OXYGEN THERAPY
Dr Waqas Ahmed
PGR Pulmonology
healthcare and
emergency settings
Oxygen therapy is a treatment for
hypoxaemia not breathlessness.
Aim is to achieve normal or near normal
oxygen saturations for all acutely ill patients.
Oxygen should be prescribed to achieve a
target saturation of 94–98% for most acutely
ill patients or 88–92% for those at risk of
hyper-capnic respiratory failure
1. Assessing patients:
For critically ill patients, high concentration
oxygen should be administered immediately.
Supplemental oxygen is given to improve
oxygenation, but it does not treat the
underlying causes of hypoxaemia which
must be diagnosed and treated as a matter
of urgency.
The oxygen saturation should be checked by
pulse oximetry in all breathless and acutely
ill patients, ‘the fifth vital sign’
(supplemented by blood gases when
2. Target Oxygen prescription:
Oxygen should be prescribed to achieve a
target saturation of 94–98% for most acutely
ill patients or 88–92% or patient-specific
target range for those at risk of hypercapnic
respiratory failure.
Use appropriate devices and flow rates in
order to achieve the target saturation.
O2 therapy is either ‘controlled’ or
‘uncontrolled’.
3. Weaning and discontinuation of oxygen
therapy:
Oxygen should be reduced in stable patients
with satisfactory oxygen saturation.
Oxygen should be discontinued once the
patient can maintain saturation within or
above the target range
Uncontrolled Use
1. Uncontrolled and high- flow O2 thought to
be important, (Deliver 15 L/ min oxygen via
a non- rebreathe mask initially in these
situations) e.g. In:
• Shock, sepsis, major trauma
• Cardiac arrest and during resuscitation
• anaphylaxis
• CO or cyanide poisoning (oxygen
saturations unreliable)
• Pneumothorax
• Severe hypoxaemia i.e. SaO2 <85%
When a reliable saturation can be obtained
oxygen can often be weaned to achieve
SaO294–98%
In critical illness and with hypoxaemia an
arterial blood gas should be obtained as
early as possible.
British thoracic Society (BtS) guidelines
advise not to remove oxygen to obtain an
arterial blood gas on room air in acute
settings.
Moderate hypoxia (i.e. SaO2 <94% but
above 85%) can be treated with either nasal
cannulae or face mask oxygen aiming for
SaO2 94–98%.
Commonly arises:
Pneumonia
asthma
acute heart failure
Pulmonary embolus (PE)
Controlled use
Controlled Use when extra O2 is required,
but ventilation critically depends on hypoxic
drive (BTS guidelines recommend targeting
SaO2 88–92%)
1. Exacerbations of chronic obstructive
pulmonary disease (COPD) (particularly
when there has been a chronically raised or
previously raised PaCO2, as evidenced by a
significant base excess/ raised bicarbonate
or documented previously high CO2)
2. Exacerbations of cystic fibrosis (CF)
3. Exacerbations of ventilatory failure due to
obesity hypoventilation syndrome, scoliosis,
⚠️
There is increasing evidence that
indiscriminate use of O2 in some medical
emergencies may actually be harmful and
should only be used if the patient is
hypoxaemic (<94%, and then to achieve no
higher than 98%).
High O2 levels can be toxic through release
of free radicals, and this may be the
mechanism of damage in some of the
following situations.
1. Ischaemic heart disease, including
myocardial infarction (MI)
2. Stroke
3. Post- cardiac arrest, once stable
4. Sickle cell crisis
5. Obstetric emergencies
6. Most poisonings (other than carbon
monoxide (CO) or cyanide) e.g. Paraquat
7. Metabolic or renal acidosis with shortness
of breath (SOB).
O2 therapy for Non-Hypoxic
conditions
Indicated in carbon
monoxide poisoning
where the carbon
monoxide has
combined with the
haemoglobin to form
carboxyhaemoglobin.
O2 therapy for Non-Hypoxic
conditions
To resolve
pnuemothorax in those
who do not require a
chest drain.
By over oxygenating
the patient
(hyperoxaemia) it
changes the pressure
gradient in the
pulmonary capillaries
which draws air out of
the pleural cavity.
Signs and symptoms of
oxygen toxicity
• Oxygen toxicity affects the
human body in different ways
depending on the type of
exposure.
• Short exposures to high partial
pressures at greater than
atmospheric pressure can lead
to central nervous system
toxicity.
• Occular and pulmonary toxicity
results from longer exposure at
normal atmospheric pressure.
CNS Toxicity
Visual disturbance
Nausea
Irritability
Anxiety
Mood Changes
Confusion
Pulmonary/Occular
Exposure tunnel vision,
Ringing in ears
Nausea
Dizziness
Twitching
Seizures
Oxygen Therapy
OXYGEN THERAPY
Simple face mask
Venturi system
Nasal cannulae
Reservoir mask
High flow oxygen
Nasal Cannulae
Oxygen flow % Oxygen
rate (L/min) delivered
1 24
Nasal
2 28 cannulae/prongs/cathe
ters are uncontrolled
3 32 and deliver
unpredictable levels of
4 36
O2 (depending on flow
5 40 rate, minute
ventilation, and oral vs
6 44 nasal breathing).
titrate using an O2
saturation monitor.
Face Mask
Oxygen flow % Oxygen Standard O2 face
rate (L/min) delivered
2 24 mask (sometimes
4 35 called high- flow
6 50 mask). Set the O2
8 55 regulator to at least 4
10 60 L/ min, much more if
very breathless (to
prevent dilution by
air drawn into mask
by high inspiratory
flows via exit holes).
Venturi
FiO2 is controlled through a Venturi mask—
O2 is directed through a narrow nozzle and
exits at speed, lowering the air pressure at
this point. This draws in surrounding air,
diluting the FiO2
a proper Venturi mask mixes O2 and air in
the same proportion, regardless of the O2
flow
Non- rebreathe reservoir masks
non- rebreathe reservoir masks can deliver
FiO2 values over 60% by means of a soft
plastic bag between the end of the tubing
and mask, plus one- way valves between the
bag and mask and on the mask exit ports.
This mechanism ensures that most of the
inspired air is pure O2. the ability of the
reservoir to empty on inspiration briefly
allows higher inspiratory flows than the
actual O2 regulator setting, and the bag
valve prevents inhalation of most exhaled
CO2; the mask exit valves close, preventing
air inhalation.
High Flow oxygen
Optiflow
Very high FiO2 requires a tight seal and is
generally delivered with high f low nasal
oxygen or continuous positive airway
pressure (CPaP) masks (using pressures of
about 5– 7 cmH2O). This ensures no air is
entrained through blow- off vents or leaks,
as well as improving ventilation- perfusion
(V/ Q) matching by recruiting collapsed
alveoli.
High flow nasal oxygen
(HFNO)
Allows delivery of high FiO2 with high flow
rates, typically up to 60 L/ min
• High flow rates mean that positive
pressure is delivered and this equates to
CPAP of up to 7 cmH2O (~1 cmH2O/ 10L/
min flow). This will be impacted by mouth
leak
HFnO is therefore often used in patients with
hypoxic non- hypercapnic respiratory failure
(t1rF) despite high- flow oxygen via a non-
rebreathemask.
Home Oxygen therapy
Long- term oxygen therapy (LTOT) : to treat
select patients with chronic hypoxia,
requiring >15 h/ day, with the evidence base
from two randomized trials
Ambulatory oxygen therapy (AOT)
Nocturnal oxygen therapy (NOT)
Short- burst oxygen therapy (SBOt)
LTOT
Two landmark trials of LTOT in the 1980s—
the British MRC Working Party trial and the
American Nocturnal O2 Therapy Trial (NOTT)
established the value of LTOT.
Oxygen concentrator
Indications for LTOT
LTOT is the provision of O2 therapy to
patients with a chronically low PaO2 (≤7.3
kPa, or ≤55 mmHg, or SaO2 ≤≈88%) for
≥15 h a day (to include the night, when
usually most hypoxic), with the aim of
achieving an awake PaO2 >8 kPa, or
>60 mmHg, or SaO2 >≈91%. PaCO2 levels
can be normal or raised.
LTOT can also be prescribed if the PaO2 is
7.3– 8 kPa, if associated with 2°
polycythaemia or pulmonary hypertension
1. COPD
2. Severe chronic asthma
3. Interstitial lung disease (ILD)
4. CF
5. Bronchiectasis
6. Pulmonary vascular disease
7. Pulmonary portohypertension
8. Pulmonary malignancy
9. Chronic heart failure.
In addition, it can be prescribed for
nocturnal hypoventilation, usually in
conjunction with nIV or CPAP, e.g. In:
1. Obesity
2. neuromuscular or other restrictive
disorders
3. Osa treated with CPAP therapy but with
continuing hypoxia.
Additional benefits of LTOT include:
1. reduction of 2° polycythaemia
2. Improved sleep quality by reducing
hypoxia- associated brain arousals
3. reduced cardiac arrythmias, and
potentially reducing the risk of nocturnal
sudden death
4. reduced sympathetic outflow, leading to
improved renal function, with increased salt
and water excretion, and reduced
Assessment for LTOT
1. Should occur when patients are stable and
at least 8 weeks have passed since any
exacerbation of their condition
2. Fully optimized treatment
3. two sets of arterial gases are taken at least
3 weeks apart to ensure that the patient
remains sufficiently hypoxic to merit LTOT
4. Blood gases are also taken after 30 min on
supplemental O2 to ensure the target PaO2
has been reached.
Ambulatory oxygen therapy
(AOT)
Ambulatory oxygen therapy (AOT) Provision
of supplemental O2 during exercise and
activities of daily living. this may be on its
own or in addition to LTOT. the evidence for
AOT is limited, showing improvements in
laboratory- based exercise performance only.
AOT has not been shown to have long- term
benefits on dyspnoea, exercise capacity,
functional capacity, time away from home
Ambulatory oxygen should not be routinely
offered and should only be considered as
part of a structured programme of exercise
such as pulmonary rehabilitation.
AOT should not be considered for patients
who are housebound.
Short burst oxygen therapy
(SBOT)
Short-burst O2 is now rarely justified. It may
be required for transient situations, such as
during exacerbations, but usually either the
patient is sufficiently hypoxic to require LTOT
or they are not.
If it is considered, then proof of efficacy
should be sought, particularly given its
expense.
SBOT at 12 L/ min should be considered
for cluster headache.
