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INSIDE
Measuring oxygen
levels in the body
Normal and
deficient oxygen
levels
Investigations
Oxygen delivery
systems
Cost and practical
advice
The author
Associate Professor
Matthew T Naughton,
head, general respiratory
and sleep medicine,
department of allergy,
immunology and
respiratory medicine, Alfred
Hospital and Monash
University, Victoria.
Oxygen therapy
Background
IN 1674, John Maylow observed the death of a
mouse in a sealed bell containing a burning candle,
thus identifying the importance of hypoxia. In 1775,
Joseph Priestly observed a candle’s flame was dependent upon ‘phlogiston’ and would not burn in the
presence of ‘dephlogisticated air’. He concluded that
“pure air might be peculiarly salutary to the lungs in
certain morbid cases”.
In 1895, liquid air became available and, later,
oxygen was used to treat chlorine poisoning in WWI.
Oxygen became a therapeutic tool in the 1920s, with
the work of Dr Alvan Barach, who recognised the
association between hypoxaemia and the oedema of
right heart failure, and the benefits of oxygen therapy
in patients with COPD.
In the 1960s, long-term oxygen therapy was
observed to reverse polycythaemia. In the 1980s, two
landmark papers on use of this type of therapy in
COPD were published (see page 32), cementing its
use in severe COPD. Since then, the indications have
broadened to other causes of hypoxia-related dyspnoea, although the weight of evidence in favour of its
use for such causes is not great.
At sea level, the air we breathe contains 21%
oxygen, with the balance mainly as nitrogen. It exerts
a pressure of 1 atmosphere, or 760mmHg.
A pressure gradient of 713mmHg (760 minus water
vapour pressure of 47mmHg) drives oxygen across
the pulmonary alveolar membrane into the pulmonary capillary. This occurs in the first third of the
0.75 second transit time that deoxygenated hypercapnic blood has in contact with aerated alveoli.
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How are oxygen levels in the body measured?
The oxygen-dissociation
curve
The oxygen dissociation curve
summarises the relationship
between the PaO2 and the
SaO2 or SpO2 (figure 1).
The curve may shift to the
right, aiding the unloading
Figure 1: Oxygen dissociation curve. Note that a shift of the
curve to the right, which aids oxygen unloading from the
haemoglobin molecule, occurs with fever, acidosis,
polycythaemia (higher 2,3 DPG levels) and hypercapnia. A PaO2
level of about 60mmHg should equate to an SaO2 of 90%.
Figure 2: Sampling arterial blood gases. A: Allen’s test to ensure
both radial and ulnar arteries are patent. B: Collection
of sample with a 25-gauge needle.
A
100
Oxyhaemoglobin saturation
(Sp02, %)
IN the blood, oxygen levels
can be measured directly by
arterial puncture, as either
partial pressure of oxygen dissolved in arterial blood (PaO2
[in mmHg]), or as the oxygen
saturation of arterial haemoglobin (SaO2 [%]). The association of PaO2 and SaO2 is
illustrated by the oxygen dissociation curve (figure 1).
Indirectly, oxygen levels can
be measured by pulse oximetry, as oxygen bound to
haemoglobin (SpO2 [%]).
Arterial blood gases are
usually measured from samples taken from the radial
artery after an Allen’s test to
ensure both radial and ulnar
arteries are patent (figure 2).
The sample is collected with
a 25-gauge needle into a
vented heparinised syringe.
Local anaesthetic can be
used to minimise discomfort
during collection of the
sample. After collection it is
important to evacuate air
from the syringe, which is
then capped and mixed to
ensure the sample is mixed
with heparin.
Sampling of arterial blood
gases provides additional
information about oxygen
levels, such as PaO2, SaO2,
PaCO2 and pH. Usually, levels
of blood glucose, bicarbonate
and haemoglobin varieties
(carboxyhaemoglobin and
methaemoglobin) can also be
measured with this sample.
Pulse oximetry (figure 3) is
an indirect and non-invasive
means of measuring the percentage of haemoglobin
bound to oxygen (SpO2). This
portable device uses a detector
placed on the finger or an ear
lobe to measure the absorption of two wavelengths of
light (by oxyhaemoglobin and
reduced haemoglobin) from
two light-emitting diodes
during a pulse wave across
arterialised blood in a capillary bed.
The proportion of oxygensaturated haemoglobin molecules relative to the total
available haemoglobin molecules provides the SpO 2
value as a percentage. This
measures functional saturation and ignores abnormal
haemoglobin species such as
carboxyhaemoglobin and
methaemoglobin.
Oximeter data are robust
and stable and, provided they
display a crisp waveform with
a pulse that matches the ECG,
reasonably accurate readings
can be obtained. Hypotension,
darkly painted finger nails,
dyes (methylene blue), hyperbilirubinaemia and movement
artefact can provide false readings.
80
60
40
20
further manipulated (beneficially or detrimentally) by centrally acting drugs such as narcotics, and vasoactive drugs
such as salbutamol. Common
medical conditions that alter
VQ matching are COPD,
pneumonia, post-operative
atelectasis, bronchiectasis, pulmonary embolus and cardiogenic pulmonary oedema.
Low levels of oxygen therapy, such as 1-2L/min, easily
correct this form of hypoxaemia.
0
0
20
40
60
80
Diffusion impairment
100
Partial pressure of oxygen (Pa02, mmHg)
of oxygen from haemoglobin molecules in conditions
such as acidosis, fever, polycythaemia (via elevated 2,3diphosphoglycerate) and
hypercapnia.
A left shift because of alkalosis, anaemia, elevated carboxyhaemoglobin level or
hypocapnia results in oxygen
being held more strongly by
the haemoglobin molecule.
Haemoglobinopathies can
also shift the oxygen dissociation curve by altering the O2binding affinity of haemoglobin molecules.
What are normal
oxygen levels?
In young healthy people the
PaO2 and SpO2 should be 85100mmHg and >95%, respectively (figure 1). During sleep,
in normal subjects values may
drop to as low as 80mmHg
and 95%, respectively.
When is a low oxygen level
of concern?
Respiratory failure is defined
as a PaO2 <60mmHg or SpO2
<90%. With severe stable disease, PaO2 may be as low as
45-60mmHg, and SpO2 may
fall to 80-90%. With acute
deterioration, these values
may fall to as low as
35mmHg and 65-80%,
respectively. Patients are usually unconscious when PaO2
reaches 30mmHg or SpO2
drops to 60%.
Low oxygen levels can
have several effects (table 1).
Acute hypoxaemia results in
confusion, dyspnoea, loss of
consciousness, and elevation
in pulmonary and systemic
blood pressure. Chronic
hypoxaemia results in pulmonary hypertension, right
heart failure (cor pulmonale)
and
secondary
polycythaemia.
Causes of low
oxygen levels
Hypoxaemia arises from five
possible causes:
■ Reduced fractional inspired
O2.
■ Hypoventilation.
■ Perfusion/ventilation
inequality.
■ Diffusion impairment.
■ Shunt effects.
Table 1: Effects of
hypoxaemia
Acute
■ Dyspnoea
■ Pulmonary
vasoconstriction
■ Tachycardia
■ Diastolic dysfunction
■ Confusion
■ Poor judgment
■ Nausea, vomiting
■ Loss of consciousness
Chronic
■ Right heart failure
■ Cor pulmonale
■ Polycythaemia
Inhalation of hypoxic air
Hypoxaemia from the inhalation of hypoxic air (or gas)
occurs most often when
people are trapped in
enclosed containers with
poor ventilation or ‘hyopoxic
air’. Another cause is exposure to hypobaric air at high
altitude.
To restore normal oxygen
content, the inspired oxygen
concentration should be
increased to more than 21%
by the use of supplemental
oxygen cylinders or by
increasing the partial pressure
(by descending to lower altitude).
If these measures are
unavailable, pulmonary
oedema may result and periodic breathing (a waxing and
waning pattern similar to that
seen in heart failure patients
with Cheyne-Stokes respiration) may develop during
sleep. In such situations, acetazolamide (Diamox) may help
via a diuretic effect and stimulation of ventilation through
metabolic acidosis.
B
Shunt effects
Figure 3. Two varieties of portable oximeters.
A: Battery-operated Nonin 8500 pulse oximeter (Nonin Inc,
Minneapolis, MN). B: Battery or electrically powered Oxypleth
Pulse Oximeter with built-in memory (Novametrix Medical
Systems, Wallingford, CT).
A
Perfusion/ventilation inequality
Hypoxaemia may occur when
there is an imbalance of airflow (ventilation) and blood
Blood shunted from the right
to the left heart chambers can
avoid oxygenation and result
in hypoxaemia. Such conditions include:
■ Cardiac shunts (atrial septal
defect, ventricular septal
defects, patent ductus arteriosus, patent foramen
ovale).
■ Scleroderma.
■ Arteriovascular malformations (eg, Osler’s disease).
■ Severe liver disease.
Characteristically,
in
patients with significant shunt,
high concentrations of oxygen
therapy (100% oxygen for 15
minutes) only partly improve
hypoxaemia.
Respiratory failure
B
Hypoventilation
Hypoventilation in normal
lungs can lead to hypoxaemia.
This can occur in stroke, drug
overdose or as a drug side
effect, and in muscle or nerve
pathology (diaphragm paresis). Such patients are best
served with ventilation assistance (eg, non-invasive ventilatory support).
Abnormalities of the alveolicapillary membrane function
causing hypoxaemia are seen
most commonly in idiopathic
pulmonary fibrosis and other
conditions in which there is
widespread lung parenchymal
disease (eg, lymphangitis carcinomatosa, Pneumocystis
carinii pneumonia). Moderate-to-high concentrations of
oxygen therapy (2-15L/m) are
required to overcome hypoxaemia in such patients.
flow (perfusion) matching in
the lung (V/Q mismatch).
The lungs have a remarkable capacity to maintain a
precise gradient of blood and
gas flow, which allows optimal exchange of oxygen and
carbon dioxide. The matching
of airflow and blood flow
responds to gravity in different
postures (upright, seated,
supine, upside down) by
changing the distribution of
blood and gases.
This delicate balance can be
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Respiratory failure is a clinical
diagnosis that is supported by
either arterial blood gases or
oximetry readings.
Type-one respiratory failure
is defined as hypoxaemia with
normal or reduced CO2 levels
and in this group oxygen therapy should be trialled. Typetwo respiratory failure,
defined as hypoxaemia with
hypercapnia, should be
treated with ventilatory assistance — either invasive, via
intubation, or non-invasive,
via face or nose mask — plus
oxygen therapy if required.
Chronicity of hypoxaemia
can be gauged by pH levels
on arterial blood gas analysis.
Chronicity of hypercapnia can
be gauged by elevated bicarbonate. Acute hypoxaemia or
hypercapnia is usually indicated by the development of
lactic acidosis on arterial
blood gas sample (pH <7.35).
A rule of thumb in respiratory failure is that if PaCO2
rises by 10mmHg, the pH
falls acutely by only 0.1 and,
in the long term, is compensated by a 3mmol/L rise in
bicarbonate level.
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how to treat - oxygen therapy
Oxygen therapy
Pressure versus
concentration
What are the aims of
oxygen therapy
The aims of oxygen therapy
are to achieve normoxia
(SpO 2 >90% or PaO 2
>60mmHg), reduce dyspnoea and alleviate polycythaemia, right heart failure
and pulmonary hypertension.
Who benefits from
oxygen therapy?
Long-term oxygen therapy
Long-term oxygen therapy
(LTOT) is defined as the use
of supplemental oxygen for
more than 15 hours/day, ideally 24 hours/day, usually at
preset and fixed flows of
0.5-5.0L/min.
COPD: Most commonly,
LTOT is indicated for severe
COPD in which the PaO2 is
<55mmHg when awake, at
rest and on optimal medical
management (see Summary:
optimal management of
COPD, page 34).
It can also be prescribed if
the PaO2 is <60mmHg (or
SpO 2 <90%) in polycythaemia,
pulmonary
hypertension or cor pulmonale. There is level-1 evidence of improved survival,
reduced level of right heart
failure, improved quality of
life and neuropsychological
functioning, improved exercise performance and maintenance of independent
activities of daily living in
these patients.
Two trials conducted in
the 1980s are the backbone
32
Pressure
Indications
Normobaric oxygen
1 atmosphere
Dyspnoea
Portable
Cost
Yes
Inexpensive
Hyperbaric oxygen
2-2.8 atmospheres
Nitrogen narcosis, carbon
monoxide poisoning,
chronic ulceration
No
Expensive
Cumulative survival data from the North American Oxygen Therapy Trial
(NOTT) (12 vs 24 hours of oxygen) and the UK Medical Research Council (MRC)
Trial (nil vs 15 hours of oxygen) trials in patients with COPD. (Adapted from Rees PJ, Dudley F.
ABC of oxygen: oxygen therapy in chronic lung disease. BMJ 1998; 317:871-74).
100
O2 24 h/day
90
O2 15 h/day
80
Table 3: Indications for long-term supplemental
(normobaric) oxygen
Proven
COPD
■ PaO2 <55mmHg or
■ PaO2 <60 mmHg with concurrent:
— Cor pulmonale
— Polycythaemia
— Pulmonary hypertension
Not proven
■ Cystic fibrosis
■ Congestive heart failure
■ Bronchiectasis
■ Pulmonary hypertension (primary or secondary)
■ Scleroderma
■ Hypoxaemic congenital heart disease
■ Sleep apnoea
of support for the use of
LTOT in COPD. The Medical Research Council study,
published in 1981, studied
patients with an FEV 1 of
0.7L, modest pulmonary
hypertension (a mean pressure of 34mmHg), PaO2 of
50mmHg, and PaCO 2 of
55mmHg.1
Thirty of the 45 subjects
in the control group who
had no oxygen therapy died,
compared with 19 out of 42
in the active group treated
with oxygen 15 hours daily.
The predicted five-year survival in the control group
was only 18% and the average annual percentage mortality risk was 30%, reflecting the poor prognosis of
this condition.
The pulmonary artery
pressure was unchanged in
the group on oxygen but
rose by a mean of
2.7mmHg/year in the control group.
The Nocturnal Oxygen
Therapy Trial conducted in
North America recruited
patients with an FEV1 of
0.7L and pulmonary artery
pressure of 30mmHg.2 The
study compared 12 hours of
overnight oxygen with continuous oxygen (in practice,
17.7 hours/day).
Annual mortality was
21% in the overnight
oxygen group compared
with 11% in the continuous
oxygen group. At six
months the pulmonary
artery pressure at rest in the
continuous oxygen group
had fallen slightly.
The two trials were not
blinded with respect to the
air cylinders used but are
accepted as adequate evidence that LTOT improves
prognosis in COPD.
The combined results of
the two trials suggests that
the nearer the use of oxygen
is to 24 hours/day, the better
| Australian Doctor | 20 August 2004
O2 12 h/day
Cumulative % survival
OXYGEN therapy can be
delivered in two forms — as
an increased pressure (>1
atmosphere) or at an
increased concentration
under normobaric conditions (table 2).
The former, known as
hyperbaric oxygen therapy,
is delivered via a hyperbaric
chamber at 2-2.8 atmospheric pressures with up to
100% oxygen.
Hyperbaric oxygen is used
to treat conditions such as
nitrogen narcosis, acute
carbon monoxide poisoning,
gas gangrene, ischaemic skin
grafts and other slowly healing peripheral limb ulcers. It
is also increasingly used by
sports physicians to speed
recovery time for elite
sportspeople with soft tissue
injuries.
Complications of hyperbaric oxygen therapy include
barotrauma such as pneumothorax , oxygen toxicity,
seizures and changes in
visual acuity.
Increased oxygen concentration delivered by cylinders
or oxygen concentrators
under normobaric conditions is the form of oxygen
therapy that most medical
practitioners will come into
contact with. The remainder
of this article refers to this
type of therapy.
Table 2: Oxygen delivery systems
70
Controls (no added O2)
60
50
40
30
20
10
0
O
the outlook. If oxygen is
used for at least 15
hours/day, the pulmonary
artery pressure may fall, and
at least the expected rise
seems to be prevented.
In addition to the
improved prognosis, there are
mild neuropsychological benefits and improvements in
quality of life. The mechanism of this improvement in
prognosis is unclear. Changes
in pulmonary artery pressure
are not great, and improved
survival might be related to
reduction in arrhythmias
related to hypoxia.
The effects of long-term
oxygen in COPD have been
extended to include other
respiratory conditions,
although no evidence of
clear benefit exists.
Other conditions: LTOT is
used in many other conditions that have hypoxiainduced dyspnoea as part of
their symptomatology (see
table 3) but where evidence
of the benefit is either lacking or negative.
Pulmonary conditions
include cystic fibrosis, interstitial lung disease, bronchiolitis obliterans, bronchiectasis, pulmonary hypertension
and recurrent pulmonary
emboli. Guidelines for eligibility are similar to those for
COPD.
Patients with ‘brittle’
asthma, or those with severe
asthma who are geographically isolated, are considered
for the provision of oxygen
cylinders for emergency use
while awaiting ambulance
assistance.
Patients with lung cancer
often complain of dyspnoea,
which much of the time is
not related to hypoxaemia.
Often it relates to weight
and muscle loss, irritation of
lung parenchyma (eg, lymphangitis), aspiration, fibrosis related to radiotherapy or
10
chemotherapy, or the underlying and pre-existing
COPD.
Obstructive sleep apnoea
is not an indication for
LTOT. It is best treated with
positive airway pressure or
other measures to alleviate
the upper airway obstruction. However, on occasions
when it coexists with COPD,
LTOT is given with positive
airway pressure during sleep.
Cardiac conditions, including congenital heart disease
and severe left-sided cardiac
failure with chronic pulmonary oedema, may also
require LTOT. Central sleep
apnoea in the setting of heart
failure and Cheyne-Stokes
respiration may benefit from
overnight LTOT.
Less common indications
include conservatively managed small pneumothoraces
and pneumatosis coli, a condition in which small bubbles of nitrogen-filled gas
form in the intestinal wall.
Increased concentrations of
oxygen in the blood are
thought to reduce these gas
bubbles.
Intermittent oxygen for
exercise
Supplemental oxygen can be
prescribed to help in the
rehabilitation of non-hypoxaemic patients with lung disease who become hypoxaemic on exertion (SpO 2
<90%) and whose exercise
capacity (eg, the distance
walked, or time at a certain
cadence on an exercise bike)
improves by >50% with
oxygen therapy, compared
with room air.
The exercise capacity is
usually established in a
blinded and randomised
fashion, with nasal cannulae (connected to air or
oxygen), an oximeter and
exercise (treadmill [sixminute walk], shuttle test or
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20
30
Time (months)
40
exercise bike).
Oxygen for air travel
During long flights, cabin
pressure may drop to the
level equivalent to an altitude of 2400 metres (about
8000 feet), analogous to an
inspired oxygen concentration of 15% at sea level.
Patients with respiratory
and/or cardiac compromise
may be at risk of hypoxaemia on such flights.
Risk of hypoxaemia can
be assessed by the hypoxic
altitude simulation test
(HAST), during which
oxygen levels are observed
while the subject breathes a
gas mixture of 15% oxygen,
with the balance as nitrogen,
for 5-15 minutes in an
oxygen hood. Depending on
the equipment used, supplemental oxygen requirements
can also be assessed.
Airlines need to be contacted well in advance if
oxygen therapy is required
during flight. Most airlines
require medical clearance
forms to be completed
before accepting carriage of
the passenger.
The airlines provide cylinders for international flights.
For domestic flights, passengers can provide their own
oxygen (checked before
departure by airline engineers), although some
domestic airlines also provide
oxygen.
Depending on the length
of the flight, purchase of an
additional seat may be
required to carry the oxygen
cylinders.
Most patients with stable
respiratory disorders already
on LTOT do not need additional flow rates for air
travel.
Oxygen at night
Patients with significant nocturnal hypoxaemia, as determined by continuous pulse
50
60
oximetry or sleep studies,
may benefit from LTOT. In
patients with COPD but no
daytime hypoxaemia or
sleep apnoea, nocturnal
oxygen over three years has
been found to reduce pulmonary artery pressures but
not alter survival.
In general, if hypoxaemia
(SpO 2 <90%) occurs for
more than 5% of the night
in the absence of sleep
apnoea or hypercapnia, supplemental nocturnal oxygen
can be considered.
Nebulisers
Nebulisers for use with
bronchodilators can be
either electrically or gas
driven. Gas-driven nebulisers require about 4-8L/min
gas flow to operate. Usually,
high-flow air is preferable to
drive nebulisers, particularly
in the case of patients with
COPD, in whom avoidance
of oxygen-induced hypercapnia is the aim. Patients
with life-threatening asthma
may run their nebulisers
with high-flow oxygen.
Contraindications to
oxygen therapy
Contraindications to oxygen
therapy include:
■ Patients with dyspnoea in
the absence of hypoxaemia.
■ Current smokers.
■ Inadequately
treated
patients (such as those
using insufficient doses of
bronchodilators).
■ Heart failure (untreated or
yet to be excluded).
■ Patients insufficiently motivated to undertake the discipline required in oxygen
therapy.
Carbon monoxide has an
affinity for haemoglobin 240
times greater than that of
oxygen, so high blood levels
(associated with smoking)
may take up to four weeks
to abate.
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Investigations
Initial investigations
INITIALLY it is important
to establish the nature and
severity of lung disease and
determine whether it is
responsible for hypoxaemia
and dyspnoea. Determine
whether the patient has been
optimally managed and
undergone pulmonary reha-
bilitation.
Organise an ECG, CXR,
lung function tests, echocardiogram (left and right heart
function and pulmonary
pressures).
Establish haemoglobin
levels: if the patient has
anaemia, this needs further
investigation, because it may
be the cause of dyspnoea. If
they have polycythaemia,
repeat the blood count after
three months’ LTOT to see
whether it abates, and, if
successful, consider lifelong
LTOT.
An
assessment
of
overnight oxygen levels may
also be required. Consider
pulmonary emboli if the
patient is immobile.
Subsequent reviews
At one month, almost 50%
of all patients initiated on
LTOT for an exacerbation
of their condition improve
spontaneously with medical
therapy (ie, after a course of
bronchodilators, antibiotics,
steroids, rehabilitation and
correction of coexistent medical problems) and no longer
require LTOT.
An arterial blood gas measurement at this time also
allows assessment of hypercapnia.
An important aspect of
clinical management of
patients receiving LTOT is
an annual review of oxygen
treatment to assess ongoing requirements (via
oximetry or, if required,
arterial blood gas measurements), adherence to treatment and any side effects
of treatment.
How is oxygen delivered?
LONG-term oxygen therapy is delivered via a concentrator or cylinders
(figure 5, table 4).
The oxygen concentrator is an
electrically driven floor-standing
pump that entrains room air
through a molecular sieve filter and
extracts nitrogen, thus providing
95-99% pure oxygen at flow rates
of 1-2L/min, or 75% oxygen at
5L/min.
The devices weigh 10kg, stand
about 0.75m tall and are on wheels
so they can be rolled about a home.
They have an hour meter to allow
objective assessment of adherence
to treatment. In some Australian
states, concessions from the electricity provider are available when
they are in use.
Small, easily carried batterydriven concentrators have recently
become available. These devices
cost about $8000 and are limited
by the battery life to about one
hour’s use.
Oxygen cylinders contain compressed oxygen and deliver 100%
oxygen at the outlet. The cylinders
range in size from C to G (table 4).
They have the capacity to provide
high-flow pure oxygen at rates only
limited by the attached regulator.
Recent developments have
reduced the weight of the cylinders
and the overall device so that they
can be easily used for mobile
patients, either as a carry bag or in
a trolley.
Oxygen concentrators have a
built-in flow meter, usually with a
maximum flow-rate capacity of
5L/min. They can be set at lower
maximum levels to avoid excessive
flow rates.
Oxygen cylinders have flow
Figure 5: Oxygen concentrator (top)
and C-sized cylinder on wheelchair
(below).
Figure 6: Gas flow regulators. From
left to right: low-flow oxygen
(0-2.5L/min), high-flow oxygen
(0-15L/min), and high-flow air
regulators (0-15L/min).
Figure 7: Pulsed system
oxygen-conserving device.
Oxygen-conserving devices
Two types of oxygen-conserving
devices exist — a reservoir system,
and the more commonly used pulse
system (figure 7). The devices are
placed between the patient and the
oxygen source to ensure the oxygen
is delivered only during inspiration
and not wasted during expiration.
They are valuable for use with
cylinders, especially portable systems, where they can increase the
life of a C-sized cylinder 3-7-fold (210 hours), depending on the chosen
device.
They can be triggered by negative
pressure sensed by the nasal prongs
at the nares during an inspiratory
effort, so they may not trigger if the
patient mouth breathes.
Oxygen-conserving devices may
be useful for patients with an oxygen
concentrator who require higher
flows than can normally be delivered (ie, >5L/min), by collecting the
oxygen during the patient’s expiration.
The oxygen interface
Table 4: Oxygen cylinders
and contents
Size
3
Volume (m ) Duration
of use at
flow rate
of 2L/min
Traveller 0.3-0.6
1-2 hours
C
0.55
3 hours
D
1.5
11 hours
E
3.8-5.2
30 hours
G
7.6-8.8
48 hours
meters attached to the pressure regulator (figure 6). Three flow meters
are available for low (0.52.5L/min), medium (0-15L/min) or
high flows (0-30L/min). Low flow
rates are generally used in patients
in whom oxygen induced hypercapnia is being avoided.
Liquid oxygen systems are available in large hospitals and conserve
space by storing oxygen in liquid
form in large permanently standing structures. The oxygen is delivered from the tanks through coils,
where it vaporises and flows to the
wall outlets.
The oxygen delivery ‘interface’ may
be nasal prongs, oxygen mask, transtracheal, or nasal trough. The most
common are nasal prongs, which are
convenient and comfortable, with
flow rates up to 6L/min, and which
can be worn while eating.
In patients requiring LTOT, the
inspired concentration of oxygen can
vary from 24% to 35% at 2L/min.
Some oxygen cannulae can be incorporated into eye wear, making the
LTOT less conspicuous.
Simple oxygen masks are used if
the required flow rate is greater than
6L/min, to avoid nasal irritation at
high gas-flow rates.
Masks should be avoided for
flows of <5L/min, as rebreathing of
CO2 may occur. Rebreathing can be
prevented by making large holes on
the side of the mask to allow
‘entrainment’ of room air to mix
with the oxygen
Masks, which can also be used
with humidification, are less comfortable and can cause perspiration.
In acute situations when highflow oxygen is required (eg, cardiogenic pulmonary oedema, pulmonary embolus), special Venturi
masks have the capacity to control
the amount of entrained air with a
specific flow of oxygen, up to
40L/min.
Oxygen can also be delivered by
a trans-tracheal approach. A minitracheostomy is made, through
which a fine bore catheter is placed
long term, and oxygen directly bled
into the trachea.
An advantage of this system is
that it can be worn inconspicuously
under a shirt or cravat. Also, higher
concentrations of inspired oxygen
can be achieved because of the
patient inhales greater amounts of
oxygen.
Oxygen can also be delivered to
patients with large tracheostomies
via tracheostomy hoods.
Such patients require artificial
humidification of their oxygen,
because their normal humidification
system is lost (as are their basic
normal airway defence mechanisms,
such as coughing).
Humidification is rarely needed at
domiciliary flow rates of <5L/min.
Dryness at the nares may be relieved
by the use of non-petroleum-based
gels or ointments (eg, ointments
made from sesame seed oil).
Hazards of oxygen therapy
Patient safety issues
ALTHOUGH oxygen is
not flammable, it is an
essential component of fire,
and fires will start more
easily and burn more
intensely in the presence of
high concentrations of
oxygen.
Oxygen should therefore
be used with extreme caution near heat sources
(heaters, electric blankets) or
naked flame (pilot lights,
candles, smokers or open
fires). Severe facial burns
requiring skin grafts have
been reported in COPD
patients who smoke and use
intranasal oxygen.
Oxygen should be used in
well-ventilated areas to
reduce elevated concentrations.
Tubing from either concentrators or cylinders is
often long (about 10m) and
trails behind the patient in
their home, creating a tripping hazard.
Patients should be educated in the safe handling of
gas cylinders and concentrators by the oxygen supplier
at the time of delivery.
Because of the potential hazards of oxygen therapy,
patients should receive continuing education on LTOT
and hazard avoidance.
Although fires precipitated
by LTOT are rare, when
Patients should
be advised to
treat oxygen
therapy like a
drug.
they do occur, it is often in
patients who have restarted
smoking.
Medical issues
Patients need to be educated
on the reasons for oxygen
therapy, safety aspects and
any new changes in technology. Patients should be
advised to treat oxygen therapy like a drug, and as such
be reviewed regularly.
At flows as low as 24L/min (<35% concentration), oxygen therapy can be
associated with hypercapnia,
especially in COPD patients
(see Author’s case study).
Such patients generally have
mild stable hypercapnia that
is exacerbated by the acute
application of high-flow
oxygen.
The mechanisms for developing acute hypercapnia are
complex and include:
■ An increased dead space.
■ V/Q mismatch.
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Loss of ventilation drive.
Anxiolysis and propensity
to sleep (and further
hypoventilate).
■ Dislodged CO 2 from the
haemoglobin molecule, elevating the PaCO2 (Haldane
effect).
Symptoms of mild hypercapnia are blurred vision and
early morning headaches,
whereas severe hypercapnia
causes confusion and loss of
consciousness. Patients
should minimise use of sedatives, narcotics, antiepileptics
and alcohol if possible.
Patients receiving LTOT
may become housebound
and develop associated
psychological problems
■
■
and social isolation.
At high flow rates (eg,
>60% inspired oxygen),
oxygen therapy can be associated with pulmonary
(atelectasis and fibrosis), cardiac and ocular pathology.
Complications include
ocular effects such as retrolental fibroplasia and disturbed vision, reported
mainly in children and
infants exposed to high concentrations of oxygen. In
adults, blurred vision as well
as confusion, headaches,
vomiting and loss of consciousness may result from
hypercapnia.
Cardiac consequences are
cont’d next page
20 August 2004 | Australian Doctor |
33
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how to treat - oxygen therapy
from previous page
only now starting to be
identified. In patients with
left heart failure, high levels
(>40% or >5L/min) of
inspired and blood oxygen
levels result in reduced cardiac output and elevation in
pulmonary capillary wedge
pressure (indicating worsening heart failure).
The mechanisms are
poorly understood but may
reflect loss of beneficial
heightened chemosensitivity
input to the brainstem cardiovascular control centre,
or the development of
oxygen radicals, which are
toxic to endothelium and
interfere with release of
nitric oxide.
Thus, any patients with
congestive heart failure using
devices other than normal
intranasal oxygen should be
closely watched for adverse
effects.
Consideration of ability to
drive should be made on a
case-by-case basis. Ideally,
patients who feel breathless
while driving should not
attempt to drive.
Detection of smoking
Cigarette smoking causes
many conditions that might
ultimately require LTOT.
Unfortunately, many addicted
patients are unable to quit
smoking despite disabling dyspnoea.
Guidelines for the provision of oxygen from government funding exclude current smokers. This is because
cessation of smoking and
subsequent reduction in
carbon monoxide binding to
haemoglobin molecules
results in greater capacity for
oxygen carriage (which
might take four weeks) and
often results in near normalisation of PaO2 and SpO2
level, thus negating the need
for LTOT.
Obviously, smokers in the
household of a patient
receiving oxygen therapy
present a fire risk.
Evidence of smoking can
be established by measuring
carboxyhaemoglobin in arte-
rial blood gases (normal
<0.1%; exposure to smoke,
car fumes, passive smoking
0.1-5%; smokers >5%).
Alternatively, a spot urine
test can be analysed for
cotinine, a byproduct of
nicotine. False-positive urinary
cotinine result may occur in
the presence of nicotine
replacement therapy (patches
or gum) or exposure to highconcentrate passive smoke.
Cost and practical advice
Set-up
OXYGEN therapy requires assessment of the patient and approval
by a respiratory physician. When
a patient meets the criteria for
oxygen therapy, applications can
be placed with the district health
care service.
Patients are usually provided
with an oxygen concentrator and a
single, back-up D-sized cylinder.
Oxygen equipment is usually
rented via external oxygen companies. Prices start from $90 a month
for an oxygen concentrator. Concentrators cost about $2600.
Rental for an oxygen cylinder with
an oxygen-conserving device and
trolley is about $60 a month.
Prices vary from company to
company, state to state, and often
according to whether the equipment is government or privately
funded. Some companies charge
delivery fees and others charge
separate refill fees for portable
cylinders.
Rental for an oxygen
cylinder with an
oxygen-conserving
device and trolley is
about $60 a month.
Medical review
Annual review is recommended to
ensure adherence to oxygen therapy, maintenance of SpO2 >90%
and absence of side effects (mainly
hypercapnia).
Equipment review
Annual servicing is required by the
oxygen distribution company at a
prescribing physician.
Standard concentrators need to
be serviced about every 20,000
hours, portable concentrators
about every 5000-10,000 hours.
Exposure of the concentrator to
water (humidity) may reduce the
lifespan of the nitrogen filter.
Funding for long-term
oxygen therapy
cost borne by the health care
provider (eg, Program of Appliances for Disabled People in Victoria) at which time, usage is
recorded and reported back to the
Funding for LTOT is provided for
patients who are medically eligible
and in some cases there are asset
and income criteria. Most sources
impose funding limits per month
per patient.
Australian state funding sources
include public hospitals, where
Author’s case study
A 48-YEAR-old man with
severe smoking-related
emphysema (FEV1 of about
500mL) was treated with
maximal medical therapy
(an anticholinergic, inhaled
steroid and long-acting bronchodilator) and 1L/min
oxygen intranasally. He had
recently stopped smoking
(negative urinary cotinine
and carboxyhaemoglobin
<0.1%).
While driving to hospital,
the patient was caught in
dense traffic, inhaled exhaust
fumes, developed acute
bronchospasm and called an
ambulance for help. He was
administered high-flow
oxygen (10L/min) via a standard face mask and transferred to the hospital’s emergency department.
On arrival he was unconscious, normotensive and
tachycardic, with an SpO2 of
99%. A CXR in emergency
(figure 8) and a previously
conducted high-resolution
CT scan of the chest (figure
9) confirmed severe COPD
without acute changes. His
ECG showed sinus tachycardia. Arterial blood gases
(figure 10) revealed severe
type 2 respiratory failure
(elevated PaCO 2 and low
pH).
Intubation was considered
but, in view of his extremely
severe COPD, he was started
on non-invasive ventilatory
support and his inspired
oxygen reduced to a level
providing an SpO2 of 90%.
In four hours his conscious
state improved and in three
34
Figure 8: Chest X-ray
showing severe
hyperinflation, as
indicated by the presence of
more than six ribs anteriorly
or 10 ribs posteriorly.
| Australian Doctor | 20 August 2004
entitlements may vary from state
to state, and aids and equipment
programs, for which eligibility criteria may vary from state to state.
Australian federal funding
sources include the Department of
Veterans’ Affairs, a residential care
subsidy for residents of federally
accredited nursing homes or hostels, and funding through an
extended aged-care in the home
package.
Other sources include some
health insurance companies, WorkCover or the Transport Accident
Commission (or state equivalent),
when oxygen is required as a result
of a work or motor vehicle injury,
respectively.
Summary
The most common indication (about 75%) for long-term
oxygen therapy (LTOT) is COPD.
■ Eligibility for LTOT is a PaO2 <55mmHg, or <60mmHg on
room air with signs of right heart failure, polycythaemia or
pulmonary hypertension, in an optimally treated non-smoking
patient.
■ Oxygen concentrators are the most efficient delivery system;
rental cost is about $100 a month.
■ 50% of COPD patients started on LTOT in hospital can stop
after one month.
■ LTOT improves quality of life and survival in COPD.
■ Evidence to support LTOT in other conditions is limited and
based on COPD data.
■ Evidence of current smoking can be obtained by finding an
elevated carboxyhaemoglobin level on arterial blood gas
analysis, or by a positive cotinine finding in a spot urine test.
■ Early morning global throbbing headache and blurred vision
(and ultimately loss of consciousness) may result from hypercapnia. Hypercapnia can be minimised by keeping SpO2
92%, and avoiding factors that might suppress respiratory
drive, such as drugs (sedatives, alcohol, antiepileptics), metabolic alkalosis (steroids, diuretics), obesity, obstructive sleep
apnoea, and medical conditions such as Cushing’s syndrome
and hypothyroidism.
■
Figure 9: High-resolution CT scan of chest showing severe
emphysema.
Figure 10. Arterial blood gas profile showing extreme
hypercapnic acidosis related to hyperoxia, with improvement in
respiratory failure after introduction of non-invasive ventilatory
support and low-flow oxygen to keep SpO2 >90%.
Optimal management of COPD
■ Stop smoking.
■ Consider alpha-1 antitrypsin deficiency.
■ Assess disease severity.
■ Search for and treat coexistent medical disorders (eg, obesity,
diastolic dysfunction, anaemia, hypothyroidism, sleep
apnoea).
■ Institute pulmonary rehabilitation.
■ Maximise use of inhaled anticholinergics, bronchodilators and
steroids (correct technique).
■ Minimise oral steroid use (3-10 days maximum for acute
exacerbation).
■ Arrange vaccination (annual influenza and five-yearly pneumococcal vaccination).
■ Consider palliative surgical procedures (transplantation, lung
volume reduction surgery) in extreme cases.
days he was discharged
home on oxygen therapy
and nocturnal non-invasive
therapy.
Issues of importance from
this case are:
■ The brittle nature of severe
COPD.
The development of
oxygen-induced hypercapnia.
■ The avoidance of intubation and intensive
care with the use of
non-invasive ventilatory
support.
■
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What not to miss in patients on established LTOT
■ Hypercapnia in patients using excessive LTOT flow rates.
■ Inadequate time spent on LTOT (should aim for
15-24 hours/day).
■ Development of cardiac dysfunction.
■ Progression of underlying lung disease.
■ Ongoing cigarette smoking.
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how to treat - oxygen therapy
GP contribution
Case study
DR MARTINE WALKER
Mosman, NSW
JIM was a 73-year-old retired
historian. Our practice inherited Jim after the departure of
his long time GP to the north
coast. He had never smoked
but by the time I met him Jim
had severe emphysema from
alpha-1 antitrypsin deficiency.
He was a veteran who had
served in the New Guinea jungles in WWII. He had a
devoted wife and two married
children.
Despite maximal medical
therapy including anticholinergics, steroids, beta-agonists
and antihypertensives, Jim’s
deteriorating respiratory function became evident as he
found even the smallest exertions exhausting.
He began waking with
headaches,
presumably
because of hypoxia. After
assessment by a respiratory
physician, which included
arterial blood gases, Jim was
found to fit the criteria for
home oxygen, which he used
initially for 16 hours a day.
With his motor scooter,
which was eventually supplied
by the Department of Veter-
ans’ Affairs, Jim was a familiar site around our area —
oxygen cylinder on board.
He became frustrated with
the limitations in mobility
associated with his portable
oxygen cylinders. He was
particularly put out that he
could no longer commute to
the university, where he had
continued to be involved
with research. Airlines were
particularly unco-operative
in Jim’s attempts to attend
conferences, cylinders in
tow.
After two years on oxygen
Jim developed a lower respiratory tract infection, which
was initially thought to be a
reactivation of TB. After a
distressing hospital stay, Jim
requested that all supports be
withdrawn. He died peacefully at home with his wife
and children around him.
Questions for the author
Assuming LTOT will have an
increasing role as the community ages, are there any
impending advances to make
LTOT less intrusive on daily
life?
Smaller lighter oxygen
cylinders and concentrators
have been, and will continue
to be, developed. Small tracheostomies with a single cannula can be used (‘minitrach’),
which can be quite inconspicuous with a collared shirt or
cravat. Unfortunately, there is
a considerable extra cost and
risk associated with minitrachs, which limit their general
use.
Clearly, discussion assessing quality versus quantity of
life need to be conducted as
part of the palliative care
aspects of end-stage lung disease. In such patients who are
comfortable without supplemental oxygen, the use of
oxygen should be reassessed.
Patients in our practice find
crusting of their nose and
dryness of their airways significant problems in their use
of LTOT. What hints do
you have to solve these and
the other practical problems
associated with LTOT?
For oxygen flow rates
< 3L/min, humidifiers are
not required. Crusting for
the nose can best be treated
with non-petrochemical topical gels such as sesame seed
oil (eg, Nozoil, distributed
by ENT Technologies Pty Ltd,
West Perth), RoEzit gel (available from BOC Gases, Australia) or saline nasal sprays.
Could you comment on the
use of LTOT in children
(eg, premature babies who
have had long periods of
ventilation). How long on
average do they require
oxygen therapy? Are there
any special issues or concerns with respect to LTOT
in babies?
I am not a paediatrician
and do not look after such
patients. However, in general,
most paediatricians would be
concerned about the toxic side
effects of medium- to longterm moderate-to-high flow
oxygen (retrolental fibroplasia and pulmonary toxicity).
However, these toxic side
effects are problematic with
flows used in intensive care
wards, rather than the flow
rates seen in the ambulatory
patient population.
Further reading
available on request
References
1. Report of the Medical
Research Council Working
Party. Long-term domiciliary
oxygen therapy in chronic
hypoxic cor pulmonale complicating chronic bronchitis
and emphysema. Lancet
1981; 1:681-86.
2. Nocturnal Oxygen Therapy Trial Group. Continuous
or nocturnal oxygen therapy
in hypoxaemia chronic
obstructive lung disease.
Annals of Internal Medicine
1980; 93:391-98.
Online resources
The BOC Group:
www.boc.com
Air Liquide Australia Limited: www.airliquide.com.au
Acknowledgement
Ms Brigitte Borg, respiratory
scientist, Alfred Hospital, for
reading the manuscript and
adding valuable and practical
comments.
Australian Doctor
How To Treat CPD
Instructions
Earn 2 CPD points by completing this quiz online or on the attached card. Mark your
answers on the card and drop in the post (no stamp required) or fax to (02) 9422 2844.
For immediate feedback click the ‘Earn CPD pts’ link at www.australiandoctor.com.au
Note that some questions have more than one correct answer. The mark required for CPD
points is 80%. Your CPD activity will be updated on your RACGP records every January,
April, July and October.
1. Pulse oximetry measures the percentage
of oxygen bound to haemoglobin (SpO2).
Which ONE statement about pulse
oximetry and the assessment of SpO2 is
false?
a) Respiratory failure is present if SpO2
is <90% . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
b) Abnormal haemoglobin varieties (eg,
carboxyhaemoglobin and methaemoglobin) can
be assessed by pulse oximetry . . . . . . . . . . .❏
c) Pulse oximetry is an indirect and noninvasive method of assessing oxygen levels in
the body . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
d) The presence of hypotension may make the
measurement of SpO2 inaccurate . . . . . . . . .❏
2. Brian, 65, is a heavy smoker. He has had
COPD for some years and is now
housebound. Coexistent medical disorders
have been excluded. To optimise Brian’s
management, which ONE action are you
least likely to take?
a) Give annual influenza vaccination and fiveyearly pneumococcal vaccine . . . . . . . . . . . .❏
b) Perform pulmonary function tests . . . . . . .❏
c) Advise him to use regular oral
steroids . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
d) Encourage him to participate in pulmonary
rehabilitation if this is available locally . . . . . .❏
HOW TO TREAT
3. Brian claims he will stop smoking if
oxygen is provided to improve his symptoms.
He understands that there is no government
funding for oxygen if he continues to smoke.
Which ONE statement concerning carbon
monoxide and smoking is true?
a) Carbon monoxide has an affinity for
haemoglobin 10 times greater than that of
oxygen . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
b) High carbon monoxide levels rapidly
decrease over five days after cessation of
smoking . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
c) PaO2 and SpO2 may be nearly normalised
after smoking cessation . . . . . . . . . . . . . . . .❏
d) Measuring arterial blood gases is the only
way to check that he has stopped
smoking . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
4. Brian’s PaO2 on maximal inhaled therapy
is 58mmHg. He has not smoked for six
weeks and this is confirmed on
measurement of arterial blood gases. Under
which THREE circumstances could Brian
receive government-funded long-term
oxygen therapy?
a) Polycythaemia . . . . . . . . . . . . . . . . . . . . . .❏
b) Pulmonary hypertension . . . . . . . . . . . . . .❏
c) COPD . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
d) Cor pulmonale . . . . . . . . . . . . . . . . . . . . .❏
5. Dorothy, 58, has emphysema secondary
to alpha-1 antitrypsin deficiency. She has
never smoked and has been compliant
with adequate doses of inhaled
medications. After hospital admission for
an acute exacerbation of COPD, oxygen
therapy has been prescribed, as well as
oral steroids for one week. Regarding
long-term oxygen therapy, which ONE
statement is true?
a) Long-term oxygen therapy involves use of
oxygen for 12 hours/day . . . . . . . . . . . . . . . .❏
b) Dorothy’s SpO2 or PaO2 should be
reassessed after four weeks . . . . . . . . . . . . .❏
c) Long-term oxygen therapy is indicated in
obstructive sleep apnoea . . . . . . . . . . . . . . .❏
d) There is evidence that long-term oxygen
therapy is beneficial in other conditions
such as interstitial lung disease and cystic
fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
6. Dorothy requests information about
various options in long-term oxygen therapy.
Which ONE statement about oxygen therapy
is not true?
a) Oxygen concentrators are the most efficient
delivery system . . . . . . . . . . . . . . . . . . . . . . .❏
b) Oxygen should always be delivered by
mask . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
c) Oxygen-conserving devices are useful with
oxygen cylinders . . . . . . . . . . . . . . . . . . . . . .❏
d) Annual review is recommended . . . . . . . .❏
7. Dorothy begins oxygen therapy. The
following week she complains of early
morning headaches as well as some
blurred vision. Arterial blood gases
confirm hypercapnia. Which ONE of the
following is least likely to have
contributed to this?
a) Alcohol consumption . . . . . . . . . . . . . . . .❏
b) Use of excessive long-term oxygen therapy
flow rates . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
c) Nocturnal sedation . . . . . . . . . . . . . . . . . .❏
d) Use of regular paracetamol . . . . . . . . . . . .❏
8. Under which ONE of the following
circumstances is oxygen therapy least likely
to be beneficial?
a) In the patient who becomes hypoxic
(SpO2 <90%) with exercise . . . . . . . . . . . . . .❏
b) Dyspnoea due to congestive cardiac
failure . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
c) Dyspnoea secondary to radiotherapyinduced fibrosis . . . . . . . . . . . . . . . . . . . . . . .❏
d) Significant nocturnal hypoxia . . . . . . . . . .❏
9. John, 52 and healthy, is attempting to
climb Mt Kilimanjaro. He has developed
some confusion and mild dyspnoea. Which
TWO options are indicated to relieve his
symptoms?
a) Increase inspired oxygen concentration to
21% by use of an oxygen cylinder . . . . . . . .❏
b) Descend . . . . . . . . . . . . . . . . . . . . . . . . . .❏
c) Use bronchodilators . . . . . . . . . . . . . . . . .❏
d) Provide moderate to high concentrations of
oxygen therapy (5-15L/min) . . . . . . . . . . . . .❏
10. Low levels of oxygen therapy (1-2L/min)
easily correct the hypoxaemia related to
conditions causing V/Q mismatch. In which
ONE condition does V/Q mismatch not
occur?
a) Pulmonary embolus . . . . . . . . . . . . . . . . .❏
b) Idiopathic pulmonary fibrosis . . . . . . . . . .❏
c) COPD . . . . . . . . . . . . . . . . . . . . . . . . . . . .❏
d) Bronchiectasis . . . . . . . . . . . . . . . . . . . . .❏
NEXT WEEK
Editor: Dr Lynn Buglar
The next How to Treat investigates the safety and risks associated with the administration of blood and blood products in Australia. The authors are Dr Joanne
Co-ordinator: Julian McAllan Pink, National Transfusion Medicine Service manager, Australian Red Cross Blood Service; and Dr Denis Spelman, head of the microbiology department and
deputy director of the infectious diseases unit, Alfred Hospital, Melbourne, Victoria.
36
| Australian Doctor | 20 August 2004
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