Oxygen therapy involves administering oxygen at concentrations higher than in ambient air to treat hypoxemia or hypoxia. It works by increasing oxygen content in the blood and oxygen flux to tissues. While beneficial, high concentrations of oxygen can cause toxicity issues like pulmonary toxicity from exposure to partial pressures over 50kPa and CNS toxicity over 1 atmosphere. Care must be taken to avoid complications like hypoventilation, retinopathy of prematurity, absorption atelectasis, and fire hazards.
Oxygen Therapy andToxicity
PRESENTER
Dr Krishna Dhakal
Second year Resident
Department of Anesthesiology and Intensive Care
NAMS
MODERATOR
Dr. Santosh Parajuli
Department of Anesthesiology
Shahid Gangalal National Heart Centre
2.
Learning Objectives
• ToDefine oxygen therapy
• To Explain the indication of oxygen therapy
• To know briefly about oxygen cascade
• To List the sources of oxygen
• To Classify and explain the sources of oxygen delivery devices
• To Explain the hazards of oxygen
3.
Introduction
Oxygen therapy
It isthe administration of oxygen at concentrations greater
than that in ambient air (20.9%) with the intent of treating or
preventing the symptoms and manifestations of hypoxemia or
tissue hypoxia.
4.
Goals of OxygenTherapy
• Correct documented or suspected hypoxemia
• Decrease the symptoms associated with chronic hypoxemia
• Decrease the workload hypoxemia imposes on the
cardiopulmonary system
• Removal of entrapped gas from the body cavities and vessels.
5.
Indication
• Documented Hypoxemia
•Adults, children and infants > 1 month of age.
• Pao2< 60mm Hg
• Sao2 < or Spo2 < 92% at rest breathing room air
• Neonates
• Pao2< 50mm Hg
• Sao2 < or Spo2 < 88% at rest in room air
• COPD, Myocardial Infarction, pulmonary edema, ALI, ARDS,
pulmonary fibrosis, cyanide poisoning, carbon monoxide poisoning.
• Perioperative and postoperative period with general anaesthesia
• Prior to tracheal suctioning or bronchoscopy
• Severe Trauma
• Any clinical suspicion of hypoxemia or hypoxia
6.
Oxygen Cascade
The processof declining oxygen tension from atmosphere to mitochondria
Atmosphere air (dry) (159 mm Hg) [ PIO2=PB x FIO2]
↓ humidification
Lower resp tract (moist) (150 mm Hg) [ PIO2=(PB-PH2O) x FIO2 ]
↓ O2 consumption and alveolar ventilation
Alveoli PAO2 (104 mm Hg) [ PAO2= PIO2- PaCO2/RQ]
↓ venous admixture
Arterial blood PaO2 (100 mm Hg)
↓ tissue extraction
Venous blood PV O2 (40 mm Hg)
↓
Mitochondria PO2 (7 – 37 mmHg)
7.
The Alveolar arterialgradient
PAO2=104 mmHg PaO2=100mmHg
Venous admixture
A-a = 4 -25 mm Hg
PaO2 = 120 − Age/3
Alveolar
Air
Arterial
Blood
8.
The A-a Gradient
●The alveolar-to-arterial O2 partial pressure gradient (A–a
gradient) is normally less than 15 mm Hg
● PaO2 = 120 − Age/3
The A–a gradient for O2 depends on
● the amount of right-to-left shunting,
● the amount of V/Q mismatch, and
● mixed venous O2 tension
● The A–a gradient for O2 is directly proportional to shunt
9.
How Does OxygenTherapy Work?
• Oxygen Transport
• Oxygen content
• Oxygen flux
• Oxygen uptake
• O2 extraction ratio
10.
Oxygen cascade
Venous Admixture
(physiological shunt)
• V/Q mismatch Normal True shunt
• Bronchial vein Thebesian vein
• Normal : upto 5 % of the cardiac output
Oxygen Flux
Amount ofof O2 leaving left ventricle per minute.
Do2 =CO x Cao2
= CO × SaO2 x Hb conc x 1.34
= 5000 x 0.97 x 15.4 x 1.34 /100
= 1000 ml/min
CO = cardiac output in ml per minute.
Do2 = oxygen flux
15.
Oxygen Uptake (VO2)
•When blood reaches the systemic capillaries, oxygen
dissociates from hemoglobin and moves into the tissues.
The rate at which this occurs is called the oxygen uptake
(Vo2).
• VO2 = CO X ( CaO2 – CvO2 )
= CO X 1.34 X Hb X ( SaO2 – SvO2 )
• Normal VO2 = 200–300 mL/min or 110–160 mL/min/m2
16.
• The fractionof the oxygen delivered to the capillaries
that is taken up into the tissue .
• An index of the efficiency of oxygen transport.
• O2ER = VO2 / DO2
= CO x C(a-v)o2
CO x Cao2
= SaO2 - SvO2 / SaO2
• Normal - 0.25 (range = 0.2–0.3)
Oxygen-Extraction Ratio (O2ER)
Oxygen cylinders
• Medicalgas distribution systems
• Central supply(G and H type cylinders)
• Patients transport, resuscitation, anesthesia machine (
E type)
Oxygen Source
Central supplysystem :
• Located outdoors,
restricted area
• Cylinder banks
connected to a common
manifold
• Primary and secondary
supply
• Reserve supply away
from main supply
22.
Oxygen concentrators
• Basedon Pressure swing
adsorber technology (adsorbs
nitrogen onto the molecular seive
made of zeolite)
• Deliver 90-96% oxygen
• Remote location , Domiciliary
use
23.
Advantages:
• Cost effective,simple to use, portable
• Not affected by altitude changes
• Compatible with anaesthesia machine, vaporisers,
ventilators
Disadvantages:
• Maintanence: regular servicing of compressor,
filters
• Device malfuntion : excessive noise, overheating,
shut down
• Argon accumulation
24.
O2 Delivery System
•Classification
DESIGNS
Low- flow system
Reservoir systems
High flow system
Enclosures
PERFORMANCES (Based on predictability and
consistency of FiO2 provided)
Fixed
Variable
25.
Oxygen flow rateand concentration
Respiratory Distress Non respiratory Distress
Minute vol
(RR x TV)
20 l/min
(40bpm x 500ml)
5 l/min
(10bpm x 500ml)
O2 flow rate 2 l/min 2 l/min
Oxygen concentration 2 l/min of 100% oxygen
+
18 l/min air drawn into
mask (21%)
=
20 l/min minute volume
FiO2 =
(1.0x2) + (0.21x18) / 20
= 0.38 (38.8%)
2 l/min of 100% oxygen
+
3 l/min air drawn into mask
(21%)
=
5 l/min
FiO2 =
(1.0x2) + (0.21x3) / 5
= 0.53 (53%)
26.
Low flow system
•The gas flow is insufficient to meet patient’s peak
inspiratory and minute ventilatory requirement
• O2 provided is always diluted with air
• FiO2 varies with the patient’s ventilatory pattern
• Deliver low and variable FiO2 → Variable performance
device
27.
High flow system
•The gas flow is sufficient to meet patient’s peak
inspiratory and minute ventilatory requirement.
• FiO2 is independent of the the patient’s ventilatory
pattern
• Deliver low- moderate and fixed FiO2 → Fixed
performance device
28.
Low Flow orVariable performance equipment
• Nasal cannula
• Nasal mask
• Simple Oxygen mask
• Oxygen tent
• Mask with gas reserviour
I. Partial rebreathing
II. Non-rebreathing
High flow or fixed performance equipment
• Anaesthesia bag (Bag mask valve system)
• Venturi mask (with or without nebulliser)
29.
Nasal cannula
● Aplastic disposable device consisting of two tips or
prongs 1 cm long, connected to oxygen tubing
● Inserted into the vestibule of the nose
● FiO2 – 24-40%
● Flow – 1-6 L/min
30.
Nasal Cannula
Advantages
• Easyto use, well tolerated by most patients
• Patients can eat, drink and talk.
• May be used in patients with COPD requiring long term
oxygen therapy.
Disadvantages
• May cause pressure sores around ears and nose.
• May dry and irritate nasal mucosa.
• Not able to achieve high concentrations of inhaled O2 in
patients who have a high minute ventilation.
• Most of the oxygen wasted.
• May not be good for mouth breather
31.
Reservoir systems
● Reservoirsystem stores a reserve volume of O2, that equals or
exceeds the patient’s tidal volume
● Delivers mod- high FiO2
● Variable performance device
● To provide a fixed FiO2, the reservoir volume must exceed the
patient’s tidal volume
Examples:
● Reservoir cannula
● Simple face mask
● Partial rebreathing mask
● Non rebreathing mask
● Tracheostomy mask
32.
Reservoir masks
● Commonlyused reservoir system
● Three types
● Simple face mask
● Partial rebreathing masks
● Non rebreathing masks
33.
Simple face masks
●Reservoir - 100-200 ml
● Variable performance device
● FiO2 varies with
● O2 input flow,
● mask volume,
● extent of air leakage
● patient’s breathing pattern
● FiO2: 40 – 60%
● Input flow range is 5-8 L/min
● Minimum flow – 5L/min to
prevent CO2 rebreathing
34.
Simple Face Mask
Merits
●Moderate but variable FiO2.
● Good for patients with blocked nasal passages and mouth breathers
● Easy to apply
Demerits
● Uncomfortable
● Interfere with further airway care
● Proper fitting is required
● Rebreathing (if input flow is less than 5 L/min)
Oxygen Flow
Rate(L/Min)
FiO2
5-6 0.4
6-7 0.5
7-8 0.6
35.
Partial rebreathing facemask
• During inspiration: Draws air
from the mask, from the bag,
holes in the side of the mask.
• During expiration: First one
third of exhaled gases (from
anatomical dead space) will flow
back into the reservoir bag
• High enough O2 flow to keep the
bag from deflating more than one
third its volume during
inspiration, then exhaled CO2 will
not accumulate in the reservoir
bag.
• Maximum FiO2 of 0.7 to 0.8
• FGF > 8L/min
36.
Nonrebreathing Face Mask
●Has 2 unidirectional valves
● Expiratory valves prevents
air entrainment
● Inspiratory valve prevents
exhaled gas flow into
reservoir bag
● FiO2 : 0.80 – 0.90
● FGF : 10 – 15L/min
● To deliver ~100% O2, bag
should remain inflated
● Factors affecting FiO2
● Air leakage and
● Pt’s breathing pattern
37.
Tracheostomy Collar/ Mask
•Inserted directed into
trachea
• Is indicated for chronic o2
therapy
• O2 flow rate 8 to 10L
• Provides good humidity
• Comfortable ,more efficient
• Less expensive
38.
High flow systems
Thegas flow is sufficient to meet patient’s peak inspiratory and
minute ventilatory requirement.
FiO2 is independent of the the patient’s ventilatory pattern
Deliver low- moderate and fixed FiO2 → Fixed performance
device
Examples:
Air entrainment devices
39.
Principle:
Based on Bernoulliprinciple –
A rapid velocity of gas exiting from a restricted orifice will
create subatmospheric lateral pressures, resulting in
atmospheric air being entrained into the mainstream.
Entrainment Ratio:
Air = 100 - %O2
O2 %O2 - 21
Complications of Oxygentherapy
1. Oxygen toxicity
2. Depression of ventilation
3. Retinopathy of Prematurity
4. Absorption atelectasis
5. Fire hazard
43.
Oxygen Toxicity
• Oxygentoxicity is a condition resulting
from the harmful effects of breathing
molecular oxygen (O2) at
increased partial pressures.
• The metabolites of oxygen are more
damaging than the parent molecule
itself.
• These are formed in the process of
conversion of O2 to water in the ETC
(electron transport chain) in
mitochondria.
• The superoxide and hydroxyl radicals
are free radicals → very active
chemically
CNS effects
● Alsoknown as Paul Bert effect
● Central nervous system toxicity - caused by short exposure to
high partial pressures of oxygen at greater than atmospheric
pressure(> 1 atm pressure)
● Symptoms may include disorientation, brief periods of
rigidity→ convulsions and unconsciousness, and seizures.
● Visual changes esp. tunnel vision, tinnitus, etc. are also
common
Oxygen toxicity,JIACM 2003; 4(3): 234
47.
Pulmonary effects
• Alsoknown as
Lorraine Smith’s effect
• First organ to be
exposed to high
concentration of O2
• Pulmonary toxicity
occurs only with
exposure to partial
pressures of oxygen
greater than 0.5 bar
(50 kPa)
ARDS like features
48.
• Tracheobronchitis, orinflammation of the upper airways most
common findings,
• Others: cough, substernal chest pain, ARDS like features
• Preterm newborns are known to be at higher risk
for bronchopulmonary dysplasia with extended exposure to
high concentrations
50.
How much O2is safe?
100% - not more than 12hrs
80% - not more than 24hrs
60% - not more than 36hrs
Goal should be to use lowest possible FiO2
compatible with adequate tissue oxygenation
Hypoventilation
• COPD patientswith chronic CO2 retention.
• Altered respiratory drive dependent on relative hypoxemia.
• Correction of hypoxemia leads to loss of respiratory drive.
• Increase oxygen concentration by 4-7% (i.e. Fio2 0.32-0.36)
with a goal of achieving Spo2 by 90-93%.
• Venturi mask when possible
59.
Retinopathy of prematurity(ROP)
Premature or low-birth-weight infants
who receive supplemental O2
↑PaO2
↓
retinal vasoconstriction
↓
necrosis of blood vessels
↓
new vessels formation
↓
Hemorrhage → retinal
detachment and blindness
To minimize the risk of ROP - PaO2
below 80 mmHg
60.
Absorption atelectasis
• Largevolume of nitrogen
in the lungs is replaced
with oxygen,
• Oxygen is subsequently
absorbed into the blood,
• The effect is reducing the
volume of the alveoli,
resulting in a form of
alveolar collapse known
as absorption atelectasis
61.
Risks of fire
•Improper use of oxygen
• Incorrect design of oxygen systems
• Incorrect operation and maintenance of oxygen
system
62.
Summary
• Oxygen therapyis administration of oxygen in concentration
greater than that of environment (>20.9%).
• Oxygen can be obtained from different sources including
environment employing several industrial/non-industrial
techniques.
• It is very important to be aware the varying FiO2 with variable
performance devices and it is important to choose devices
appropriate for the patient.
• Oxygen in concentrations higher than required to maintain
normal PaO2 is associated with toxicity.
• The potential hazards of oxygen therapy are: absorpotion
atelectasis, CNS/Respiratory problems, depression of
ventilation, ROP, and fire hazards.
• Goal should be to use lowest possible FiO2 compatible with
adequate tissue oxygenation
63.
Bibliography
• Marinos, TheICU Book, 4th Edition
• Barash, Paul G Cullen’s Clinical Anesthesia, 7th edition
• Mikhail & Morgan’s Clinical Anesthesiology, 5th edition
• Carvalho M, Soares M, Machado HS. Paradigms of Oxygen
Therapy in Critically Ill patients. J Intensive & Crit Care
2017,3:1
• Internet : Wikipedia.org , Uptodate
• BTS Guidelines for oxygen use in adults in healthcare and
emergency settings -2017
Editor's Notes
#7 With every breath the inspired gas mixture is humidified at 37.c in the upper airway
Water vapor pressure is depend only upon temperature ans is 47mm hg
PaO2 = pio2- paco2/RQ
#8 refers to the blood entering the arterial system without passing through ventilated areas of lung causing the PO2 of arterial blood to be less than that of alveolar PO2.
Normally 15mmhg
A-a gradient for o2 is directly proportional to the rt-lt shunting , but progressively increases with age up to 20–30 mm Hg
#9 but progressively increases with age up to 20–30 mm Hg
#10 The transport of oxygen from the lungs to metabolizing tissues can be described by using
four clinical parameters: (a) the concentration of oxygen in blood, (b) the delivery rate of
oxygen in arterial blood, (c) the rate of oxygen uptake from capillary blood into the
tissues, and (d) the fraction of oxygen in capillary blood that is taken up into the tissues.
#11 VENOUS ADMIXTURE is the result of mixing of shunted non-reoxygenated blood with reoxygenated blood distal to the alveoli. The shunted blood is a result of 1) Anatomic shunts and 2) shunt-like effects.
#12 Pasteur point – The critical level for aerobic metabolism to continue
(1 – 2 mmHg PO2 in mitochondria)
#14 arterial Po2 (Pao2) as an indication of how much oxygen is in the blood. the hemoglobin concentration is the principal determinant of the oxygen content of blood. Hemoglobin saturation is the amount of O 2 bound as a percentage of its total O 2 -binding capacity. P 50 , the O 2 tension at
which hemoglobin is 50% saturated A rightward shift in the oxygen–hemoglobin dissociation curve lowers O 2 affinity, displaces O 2 from hemoglobin, and makes more O 2 available to tissues;.
50% hb: 50% Cao2
50% pao2 : 18 % cao2
#16 Cardiac index (CI) is a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA), thus relating heart performance to the size of the individual. The unit of measurement is litres per minute per square metre (L/min/m2)
#20 O2 is packaged and shipped as a high pressure gas in seamless steel or aluminum cylinder .
In cylinder charged with gaseous oxygen , the pressure in the container is related both to temperature and the amount of o2 in the container.
Full high pressure cylinder normally contain gas at 2200psig at 21’c.
#22 Cylinders may be used various ways . For eg in a manifold system large sized cylinders are linked together to supply medical oxygen to medical pipelines which then lead directly to the bedside.
#23 Zeolite is hydrated aluminium silicates of the alkaline earth metals in a powder or granular form.
#26 The larger the VT or faster the respiratory rate, the lower the FiO2.
The smaller the VT or lower the respiratory rate, the higher the FiO2.
#27
Low-fl ow systems are adequate for patients with stable brathing pattern
• Minute ventilation less than ∼8–10 L/min
• Breathing frequencies less than ∼20 breaths/min
• Tidal volumes (V T ) less than ∼0.8 L
• Normal inspiratory fl ow (10–30 L/min).
#28 Indicated for patient who requires
Consistent fio2
Flows - 30 - 40 L/min (or > 3 times patient’s minute ventilation) thus provides a fixed FiO2.
#30 Use for long term o2 therapy .
After exhalation 02 from the nasal cannula fill the nasopaharynx. And during inspiration o2 and entrained air are drwan into the trachea.
If > 5lit /min poorly tolerated by pt beacause of discomfort of gas jetting into the nasal cavity and because of drying and crusting of nasal cannula.
The major disadvantage of nasal prongs is the inability to achieve high concentrations of inhaled O2 in patients who have a high minute ventilation
#44 Paul Bert, a French physiologist, first described oxygen toxicity in 1878. Also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning.
#47 Twitching of perioral and small muscles of the hand
Intense peripheral vasoconstriction due to hyperoxia and diaphragmatic twitching can result in facial pallor & “Cogwheel breathing respectively
Vertigo and nausea followed by altered behaviour, clumsiness, and finally convulsions(tonic-clonic
#48 Normal humans, the first signs of toxicity appear after 10 hours of oxygen at 1 ATA
Oxygen toxicity,JIACM 2003; 4(3): 234
#50 The curves show typical decrement in lung vital capacity when breathing oxygen. Lambertsen concluded in 1987 that 0.5 bar could be tolerated indefinitely.
#51 Many studies believe fio2 level lower than 0.6-0.7 are safe
#56 This article published In scientific research publishing in madrid spain ..they havelooked over published studies to try to describe the current situation and future proscpects of 02 therapy in critical care
#57 Hindawi journal in 2011 … conducted by j mach et al ..open access review article
#58 It’s a review article published in 2016 December27 in imedpub journal of Portugal…they had compiled various metanalysis in multicentered of patient wit stroke patient,acute mi ..patient with resusciatation following cardiac arrest neonatal resuscitation and patient treated in critical care…..
#59 Peripheral chemoreceptor-carotid body and aortic arch..respond primarily to lack of o2..when pao2 fall below 100 mm hg ,neural activity from these receptor begin to increase..however it is not until pao2 reches 60-65 mm hg neural activity increase substantially to augment MV..thus those pt like copd that depend on hypoxic vent drive if pao2 increase by >65 mm hg ,vent drive diminishs and pao2 fall until ventilation again stimulated by arterial hypoxemia…
#60 In preterm infants, the retina is often not fully vascularised.
Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally.
Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment