndrome (constricted pupil, ptosis, and
absence of sweat gland activity on that side of the face).
Central venous catheters inserted in the internal jugular
vein pose a number of nursing challenges, particularly in
relation to beard growth; diaphoresis; and poor control of
oral secretions, which can cause fixation problems and the
need for repeated dressing changes.
The subclavian approach is used often, perhaps because
of a reported lower risk of catheter-related bloodstream
infection.55–57 Coagulopathy is a significant contraindication
for this approach, as puncture of the subclavian artery is a
known complication. There is also a risk of pneumothorax,
which rises if the patient is receiving intermittent positive
pressure ventilation (IPPV).56 Complications of any central
venous access catheters include air embolism, pneumothorax,
hydrothorax and haemorrhage.53
Pulmonary artery pressure (PAP) monitoring. Pulmonary
artery pressure monitoring began in the 1970s, led by Drs
Swan, Ganz and colleagues,58 and was subsequently adopted
in ICUs worldwide. Pulmonary artery catherisation facilitates
assessment of filling pressure of the left ventricle through
the pulmonary artery wedge (occlusion) pressure (see Figure
7.12).54,59 By using a thermodilution pulmonary artery
catheter (PAC), cardiac output and other haemodynamic
measurements can also be calculated. PAP monitoring is
A
B
C
FIGURE 7.12 Pulmonary artery catheter29 (published with permission)
CHAPTER 7
a diagnostic tool that can assist in determination of the
nature of a haemodynamic problem and improve diagnostic
accuracy.
The beneficial claims of PAP monitoring have, however,
been questioned, with some proposing a moratorium.60,61
In response, two consensus conferences were held in the
USA to make recommendations for future practice. These
concluded that there was no basis for a moratorium on the
use of PACs; instead, education and knowledge about the
use of this technology must be standardised and monitored.
Further research was indicated, particularly focusing on the
use of PACs and ARDS, and congestive cardiac failure.62,63
More recently, an observational cohort study of 7310
patients found that PAC use was not associated with an
overall higher mortality, although the authors concluded
that severity of illness should be examined when considering
the use of this measurement tool.64 A systematic review is
currently underway through the Cochrane Collaboration
to synthesise the available evidence relating to the effects
of PACs on mortality and cost-of-care in adult intensive
care patients.65 In the meantime, proponents for continuing
clinical use of the PAC argue that it provides a physiological
rationale for diagnosis and assists in the titration of therapies
such as inotropes, which would otherwise be potentially
dangerous.41,59,62
PAP monitoring is indicated for adults in severe
hypovolaemic or cardiogenic shock, where there may be
diagnostic uncertainty, or where the patient is unresponsive
to initial therapy. The PAP is used to guide administration of
fluid, inotropes and vasopressors. PAP monitoring may also
be utilised in other cases of haemodynamic instability when
diagnosis is unclear. It may be helpful when clinicians want
■
Assessment, monitoring and diagnostics
to differentiate hypovolaemic from cardiogenic shock or,
in cases of pulmonary oedema, to differentiate cardiogenic
from non-cardiogenic origins.66 It has been used to guide
haemodynamic support in a number of disease states such
as shock, and to assist in assessing the effects of fluid
management therapy. 45,59
Complications do arise from PACs, as these catheters share
all the complications of central lines and are additionally
associated with a higher incidence of dysrhythmia (particularly
due to cold bolus injectate, which irritates myocardium), valve
damage, pulmonary vascular occlusion, emboli/infarction
(reported incidence of 0.1%–5.6%) and, very rarely, knotting
of the catheter.53
A number of measurements can be taken via the PAC,
either by direct measurement, for example using pulmonary
capillary wedge pressure (PCWP), which is an estimate of
left ventricular preload (LVEDV) or through calculation
of derived parameters, such as cardiac output (CO) and
cardiac index (CI)45(see Table 7.2 for descriptors and normal
values).
Pulmonary capillary wedge pressure (PCWP) monitoring. Pulmonary capillary wedge pressure, or pulmonary
artery occlusion pressure (PAOP), is measured when the
pulmonary artery catheter balloon is inflated with no more
than 1–1.5 mL air. The inflated balloon isolates the distal
measuring lumen from the pulmonary arterial pressures,
and measures pressures in the capillaries of the pulmonary
venous system, and indirectly the left atrial pressure. The
PAP waveform looks similar to that of the arterial waveform,
with the tracing showing a systolic peak, dicrotic notch
and a diastolic dip (see Figure 7.13). When the balloon is
Flow-directed
catheter
Pressure
Right atrium
Right ventricle
125
Pulmonary artery
Pulmonary artery wedge (PAOP)
30
mm Hg
20
mm Hg
10
mm Hg
0
mm Hg
FIGURE 7.13 Pulmonary artery pressure and wedge waveforms29 (published with permission)
126
SECTION 2
■
Principles and practice of critical care
inflated, the waveform changes shape and becomes much
flatter in appearance, providing a similar waveform to the
CVP. There are two positive waves on the tracing: the first
reflects atrial contraction, and the second reflects pressure
changes from blood flow when the mitral valve closes and
the ventricles contract.67 The PCWP should be read once
the ‘wedge’ trace stops falling at the end-expiratory phase
of the respiratory cycle (see Figure 7.13).
If balloon occlusion occurs with <1 mL air, then the
balloon is wedged in a small capillary and consequently will
not accurately reflect LA pressure. Conversely, if 1.5 mL air
does not cause occlusion, the balloon may have burst (which
can result in an air embolus) or it may be floating in a larger
vessel. If balloon rupture is suspected, no further attempts
to inflate the balloon should be made, and interventions to
minimise the risk of air embolism should be initiated; the
patient should be positioned to the left lateral with headdown tilt.68 Note: it is essential that the balloon be deflated
as soon as the wedge has been recorded, as continued
occlusion will cause distal pulmonary vasculature ischaemia
and infarction.69
Left atrial pressure (LAP) monitoring. Left atrial pressure
monitoring directly estimates left heart preload, but requires
an open thorax to enable direct cannulation of the atrium.
It is used only in the postoperative cardiac surgical setting,
although such use is infrequent since the widespread use of
PAC. Complications, recorded in a large retrospective study,
occurred in just 0.2% of patients,70 although other modes of
monitoring can also be used to achieve comprehensive left
atrial assessment, such as Doppler echocardiography.71
AFTERLOAD
As previously noted, afterload is the pressure that the ventricle
produces to overcome the resistance to ejection generated
in the systematic or pulmonary circulation by the arteries
and arterioles. It is calculated by cardiac output studies: left
heart afterload is reflected as systemic vascular resistance
(SVR), and right heart afterload is reflected as pulmonary
vascular resistance (PVR) (Table 7.2).
Systemic and pulmonary vascular resistance. Systemic vascular
resistance is a measure of resistance or impediment of the
systemic vascular bed to blood flow. An elevated SVR can
be caused by vasoconstrictors, hypovolaemia or late septic
shock. A lowered SVR can be caused by early septic shock,
vasodilators, morphine, nitrates or hypercarbia. Afterload is a
major determinant of blood pressure, and gross vasodilation
causes peripheral pooling and hypotension, reducing
SVR. The precise estimation of SVR enables safer use of
therapies such as vasodilators (e.g. sodium nitroprusside)
and vasoconstrictors (e.g. noradrenaline).11
Pulmonary vascular resistance is a measure of resistance
or the impediment of the pulmonary vascular bed to blood
flow. An elevated PVR (‘pulmonary hypertension’) is caused
by pulmonary vascular disease, pulmonary embolism,
pulmonary vasculitis or hypoxia. A lowered PVR is caused by
medications such as calcium channel blockers, aminophylline
or isoproterenol, or by the delivery of O2.10,11
CONTRACTILITY
Contractility reflects the force of myocardial contraction, and
is related to the extent of myocardial fibre stretch (preload see
above) and wall tension (afterload, see above). It is important
because it influences myocardial oxygen consumption.
Contractility of the left side of the heart is measured by
calculating the left ventricular stroke work index (LVSWI),
although the clinical use of this value is not widespread.
Right ventricular stroke work index (RVSWI) can be similarly
calculated. Contractility can decrease as a result of excessive
preload or afterload, drugs such as negative inotropes,
myocardial damage such as that occurring after MI, and
changes in the cellular environment arising from acidosis,
hypoxia or electrolyte imbalances. Increases in contractility
arise from drugs such as positive inotropes.72
CARDIAC OUTPUT
The variety of cardiac output measurement techniques
has grown over the past decade73 since the development of
thermodilution pulmonary artery catheters, pulse-induced
contour devices, and less invasive techniques such as Doppler.
As many critically ill patients require ventilatory support, the
associated rises in intrathoracic pressure, as well as changing
ventricular compliance, make accurate haemodynamic
assessment difficult with the older technologies. Therefore,
volumetric measurements of preload, such as right ventricular
end-systolic volume (RVESV), right ventricular end-diastolic
volume (RVEDV) and index (RVESVI/RVEDVI) as well as
measurements of right ventricular ejection fraction (RVEF)
are now being used to more accurately determine cardiac
output. The parameters RVEF, CO and/or CI, and stroke
volume (SV) are generated using thermodilution technology,
and from these the parameters of RVEDV/RVEDVI and
RVESV/RVESVI can be calculated (see Table 7.2 for normal
values).13 The availability of continuous modes of assessment
has further improved a clinician’s ability to effectively treat
these patients.13
Thermodilution cardiac output. Cardiac output (CO) and
associated pressures such as global end-diastolic volume50 can
be calculated using a thermodilution PA catheter. Intermittent
measurements obtained every few hours produce a snapshot
of the cardiovascular state over that time. By injecting a
bolus of 5–10ml of crystalloid solution, and measuring
the resulting temperature changes, an estimation of stroke
volume is calculated. Cold injectate (run through ice) was
initially recommended, but studies now support the use of
room temperature injectate, providing there is a difference
of 12º Celsius between injectate and blood temperature.74
Three readings are taken at the same part of the respiratory
cycle (normally end expiration), and any measurements that
differ by more than 10% should be disregarded (see Table 7.2
for normal values). Since the 1990s, the value of having
continuous measurement of cardiac output has been recognised 59and this has led to the development of devices which
permit the transference of pulses of thermal energy to
pulmonary artery blood; the pulse-induced contour method.71
Pulse-induced contour cardiac output. Pulse-induced contour
cardiac output (PiCCO) provides continuous assessment of
CHAPTER 7
CO, and requires a central venous line and an arterial line
with a thermistor (not a PAC).75A known volume of thermal
indicator (usually room temperature saline) is injected into
the central vein. The injectate disperses both volumetrically
and thermally within the cardiac and pulmonary blood. When
the thermal signal is detected by the arterial thermistor, the
temperature difference is calculated and a dissipation curve
generated.76 From these data, the cardiac output can be
calculated. These continuous cardiac output measurements
have been well researched over the past 10 years and appear
to be equal in accuracy to intermittent injections required
for the earlier catheters.73,77,78 The parameters measured by
PiCCO75 include:
• Pulse-induced contour cardiac output—derived normal
value for cardiac index 2.5–4.2 L/min/m2.
• Global end-diastolic volume (GEDV)—the volume of
blood contained in the four chambers of the heart;
assists in the calculation of intrathoracic blood
volume. Derived normal value for global end-diastolic
blood volume index 680–800 mL/m2.
• Intrathoracic blood volume (ITBV)—the volume of
the four chambers of the heart plus the blood volume
in the pulmonary vessels; more accurately reflects
circulating blood volumes, particularly when a patient
is artificially ventilated. Derived normal value for
intrathoracic blood volume index 850–1000 mL/m2.
• Extravascular lung water (EVLW)—the amount of
water content in the lungs; allows quantification of
the degree of pulmonary oedema (not evident with
X-ray or blood gases). Derived normal value for
extravascular lung water index 3.0–7.0 mL/kg.
EVLW has been shown to be useful as a guide for fluid
management in critically ill patients.74 An elevated EVLW
may be an effective indicator of severity of illness, particularly
CI (l/min/m2)
Results
Assessment, monitoring and diagnostics
>3.0
<700
<850
>700
>850
<700
<850
>700
>850
<10
>10
<10
>10
<10
>10
V+
V+!
Cat
Cat
Cat
V–
V+
V+!
<10
>10
Therapy
V–
Target
1. GEDI (ml/m2)
or ITBI (ml/m2)
2. Optimise SVV (%)*
GEF (%)
or CFI (1/min)
ELWI (ml/kg)
(slowly responding)
V+ = volume loading (! = cautiously)
>700 700–800 >700 700–800
>850 850–1000 >850 850–1000
<10
<10
<10
<10
>25
>4.5
>30
>5.5
>25
>4.5
≤10
V- = volume contraction
127
after acute lung injury or in ARDS, when EVLW is elevated
due to alterations in hydrostatic pressures.79 Other patients
at risk of high ELWV are those with left heart failure,
severe pneumonia, and burns. There may be an association
between a high EVLW and increased mortality, the need
for mechanical ventilation and a higher risk of nosocomial
infection.79 A decision tree outlining processes of care
guided by information provided by PiCCO is provided in
Figure 7.14.
PiCCO removes the impact of factors that can cause
variability in the standard approach of cardiac output
measurement, such as injectate volume and temperature,
and timing of the injection within the respiratory cycle.80
The additional fluid volume injected with the standard
technique is significant in some patients; with the continuous
technology this is eliminated. A further advantage is that
virtually real-time responses to treatment can be obtained,
removing the time delay that was a potential problem with
standard thermodilution techniques.71
An arterial catheter is widely used in critical care to enable
frequent blood sampling and blood pressure monitoring, and
is used to measure beat-by-beat cardiac output, obtained
from the shape of the arterial pressure wave. The area under
the systolic portion of the arterial pulse wave from the end
of diastole to the end of the ejection phase is measured and
combined with an individual calibration factor. The algorithm
is capable of computing each single stroke volume after being
calibrated by an initial transpulmonary thermodilution.
PiCCO preload indicators of intrathoracic blood volume
(ITBV) and global end-diastolic volume (GEDV) are more
sensitive and specific to cardiac preload than the standard
cardiac filling pressures of CVP and PCWP, as well as right
ventricular end-diastolic volume.50 One advantage of ITBV
and GEDV is that they are not affected by mechanical
<3.0
GEDI (ml/m2)
or ITBI (ml/m2)
ELWI (ml/kg)
■
>700 700–800
>850 850–1000
<10
<10
>30
>5.5
≤10
Cat = catecholamine / cardiovascular agents
*SVV only applicable in ventilated patients without cardiac arrhythmia
Without guarantee
FIGURE 7.14 PiCCO decision tree (published with permission, Pulsion Medical Systems)
700–800
850–1000
<10
<10
OK!
≤10
≤10
128
SECTION 2
■
Principles and practice of critical care
ventilation and therefore give correct information on the
preload status under almost any condition. Extravascular
lung water correlates moderately well with severity of
ARDS, length of ventilation days, ICU stay and mortality,81
and appears to be of greater accuracy than the traditional
assessment of lung oedema by chest X-ray. Disadvantages
of PiCCO include its potential unreliability when heart
rate, blood pressure and total vascular resistance change
substantially.13,75
Oesophageal Doppler monitoring. Oesophageal Doppler
monitoring, often referred to as transoesophageal
echocardiography (TOE), also enables calculation of cardiac
output82 from assessment of stroke volume and heart rate, but
uses a less invasive technique than those outlined previously.
Stroke volume is assessed by measuring the flow velocity
and the area through which the forward flow travels. Flow
velocity is the distance one red blood cell travels forward
in one cardiac cycle, and the measurement provides a time
velocity interval (TVI). The area of flow is calculated by
measuring the cross-sectional area of the blood vessel or
heart chamber at the site of the flow velocity management.83
TOE can be performed at the level of the pulmonary artery,
mitral valve or aortic valve.
Doppler principles are that the movement of blood
produces a waveform that reflects blood flow velocity, in
this case in the descending thoracic aorta, by capturing the
change in frequency of an ultrasound beam as it reflects off
a moving object (see figure 7.15).32 This measurement is
combined with an estimate of the aorta’s cross-sectional area
for the stroke volume, cardiac output and cardiac index to
be calculated, using the patient’s age, height and weight.84
Oesophageal Doppler monitoring provides an alternative
for patients who would not benefit from PAC insertion,84
and can be used to provide continuous measurements under
certain conditions: the estimate of cross-sectional area must
be accurate; the ultrasound beam must be directed parallel
to the flow of blood; and there should be minimal variation
in movement of the beam between measurements. There is
some debate at present among clinicians about the accuracy
of TOE when compared with thermodilution technique
for calculating cardiac output.85–87 However, Australian
research purports that this technology has become and will
continue to be an invaluable tool in critical care.82 This
form of monitoring can be used perioperatively and in the
critical care unit, on a wide variety of patients. It should
not, however, be used in patients with aortic coarctation or
dissection, oesophageal malignancy or perforation, severe
bleeding problems, or with patients on an intra-aortic
balloon pump.84
The Doppler probe that sits in the oesophagus is
approximately the size of a nasogastric tube, is semirigid
and is inserted using a similar technique.84 The patient is
usually sedated but it has been used in awake patients.88 In
such cases, however, the limitation is that the probe is more
likely to require more frequent repositioning.83
The waveform that is displayed on the monitor is triangular
in shape (see Figure 7.15) and captures the systolic portion
of the cardiac cycle—an upstroke at the beginning of systole,
the peak reflecting maximum systole, and the downward
slope of the ending of systole. The waveform captures realtime changes in blood flow and can therefore be seen as an
indirect reflection of left ventricular function.84 Changes to
haemodynamic status will be reflected in alterations in the
triangular shape (see Figure 7.15).
Transthoracic bioimpedance. Transthoracic bioimpedance
(impedance cardiography) is another form of non-invasive
monitoring used to estimate cardiac output, and was first
introduced by Kubicek in 1966.89 It measures the amount
of electrical resistance generated by the thorax to highfrequency, very-low-magnitude currents. This measure is
inversely proportional to the content of fluid in the thorax:
if the amount of thoracic fluid increases, then transthoracic
bioimpedance falls.32 Changes in cardiac output can be
reflected as a change in overall bioimpedance. The technique
requires six electrodes to be positioned on the patient: two
in the upper thorax/neck area, and four in the lower thorax.
These electrodes also monitor electrical signals from the
heart.
Overall, transthoracic bioimpedance is determined by:
(a) changes in tissue fluid volume; (b) volumetric changes
in pulmonary and venous blood caused by respiration; and
(c) volumetric changes in aortic blood flow produced by
a) Decreased preload
a) Increased preload
Fluids
b) Poor contractility
b) Increased contractility
Inotropes
c) High afterload (high SVR)
c) Decreased afterload
Vasodilators
FIGURE 7.15 Oesophageal Doppler waveforms83 (published with
permission)
CHAPTER 7
myocardial contractility. Accurate measurements of changes
in aortic blood flow are dependent on the ability to measure
the third determinant, while filtering out any interference
produced by the first two determinants. Any changes to
position or to electrode contact will cause alterations to the
measurements obtained, and recordings should therefore be
undertaken with the electrodes positioned in the same location
as previous readings. Caution is required for patients with
high levels of perspiration (which reduces electrode contact),
atrial fibrillation (irregular R-R intervals makes estimation
of the ventricular ejection time difficult), or pulmonary
oedema, pleural effusions or chest wall oedema (which alter
bioimpedance readings irrespective of any changes in cardiac
output). The use of transthoracic bioimpedance in critically ill
patients is variable, due in part to limitations of its usefulness
in patients who have pulmonary oedema.90–93
RESPIRATORY MONITORING
Respiratory insufficiency is one of the main reasons for
admission to a critical care unit, as either a potential or
actual problem, so comprehensive respiratory monitoring
is essential.18 Critical care nurses need to utilise evidence in
their practice to expand their roles and act on findings arising
from accurate and comprehensive assessment. Patients with
respiratory problems have a wide range of symptoms, some
of which are not directly associated with the respiratory
system. (Further information relating to respiratory diseases
and other conditions that cause respiratory symptoms is
provided in Chapter 11.) A thorough assessment, followed
by accurate ongoing monitoring, enables early detection of
condition changes and assessment of the impact of treatment.
This section focuses on the main aspects of respiratory
monitoring and the tools used, including arterial blood gas
(ABG) analysis, capnography and pulse oximetry to assess
the efficiency of the patient’s gas transfer mechanisms.18
Pulse oximetry
Pulse oximetry is a non-invasive device that measures
peripheral (capillary) saturation of haemoglobin by oxygen.
The technology is now generally regarded as standard for
critical care units24 and is recognised as being one of the
major advances in clinical monitoring.94,95 It works by using
select wavelengths of light and, as arterioles empty during
diastole, differentiation of infrared light absorption by
blood is recorded using a pulse oximeter probe.96 The signal
emitted is measured over five pulses, causing a slight delay
when monitoring. Two wavelengths of light are emitted,
red and infrared, from a diode (positioned on one side of
the probe) to a photodetector (positioned on the opposite
side). Well-oxygenated blood absorbs light differently from
deoxygenated blood, with the oximeter determining the
amount of light absorbed by the vascular bed and calculating
the saturation of oxygen in those capillaries (SpO2). SpO2
and heart rate are continuously displayed on the monitor
as digital readings. Normal SpO2 is greater than 97%. The
probes used to emit the infrared light source can be sited
■
Assessment, monitoring and diagnostics
129
on a finger, toe or ear. The probes used in pulse oximetry
generate heat which, in extreme cases, may cause burns,
especially in patients with poorly perfused peripheries. A
frequent change of probe positions is required.97,98 Perfusion
of the site also needs to be assessed, along with other visual
observations of the probe site.
Pulse oximetry alone, however, does not provide all the
information needed on ventilation status and acid–base
balance. Therefore, arterial blood gases are also needed
periodically to assess other parameters. Other limitations
arise with oximetry monitoring:
• Peripheral vasoconstriction results in poor perfusion,
causing poor flow and less accurate signals.99
• Cardiac dysrhythmias can impair perfusion and flow.
• Shivering and other movements may give poor or
inaccurate readings.95
• The presence of high levels of bilirubin, dark skin and
nail varnish may cause underestimation of SpO2, as
light is absorbed in these circumstances.98
• External light can overestimate SpO2, especially
fluorescent light and heat lamps; ear probes in
particular may detect overhead lighting.
• Dyshaemoglobins such as carboxyhaemoglobin levels
above 3% cause overreading, making SpO2 monitoring
unreliable.7,100
• When hypercapnia is present (e.g. in patients with
COPD), SpO2 monitoring alone is unreliable.97
Pulse oximetry is subject to low-level accuracy, and when
the SpO2 is below 80% its use is unproven.7 It is therefore
important that when SpO2 appears to be abnormal, the
arterial blood is sampled and gases are checked.
Ventilation monitoring
Mechanical ventilation is a common intervention used in
ICUs for patients with respiratory failure or who require
respiratory support (see Chapter 11). The recent major
advances in ventilation technology challenge all critical
care clinicians.101,102 Many mechanical ventilators now offer
integrated graphic displays, usually as waveforms that plot
one of three parameters against time:103–105
• airway pressure vs time;
• inspiratory and expiratory flow vs time; or
• inspiratory and expiratory tidal volume vs time.
Also available are data describing:
• pressure vs volume loops; and
• flow vs volume loops.
Respiratory waveforms are normally displayed on the
ventilator screen, and most systems provide the flexibility
to adjust the vertical and horizontal axis, allowing the user
to examine more closely particular sections and to fine-tune
the ventilator settings. This can help in assessing patient–
ventilator synchrony, assist in the setting of appropriate
inspiratory/expiratory times, and determine the extent
of increased airway resistance. Circuit leaks can also be
identified through these data and the waveforms can be
used to explain the different ventilation modes, utilising
graphic analysis. Pressure vs volume loops may also be used
to ascertain lung compliance, with lower inflection points
guiding positive end-expiratory pressure (PEEP) application
130
SECTION 2
■
Principles and practice of critical care
Practice tip
Clinicians should familiarise themselves with their unit’s
ventilator graphic package. These are generally intuitive, and
the manipulation of the various screens has no impact on actual
ventilator settings. Confidence builds with basic familiarisation.
This process in itself may constitute a good topic for a clinical
workshop conducted in your ICU.
and with upper inflection point providing a guide to lung
overdistension.7,106
PRESSURES
Understanding the various pressure displays is an important
aspect of ICU nursing practice.103 For instance, in volumecycled ventilation, peak inspiratory pressure does not
always represent peak alveolar pressure, especially when
there is increased inspiratory airways resistance. In such
cases, pause or plateau pressure is more reflective of the
pressure in the alveoli; this is when there is no influence of
inspiratory flow on the pressure readings. In pressure control
mode,107,108 the alveolar pressure cannot be inferred until
inspiratory flow has fallen to the zero baseline, just prior to
exhalation. Significant differences between peak inspiratory
and end-inspiratory pressures require examination of the
expiratory flow waveform to investigate the reasons for
any increase in inspiratory resistance. Many valuable lung
mechanics properties can be derived from knowing these
simple values. Knowing these different pressures displayed
by the waveforms allows the ventilator’s lung mechanics
software packages to calculate many useful parameters,
such as static lung compliance, inspiratory and expiratory
airways resistances. These derived parameters may further
guide therapeutic interventions.
WAVEFORMS
Each of the ventilation waveforms requires careful analysis.103
A clinician can examine the airway pressure and the flow
screens to assess whether the patient is triggering a breath,
the level of the baseline pressure, the modality of ventilation,
extent of patient synchronisation with the ventilator breath,
and evidence of gas trapping.103 These are described further
below.
Airway pressure vs time. The morphology of this waveform
depends on which ventilation strategy is chosen (volume or
pressure), and whether the patient is generating spontaneous
breaths.109 Pressure–time waveforms110 reflect inspiratory and
expiratory phases and can be used to facilitate calculation of
inspiratory time, breathing rate, peak airway pressure, alveolar
pressure (with co-analysis of the flow waveform) and
PEEP (see Figure 7.16). With pressure–time waveforms,
the vertical axis represents pressure and the horizontal
represents time.
The resting value in expiration represents the PEEP
setting or the baseline pressure. The breath then moves
into the inspiratory phase, which is triggered either by time
(ventilator set rate) or by the patient’s inspiratory effort.
Patient effort can be sensed either by a pressure drop relative
to PEEP (pressure triggering) or by direct patient inspiratory
flow (flow triggering). This effort should be minimal and
not cause the PEEP to drop by more than 2–3 cmH2O at the
start of inspiration.103 The ventilator should respond quickly
to this effort with a rapid rise in airway pressure. A slow
rise, possibly only at the end of inspiration, implies that the
patient is wanting more inspiratory flow and volume than
the ventilator can, or has been programmed to, deliver; this
is more common in volume-targeted ventilation modes than
in pressure-targeted modes.103,108 In pressure-targeted modes
(pressure control, pressure support) inspiratory flow is not
set; the patient is allowed to take flow from the ventilator’s
demand system, commonly up to 200 L/min.110
The airway pressure graphic represents what is occurring
on the ventilator side of the endotracheal tube. Alveolar
pressure will lag in time from what is seen on the ventilator
Pressure
(mbar)
Peak pressure
C
.
‘Resistance pressure’ (R .V)
D
B
Resistance
Pressure
.
(R . V)
A
E
Plateau pressure
Gradient
.
V/C
Flowphase
‘Compliance pressure’ (VT/C)
Pause
phase
F
‘PEEP’
Time (s)
Inspiration time
Expiration time
(V insp = const.)
FIGURE 7.16 Airway pressure vs time (published with permission, Dräger Medical)
CHAPTER 7
Practice tip
If there appears to be inconsistent triggering of the ventilator
by the patient despite the patient breathing regularly, check
the expiratory flow waveform. If this has failed to return to the
zero baseline there may be gas trapping. Ventilation should
be adapted to ensure that the patient expires all inspired tidal
volume, e.g. by increasing expiratory time. Gas trapping may
result in patient fatigue or cardiac embarrassment.
screen and, depending on airway resistance, may bear no
resemblance to the pressures being displayed.110 For example,
the presence of auto-PEEP (pressure inside the alveolus
not routinely seen on the ventilator expiratory pressure
waveform) may cause the patient to make inspiratory efforts,
which the ventilator fails to detect, resulting in no breath
being delivered. This increases the work of the breathing,
which for some patients (e.g. those with severe asthma) may
increase morbidity and mortality.111,112 Significant levels of
auto-PEEP may also cause a reduction in cardiac output, as
this pressure in the chest is impeding venous return. When
any form of artificial ventilation is applied, expiratory time
must be long enough to ensure that all the gas delivered is
exhaled before the next breath is delivered. If this is achieved,
auto-PEEP will be minimised.
Assessment, monitoring and diagnostics
■
Volume
Volume-oriented
Time
Flow
Time
Pressure
Time
Volume
Flow vs time. With flow–time waveforms, flow is plotted
on the vertical axis, while time is on the horizontal.103
This waveform assists with detecting levels of auto-PEEP
as well as the patient’s reponse to medications such as
bronchodilators. 111 Two components are displayed,
inspiratory and expiratory flows (see Figure 7.17). The
inspiratory waveform is generated from the inspiratory
flow transducer commonly located inside the ventilator just
prior to the inspiratory outlet port. The inspiratory flow
waveform’s shape and peak value depends on a number of
factors:
• the ventilatory strategy chosen (i.e. volume vs
pressure);
• the programmed inspiratory time;
• the selected inspiratory flow waveform; and
• the presence of spontaneous breathing.
The inspiratory waveform is unique to the type of breath
and will therefore be different for pressure, volume or
spontaneous breathing.103 In volume modes of ventilation, the
flow pattern is generally stable throughout the breath, thus
reflecting the constant speed of gas delivery. This generates
a square low waveform. Flow should start from the zero
baseline, reach its peak and then, at the point at which
exhalation commences, the value is read by the exhalation
flow transducer (commonly located in the distal section of
the expiratory limb, after the exhalation valve). In pressure
modes, the flow is higher at the beginning of the breath
than at the end, generating a tapering flow waveform as the
lungs fill.103 Spontaneous breath waveforms have a similar
shape to those of pressure modes, but they are generally
more rounded.103
In the normal expiratory flow waveform, a sharp peak
expiratory flow value, depicted below the zero baseline, is
131
Pressure-oriented
Time
Flow
Time
Pressure
Time
Flow
phase
Pause
phase
Inspiration
Flow
phase
Pause
phase
Expiration
FIGURE 7.17 Pressure, flow and volume vs time (published with
permission, Dräger Medical)
Flow
■
Principles and practice of critical care
Flow
E xp
irato
ry
Time
Tidal volume m/sec
SECTION 2
Tidal volume m/sec
Ins
pira
tor
y
132
Time
(sec)
0
Leak
volume
Time
(sec)
0
FIGURE 7.19 Tidal volume vs time, with and without leak
FIGURE 7.18 Expiratory flow curve in the case of increased
expiratory resistance (published with permission, Dräger Medical)
recorded, followed by the flow returning promptly to zero,
prior to the next inspiratory effort. If this waveform fails to
return to the baseline before the next breath, this indicates
that not all of the previous volume has been exhaled, which
leads to ‘gas trapping’.112 This can result in significant levels
of ‘inadvertent’ or ‘auto-PEEP’, which has the potential to
adversely affect a patient’s haemodynamics and prevent the
patient from synchronising breaths with the ventilator.112
In such circumstances, the patient has to overcome the set
trigger sensitivity, as well as the auto-PEEP value, and this
can be distressing for some patients.
For some forms of intervention, such as bronchodilator
therapy, the expiratory flow waveform provides information
on therapeutic effect.111,112 In other circumstances, such as
when a patient is suffering from acute asthma, the flow
waveform indicates gas trapping (see Figure 7.18).111,112
The flow waveform can also be helpful when investigating
internal faults within the ventilator and its circuitry. Normally
the exhaled tidal volume should equal the inspired tidal
volume. If this is not the case, a reason should be found for
the discrepancy. If there is a leak in the ventilator circuitry
(including the ETT cuff), gas trapping may be occurring.
If, after all investigations, no reason for the leak can be
found, consider whether the flow transducer may be out of
calibration or damaged. Exhalation flow transducers are
commonly part of the ventilator circuit, and care needs to be
taken with their sterilisation, as this can result in transducers
being out of calibration. Some ventilator manufacturers avoid
this by placing a hydrophobic viral/bacterial filter before the
exhalation flow transducer, thus protecting it from damage.
If a viral/bacterial filter is used in the expiratory limb of
the ventilator, regular checking of its resistance should be
performed so as to avoid patient-triggering problems. Many
modern ventilators have their triggering site located in the
expiratory limb of the ventilator, possibly on the other side
of an expiratory viral/bacterial filter.
Tidal volume vs time. In this graphic, the inspiratory and
expiratory flow waveforms are mathematically integrated,
yielding inspiratory tidal and expiratory tidal volume
waveforms. This waveform (see Figure 7.19) starts from
a baseline of the functional residual capacity (FRC) of the
lung, then rises as inspiratory flow is delivered, to reach
the inspiratory tidal volume. Once the inspiratory time
has elapsed, the waveform falls back towards baseline as
exhalation occurs. It is usually the expiratory tidal volume
waveform that is displayed on the ventilator monitor; however,
some ventilators offer both inspiratory and expiratory tidal
volume displays. Having both these volumes displayed can
be useful, especially when you are trying to minimise a
leak through a bronchopleural fistula. It is then possible to
quantify the leak and have this recorded and trended in the
patient’s record.
The tidal volume waveform is also useful in troubleshooting
circuit leaks (see Figure 7.19); if it fails to return to its baseline,
the clinician should look for a leak in the circuit–patient
interface. However, an elevated baseline can also be caused
by an incorrectly calibrated or damaged expiratory flow
transducer. The tidal volume graphic may also be useful in
detecting the presence of pulmonary leaks via intercostal
catheters.113,114
Pressure vs volume loop. This graphic represents the dynamic
compliance between the lungs and the ventilator circuit.
The two parameters, airway pressure and tidal volume, are
plotted against each other; the ascending limb of the loop
represents inspiration and the descending limb represents
expiration (see Figure 7.20).
As inspiratory pressure rises, there is initially little
change in delivered tidal volume. However, as inspiratory
pressure continues to rise, tidal volume suddenly increases
as alveoli are recruited, causing a change in the slope of
this inspiratory limb. This represents lung expansion with
tidal volume recruitment. As the lung reaches its capacity,
there is a flattening at the top of this pressure–volume
Volume
Expiration
B
Inspiration
A
Pressure
FIGURE 7.20 Pressure vs volume loop (published with
permission, Dräger Medical)
CHAPTER 7
loop, representing wasted and possibly injurious pressures.
Expiration commences, as reflected in the expiratory limb
of this loop. If pressure is allowed to return to zero the lung
units will collapse, requiring further inflation on the next
breath. Current ventilation strategies favour preventing
the end-expiratory volume from going too low and the
inspiratory volume going too high, with optimal operation
within this region.115–118 The sudden change in volume on
the lower portion of the inspiratory loop, representing
lung recruitment, may be used as a reference point at
which to set a patient’s PEEP, or slightly above this value,
to avoid repeated alveolar stretch and possible alveolar
damage.106,117
The expiratory part of the loop has been the subject
of recent research, which suggests that this limb of the
pressure–volume loop may offer more important clinical
information than the inspiratory limb.117,119–121 The expiratory
loop represents lung de-recruitment; the point at which
this occurs may be a more accurate PEEP reference point.
However, more evidence is needed to support this, and for
the time being clinicians will continue to examine the loops
for the inflection point on the inspiratory limb to help set
optimal PEEP.122–124
The area between the loops represents the resistance to
inspiration and expiration, known as hysteresis. The slope
of the line drawn between the ‘no flow’ points of the loops
represents the compliance of the lung/thorax; the flatter the
line, the lower the compliance.125
■
Assessment, monitoring and diagnostics
133
END-TIDAL CARBON DIOXIDE MONITORING
End-tidal carbon dioxide levels can be monitored using
capnography, which is defined as ‘the graphical and numerical
representation of carbon dioxide concentration during the
respiratory cycle’,126 and capnometry (the digital display
of carbon dioxide measurement). Such technology is now
widely available in the critical care environment.127 The first
device was used in 1943 by Luft,123 and over the ensuing
years this technology has become smaller, more accurate and
affordable. With the reliability of capnometry to differentiate
between endotracheal and oesophageal intubation, it has
been proposed as standard practice for the confirmation of
endotracheal tube placement in ICU.128,129
There are a number of methods to determine end-tidal
CO2 tension (PETCO2),130,131 but the infrared determination
appears most popular among monitoring manufacturers.
Infrared rays have a wavelength >1.0 µm, and carbon dioxide
is able to selectively absorb wavelengths of 4.3 µm. The
end-tidal CO2 monitor compares the absorbed value to a
known standard and the result is displayed in digital form
(capnometry), or more commonly in graphic form.
There are two common methods of determining PETCO2
using infrared technology:132
1. Mainstream sampling. The PETCO2 housing and sensor
head are in direct contact with the patient’s exhaled
gases (see Figure 7.21) and, as these are located in the
airway, they respond quickly to changes in PETCO2.
To prevent moisture from affecting the measurement,
CO2-sensor
Patient
Cuvette
FIGURE 7.21 Mainstream PETCO2 Ventilator setup (published with permission, Dräger Medical)
134
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■
Principles and practice of critical care
the sensor is usually heated; however, sputum may
migrate over the sampling windows and interrupt
measurement. These sensors/housings have over time
become less bulky, reducing traction on the airway.
2. Sidestream sampling. The PETCO2 sensor is located in
the main unit itself and a small pump, with a sampling
tube attached to a T piece located in the breathing
circuit, diverts sampled exhaled gases to the sensor.
Special tubing that allows moisture to escape prior
to the sensor should be used when using a sidestream
system, as this ensures more consistent results. For
accuracy, ideal sampling rates should be 50–200 mL/
min.132,133
As with all monitoring modalities, a thorough understanding
of this technique and its limitations is necessary.133 It is also
essential that the system be calibrated appropriately before
use. Potential sources of inaccuracy when using PETCO2
monitoring include:
• Humidity. The presence of water in either system may
falsely elevate the reading, but using semipermeable
tubing should minimise this. If the ventilator circuit
produces a lot of water, attention should be directed
to improving the efficiency of the humidifier–heater
wire interface. It is preferable to run inspiratory and
expiratory heater wires with full saturation of gases.
• Atmospheric pressure. Partial pressure does have an
effect on the displayed value of CO2; many monitoring
systems have a direct measurement of the presiding
barometric pressure and include this value in the
calculation of the displayed value of CO2. Periodic
checks should be undertaken to determine that
the machine-calculated value agrees with a known
accurate independent monitor; a good source of these
values is the local weather bureau/authority, and
the hospital laboratories are another good source of
barometric pressure readings. If a system requires a
value to be input for barometric pressure, this will
need checking on a regular basis. Reduced atmospheric
pressure also adversely affects the pumping of gas
through the sampling chamber, as well as appearing
to trigger an ‘air-leak’ error in some machines.134 It
appears that altitude levels above 3600 metres cause
malfunctions to occur.134
• Nitrous oxide. The presence of this gas in the patient
circuit can falsely elevate the PETCO2 reading, as
the wavelength of N2O is close to that of CO2. Most
current monitors allow compensation for the presence
of this gas in the breathing circuit.
• Oxygen. At levels above 60% there is some collision
with CO2, causing a falsely low PETCO2 reading.
Many monitors minimise this effect by adjusting for
the presence of high oxygen levels above a certain
percentage; however, the clinician may have to turn on
this feature.
Relationship of PaCO2 to PETCO2. In normal human physiology
the PaCO2 is 2–5 mmHg higher than PETCO2. A difference
that exceeds this range indicates increases in alveolar dead
space and subsequent ventilation (V) to perfusion (Q)
mismatch. Research suggests that clinicians should not
rely solely on PETCO2 for monitoring of carbon dioxide
tension, due to the unreliability of current technology.126
Changes noted in PETCO2 should prompt ABG analysis,
because the arterial/end-tidal carbon dioxide gradient is
not constant.126
Capnogram interpretation. The capnogram represents the
dynamic readings presented to the sensor in a graphic form,
commonly PETCO2 versus time (see Figure 7.22). However,
greater information about dead space (both anatomical and
physiological) can be interpreted if PETCO2 is plotted against
exhaled volume, using a flow sensor mounted between the
endotracheal tube and the ventilator Y piece.
There are five phases (0–IV) possible on the
capnogram:
• 0—represents the inspiratory phase where fresh gas
enters the airway and lungs; this produces a rapid
downstroke to a zero baseline from phase III (or IV if
present).
• I—represents the start of expiration of CO2 free gas
(dead space).
• II —normally has a steep rise, where there is a mixing
of dead space gas (CO2 poor) and alveolar (CO2 rich)
gas.
• III—a plateau pressure with a positive slope is reached
as alveoli continue to expel CO2.
• IV—the closing volume at deep expiration results in a
further rise in CO2. This phase is rarely seen except in
patients who are pregnant or obese.130,131
Common abnormalities in PETCO2 waveforms. In normal
subjects there is a balance between ventilation (excretion
of CO2 from alveolus) and perfusion (delivery of CO2 to
alveolus). This produces the normal gap seen between PaCO2
and PETCO2 of 2–5 mmHg. Where there is disturbance of
PCO2
I
II
III IV
0
Practice tip
During calibration of PETCO2 monitoring it is important to allow
the system to warm up, to zero and reference the sensor head,
as well as to calibrate the sensor housing outside the patient
circuit away from any exhaled carbon dioxide. Failure to perform
these calibrations appropriately will result in erroneous values
and may influence clinical management.
Time
FIGURE 7.22 Typical capnograph waveform
CHAPTER 7
Waveform
ETCO2
(mmHg)
(kPa)
CO2 curve shapes
80 10.0
60 8.0
6.0
40
4.0
20 2.0
4
8
Waveform
ETCO2
(kPa)
CO2 curve shapes
80 10.0
60 8.0
6.0
40
4.0
20 2.0
4
8
12 s
Possible causes
Respiratory depression caused by drugs
Metabolic alkalosis (respiratory compensation)
Insufficient minute ventilation
Waveform
ETCO2
(mmHg)
(kPa)
CO2 curve shapes
80 10.0
60 8.0
6.0
40
4.0
20 2.0
4
8
Assessment, monitoring and diagnostics
135
the balance this normal relationship does not hold true (see
Figure 7.23). There may be an increase of physiological
dead space, for example with pulmonary embolism, PEEP
or a fall in cardiac output. When this occurs the difference
between PaCO2 and PETCO2 increases. This difference can
be quantified by drawing an arterial blood gas and noting
the PETCO2 value displayed on the bedside monitor at the
same time; if the respiratory disease remains stable, this gap
appears to remain constant.130,135
12 s
Possible causes
Accidental extubation
Complete obstruction of the airways
Disconnection
Oesophageal intubation (drop after 1–2 tidal volumes)
(mmHg)
■
12 s
Possible causes
Asthma
Ventilatory maldistribution (asynchronous emptying)
Asthmatic bronchitis
Waveform
NEUROLOGICAL
MONITORING
The management of patients with head injuries and other
cerebral disorders complicated by raised intracranial pressure
has advanced significantly in recent years.17 Although primary
damage to the brain tissue is usually irreversible, secondary
damage arising from ischaemia and hypoxia can be treated.
Assessment and ongoing monitoring of the neurological
system, to ensure that complications are identified and
treated early, remains key to the care of these patients, as it
is important to minimise sustained damage to cerebral tissue.
The importance of maintaining optimal cerebral perfusion
pressure in patients with severe head injuries is now widely
acknowledged, and intracranial pressure (ICP) assessment
is a vitally important component of care.136 Raised ICP
leads to a progressive fall in cerebral perfusion pressure
and is the dominating cause of death in such patients.
However, monitoring cerebral perfusion pressure and
subsequent oxygenation at the bedside is challenging, and
it is still unclear which method produces the most valid
estimate of the balance between cerebral oxygen delivery
and demand.137,138
A number of forms of monitoring are used in Australasian
critical care units, including cerebral function monitoring,
jugular venous bulb oximetry, near-infrared spectroscopy
(NIRS), and intracranial pressure monitoring. However, all
patients in whom a neurological problem is suspected will
undergo initial assessment of level of consciousness, often
using the Glasgow Coma Scale.
P
Glasgow Coma Scale
Possible causes
CO2 rebreathing
The Glasgow Coma Scale (GCS) was originally devised in
1974 by Teasdale and Jennett139 to establish an objective,
quantifiable measure to describe the prognosis of a patient
with a brain injury. The GCS (see Table 7.3) requires a series
of observations to be recorded that assess consciousness by
measuring arousal, which depends on brainstem function;
and cognition, or awareness, which depends on cerebral
hemisphere function. In 2003, the UK National Institute
for Clinical Excellence stipulated the use of the GCS for
assessment and classification of all head-injured patients140,141
Head injuries can be classified into three categories according
to GCS scores: minor, moderate, and severe (see Table 7.4).
The GCS includes scoring of separate subscales related
to eye opening, verbal response and motor response. In
t
FIGURE 7.23 PETCO2 waveforms (published with permission,
Dräger Medical)
136
SECTION 2
■
Principles and practice of critical care
TABLE 7.3 Glasgow Coma Scale139,141
Response
Best eye response
Best verbal response
Best motor response
TABLE 7.4 Head injury
Score
classification180,181
No eye opening
1
Severe head injury
GCS score of 8 or less
Open to pain
2
Moderate head injury
GCS score of 9–12
Open to verbal
command
3
Minor head injury
GCS score of 13–15
Open spontaneously
4
No verbal response
1
Incomprehensible sounds
2
Inappropriate words
3
Confused
4
LIMB MOVEMENT
Oriented
5
No motor response
1
Extension to pain
2
Flexion to pain
3
Withdrawal from pain
4
Localising pain
5
Obeys commands
6
Localised cerebral injury or damage may impair the movement
of an individual limb or limbs. Increasing damage may be
reflected in a deteriorating pattern of movement. Instructing
the patient to move the limb laterally on the bed, lifting
against gravity, or against your resistance, are techniques
used to assess limb movement. The left and right side should
be assessed separately and if the patient is unable to follow
instructions, movement can be assessed in response to pain.
The type of movement observed can be classified as:
• normal power—movements are appropriate to the
normal muscle strength for that patient;
• mild weakness—moves with difficulty against
resistance and has difficulty fully lifting against gravity;
• severe weakness—moves a limb laterally but has great
weakness against gravity and is unable to move against
resistance.
Abnormal responses to stimulation may be noted that are
indicative of tissue damage:
• spastic flexion—the arm slowly bends at the elbow
and is very stiff;
• extension—the limb straightens at the elbow or knee
joint.
applying the GCS it is important to note that accuracy will
be affected if the patient is receiving anaesthetic agents or
sedation.
Monitoring consciousness is simple and non-invasive
using this tool, which aids in the detection of those patients
most at risk of developing raised intracranial pressure (see
Chapter 12).
PUPILLARY ASSESSMENT
Pupillary responses, including pupil size and reaction to light,
are important neurological observations. Normal pupils are
round and equal in size, with an average size of 2–5 mm in
diameter. The millimetre scale to estimate the size of each
pupil should be indicated on the neurological observation
chart. The shape of each pupil should also be noted.140,142
The immediate constriction of the pupil when light is
shone into the eye is referred to as the direct light reflex.
Withdrawal of the light should produce an immediate and
brisk dilation of the pupil. Introduction of the light into one
eye should cause a similar constriction to occur in the other
pupil (consensual light reaction).140
Other points to consider when conducting pupillary
observations include the following:140
• Pinpoint non-reactive pupils are associated with opiate
overdose.
• Non-reactive pupils may also be caused by local
damage.
• Atropine will cause dilated pupils.
• One dilated or fixed pupil may be indicative of
an expanding or developing intracranial lesion,
compressing the oculomotor nerve on the same side of
the brain as the affected pupil.
•
A sluggish pupil may be difficult to distinguish from
a fixed pupil and may be an early focal sign of an
expanding intracranial lesion and raised intracranial
pressure. A sluggish response to light in a previously
reacting pupil must be reported immediately.
The frequency of neurological observations is dependent on
the patient’s condition and clinical judgment.
Although used worldwide, the value of the GCS has been
challenged.143,144 Discrimination is poor when monitoring
changes in levels of consciousness, and it may be unreliable
in the middle-range scores. Individual ability to undertake the
required components of the assessment can cause variations
to occur: motor weakness is a subjective assessment, as is
pupil size, as comprehensive guides are not available. The
assessment of responses to painful stimuli has resulted in
reports of unnecessary pressure being used, while for some
patients who are deeply unconscious, insufficient pressure
may be used to elicit a response. Additionally, the stimuli
used may conflict with other requirements or interventions,
such as the need for rest to minimise raised ICP.142
Cerebral function monitoring
The electroencephalogram has been used for many years to
assess neurological function by recording electrical signals
emitted from the brain, particularly those impulses from
CHAPTER 7
the surface of the brain that reflect the current awareness
state (e.g. awake, asleep or sedated). Waves produced by
the electrical impulses are displayed on a monitor and
can then be interpreted by examining the frequency and
morphology of each wave or series of waves. Some cerebral
function monitors are used to assist in determining sedation
levels or for analysing pattern changes in sedation, especially
if different drugs have been used to induce sedation.145
Use of the EEG in critical care units has been variable, but
the introduction of continuous EEG monitoring to assess
and monitor a patient with brain injury or acute ischaemia
enables prevention of further complications.146 In the USA
and some other countries, EEG is considered useful for
confirming suspected brain death and other brainstem
injuries.147 (Brain death is discussed in more detail in Chapter
21.)
Intracranial pressure monitoring
Invasive measures for monitoring intracranial pressure (ICP)
are commonly used in patients with a severe head injury or
after neurological surgery. The head injury management
guidelines published by the Brain Trauma Foundation in
2000148,149 recommend intraventricular ICP measurement
as the first-line approach to monitoring ICP. However,
a Cochrane Systematic Review150 did not find sufficient
data to reach a conclusion about the value of routine ICP
monitoring in patients with acute coma, due to the small
size of existing trials.
There are a few absolute contraindications to ICP
monitoring—severe coagulopathy and other conditions that
are associated with a high risk of intracranial haemorrhage
that can occur when the monitoring catheter is inserted.151
Other conditions to be carefully considered before ICP
monitoring devices are used include severe infection, severe
haemodynamic instability, open scalp or skull wounds around
the proposed insertion site, immunosuppression, and small
ventricles (seen on CT or MRI).152
ICP measurements are used to estimate cerebral perfusion
pressure (CPP). Mean CPP is calculated by subtracting the
mean ICP from the mean arterial blood pressure153 and
represents the blood pressure gradient across the brain.
CPP is usually maintained between approximately 70 and
85 mmHg, although target levels for each patient will be
individualised based on usual blood pressure levels and
cerebral pathophysiology (see further reading, Vespa 2003).
Reduced cerebral perfusion pressure (i.e. below 50 and 60
mmHg) results in inadequate cerebral blood flow and the
potential for ischaemic changes. ICP monitoring devices can
be inserted in epidural, subdural, subarachnoid, parenchymal
or ventricular locations.154 Intraventricular monitoring is still
considered to be the gold standard, although parenchymal
catheterisation is now more common as it is generally
faster and technically easier.154 Intraventricular catheters
are usually inserted into the foramen of Munro (the duct
joining the lateral and third ventricle that is in alignment
with the middle of the ear).
This monitoring requires the use of a pressure transducer,
three types of which are in use: external strain gauge, cathetertip strain gauge, and catheter-tip fibreoptic technology.
■
Assessment, monitoring and diagnostics
137
External strain-gauge transducers connect to the intracranial
space via fluid-filled lines, whereas catheter-tip transducers
are inserted into the brain. External strain-gauge transducers
are considered accurate and can be recalibrated, but they
are susceptible to blockages, which increases inaccuracy.
Catheter-tip transducers, of either strain-gauge or fibreoptic
technology, have to be calibrated prior to insertion and cannot
be recalibrated. However, these are generally easier to use
because they do not require the patient’s head elevation to
be static.152
The choice of catheter depends on unit policy and
available equipment, the level of accuracy needed, anticipated
duration of monitoring, and the infection risk to the patient.
Intraventricular catheters with a burr hole have been the
gold standard for several years now and are associated
with low infection risks if the duration of placement is less
than 72 hours. The infection risk is highest with fluid-filled
monitoring devices, and so the preferred systems use closed
circuits. Bolts measure subdural pressure, and, as they do
not penetrate the ventricle, are associated with a lower risk
of infection; however, the traces produced tend to be less
reliable and clear.153
Fibreoptic catheters produce a pulse and trend waveform,
and are considered more reliable than bolts in the short term.
They have a catheter-tip transducer that must be calibrated
by zeroing relative to atmospheric pressure. In general this
is performed prior to insertion, as some catheter types do
not allow in-vivo zeroing. A slight drift of ±2 mmHg is
to be expected for the first day after insertion and then
±1 mmHg thereafter, although in reality the drift may be
greater than this.155 The fibreoptic catheters usually have a
drainage channel, which can be used to remove fluid and
ease intracranial pressure. Once they are positioned, the
catheter needs to be marked so that any migration can be
readily observed.137
Equipment can be tested by applying jugular venous
pressure momentarily, which will cause the ICP to rise quickly.
For monitoring purposes systolic and diastolic pressures
can be obtained, but normally mean values are recorded.
Normal ICP ranges from 5 to 20 mmHg, although as stated
earlier transient elevations of up to 40 mmHg can occur
from everyday activities such as sneezing. Pressures that
remain above 20–25 mmHg should be actively treated. These
probes can also record tissue oxygen tension, the normal
values of which range from 25 to 45 mmHg. Reductions in
tissue oxygen tension have been reported to be associated
with adverse events and poor outcome, but there is lack
of agreement on the value of this measurement 138 (see
Chapter 12 for further discussion of clinical states and
management).
PULSE WAVEFORMS
Interpretation of waveforms that are generated by the
cerebral monitoring devices is important in the clinical
assessment of intracranial adaptive capacity (the ability of
the brain to compensate for rises in intracranial volume
without raising the ICP).156 Cardiac pulse waves are detected
and transmitted as continuous waveforms on a cerebral
monitoring system (see Figure 7.24). The cardiac waves reach
the cranial circulation via the choroid plexus and resemble
138
SECTION 2
■
Percussion
(arterial)
P1
Principles and practice of critical care
Tidal
(rebound)
P2
Dicrotic
P3 (venous)
P2
P1
P3
FIGURE 7.24 Intracranial pressure monitoring: above, lowpressure wave, compliant cranium; below, high-pressure wave,
non-compliant cranium184 (published with permission)
the waveforms transmitted by arterial catheters, although
the amplitude is lower.
There are three distinct peaks seen in the ICP
waveform:154
• P1—the percussion wave, which is sharp and reflects
the cardiac pulse as the pressure is transmitted from
the choroid plexus to the ventricle;
• P2—the tidal wave, which is more variable in nature
and reflects cerebral compliance and increases in
amplitude as compliance decreases; and
• P3—which is due to the closure of the aortic valve and
is known as the dicrotic notch.
It is important that the waveform be continuously observed,
as changes in mean pressure or in waveform shape usually
require immediate attention. In acute states such as head
injury and subarachnoid haemorrhage, the value of ICP
depends greatly on the link between monitoring and therapy,
so close inspection of the trend of the ICP and the details
derived from the waveform is extremely important. 153
Simple ongoing visual assessment of the ICP waveform
for increased amplitude, elevated P2 and rounding of the
waveform provides non-specific information suggestive
of decreased intracranial adaptive capacity and altered
intracranial dynamics.146,149
Inaccuracies in ICP readings can occur, and may be due
to CSF leaks around the insertion site, obstruction of the
intraventricular catheter or bolt, the difference in height
between the bolt and the transducer (occurs in external straingauge transducers) and kinks in the tubing. In the strain-gauge
transducer that connects to fluid-coupled systems, bubbles or
air in the tubing will result in dampening of the waveform.
Also interventions and environmental stimuli can cause an
increase in the ICP, and thus particular events that do trigger
a rise in ICP need to be minimised or prevented.157
Jugular bulb oximetry
Jugular venous catheterisation is used in neurological units
for the routine monitoring of a head-injured patient.157 It
facilitates the assessment of jugular venous oxygenation
(SjvO2), cerebral oxygen extraction (CEO2), and arteriovenous
difference in oxygen (AVDO2). All of these variables indicate
changes in cerebral metabolism and blood flow, and therefore
the catheter generates continuous data that reflect the balance
between supply and demand of cerebral oxygen.158 As this
form of monitoring increases in popularity in ICUs, it is
important that nurses and doctors understand the rationale
for using such technology, the data generated and the care
required.159
The catheter is inserted using the same sterile technique
used for central venous catheters but in a retrograde (supine)
direction in the jugular vein.160 Usually the right jugular
vein is chosen, as it is slightly larger than the left and
provides readings that are more representative of overall
brain function.161 The catheter tip is advanced so that the
tip sits in the bulb of the internal jugular vein. Correct
positioning is confirmed by X-ray; the tip of the catheter
should be located at the border of the first and second cervical
spine and medial to the mastoid process.161,162
The normal requirement for cerebral oxygen delivery is
consumption at 35%–40% of available oxygen, giving a
normal SjvO2 of 60%–65%. Changes in SjvO2 reflect changes
in cerebral metabolic rate and cerebral blood flow; however,
as it is a global measure it does not detect regional ischaemia.
A high SjvO2 is indicative of increased cerebral blood flow,
reduced oxygen consumption, and hyperventilation. Low
SjvO2 levels suggest that cerebral perfusion is reduced, with
levels below 40% indicative of global cerebral ischaemia.
However, caution must be used when interpreting values
generated using this method, as high values might also
imply an increase in arteriovenous shunting secondary to
vasoconstriction or maldistribution of blood flow.138
As noted above, the major limitation of SjvO2 monitoring
is that it is a global measure of cerebral oxygenation.163 As a
result, smaller areas of ischaemia are not detected unless these
are of sufficient magnitude to affect global brain saturation. It
is possible therefore that regional ischaemia may be missed.158
This form of monitoring requires frequent recalibration to
ensure accurate measurements. Catheter migration interferes
with signal quality, and medical intervention is required
to reposition the catheter. The position of the patient also
affects signal quality, and ideally the patient should be nursed
supine with a head elevation of 10°–15° and at least a neutral
head alignment. It is important that measurement errors be
excluded when abnormal readings are noted; algorithms
have been developed to assist nurses when caring for patients
with jugular bulb oximetry.159,161
NEAR-INFRARED SPECTROSCOPY
Near-infrared spectroscopy (NIRS) is a non-invasive method
of monitoring continuous trends of cerebral oxygenated and
deoxygenated haemoglobin by utilising an infrared light
beam transmitted through the skull. Normal saturations
would be 70%. The clinical use of NIRS is constrained by
potential sources of error, which include contamination of the
CHAPTER 7
signal by the extracerebral circulation (such as in the scalp),
extraneous light, and the presence of extravascular blood
arising from subarachnoid or subdural haemorrhage.164
BEDSIDE/LABORATORY
INVESTIGATIONS
In recent years, advances in technology have enabled more
point-of-care testing to occur. However, there are still times
when laboratory investigations are required. This section
focuses on the key bedside and laboratory investigations
required to manage critically ill patients.
Arterial blood gases
Arterial blood gases (ABGs) are one of the most commonly
performed laboratory tests in ICUs and other critical care
areas, and ABG analysis is an important clinical skill. ABG
measurements are essential for assessing oxygenation/gas
exchange and ventilation and, accordingly, all ICUs are
recommended to have a blood gas analyser as a minimum
standard to facilitate assessment and monitoring of respiratory
function.24 Despite this familiarity, interpretation of the blood
gases can be difficult, and it is important that this is done
with accuracy and speed. (Further details of the application
or utilisation of this form of monitoring are provided in
Chapter 11.)
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Assessment, monitoring and diagnostics
139
ABGs are measured to determine the status of the acid–
base balance and oxygenation, and include measurement of
the PaO2, PaCO2, acidity (pH) and bicarbonate (HCO3-).
Blood for ABG analysis is sampled by arterial puncture or,
more commonly in critically ill patients, from an arterial
catheter in the radial or femoral artery. Both techniques are
invasive and allow only intermittent analysis. Continuous
blood gas monitoring is possible if a fibreoptic sensor or an
oxygen electrode is inserted into the arterial catheter system.
The advantage of the arterial catheter is that it facilitates
ABG sampling without repeated arterial punctures. Normal
values for ABGs are given in Table 7.5.
When assessing ABGs, a number of questions should
be asked:165
• Does the PaO2 level show hypoxaemia?
• Does the pH level fall on the acid or alkaline side of
7.4 (i.e. 6.9 ↔ acid ↔ 7.4 ↔ alkaline ↔ 7.9)?
• Does the PaCO2 level show respiratory acidosis or
alkalosis?
• Does the HCO3- show metabolic acidosis or alkalosis?
• Re-examine the pH: is it compensated or
uncompensated?
— pH is abnormal, along with the abnormal PaCO2
and the HCO3– = uncompensated condition;
— pH is normal but the PaCO2 and the HCO3– are
abnormal = compensated condition (the body has
had time to restore pH levels to normal).
The following points of interpretation should be noted.
(More detailed information related to the pathophysiology
can be found in Chapter 11.)
TABLE 7.5 Arterial blood gas normal values166
Blood gas
measurements
Description
Normal value
Temperature (T)
Default setting is 37°C. No consensus on analysis according to patient
temperature. Consistency of greater importance.
37°C
Haemoglobin (Hb)
Samples need to be fully mixed so should be constantly agitated until
analysed.
Females 115–165
g/L
Males: 130–180
g/L
Acid–base status (pH)
Overall acidity or alkalinity of blood.
7.36–7.44
(36–44 nmol/L)
Carbon dioxide
(PaCO2)
Partial pressure of arterial CO2.
4.5–6.0 kPa
35–45 mmHg
Oxygen (PaO2)
Partial pressure of arterial oxygen.
11–13.5 kPa
80–100 mmHg
(varies with age)
Bicarbonate (HCO3–)
Standard bicarbonate is usually used to assess metabolic function; this is
calculated by removing the respiratory component from the HCO3– .
22–32 mmol/L
Base excess (BE)
The number of molecules of acid or base that are needed to return 1 litre
of blood to the normal pH (7.4): it measures acid–base balance. As with
HCO3–, standard BE is more useful for accurate assessment of metabolic
components.
-3 to +3 mmol/L
Saturation (SaO2)
Haemoglobin saturation by oxygen in arterial blood.
>94%
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Principles and practice of critical care
Lowered PaO2 is seen with hypoventilation,
ventilation/perfusion mismatch, alveolar-capillary
block and right-to-left shunts.
• Raised PaO2 may be seen with hyperventilation or
oxygen therapy.
• Lowered PaCO2 (respiratory alkalosis) is usually a
compensatory phenomenon in metabolic acidosis, but
may be a primary abnormality; in both situations it is
due to hyperventilation.
• Raised PaCO2 (respiratory acidosis) occurs in
respiratory failure, but is also seen as a compensatory
phenomenon, caused by hypoventilation, in metabolic
alkalosis.
• Lowered pH indicates a net acidaemia and raised pH
indicates a net alkalaemia. The acid–base balance
component (be it metabolic or respiratory) is in
the same direction as the pH and is the primary
abnormality in acid–base imbalance.
• Base excess is decreased in metabolic acidosis and
compensated respiratory alkalosis. It is increased
in metabolic alkalosis or compensated respiratory
acidosis.
• Alveolar-arterial PO2 difference is elevated in all causes
of hypoxia except hypoventilation.166
Errors can be caused by sampling techniques. Commonly in
Australasia, premixed, dry heparin syringes are the preferred
choice, filled to 0.3–0.6 mL. One millilitre of arterial blood
is collected anaerobically in a heparinised syringe and
transported rapidly to the laboratory, or to the blood gas
analyser in the ICU, in a capped syringe with the needle
removed.166 Some blood gas syringes still contain liquid
heparin, and are prone to producing dilutional inaccuracies
if the excess heparin is not expelled once the internal surfaces
of the syringe have been coated with the solution; only
enough to fill the hub of the syringe should remain. Too
much heparin can lower CO2 and HCO3- readings. The
syringes that contain dried heparin minimise this problem.
Dilution can also occur from the saline in the flush solution
of the arterial line, if too little is withdrawn prior to arterial
blood sampling.
The amount of blood that needs to be withdrawn to
minimise the risk of saline dilution varies, with published
recommendations indicating that, in general, 2 mL fluid should
suffice.167 However, a recent Australian study concluded that
the blood discard volume should be twice the dead space to
ensure clinically accurate arterial blood gas and electrolyte
measurement, and to prevent unnecessary blood loss.168
Arterial blood exerts its own pressure, which is sufficient
to allow the blood to fill the syringe to the required level;
thus, negative pressure should be avoided, as this causes
frothing. Any excess air will cause inaccurate readings and
should be expelled before the syringe is capped with a hub;
covering with a hub prevents further contamination with air.
The sample must be analysed within 10 minutes if it is not
packed in ice, or within 60 minutes if iced, as delays cause
degradation of the sample. Degradation also occurs if the
sample is shaken; it should be gently rolled between fingers to
mix the sample with the heparin and prevent clotting.167
Other modes of assessment and monitoring are used in
some ICUs that provide alternative or additional modes of data
collection and may become more widely used in the future.
Transcutaneous and transconjunctival oxygen monitoring
are being used in neonates but are proving to be of less value
for ongoing monitoring of adult patients with hypotension
or shock.7 Transcutaneous carbon dioxide monitoring is
also less effective in critically ill adults, but there may be
indication for its use in stable patients during weaning from
artificial ventilation, or for the monitoring of CO2 during
apnoea testing for brain death. Capnometry, particularly
the measurement of end-tidal CO2, is being used to measure
true alveolar carbon dioxide; but, as highlighted previously,
its value is limited in general critically ill patients.126 New
technologies are not yet proving superior to those existing
diagnostic or monitoring modalities.7
Full blood count
The full blood count (FBC) assesses the status of three major
cells that are formed in the bone marrow: red blood cells
(RBC), white blood cells (WBC), and platelets.
Although normal values have been given (see Appendix C),
for critically ill patients changes will occur in certain
conditions. For example, Hb is reduced in the presence
of haemorrhage and also in acute fluid overload causing
haemodilution. Haemoconcentration can occur during
acute dehydration, which would show as a high Hb. Similar
conditions will also affect the haematocrit. WBC levels will
be elevated during episodes of infection, tissue damage and
inflammation. When infections are severe, the full blood
count will show a dramatic rise in the number of immature
neutrophils. Platelets are easily lost during haemorrhage,
and clotting deficiencies are noted when the count falls to
below 20 × 109/L.166
Biochemistry
Diagnostic tests provide information at cellular and
biochemical levels that assist clinicians in determining
abnormalities and diagnosing causality. (For parameters
and normal values, see Appendix C.)
Cardiac enzymes
For patients with suspected acute myocardial infarction,
testing of the enzyme troponin T or I is now standard.
Recent studies have also revealed that cardiac troponin
levels are elevated in critically ill septic patients who do not
have evidence of MI. Further, mortality rates are higher in
troponin-positive patients than in those who are troponinnegative, suggesting that this may become an important
enzyme to measure; however, more research is still required
to refine the testing.169,170 But not all critically ill patients with
elevated cardiac troponin levels should be treated as having
myocardial infarction unless there is support from other
data.171All injured cells release enzymes, and by measuring the
levels of enzymes it is possible to determine which cells are
damaged, thus aiding diagnosis. (For details of the tests that
can be used to diagnose cardiac injury, and the management
of patients requiring cardiovascular support, refer to Chapter
10.) See Table 7.6 for parameters and normal values.
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141
TABLE 7.6 Cardiac enzymes—normal values159
Enzyme
Description
Normal value
Troponin T
Detected within 4–6 hours of infarction, peaking in 10–24
hours.
not normally detected
Creatine kinase (CK)
Levels of CK are raised in diseases affecting skeletal muscle.
It can be used to detect carrier status for Duchenne
muscular dystrophy, although not all carriers have
increased levels.
CK-MB is the first of cardiac enzymes to rise, levels peaking
in 24 hours but returning to normal within 2–3 days.
Adult female: 30–180 U/L
Adult male: 60–220 U/L
Aspartate aminotransferase
(AST)
Detection and monitoring of liver cell damage. No cardiacspecific isoenzymes; today rarely used because it is
released after renal, cerebral and hepatic damage.
<40 U/L
Lactate dehydrogenase
(LDH)
Of no value in the diagnosis of myocardial infarction.
110–230 U/L
Occasionally useful in the assessment of patients with liver
disease or malignancy (especially lymphoma, seminoma,
hepatic metastases); anaemia when haemolysis or
ineffective erythropoiesis suspected. Although it may be
elevated in patients with skeletal muscle damage, it is
not a useful in this situation. Post-AMI, cardiac-specific
isoenzyme LDH1 peaks between 48 and 72 hours.
D-Dimer
Presence indicates deep vein thrombosis, myocardial
infarction, DIC
CK-MB: 0–5% of total CK
<0.25 ng/L
DIC = disseminated intravascular coagulation.
Coagulation profiles
CHEST X-RAY INTERPRETATION
Clotting studies are often undertaken when caring for critically
ill patients, and they provide a great deal of information that
helps clinicians diagnose and treat emerging problems. (See
Appendix C for coagulation investigations and normal
results.) Samples for these tests should not be taken from
heparinised lines or using a heparinised syringe.
The chest X-ray (CXR) is one of the most commonly
undertaken diagnostic procedures in ICUs. As most X-rays
of patients in critical care are performed using portable
equipment, the results are inferior to those taken using a fixed
camera. Care must therefore be taken to minimise erroneous
interpretations of subtle changes that have occurred due to
overexposure or suboptimal technique. Chest X-rays can be
taken looking at the chest via the posterior-anterior (PA) (see
Figure 7.25) or anterior-posterior (AP) view.
Patients should ideally be positioned sitting or semierect
for this procedure. Supine images can be taken but are less
effective at revealing gravity-related abnormalities such
as haemothorax. Lateral views of chest X-rays can also
be taken to view lesions in the thorax (see Figure 7.26).
Interpretation of the CXR in the critical care unit should
follow a systematic process that is designed to identify
common pathophysiological processes, as well as the location
of catheters and other additional items (see Table 7.7).
DIAGNOSTIC PROCEDURES
Data generated from many sources are used to determine
the cause of illness, the severity of the illness episode,
relevant co-morbidities, and the appropriateness of various
interventions. Response to treatment also has to be evaluated
to determine clinical progress. The diagnostic tests outlined
above generate valuable information, but other modalities
may be utilised in critical care units to provide additional
data that will assist the diagnostic process.
X-Rays
X-rays are widely used in critical care, and images are
produced by directing short-wavelength X-rays at the body.
Dense structures absorb these rays most and so appear as
light areas on the image. Hollow air-containing organs and
fat absorb fewer rays and so show up as dark areas. X-ray
images are very useful for visualising hard, bony structures
and revealing abnormal, dense structures in the lungs.172
172,173
Common abnormalities that can be detected by chest
X-rays include:
• Lobar collapse or atelectasis. The image will reveal all
or some of the following features: loss of lung volume,
displacement of fissures and vascular markings,
mediastinal and tracheal shift to the affected side, and
diaphragmatic elevation or obscurity.
• Barotrauma. The commonest form is pneumothorax.
Features to look for include a white, visible air–lung
divide, mediastinal shift to the opposite side (seen in
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FIGURE 7.25 Chest X-ray, PA view (published with permission, University of Auckland Faculty of Medical and Health Sciences)
FIGURE 7.26 Chest X-ray, lateral view (published with permission, University of Auckland Faculty of Medical and Health Sciences)
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TABLE 7.7 Guide to normal chest X-ray interpretation173
Technical issues
• Check X-ray belongs to correct patient; note date and time of film.
• Ensure you are viewing X-ray correctly (i.e. right and left markings correspond to thoracic
structures).
• Determine whether X-ray was taken supine or erect, and whether PA or AP.
• Check X-ray was taken at full inspiration (posterior aspects of 9th/10th ribs & anterior aspects of
5th/6th ribs should be visible above diaphragm).
• Note the penetration of the film: dark films are overpenetrated and may require a strong light to
view; white films are underpenetrated; good penetration will allow visualisation of the vertebrae
behind the heart.
Bones
• Check along each rib from vertebral origin, looking for fractures.
• Ensure clavicles and scapulas are intact.
Mediastinum
• Check for presence of trachea and identify carina (approximately level of 5th–6th vertebrae).
• Check width of mediastinum: should not be more than 8 cm.
Apex
• Ensure blood vessels are visible in both apices, particularly looking to rule out pneumothoraces
that present as clear black shading on the X-ray. Erect X-rays are essential to facilitate visibility of
pneumothoraces.
Hilum
• Check for prominence of vessels in this region: it generally indicates vascular abnormalities such as
pulmonary oedema or pulmonary hypertension, or congestive heart failure.
Heart
• Cardiac silhouette should be not more than 50% of the diameter of the thorax, with 1/3 of heart
shadow to the right of the vertebrae and 2/3 of shadow to the left of the vertebrae; this positioning
helps to rule out a tension pneumothorax. It should be noted that, post-cardiac surgery, if the
mediastinum is left open the heart may appear wider than this; also in AP films this may be the
case due to the plate being further away from the heart.
Lung
• Identify the lobes of the lungs and determine if infiltrate or collapse is present in one or more of
them. Lobes are approximately located as follows:
—left upper lobe occupies upper half of lung;
—left lower lobe occupies lower half of lung;
—right lower lobe occupies costophrenic portion of lung;
—right middle lobe occupies cardiophrenic portion of lung;
—right upper lobe occupies upper portion of lung.
• Also look for signs of pleural effusion, which appear as a collection of fluid in the lower, usually
costophrenic, region in the erect X-ray, causing loss of visualisation of the costophrenic and/or
cardiophrenic angles. In a supine X-ray pleural effusions may have a pale white appearance across
the entire lung field.
Diaphragm
• Check levels of diaphragm: right diaphragm will normally be 1–2 cm above the left diaphragm to
accommodate the liver.
Catheters and
lines
• Identify distal end of endotracheal tube and ensure above the carina (i.e. not in the right main
bronchus).
• Trace nasogastric tube along length and ensure tip is in stomach, or below stomach if nasoenteric
tube.
• Trace all central catheters and ensure distal tip in correct location.
• Identify other lines (e.g. intercostal catheters, pacing wires) and note location.
PA = posterior-anterior; AP = anterior-posterior.
•
•
tension pneumothoraces), dark affected side with a
lack of lung markings crossing the air–lung interface.
Pleural effusion. Features include fluid meniscus,
homogeneous white density, diaphragmatic and
cardiac obscurity, no loss of hemithoracic volume,
possible shift of the mediastinum away from the large
effusion. These can be seen well when the image is
taken with the patient in an upright position.
Pulmonary oedema. This is a common abnormality
seen on X-ray, but difficult to determine if the origin is
cardiac or non-cardiac.
• Pulmonary embolism. Although not the optimal
diagnostic modality, there may be areas of infarction
seen. However, these can be mistaken for collapse or
consolidation.
Positioning of invasive catheters and other devices can be
detected on a simple X-ray if these are made of a radioopaque material.
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Ultrasound
Ultrasound imaging (or sonography) uses high-frequency
sound waves which, when probed on the body, reflect and
scatter. Ultrasound waves are produced by a piezoelectric
element, which acts as a transmitter and a receiver. Different
body tissues produce different echoes, and therefore visual
images of outlines of the body organs of interest can be
constructed. A single hand-held device is used to emit the
sound and pick up the echoes. This has many advantages
over other diagnostic techniques because it is safe, portable,
and can be easily moved over the body to scan from different
body planes. However, it does have limitations, one being that
sound waves have poor penetrating power and dissipate in air,
so structures such as the lungs or those that are surrounded
by bone do not produce good images. Ultrasound is therefore
most helpful in diagnosing abnormalities with the liver and
biliary tree, pancreas, renal tract, pelvic structures, and pleural,
abdominal and pelvic fluid collections. Echocardiography
ultrasound generates images in two ways: m-mode, which is
a one-dimensional view of the heart; and two-dimensional
devices that emit a beam which moves continually in an arc,
thereby examining a pie-shaped slice of the heart.174
DOPPLER
Doppler technology is a form of ultrasound that can
detect and measure blood flow velocity. It can be used as a
bedside diagnostic tool as well as a technique for continuous
haemodynamic monitoring. The beam is directed at moving
objects such as red blood cells, and the frequency of the
reflected sound differs from that of the transmitted sound.
The difference between the two is called the Doppler shift,
and from this can be calculated the speed and direction of
blood flow. Different modalities of Doppler are utilised:
• Continuous-wave Doppler uses two transducers for
continuous transmission and receipt of sound. This
can measure the velocity of all blood captured in the
beam, including high-velocity blood flow.
• Pulsed-wave Doppler uses one transducer to transmit a
burst of ultrasound and then receive the reflection for
a specific period of time. It can be used only to receive
sound from a target area, such as a specific area of the
heart. It is commonly used for recording high-velocity
flow, such as through a stenotic valve.
• Colour Doppler uses the same pulsed-wave technology
but directs the beam onto many hundreds of tiny
sample regions. The blood flow in each of these is
analysed separately and displayed in colour. Blood
flow towards the transducer is displayed in red, while
the away flow is blue. Data are displayed in real time and
facilitate the detection of many problems, including
valvular regurgitation, turbulence and septal defects.175
Computerised tomography
Computerised tomography (CT) scanning techniques were
introduced in the 1970s. A patient is slowly moved supinely
through a doughnut-shaped machine and X-rays are emitted
from a tube that surrounds the body of the scanner. These
beams are directed onto a specific part of the body and
slice through to achieve a detailed cross-sectional picture of
the consecutive body regions that have been scanned. CT
images are produced with great clarity and revolutionised
the diagnosing of the location and severity of head trauma
and bleeds. A CT assists in evaluation of many problems
affecting the brain, abdomen and skeletal systems. Ultrafast
CT scanners are used in dynamic spatial reconstruction,
which provides three-dimensional images of the body’s
organs from any angle, as well as facilitating the review of
movements and volume within the organ, at normal speed
and at a specific moment in time.
Another computer-assisted diagnostic X-ray technique is
digital subtraction angiography, which produces a detailed
view of diseased blood vessels. This has been particularly
useful in diagnosing blockages in the vessels that supply the
heart wall and the brain. An image is taken before and after
contrast medium is injected into the vessel and the computer
subtracts one from the other, eliminating all the body
structures that might be blocking the view of the vessel.
Magnetic resonance imaging
Magnetic resonance imaging (MRI) uses radiofrequency
waves and a strong magnetic field rather than X-rays to
provide remarkably clear and detailed pictures of internal
organs and tissues.176 The high-contrast images of soft tissue
are clearer than those generated by X-ray or CT scans. MRI
maps hydrogen molecules in the body by subjecting these
to an extremely strong magnetic field, which causes the
hydrogen molecules to spin. The energy released by this
movement is translated into a visual image. MRI identifies
differences in the water content of body tissues, which is
useful in differentiating between the white and grey matter
in the brain. Dense structures such as the skull and vertebral
column do not appear in MRI images and so the technique
can be used to obtain detailed images of the brain, tumours
in various parts of the body, and degenerative diseases such
as multiple sclerosis. The plaques produced by this disease
are clearly visible using MRI but not in CT scans. MRI is
also good at revealing metabolic reactions, particularly those
that produce ATP molecules that are energy-rich.177
Newer variants of MRI have emerged. Magnetic resonance
spectroscopy (MRS) is able to map other elements in the
body to reveal information about the effect of disease on
body chemistry.178 Other MRI developments have included
functional MRI, which tracks blood flow into the brain in
real time. This eliminates the need for the injection of tracer
element, producing an alternative to positron emission
tomography.
MRI does have limitations: one is that it cannot be used
for patients who have implanted pacemakers, or loose
dental fillings. The magnetic force can attract these items
and dislodge them from the body.
Positron emission tomography
Positron emission tomography (PET) is a development in the
field of nuclear medicine and, through the use of injected
radioisotopes tagged with biological molecules (tracers), the
scanner locates the high-energy gamma rays that are released
CHAPTER 7
as the tracers get absorbed into the most active brain cells.
Computers analyse these emissions and produce a colour
picture of the brain’s biochemical activity.
SUMMARY
A critical care nurse, in today’s changing and challenging
healthcare environment, has to be adaptable and willing to
Clinical case study
Helen is a 23-year-old woman who has been admitted
to the ICU with respiratory distress. Her respiratory
rate is 38 breaths per minute, she is using her accessory
muscles to breathe, and she appears exhausted. Oxygen
therapy is commenced in the emergency department and
continues to be delivered at 40% after her arrival in the
ICU. Pulse oximetry reveals an SpO2 of 89% despite the
additional oxygen therapy. Given the known inaccuracy
at saturation levels of less than 90%,5 an arterial blood
sample is obtained from the femoral artery and the results
indicate uncompensated respiratory acidosis (pH 7.2,
PaCO2 = 54 mmHg (7.2 kPa), HCO3– = 20 mmol/L). A
rapid assessment indicates that Helen has a pyrexia of
40°C, recorded via tympanic thermometer, and yet she
appears cool peripherally, with poor capillary refill.
Cardiac monitoring is commenced and reveals a sinus
tachycardia, rate 130 beats/min. Assessment of blood
pressure using a non-invasive approach finds her to be
hypotensive, at 80/55 mmHg. Intravenous access has
been made in the emergency department but it is clear
that central venous access is required. Before the central
access can be obtained, the decision is taken to intubate
Helen, because her current rate and pattern of breathing
is unsustainable. It is anticipated that the commencement
of artificial ventilation will reduce oxygen demand because
the respiratory muscles will be rested.
DISCUSSION
In view of Helen’s age and the preliminary diagnosis of
septic shock, cardiac output measurements were warranted
to facilitate more accurate assessment of haemodynamic
status. Concern about the efficacy of pulmonary artery
catheters, and the inaccuracy of central venous pressure
Research vignette
Rickard CM, Couchman BA, Schmidt SJ, Dank A, Purdie
DM. A discard volume of twice the deadspace ensures
clinically accurate arterial blood gases and electrolytes
and prevents unnecessary blood loss. Crit Care Med 2003;
31(6): 1654–8 (published with permission).
ABSTRACT
Objective To determine the blood discard volume, as
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Assessment, monitoring and diagnostics
145
embrace new skills and knowledge. There is a wealth of data
that nurses can use to assist them in making both simple
and complex decisions related to the care of the critically
ill patient, as reflected in the content of this chapter on
assessment, monitoring and diagnostics. Nurses, however,
must make full use of these data,179 and to achieve this
they need to be able to quickly synthesise this information,
consider all possible reasons for any changes found, and
make decisions that are based on sound evidence wherever
possible.
by itself to predict response to IV fluid, led to a PiCCO
system being used to measure cardiac output. Therefore, a
central line and a thermistor arterial catheter were inserted.
The values obtained from this technique indicated that
preload was low, reflected by a low ITBV (725 mL/m2).
However, the EVLW was slightly elevated (8.5 mL/kg), due
to increased capillary permeability. Cardiac output (9.1
L/min) and cardiac index (4.8 L/min/m2) were elevated,
indicative of the hyperdynamic phase of sepsis.
The appropriate treatment was the administration
of IV fluids to improve preload, in conjunction with
inotropic therapy to improve the mean arterial pressure.
Helen had a urinary catheter inserted, to enable accurate
measurement of urine output in order to evaluate renal
perfusion.
A comprehensive assessment of all systems, including
biopsychological factors, was undertaken and a
multidisciplinary plan of care formulated. Respiratory
monitoring continued with the measurement of end-tidal
CO2 tension (PETCO2) as, when combined with continuous
oximetry, this can reduce the frequency of arterial blood
gas sampling.126 Helen spent a period of 2 weeks in the ICU,
during which time she required mechanical ventilatory
support for 9 days. Renal impairment was minimal and
therefore no renal support was required, as adequate
cardiac output responded rapidly to positive inotropic
and fluid therapy.
Hyperdynamic representation of septic shock is not
unusual in younger patients. However, this response
requires accurate haemodynamic monitoring because of
the instability of the cardiovascular system, so the patient’s
response to treatment must be carefully evaluated to
achieve a favourable outcome wherever possible.
a multiple of deadspace, that is required for accurate
arterial blood gas and electrolyte testing from arterial
catheters. Design Prospective, controlled, crossover
trial. Setting An 18-bed ICU of a metropolitan teaching
hospital. Patients A total of 84 critically ill patients with
20-gauge, radial arterial cannulae, pressure-monitoring
transducer set, and stable oxygenation. Interventions
System deadspace (priming volume from sampling port
to catheter tip) was established. Patients had six 0.5 mL
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arterial blood samples taken sequentially in random
order using discard volumes of 1, 1.5, 2, 2.3 and 3.6
times the deadspace (experimental values) and 5.5 times
the deadspace (control). Measurements and main results
Samples were analysed for PaO2, SaO2, pH, PaCO2,
HCO3–, Na+, and K+. We performed repeated-measures
analysis of variance with post-hoc linear contrasts and
compared mean experimental and control values. The
smallest discard volumes that provided measurements
that were statistically equal to control were twice the
deadspace (PaO2, P = 0.563; SaO2, P = 0.371) and 3.6
times the deadspace (pH, P = 0.107; PaCO2, P = 0.519;
HCO3–, P = 0.10). All discard volumes tested provided
results that were statistically different from control for
Na+ (P <0.003) and K+ (P <0.001). Conclusions Many
results were statistically different from control, although
the actual discrepancies were very small. At clinically
relevant levels of measurement, there was minimal
variation between values obtained after a discard volume
of twice the deadspace and control values. The level
of error was clinically acceptable and within, or close
to, the precision limits of the blood gas analyser. Slight
fluctuation in patient variables during sampling could also
have contributed to the error. A blood discard volume
of twice the deadspace is recommended for all variables.
This will provide clinically accurate results and avoid the
deleterious effects of unnecessary blood loss.
CRITIQUE
This study investigated an often raised question that has
the potential to affect patient wellbeing, particularly those
long-term critically ill patients who have many hundreds
of blood analyses performed during their illness.
The principle of testing various multiples of the
deadspace, rather than a predetermined absolute value,
was particularly useful, as it ensures applicability of results
to multiple brands of arterial lines. The authors identified
5.5 times the deadspace for the control specimens used
in this study, although no evidence is provided as to why
this multiple was selected. This is particularly important
in the light of the result that Na+ and K+ samples drawn
after 3.6 times the deadspace had been removed, remained
statistically different from the control, and that measured
values were still trending downwards (in the case of Na+)
and upwards (in the case of K+) when all samples were
considered.
A cohort of 84 clinically stable critically ill patients
Learning activities
Learning activities 1–4 relate to the clinical case study.
1. Why is levelling of the transducer so important?
2. What are the key variables to note when
interpreting arterial blood gases?
3. What are the key points to remember when
interpreting haemodynamic monitoring results in a
patient receiving mechanical ventilation? Outline,
and provide a rationale for, the other aspects of
was enrolled in the study. Determining clinically stable
patients is difficult, although the following definition
was provided: ‘the patient had neither required nor was
anticipated to require any clinical intervention in the
30-min period before sampling or during the sampling
period’.168 While it is difficult to predict what will happen
during a future period, no emergency situation arose that
required cessation of the sampling protocol, although no
definition of what constituted an emergency situation was
provided. It is not clear why a full year was required to
enrol the patients in this study, given that the inclusion
criteria do not appear particularly limiting and that the
unit in which the work was conducted is a tertiary-level
unit with 18 beds.
The procedure described for drawing and analysing the
blood is well described and rigorous in its method. The
samples appear to have been taken as rapidly as possible,
although no indication of the time elapsed between the
first and last sample has been provided. While this may
affect the results obtained, the random order for each of
the blood samples with each patient is likely to have been
effective in preventing a systematic bias.
Results indicated that blood taken after removal
of twice the deadspace was not statistically different
from the control measurements for PaO2 and SaO2. The
measures of pH, PaCO2 and HCO3– required 3.6 times
the deadspace to be removed before measures were not
statistically different from the controls, while Na+ and K+
levels remained statistically different from the controls
after removal of 3.6 times the deadspace. Despite these
statistical differences, the authors claim that above twice
the deadspace, the differences identified were clinically
negligible, and therefore suggest that removal of twice the
deadspace is suitable to ensure accurate blood results. On
perusal of mean results the differences in blood levels for
each amount of discard volume were small (<1 mmHg
for PaO2 and PaCO2; <1 mmol/L for HCO3–; 1.1 mmol/L
Na+ and <0.2 mmol/L K+). However, there are no data
indicating the degree of difference for each individual
patient: this might have been considerable, and might
account for the statistically significant differences on the
repeated-measures analysis of variance that do take into
account differences within each individual subject. Further
examination of these differences is warranted before
assuming that the small differences in mean measurements
assure clinical accuracy.
assessment that should be undertaken in association
with haemodynamic monitoring.
4. Describe the ventilation monitoring that should
be in place when caring for a patient who has no
specific respiratory disease but is experiencing a
severe systemic disease such as sepsis. Outline the
information you will gain from that monitoring,
and how it will inform assessment and changes of
ventilation support.
CHAPTER 7
Online resources
• Diagnostic Medlab. Diagnostic handbook: the
interpretation of laboratory tests. Available from: http://
www.dml.co.nz/clin_handbook.asp
• Hammett RJH, Harris RD. Halting the growth in
diagnostic testing. Med J Aust 2002; 177(3): 124–5
(accessed 07/03/05). Available from: http://www.mja.com.
au/public/issues/177_03_050802/ham10334_fm.html
• Neurological Society of Australasia and Royal
Australasian College of Surgeons (joint publication). The
management of acute neurotrauma in rural and remote
locations, 2nd edn, 2000. Available from: http:www.
surgeons.org/Content/NavigationMenu/WhoWeAre/
ReportsandPublications/guidelinesandpositionpapers/
guidelines_end_posit.htm
• Webster NR, 2001. Monitoring the critically ill (accessed
30/12/2004). Available from: http://www.rcsed.ac.uk/
journal/vol446/44_60010.htm 30/12/2004.
• Capnography: a comprehensive educational website,
www.capnography.com
9.
10.
11.
12.
13.
14.
15.
Further reading
Dutton RP, McCunn M. Traumatic brain injury. Current
Opinion in Critical Care 2003; 9: 503–9.
Winkelman C. Effect of backrest position on intracranial and
cerebral perfusion pressures in traumatically brain-injured
adults. American Journal of Critical Care 2000; 9(6):
373–80.
Winters AC, Munro N. Assessment of the mechanically
ventilated patient: an advanced practice approach. AACN
Clinical Issues: Advanced Practice in Acute and Critical
Care 2004; 15(4): 525–33.
Vespa P. What is the optimal threshold for cerebral perfusion
pressure following traumatic brain injury? Neurosurgical
Focus 2003; 15(6): Article 4: http://www.aans.org/
education/journal/neurosurgical/dec03/15-6-4.pdf
Monitoring and hemodynamics. Critical Care Nursing
Clinics of North America vol 18(2): 145–272.
16.
17.
18.
19.
20.
21.
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