Oxygen and oxygen therapy

 Oxygen
 The Fick Principle
 Oxygen Electrode
 Oxygen Transport
 Oxyhemoglobin Dissociation Curve (ODC)
 Transport of carbon Dioxide
 Carbon Dioxide Dissociation Curve
 Oxygen Content
 Oxygen Delivery
 Postoperative Hypoxemia
 Oxygen Flux
 Oxygen Cascade
 CO Poisoning

 Hypoxia
 Oxygen Therapy and devices
 Peak Inspiratory Flow Rate
 Low Flow Systems
 High flow systems
 Performance devices
 Venturi effect
 Medium Dependency System
 Neonates and Infants
 Clean and Sterilization
 Choice of Devices
 Hazards of oxygen therapy
 Oxygen Toxicity

 Oxygen is a drug.
 It must be used meticulously & diligently.
 If abused it can cause complications.
 The major reason for O2 therapy is hypoxia.
 Hypoxia is deficiency of O2 at tissue levels.
 Hypoxemia refers to reduced O2 tension in arterial blood.
 A gas with chemical formula of O2
 Colourless, odorless, tasteless
 Boiling point -183 C
 Melting point –216.6C
 Critical temp. –118.4C , Critical pressure 736.9psi
 Constitutes about 20.95% of atmosphere

 Used to measure widely differing physiological flow
parameters.
 A substance is added or subtracted from the flow that it is
desired to measure.
 Flow of liquid in a given period of time = the amount of
substance entering or leaving the stream in the same period of
time, divided by the concentration difference before and after
the point of entry or exit.
 Two forms of indicator dilution technique can be used to
measure blood flow :-
1. An indicator is injected at a constant rate upstream and its
concentration is measured from a downstream sample after
mixing has taken place.
Flow = rate of infusion of indicator/concentration of indicator in
blood

 Nontoxic dyes such as Indocyanine green have been used for
physiological measurements of blood flow. Radioactive tracers
may also be used.
 The direct Fick principle is the basis of the calculation of cardiac
output from measurements of the steady-state oxygen
consumption of the body as follows :-
CO = Oxygen consumption/Arteriovenous oxygen content
difference
 Oxygen consumption is measured over a fixed period of time
using a volumetric method or indirectly by measuring the
inspired and expired volumes & oxygen concentrations.
 Arteriovenous oxygen content difference = Arterial oxygen
content - the mixed venous (Pulmonary artery) oxygen content

2. A slug of indicator is injected and the concentration of the
indicator is sampled continuously downstream.
 In the thermodilution measurement of cardiac output, a bolus of
saline is injected into the right atrium and a thermistor
continuously measures the temperature of the blood downstream
in the pulmonary artery.
 The CO is inversely proportional to the area under the plot of
temperature with time and is calculated using a modified
Stewart-Hamilton equation, the denominator of which is the
integral of the change in blood temperature.
 A modification of this technique uses a special catheter that
pulse-heats blood in the right side of the heart and detects the
rise in temperature in the pulmonary artery, which estimates the
continuous estimation of CO.

 The principle of the Clark-type, polarographic electrode for the
measurement of the partial pressure of oxygen (Po2) in a blood
sample involves the electrolytic reduction of oxygen at a cathode
constructed of glass-coated platinum.
 The platinum electrode is charged negatively w.r.t. a suitable
reference electrode, (Ag/AgCl2) in a solution containing oxygen.
 At the cathode, the oxygen combines with water and the
additional electrons to give hydroxyl ions in a reduction process
:-
O2 + 2H2O + 4ē →2H2O + 4ē → 4OHˉ
 The hydroxyl ions are buffered by the electrolyte (e.g. potassium
chloride) :-
4OHˉ + 4KCl → 4KOH = 4Clˉ

 At the anode of the PO2, oxidation or loss of electrons occurs.
The electrons in the process are provided by the silver anode
and chloride ions, which form silver chloride :-
4Ag + 4Clˉ → 4AgCl + 4eˉ
 The clark electrode has an oxygen-permeable, plastic
membrane covering the tip of the cathode.
 As the polarizing voltage increases, the current flow reaches a
plateau at about 0.6 to 0.8V, minimizes interference due to
electrochemical reactions with other gases and provides
sufficient voltage to drive the reaction.

 There is a linear relation between the current generated and the
concentration of oxygen in the solution.
 The dependence on temperature is controlled by using a precise
operating temperature, such as with an electronic heat source.
 The system is calibrated with two gases :-
1. Containing no oxygen and
2. Containing a known amount of oxygen

 At breathing air, oxygen reserve in a 3-L FRC is about 500 ml.
 The blood stores about 850 ml of Oxygen.
 Increasing the Inspired Oxygen Fraction (FiO2), increases
oxygen stores in the FRC to nearly 3 L which increases
dissolved oxygen but has less effect on the volume bound to
hemoglobin, as it is nearly fully saturated at breathing air.
 Oxygen is carried to the tissues by means of being dissolved in
the plasma and bound to hemoglobin.
 The amount dissolved depends on the partial pressure and
Solubility, giving 0.003 ml per 100 ml blood for each mmHg of
Po2.

 Blood substitues such as Perfluoronated hydrocarbons have a
high oxygen solubility & can carry as much oxygen as blood, at
high oxygen tensions.
 In theory, 1 gm of Hb can combine with 1.39 ml of oxygen i.e.
Hoffman coefficient but in reality, this amount is less i.e. 1.34-
1.36 ml because in vivo the heme group of a small fraction of
hemoglobin is oxidized to methemoglobin , which is unable to
release its oxygen to the tissues.
 Nitrites & Sulfonamides oxidize hemoglobin, as can a
congenital deficiency in the enzyme methemoglobin reductase.

 If the oxygen capacity of hemoglobin is 1.36 ml/gm, 15 gm of
hemoglobin can combine with 20.4 ml of oxygen – the oxygen
content.
 The oxygen saturation of Hb (SaO2) is expressed as a percentage
of the oxygen capacity :
1. O2 content = (1.36×Hb×So2/100) + (0.003×Po2)
2. O2 content= O2 bound to Hb+O2 dissolved in plasma
 Where the O2 content is given as ml O2 per 100 ml blood, Hb is
given as g per 100 ml and Po2 is given as mmHg

 The shape of the curve have important physiologic advantages :-
1. The flat upper portion implies that small changes in alveolar
oxygen (breath holding, moderate altitude) have harmful effect
on full oxygen saturation of blood.
2. At alveolar oxygen tensions of less than 70 mmHg(9.3kPa), small
reductions in capillary oxygen tension result in large reductions
in hemoglobin oxygen content, which facilitates the unloading of
oxygen from hemoglobin to supply the tissues.
3. The position of the ODC is described by the term P50, which is
the oxygen tension required for 50% saturation of hemoglobin
and is normally 27 mmHg(3.6kPa). P50 may shift to the right or
left under certain physiologic conditions.

Normal Oxyhemoglobin Dissociation Curve
97% saturation = 97 PaO2 (normal)
90% saturation = 60 PaO2 (danger)
80% saturation = 45 PaO2 (severe hypoxia)

SHIFT TO LEFT
• Increase in pH
• Decrease in CO2
• Decrease in 2.3-DPG
• Decrease in temperature
SHIFT TO RIGHT
• Decrease in pH
• Increase in CO2
• Increase in 2,3-DPG
• Increase in temperature

 A right shift means that more oxygen is unloaded at a given
Po2.
 BOHR EFFECT :- The effect of altering Pco2 is mainly
associated with change in the hydrogen ion concentration.
 Conditions associated with a right shift in the ODC are found in
active tissues, so that hemoglobin gives up its oxygen more
easily where it is needed most.
 The compound 2,3-DPG is an endproduct of red cell
metabolism and is increased :-
1. Anemia
2. Thyrotoxicosis
3. Chronic Hypoxia – Lung disease & High altitude
 Stored blood has depleted 2,3-DPG and is less effective at
oxygen delivery.

 Tension of CO2 in venous blood is 46mmHg and in alveoli the
tension is 40mmHg .
 CO2 is distributed in the following manner-
1.In solution in plasma (5%) : This quantity is responsible for
determining the tension of gas in the blood and also acts as an
intermediate between the air in alveoli and inside the red cell .
2.As carbamino compound (25%) : CO2 can combine with amino
group of Hb. - 3.5 times greater affinity to CO2 as compared to
oxy hemoglobin
3.As carbonic acid: CO2+H20↔H2CO3

4.As Bicarbonate(90)% :
Most of CO2 passes to
red cells where enzyme
carbonic anhydrase aids
its rapid hydration to
form carbonic acid .
Carbonic Anhydrase is
not found in plasma.
-Hamburger shift

 The CO2 dissociation curve relates to CO2 content of blood to
PCO2 to which it is exposed .The position of this curve depends
on the degree of O2 of the blood.
HALDANE EFFECT:
 The more deoxygenated , the blood becomes the more CO2 it
carries at given PCO2 .
 Deoxygenation of blood in peripheral capillaries facilitates
loading of CO2 while oxygenation in pulmonary capillaries
facilitates unloading of CO2.
 Hence, Venous blood carries more CO2 as compared to arterial
blood.

CO2 stores are large :
approx120L and
primarily dissolved as
CO2 and bicarbonate.
Equilibrium requires 20
to 30 mins, as compared
to O2 which requires 4
– 5 mins.
Due to large capacity of
intermediate + slow
compartments , change
in CO2 tension is
slower than its fall,
following acute

 Diffusion rate of CO2 – 20 times greater than oxygen
 PACO2 ( Alveolar CO2 Tension) = VCO2(total CO2
production ) / VA( alveolar ventilation )
Pulmonary End Capillary tension ( Pc’CO2 )= PACO2
End Tidal CO2 Tension ( PET CO2 ): clinical estimate of
CO2.
Normally, PA CO2 – PET CO2 < 5mm

 The oxygen content of the blood is that quantity of oxygen
contained in the red cell , added to the quantity , dissolved in the
plasma and is defined as the volume of oxygen in milliliters
carried in 1 dL of blood.
 Normally calculated from the equation :-
 CaO2 = Hb × 1.37 × SaO2 + 0.023 × PaO2 kPa
 (CaO2 = Hb × 1.37 × SaO2 + 0.0034 × PaO2 mmHg)
a = An arterial blood sample
CaO2 = The arterial oxygen content in ml/dL of blood
Hb = The hemoglobin concentration in g/dL of blood
1.37 = The volume of oxygen in milliliters carried by 1g of fully
saturated hemoglobin
SaO2 = The fractional hemoglobin saturation
PaO2 = Arterial oxygen tension measured in kPa or mmHg

0.023 and 0.0034 = The solubility coefficients of oxygen in plasma
(mL of oxygen per dL plasma, in kPa or mmHg respectively)
 The red cells’ contribution to oxygen content is controlled by
the concentration of active hemoglobin and by the ability of
hemoglobin to combine with oxygen i.e. the Saturation.
 The saturation depends on the partial pressure of oxygen and the
position of the oxygen dissociation curve.
Fractional hemoglobin saturation (SaO2) is defined as the ratio
of oxyhemoglobin to total hemoglobin :-
SaO2 = HbO2/(HbO2 + Hb + metHb + COHb)
Where HbO2 = Oxyhemoglobin
Hb = Reduced hemoglobin
metHb = Methemoglobin
COHb = Carboxyhemoglobin

 Multiwavelength co-oximeters are required to measure the
saturation.
Functional Saturation is used to describe hemoglobin saturation,
which ignores the presence of methemoglobin and
carboxyhemoglobin :-
fnSaO2 = HbO2/(HbO2 + Hb)
 SaO2 is provided by blood gas analysis and measures
saturation from PaO2 and the oxyhemoglobin dissociation
curve.

 Because methemoglobin and carboxyhemoglobin do not carry
oxygen, only SaO2 should be used when accurately calculating
oxygen content.
 With a hemoglobin level of 15g and normal values of PaO2 and
SaO2, the arterial oxygen content is 20 ml/dL blood, 20 vol% or
9 mmol/L.
 Normal oxygen content of blood is very similar to that of room
air at sea level.

 The total quantity of oxygen delivered to the tissues per minute
is a function of the oxygen content and the Cardiac output. The
overall flow rate of oxygen to the tissues is called the “O2
Delivery”.
 With a normal Cardiac Output of 5L/min for a 70 kg adult, there
will be a normal O2 delivery of 44.5mmol/min O2 or 1000
ml/min O2.
 Since the normal Cardiac Output depends on the size of the
patient , cardiac output is commonly indexed to body surface
area (BSA) , using a normal cardiac index(CI) of 3L/min/m2 of
O2 delivery.
CI = CO/BSA L/min/m2
O2 Delivery = CaO2 × CI × 10 ml/min/m2 O2

 In an adult patient with a normal CI of 3L/min/m2, the oxygen
delivery index would be 600 ml/min/m2 O2 or approximately 27
mmol/min/m2 O2.
 This measure of the oxygen delivery index is a value of total
oxygen transport but it does not take into consideration of the
regional variations in oxygen transport to specific organ systems.

 The most important cause is the combination of :-
1. A reduced VA/Q intraoperatively
2. Impaired postoperative ventilatory control induced by opioids.
 A reduced VA/Q shifts the PiO2 vs. SpO2 curve to the right so
that the steep part of the curve becomes a tangent to the inspired
oxygen pressure.
 Opioid administration causes a further shift to the right and this
causes a profound fall in oxygen saturation.
 So, postoperative oxygen saturation was measured continuously
overnight with patients breathing air.
 A fall in VA/Q causing a shift in the PiO2 vs. SpO2 curve to the
right, is an important factor in predisposing patients to sleep-
related hypoxemia.

 DEFINITION: The amount of oxygen leaving left ventricle per
minute in the arterial blood has been termed as oxygen flux .
 It is expressed as : Cardiac Output ×Arterial oxygen saturation ×
Hemoglobin concentration ×1.31(vol of O2 combining with 1 gm
of Hb )
 5000ml/min × 98/100 ×15.6/100g/ml ×1.31
 so, oxygen flux = 1000ml/min
 250ml of this Oxygen is used in cellular metabolism & rest
returns to lungs in mixed venous blood (75% saturated with
oxygen).

ARTERIAL OXYGEN CONTENT:
 It is predominantly in combination with Hb.
Cao2= Sao2×Hb×1.31
OXYGEN UPTAKE:
 When blood reaches the systemic capillaries, oxygen dissociates
from Hb & moves into tissues.
 rate at which this occurs is called oxygen uptake.
 normal range of Vo2 in healthy adults at rest is: 200-300ml/min
or 110-160 ml/min/m2 when adjusted for body size.

 Oxygen binds with hemoglobin but much less avidly than with
CO.
 The oxygen partial pressure of mixed venous blood entering
pulmonary capillaries is about 5.3 kPa (40 mmHg) compared
with the alveolar tension of about 13.3 kPa (100mmHg).
 Under normal conditions, the transfer of oxygen is perfusion
limited.
 If diffusion properties of the blood-gas barrier are impaired, for
example in ARDS, then diffusion equilibrium may not occur by
the end of the capillary.

 The fraction of oxygen delivered to the capillaries that is taken
up into the tissues is an index of efficiency of oxygen transport.
 Monitored with a parameter called oxygen-extraction
ratio(O2ER)
 Normally about 0.25 (range=0.2-0.3)
 So only 25% of oxygen delivered to systemic capillaries is taken
up into tissues.
 Though O2 extraction is low it is adjustable & can be increased
when oxygen delivery is impaired.

 PO2 of dry air at sea level is 21.2kpa(159mmhg)
 O2 moves down the partial pressure gradient from air through
respiratory tract, alveolar gas, arterial blood, systemic capillaries,
tissues & cell.
 It reaches its lowest level in the mitochondria where it is
consumed . Here PO2 is 0.5-3kpa(3.8-22.5mmhg)
 The steps by which PO2 decreases from air to mitochondria are
known as O2 cascade.

Dilution of inspired oxygen by water vapour:
 Concentration of atmospheric oxygen is 20.94%
 As gas is inhaled through the respiratory tract, it becomes
humidified at body temperature & added water vapour dilutes
the O2 & ↓ PO2 below its level in ambient air.
 PO2 = fractional conc’n of O2 in dry gas phase × (barometric
pressure - saturated water vapour pressure)
 PO2=0.2094(760-47)
=149mmhg.

 CO exposure produces cerebral hypoxia secondary to its
reversible combination with hemoglobin to form
Carboxyhemoglobin.
 Symptoms are related to the blood carboxyhemoglobin content,
which depends on the duration of exposure, time since exposure
and the treatment given.
 In the early stages :-
1. Throbbing headache
2. Vomiting without Diarrhea
3. Lethargy
4. Hyperventilation

 Symptoms may progress to :-
1. Convulsions
2. Coma
3. Hypoventilation
4. Bradycardia
5. Cardiovascular collapse
 In the elderly, CO toxicity may present as a cerebrovascular
accident or myocardial infarction.

 Inhalation of products of combustion.
 Faulty appliance
 Blocked flue
 Motor exhaust gas inhalation.
Because of the high affinity of CO for hemoglobin, a few breaths at
high concentrations can be fatal; 1% CO in air can kill within a
few minutes

 CO is colourless, odourless, nonirritant toxic gas
 CO toxicity due to
 Cellular hypoxia
 Direct cellular injury
 Cellular hypoxia
 CO competes with O2 for binding to Hb
 Affinity of Hb for CO x 200-250 > affinity for O2
 O2-Hb dissociation curve shift to the left
 Impaired tissue release of O2 and cellular hypoxia

 Direct cellular injury
 CNS reoxygenation injury
 Lipid peroxygenation
 Free radical formation
 CO toxicity in pregnancy
 Risk of fetal injury

Oxygen-Hemoglobin Dissociation Curve
Curve – shifted to left hyperbolic curve , decreases oxygen
carying capacity

 High level of clinical suspicion
 Serum COHb level
 Exhaled breath COHb level
 Measured by spectrophotometry
 Pulse oximetry cannot distinguish between HbO2 and COHb
 Comprehensive neurological and neuropsychological
assessment
 CO Neuropsychological Screening Battery
 CT brain to exclude other conditions

TREATMENT :-
 Removal from the source of exposure
 Administration of 100% Oxygen immediately, after taking an
anticoagulated whole blood sample for carboxyhemoglobin
estimation.
 The pregnant patient or any patient who has had symptoms s/o.
severe poisoning (including any degree of neurologic
impairment) should be treated with Hyperbaric Oxygen.
 Hyperbaric oxygen is effective in :-
A. Reducing long-term mental impairment following CO poisoning
B. Shortening the half-life of Carboxyhemoglobin
C. Preventing late neurologic sequelae

INADEQUATE O2 SUPPLY TO THE BODY TISSUES
(ENTIRE BODY) OR (LOCALIZED REGION)
HYPOXIA MEANS

 DEPEND ON:
RAPIDITY AND SEVERITY
OF THE
DECREASE OF ARTERIAL Po2

CAUSES :-
Hypoxia could be due to arterial hypoxemia or failure of the
oxygen hemoglobin transport system :-
1. Arterial Hypoxemia –
 Low inspired oxygen partial pressure (high altitude)
 Alveolar hypoventilation (Sleep apnea, Narcotic overdose,
neuromuscular disorders, anesthetics and sedatives)
 Ventilation-perfusion mismatch (atelectasis , pneumonia, Acute
Asthma)
 Right to left shunts (Pneumonia, pulmonary embolism,
Arteriovenous malformation)

2. Failure of oxygen hemoglobin transport system :-
 Inadequate tissue perfusion (Cardiac failure, myocardial
infarction, hypovolemic shock)
 Low hemoglobin concentration (anemia, trauma)
 Abnormal oxygen dissociation curve (hemoglobinopathies, high
carboxyhemoglobin)
 Increased oxygen requirements in hypermetabolic states
 Histotoxic poisoning of intracellular enzymes (cyanide
poisoning, septicemia)

CLASSIFICATION :-
1. Ischemic hypoxia - ↓ blood flow, normal CaO2
2. Hypoxemic hypoxia – CaO2
3. Hypoxic hypoxemia - ↓ PaO2, SaO2, Normal Hb
4. Anemic hypoxemia - ↓ Hb , Normal PaO2, SaO2
5. Toxic hypoxemia - ↓ SaO2, Normal PaO2 (i.e. MetHb or COHb)

1.HYPOXIC HYPOXIA:
- Dec. in O2 saturation of Hb like alveolar
hypoventilation& low FiO2.
- O2 therapy fruitful results.

- Due to low cardiac output states & vascular
occlusion.
- O2 therapy helps to less extent.

- O2 carrying capacity is reduced like
anemia,hemodilution,CO poisoning.
- O2 therapy useful to some extent.

- Due to cyanide poisoning.
- Cells cannot utilise O2.
- O2 therapy least likely useful.

WHICH PATIENTS NEED :-
American College of Chest Physicians and National Heart Lung and
Blood Institute recommendations for instituting oxygen therapy
are :-
1. Cardiac and respiratory arrest
2. Hypoxemia (PaO2 < 60mmHg, SaO2<90%)
3. Hypotension (Systolic BP<100mmHg)
4. Low Cardiac Output and metabolic acidosis
5. Respiratory distress (RR>24/min)
While providing oxygen therapy, attempts must be made to find the
underlying pathology and treat it.

TYPES :-
Depending on the cause and severity, oxygen can be supplemented
from a range of oxygen therapy devices.
1. Normobaric oxygen therapy :-
 When devices deliver oxygen at or just above atmospheric
pressure.
2. Hyperbaric oxygen therapy :-
 Patients in whom, either the oxygen carrying capacity of
hemoglobin is compromised e.g. CO Poisoning or extra tissue
oxygen is required (in severe burns and tissue infections).
 Supplemental oxygen may be delivered by dissolving it under
pressure, in plasma.

INDICATIONS :-
 Patient factors –
 Cardiorespiratory disease, elderly, shivering , obesity
 Surgical factors –
 Thoracic surgery, upper abdominal surgery
 Physiological factors –
 Hypovolemia , hypotension, anemia
 Postoperative analgesic technique –
 Patient controlled analgesia, IV Opioid infusion

CLASSIFICATION :-
1. Performance of the device –
 Fixed – Venturi mask
 Variable – Nasal prong, Face mask
2. Flows delivered by the device –
 Low flow – Nasal prongs, Face mask
 High flow – Venturi mask
3. Patient –
 Dependent – Face mask, Nasal prongs, CPAP Device
 Independent – Ventilators
4. Degree of dependency –
 Low dependency – Face mask, Nasal prongs
 Medium dependency – CPAP Mask and equipment
 High dependency – Noninvasive or IPPV

 Open ports for exhaled
gas
 Air entrained through
ports if O2 flow through
does not meet peak
inspiratory flow
O2 inlet
Exhalation
ports

 If a patient is breathing spontaneously from a T-Piece with no
reservoir and zero FGF, then all the inspired gas would be room
air.
 FGF is ↑ to 100 L/min, then all the inspired gas would be taken
from the FGF & FiO2 will be the same as the Fresh gas.
 FGF are ↓ from 100L/min, there will be a point at which the FGF
will not meet the patient’s requirements.
 FGF < peak inspiratory flow, the patient will entrain room air
which will dilute the FiO2 of the fresh gas.

 Deliver oxygen at flows that are less than the patient’s inspiratory
flow rate leading to air entrainment.
 The inhaled oxygen concentration (FiO2) may be low or high,
depending on the specific device and the patient’s inspiratory
flow rate.
 Oxygen delivery varies with the patient’s inspiratory flow i.e.
variable performance oxygen delivery systems.
 An anesthetic breathing system having a tight fitting mask and a
reservoir, can deliver a known FiO2.

 Examples :-
1. No capacity system –
 Nasal cannula , Nasopharyngeal catheters
2. Low capacity system (Capacity < 100 ml) –
 Simple and nebuliser face mask for children, Tracheostomy
mask
3. Medium capacity system (Capacity 100-250 ml) –
 Simple and nebulizer face mask for adults
4. High Capacity system (Capacity 250-1500 ml) –
 Face mask with reservoir bag
5. Very high capacity system (Capacity > 1500 ml) –
 Incubators, Oxygen hood, Oxygen tents

 Fixed-performance oxygen delivery systems as they can provide
a specific FiO2 at flows that meet or exceed the patient’s
inspiratory flow requirement.
 No defined cut-off point between low and high flow, about 10-15
L/min.
 A constant proportion of air-oxygen mixture is created in excess
of patient inspiratory flow rate and are independent of patient
factors or fit to the face.
 There is no rebreathing , as the CO2 gets washed out by the gas
flow , which constantly exceeds the patients demand.

 When the flow is less than the peak inspiratory flow, the high
flow devices become patient-dependent
 To work efficiently and to prevent air dilution, a fixed
performance device should incorporate :-
1. A large volume face piece (not < 280 ml)
2. Gas mixture flowing directly towards the nose and mouth
3. Vents positioned well away from the patient airway. e.g.
Ventimask

 Supplemental oxygen can be supplied by a variety of devices.
 The effectiveness of each device is determined by the capacity of
each device to deliver sufficient oxygen at high enough flow rate
to match the patients spontaneous inspiratory flow rate.
 In a non-intubated patient, breathing in an “open” system, the
capacity of the oxygen therapy device to meet the patient’s
inspiratory flow will determine how much room air will be
entrained.
 The FiO2 delivered from the oxygen source will be diluted by
the entrained room air. Therefore, the oxygen delivery systems
are categorized as :-
1. Variable Performance
2. High-flow fixed performance

1. Variable performance systems :-
 No control on FiO2
 Patient-dependent because the FiO2 that the patient receives will
change with changes in the respiratory parameters.
 For example, nasal catheters, nasal cannulae and masks with or
without a rebreathing bag.
2. High-flow fixed performance systems :-
 Controlled FiO2
 Patient-independent because regardless of changes in respiratory
parameters, the patient will receive a constant predetermined
inspired oxygen concentration (FiO2).
 For example, Ventimask

 If the diameter of a tube is made smaller at some point in its
length and the flow through the tube is held constant, the
velocity of the gas in the narrowed segment must increases.
 The increase in kinetic energy that enables the gas to flow
faster can only be achieved by converting some of its potential
energy, which can only be derived from the pressure within the
tube.
 In the narrowed segment, the gas flows faster and the pressure
is reduced.
 Bernouille’s equation relates the pressure gradient across a tube
and the velocity of the gas flowing through it :-
P + ρgH + 1/2ρv2 = constant
Where ρ = Density of the gas
P = Pressure
H = Height measured from a fixed point

 The pressure is approximately proportional to the square of the
flow rate.
 The most common application is found in the fixed-
performance Venturi oxygen mask.
 High-pressure oxygen from a cylinder or pipeline is acclerated
through a small-diameter tube in the base of the mask.
 At the point at which the tube emerges inside the mask, the
pressure is reduced to below atmospheric and air is entrained
which is mixed with the oxygen feed in the body of the mask.

 The concentration of oxygen received by the patient, depends on
the flow of oxygen and the diameter of the Venturi.
 The Venturi principle can also be used as a generally applicable
device to calculate the flow of gas by measuring the pressure
drop in a narrowed segment in a specially constructed and
calibrated tube.
 Other devices that are used to measure the flow of gases include
:-
1. Thermistor flowmeter (Cooled by the flow of gas)
2. Moveable-pointer peak flowmeter (a variable-orifice flowmeter)

 Used when the patient needs some amount of respiratory
assistance along with oxygen supplementation.
 It can only be used in spontaneously breathing patients.
Example, CPAP Mask.
 The CPAP device consists of a face mask with head strap, O2-
CPAP Valve, flow generator and wide bore tubings.
 The masks are available in various sizes and cover the mouth
and nose. The mask is secured with a harness.
 O2-CPAP Valves provide CPAP from 2.5-20 cm of water.

 The flow generator can be plugged into wall outlet for oxygen.
Has an ON switch, as well as a switch for adjusting the oxygen
flow and oxygen concentration.
 Wide bore tubing connects the flow generator to the mask.
 There are 2 one way valves present in the body of the face mask
:-
1. The inlet valve
2. The outlet valve to which the CPAP valve is attached.
 The facemask, CPAP valve and the wide bore tubings are for
single use only.

O2 Flow rate FiO2 O2 Flow rate FiO2 O2 Flow rate FiO2
Nasal cannula Oxygen mask Mask with reservoir
1 0.24 5-6 0.4 6 0.6
2 0.28 6-7 0.5 7 0.7
3 0.32 7-8 0.6 8 0.8
4 0.36 9 0.80+
5 0.4 10 0.80+
6 0.44

 Enclosure systems are used to provide oxygen therapy to
neonates and small infants :-
1. Oxygen hoods :-
 Transparent enclosures designed to surround the head of the
neonate or small infant.
 It has an opening for the neck and comes in different sizes.
 Hoods are well-tolerated by infants and allow easy access to
chest, trunk, and extremities.
 Due limitation of the size, these hoods can be used only in
children below 1 year of age.
 A continuous flow of humidified oxygen is supplied to the hood.
 The hoods deliver 80-90% at a flow rate of 10-15L/min.

2. Oxygen Tents :-
 Transparent enclosures in larger sizes (so-called tent houses or
huts) are available for patients who are too big for the hoods.
 The subject lies in the tent and CO2 is removed by soda lime
and water vapour by calcium chloride.
 The temperature in the tent is regulated by flowing oxygen and
air over ice chunks (to prevent accumulation of heat of
exothermic reaction).
 The tents are designed for children.
 FiO2 of 0.6-0.7 can be achieved with flow rates of 10-12
L/min.
 The air changes 20 times/hr.
 High output nebulizers can circulate cooled mist in the tent.

 As the oxygen concentrations may vary within the hood, it
should be measured as near the nose and mouth as possible.
 There is a decrease in oxygen concentration whenever the
enclosure is opened.
 Nasal oxygen may need to be supplied during feeding and
nursing care of patients who are confined to hoods.
 Flows > 7 L/min are required to wash out CO2 :-
1. Devices can be confining and isolating
2. FiO2 can vary from 0.21 to 1.0
 Temperature of the gases in the hood should be maintained to
provide a neutral thermal environment.

3. Closed Incubators :-
 Transparent enclosures that provide a warm environment for
small infants with temperature instability.
 Supplemental oxygen can be added to incubators but may result
in an increased oxygen concentration.
 The primary purpose of an incubator is to provide a temperature-
controlled environment.
 FiO2 is maintained at 0.4
 Humidified oxygen can be provided.

 Prolonged exposure to humidified oxygen may increase risk for
cutaneous fungal infection
 Hypoxia or hypercapnia can result from inadequate or loss of
gas flow.
 Temperature within enclosures should be closely monitored to
reduce the potential for cold stress or apnea from overheating in
neonates.
 Use of an improperly sized hood can result in irritation of the
infant’s skin.

1. Low-flow systems :-
 Under normal circumstances, do not present clinically important
risk of infections and do not require routine replacement on the
same patient.
 Nasopharyngeal catheters should be changed every 24 hours.
 Transtracheal catheters should be changed every 3 months.
 Reservoir system – Under normal circumstances, reservoir
systems do not present clinically important risk of infection and
do not require routine replacement on the same patient.

2. High-flow systems :-
 Large-volume nebulizers should be changed every 24 hours
when applied to patients with an artificial airway.
3. Enclosure Systems :-
 No recommendation regarding the frequency of changing
oxygen hoods and reservoirs while in use on the same patient.

 Need is determined by :-
1. Measurements of inadequate oxygen tensions.
2. Saturations by invasive or noninvasive methods.
3. The presence of clinical indicators.
 Supplemental oxygen flow should be titrated to maintain
adequate oxygen saturation as indicated by pulse oximetry SpO2
or appropriate arterial or venous blood gas values.
 Nasal cannulae and nasopharyngeal catheters are used to provide
low level supplemental oxygen. Also used to supplement oxygen
in patients who are being fed so that there is no interruption in
oxygen supplementation.

 Simple oxygen masks are used to provide supplemental oxygen
in the moderate range (0.35-0.50, depending on size & minute
ventilation) for short periods of time (e.g., during procedures,
for transport, in emergency situations).
 Air-entrainment nebulizers, can be used when high levels of
humidity or aerosol are desired.
 Partial rebreathing masks are used to conserve the oxygen
supply when higher concentrations (FiO2 > 0.4, < 0.6) are
required (e.g., during transport).
 Non-rebreathing masks are used to deliver concentrations > 0.60
 Venturi mask are used when precise FiO2 has to be delivered
e.g., COPD

Used to provide :-
 Controlled FiO2 in infants and small children.
 Controlled FiO2 and or increased heated humidity to patients
who cannot tolerate other devices.
 Controlled FiO2 when the chest, abdomen and extremities
must be accessible to caregivers.

1.Drying of mucous membrane.
2.Depression of ventilation in COPD.
3.Reversal of compensatory hypoxic vasoconstriction.
4.Atelectasis due to absorption collapse.
5.O2 toxicity.

 1.Pulmonary oxygen toxicity (Lorrain-Smith effect):
- 100%O2 given for 12 hours or more.
- 80% O2 for more than 24hrs.
- 60%O2 more than 36hrs.
- Symptoms: substernal pain , irresistable cough ,
dyspnoea , ↓ compliance, pulmonary interstitial
edema leading to fibrosis.

 2.Retrolental fibroplasia :
- Occurs when PaO2 more than 80mmhg for more
than 3 hrs in new born.
- Very premature babies are more susceptible.
- O2 saturation must be around 90-92 %.

 3.C.N.S O2 toxicity (Paul-Bert effect):
- O2 is given in hyperbaric chambers.

Exposure to ↑ Po2 damages capillary endothelium
Interstitial oedema & alveolar thickening follows
Type-1 alveolar cells are destroyed & Type-2 cells
proliferate

Exudative phase follows
Low V/Q ratio , Physiologic shunting & hypoxemia
Hyaline membrane forms in alveolar regions
Pulmonary fibrosis & hypertension develops

 AS LUNG INJURY WORSENS
BLOOD OXYGENATION
DETERIORATES
 If this progressive hypoxemia is
managed with additional oxygen, the
toxic effect worsens
 A vicious cycle sets in

OXYGEN TOXICITY
INCREASED
FiO2
LOW PaO2
INCREASED
SHUNTING

Oxygen and oxygen therapy

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