Hyperbaric oxygen therapy which is required for treatment of some clinical conditions.

1. Hyperbaric oxygen therapy
Moderator
Dr Neha Aeron ( Assistant Professor )
Presenter : Dr Gaurav Joshi (2nd yr resident)

2. Outline of discussion
• Definition
• Physics related to HBO
• History
• Physiology
• Gas laws
• Indications
• Methods of administration & Practical aspects
• Anaesthesia at HBO
• Conraindications &Toxicity

3. HYPERBARIC OXYGEN Therapy [HBOT]
3
• Hyperbaric oxygen therapy(HBOT) is defined as
administration of 100% oxygen to a patient placed
inside a chamber pressurized to greater than 1
atmosphere.
• Hyperbaric oxygen exposure(breathing O2 at
increased ambient pressure, typically 2 to 3 ATA)
causes an increase in arterial and tissue partial
pressure of oxygen with no significant change in
arterial pH and partial pressure of CO2.

4. PHYSICS AND PHYSIOLOGY
• 1 atm = 760 mm Hg = 101.3 k pa
• Atmospheric pressure can be any value – 1 atm(sea
level)
• ½ atm( 8000 feet elevation)
• 3 atm ( hyperbaric chamber)
• Therapeutic oxygen at pressure greater than 1 Atm
express HBO pressure that is Ata (atmospheric
pressure absolute)
• Hyperbaric oxygen pressure general range is 2 to 3
Ata

5. • In physical terms,compression and decompression of a given
amount of gas basically does three things.
-it changes volume
-it changes density
-it changes the partial pressures of constituent gases.
physiological responses and problems due to exposure to a
hyperbaric environment are directly from these physical
changes and are categorized as
-complications due to direct physical effects of pressure.
-secondary complications due to abnormally high volumes of
respiratory gases dissolved in the blood and tissues.

6. • Due to direct physical effects
1. Barotrauma is the term used to describe tissue
damage which may occure whenever pressure
gradient exist between tissues.
It is due to distortion of lung tissue which may
occure during decompression either within a
pressure chamber or during ascent in water.
Three clinical syndromes of pulmonary barotrauma
namely pneumothorax, interstitial emphysema and
air embolism can occure.

7. 2. Aural barotrauma-tympanic membrane perforation
3. Respiratory sinuses-sinusitis
4. Dental problems-severe toothache due to small
pockets of air exist around the roots of teeth.
5. Gas in the intestinal tract-usually gas in viscera does
not present any problem with change in environmental
pressure,on occasions fermentation continues in gut and
this produce abdominal distension,discomfort and painful
flatulence.
6. Pressure and clothing-pockets of compressed air
trapped within clothing may produce a deep impressin on
the skin.

8. secondary complications due to abnormally high
volumes of respiratory gases dissolved in the blood and
tissues.
1. nitrogen and inert gas narcosis
2. decompression sickness.

9. HISTORY
Initial discovery,,
1662 - Henshaw built first hyperbaric chamber

10. 1775 - elemental O2 discovered by Joseph Pristley

11. 1870 - surgical use of HBO by Fontain and Bent
1920 - Dragger,behrke and shaw used in decompression sickness
1950 - Boerema used Hyperbaric O2 in cardiothoracic surgery
1962 - Smith & Sharp used in CO poisoning

12. • 1926 - “steel ball hospital” cunnigham sanitarium
• 72 rooms at pressure of 3 Atm absolute.

13. • Previosly hyperbaric chambers are there only in two
centres across country
-Institute of Aerospace medicine, Banglore
-Institute of Naval medicine, Mumbai
•Today it is available in10 hospitals in the country,
they are located in Mumbai(4),Delhi Ahmedabad(2
each), Pune,Trichur (1 each).

14. Physiology
Higher the Po2 of the inspired gas,
higher is the arterial Po2
higher the amount of oxygen carried in solution
in arterial blood
• Alveolar PO2 is the principal determinant of arterial
PO2,the difference between the two is small and is
mainly due to venous admixture
• Arterial oxygen level depends on number of factors
 Properties of haemoglobin
 Cardiac output
 Regional tissue perfusion
 Diffusion of oxygen from capillaries to tissues

15. • Fresh air contains 20.93 per cent oxygen remainder being
mainly nitrogen.At sea level barometric pressure of 760 mm
Hg,the partial pressure of oxygen in inspired air is thus
158mm Hg(20.93 per cent of 760mmHg).
• When air is inspired it rapidly becomes saturated with water
vapour at body temperature and on entering lungs mixes
with alveolar gas which contains carbon dioxide.
• The water vapour and and the carbon dioxide accounts for
47 mm Hg and 40 mmHg respectively leaving 673 mmHg for
the combined pressures of oxygen and nitrogen.

16. • When oxygen alone is inspired, nitrogen is displaced from
the alveoli, leaving only the oxygen water vapour and the
carbon dioxide.
So PAo2=Pio2-PH2o-PAco2
where PAo2-alveolar partial pressure of oxygen
Pio2 - inspired partial pressure of oxygen
PAco2 - alveolar partial pressure of co2
PH2o – alveolar pressure of water vapour

17. • 1 gm of haemoglobin combines with 1.34 ml of O2.
• In a healthy individual when 100% O2 is breathed
at atmospheric pressure ,the Hb becomes fully
saturated.
• At a Hb% concentration of 14.6 gm/100ml of blood
the amount of O2 carried in combination with Hb
will be 19.6ml/100ml of blood.

18. GAS LAWS
Air under Hyperbaric conditioning obeys the
same gas laws as in the atmosphere
• Boyles law
• Daltons law
• Henry’s law

19. • Boyle’s law At constant temp and mass, volume of gas is
inversely proportional to pressure
• Vα 1/P at constant temperature
• At constant temp and mass, Density of a gas is directly
proportional to pressure
• D α P at constant temperature
• Therefore P α D
• P α 1/V
• D α 1/V
BOYLE’S LAW

20. • So at 2 atm, V decreases by 1/2 and density of gas
doubles
• At 3 atm V decreases by 1/3 and Density of gas
triples
• So During HBO,as pressure increases gas density in
lungs increases.

21. Dalton’s law
• Pressure exerted by gas equals the sum of all the
partial pressure of the constituent gases
• PT = P1 + P2 + P3 =……………Pn
• Sum of the partial pressure of all the gases in a gas
mixture can never exceed the total pressure of the
gas mixture
• Lower partial pressure at high altitude reflect
presence of less O2 and N2 molecules per volume
compared to sea level.

23. Henry’s law
• As the partial pressure of gas above the surface of a liquid
increases, more of that gas will dissolve into that liquid.
• It means solubility of a gas in solution is directly proprotional to
partial pressure of solution.
• When ambient pressure decreases ( altitude ) the partial pressure
of O2 and N2 in the body fall and fewer O2 & N2 molecules
dissolve into the blood.
• When ambient pressure increases (hyperbarism) the partial
pressure of O2 & N2 in the body increases and more O2 & N2
molecules dissolve into the blood
• This is the basics of hyperbaric oxygen therapy .

24. •Physiological effectWhen breathing room air at an
alveolar PO2 of 100mmhg, oxygen in physical solution amounts to
0.3ml /100ml blood
• If the P02 rise to 600mmhg (because the patient breath a high 02
mixture) the dissolved oxygen would be 1.8ml
• If a subject breathed O2 at 3Ata (3×760=2280mmhg) and arterial
PO2 was 2000mmhg, the dissolved oxygen would be 6ml O2 /
100ml blood
• Thus at normal atmospheric pressure the oxygen content of
arterial blood is largely dependent on the Hb content.
• When hyperbaric O2 is inhaled the Hb cannot increase its oxygen
load because it is already fully saturated, and as the PO2 rises, O2
content increase only by carriage of additional O2 as single
solution in plasma.

25. PAO2 is 100 mm Hg at atmospheric pressure
Alveolar gas equation
PAO2 = FiO2[PB-PH2O] – PACO2
R
= 0.21[760-47] - 40
0.8
= 149.7 – 50
PAO2 = 100 mm Hg
So in HBO ,patient breathing FiO2 of 0.4 at 3 atm
3x 760 = 2200 mm Hg
• PAO2 = 0.4 x (2200 mm Hg – 47 mmHg) - 40
0.8
PAO2 = 811 mm Hg
• So increase O2 carrying capacity and increase tissue
oxygenation for the treatment of ischemic conditions.

26. INDICATIONS
CLINICAL INDICATIONS
Poisoning
• Carbon monoxide
• Cyanide
Gas Bubble disease
• Air embolism
• Decompression sickness
Infections
• Gas gangrene
• Soft tissue necrotising infections
• Chronic ostemyelitis
• Intracranial abscess

27. Acute Ischemia
• Crush injuries
• Compromised skin flaps
• CRAO
• CRVO
Chronic Ischemia
• Radiation necrosis(soft tissue, radiation cystitis)
• Ischemic ulcers, including diabetic ulcers
Acute hypoxia
• Blood loss, anemia
Thermal injury
• Burns
Cancer therapy
Congenital cardiac anomalies
Peripheral vascular insufficiencies

28. POSSIBLE INDICATIONS
• Cardiopulmonary bypass surgery
• Arterial hypoxemia due to increase in
physiological shunts
• Oxygen therapy secondary to severe cardiac
disease.

29. CO POISONING
• CO has considerably greater affinity for Hb than oxygen (200 times
than o2)
• Exposure to even low concentration of CO rapidly leads to
“anaemic hypoxaemia” because the gas interferes with the ability
of Hb to transfer oxygen.
• CO shifts the oxygen-Hb saturation curve to the left side,
• CO exposure also trigger intravascular platelet neutrophil
aggregation and neutrophil activation resulting in toxicity in
multiple organ system.
• Clinical features : Headache nausea, vomiting, dizziness,
Loss of consciousness, During pregnancy it causes fetal distress
• Diagnosis : By h/o exposure and confirmation of the diagnosis by
finding an elevated HbCO level in either arterial or venous blood.

30. • Hyperbaric oxygen therapy at 2 to 3 Ata alleviate the situation in
three ways
a) It provides enough dissolved oxygen in the plasma to keep the
patient alive
b) It moves oxygen-Hb dissociation curve to the right ,thus
enabling the remaining O2Hb to give up more O2
c) It acclerates the rate of dissociation of carboxyHb to twice that
achieved by conventional treatment with 5% CO2 in O2.
• Treatment should be continued until carboxyHb is no longer
detectable in the blood
• Clearance time seems to be related to the period of exposure to
carbon monoxide rather than to the blood level of carboxyHb or
clinical condition of the patient .

31. CLOSTRIDIAL GAS GANGRENE
• Clostridial gas gangrene is a life threatening infection
mandates emergent surgical intervention i.e. HBO in
conjuction with surgery
• HBO works by inhibiting the growth of organisms thus
decrease the production of the α- toxin released from
clostridium & limits bacterial replication.

32. CANCER THERAPY
• It helps in potentiation of radiation therapy for
inoperable cancers.
• Hyperoxygenation of normal cells produces increase
in sensitivity to radiation.
• As tumor cells are hypoxic ,treatment with
hyperbaric oxygen raises their oxygen tension
leading to sensitization for radiation.
ARTERIAL INSUFFICIENCY
• Due to trauma, embolism or thrombosis there is
decreased blood supply to the tissues which leads
to anoxaemia, hyperbaric oxygen allows
improvement of flow.

33. CHRONIC NON HEALING
WOUNDS/ARTERIOLAR
INSUFFICIANCY/DIABETIC WOUNDS
• Oxygenation is required for angiogenesis, collagen
deposition, reepithelialisation, cellular respiration &
oxidative killing of bacteria thus useful in non healing
wounds.

34. CRUSH INJURY
• HBO is used in limited degree for acute traumatic
peripherial Ischemia and suturing of severed limbs.
• Reduces infection and wound dehiscence and improves
healing.
• Improves oxygenation to hypoperfused tissues
• Causes arterial hyperoxia causing vasocontriction and
decreased edema formation.

35. Decompression sickness
 Also known as bend’s , chokes, divers palsy and
cassion’s disease.
 The term decompression sickness refers to a
conditions which are results of an excessive rapid
reduction of environmental pressure and are caused
by liberation of bubbles of gas from tissues and blood
which has been supersaturated.
 At sea level nitrogen in atm air is in equilibrium with
body tissues
 When ambient pressure is raised as seen in pressure
chambers and deep sea diving, greater amounts of
gas dissolves in the tissues until after sometimes
tissue saturation is attained at higher inspired
pressure.

36.  When pressure is reduced, gas dissolved in the
tissues must be carried by the blood to the lungs for
elimination.
 If decompression is too rapid, bubble formation may
occur due to insoluble nitrogen.
Signs and symptoms of decompression sickness
EARLY SIGNS & SYMPTOMS
 Type 1: pain, which includes joint pains, with skin
manifestations with intense itching, lymphatic
occlusion may produce edema- peau- d- orange
appearance.
 Type 2: includes CNS and Cardio -pulmonary
involvement. Symptoms like chokes due to bubbles in
the pulmonary capillaries, with psychotic conditions,
visual blurring, scotoma and migranous headache,
DELAYED:
 Aseptic necrosis of bone, leads to joint deformity and
arthritic changes.

37. Treated by recompression in air
•The purpose of recompression is to provide a prompt
and lasting relief of symptoms of decompression sickness.
•The recompression procedure reduces the size of gas
bubble rapidly to reduce symptoms on subsequent
decompression.
•The increase in pressure during compression causes
compression of gas bubbles( boyle’s law)
•As a result there is outward diffusion of gases
• But if tissues are supersaturated with gases the bubble
may grow by increasing the diffusion of gases into it
from surrounding tissues.
• To prevent this ambient pressure during treatment
should be equal to the pressure of the dissolved gases in
the surrounding of bubbles.
• Most effective is administration of HBO at 3AT.A

38. • TREATMENT: High po2 results in ↑ rate of resolution of
gas bubbles because of resulting higher partial
pressure gradient for diffusion of inert gas from the
interior of the bubble into surrounding tissue or blood.
PREVENTION OF DECOMPRESSION SICKNESS
1. Limitation of pressure in the chamber: since tissues can be
moderately saturated with inert gas without the formation
of bubbles, it is possible to spend unlimited time in a
chamber at 2 Ata without the need for slow decompression.
2. Limitation of time: experience with deep sea diving has
suggested that when the time spent at a given Atm pressure
is limited, then no decompression is necessary, the longer
the period spent in a compressed envinorment the greater
the problems of decompression.

39. 3. Limitation of rate of decompression: it is apprarently safe
to be decompressed rapidly to half the original working pressure,
but a suitable pause must be made at this new pressure before
further decompression in under taken
4. Use of helium and oxygen mixture: substitution of helium for
nitrogen as the inert gas eliminates the danger of narcosis and
also reduces the problems of decompression sickness. Helium
also reduces the time required for decompression because it is
only about one-half as soluble as nitrogen in the body, and in
addition it diffuse out much more rapidly.
5. Oxygen decompression: it has already been stated that rapid
decompression to half the original pressure can be achieved with
safety. On reaching this stage, the time required at this new level
can be shortened if the subject breathes oxygen.

40. • This ensures the maximum possible gradient
between the nirogen in the tissue and zero level of
nitogen in alveoli. This will speed the elimination
of nitrogen and the decompression time will be
shortened.

41. METHODS OF ADMINISTRATION
TWO TYPES OF HYPERBARIC OXYGEN ARE IN USE
a)Monoplace: single person chamber in which only
patient is subjected to compression & the staff remain
outside.
b) Multiplace: Large operating room pressure chamber
enclosing both the patient and medical attendants
• The chamber is compressed with air which is breathed
by medical attendants, while the patient breaths 100
percent oxygen at the same ambient pressure either
from a facemask or endotracheal tube according to the
level of consciousness.
• Large pressure chambers are also used for surgery.

42. Monoplace multiplace

43. HYPERBARIC CHAMBERS

44. BASIC DESIGN REQUIREMENTS
a) Compression air pump- usually there are two
i) One pump used for rapid compression of chamber
ii)Other used to maintain ventilation of the chamber.
Compressor produces a steady rise of pressure within the
chamber because this tends to reduce the incidence of
painful effect of pressure change on middle ear and skull
sinus.
b) Climate control – there must be provision for cooling,
heating, & humidifying the air in the chamber.
c) Electric equipment – all electric equipment within
chamber must be spark proof

45. d) Anesthetic gases & oxygen: are best administered
from cylinders stored within the chamber with
facilities for spent gases to be vented.
e) Sterile instruments. There must be an air lock for
allowing instruments to be passed to and from the
chamber.

46. PRACTICAL ASPECTS OF HYPERBARIC THERAPY
• A)Patient monitoring
• despite the changes in the acoustic properties of
compressed air blood pressure measurement may be
performed without difficulty with standard
sphygnomanometer & stethoscope.
• Aneroid pressure gauge are preferred to mercury to avoid
contamination of environment
• Monitoring of ECG & intravascular pressures requires the
transducer cables plumbed through the chamber wall to
pre amplifiers outside the chamber
• To avoid pressure related malfunction of the device,
defibrillator can remain outside the chamber &
connection to patient given through voltage wiring.
• Despite the fear of fire it can be safely used in multiple
chamber but not in monoplace chamber.

47. B) IV-fluid administration
In multiphase chamber the air volume with in drip
chamber will shrink during compression phase of HBO
therapy, expand during decompression (which could force
air into the IV line).
• Therefore infusion pumps are used which are capable of
handling the pressure deferential upto 3 ATA
C) Ventilator management
Mechanical ventilation in hyperbaric environment
presents a variety of challenges.
Ideal requirements;
• Small size, no electric equipment, absence of flammable
lubricants.
• Ability to operate on a volume cycled basis over a wide
range of tidal volumes & respiratory rates.
• Ability to provide positive end expiratory pressure

48. • Measurement of respiratory conductance during
tidal breathing varies with gas density.
• As gas density increases the lung conductance
decreases by 50% which is equivalent to doubling
the pulmonary resistance lead to increase in
physiological dead space.
• If ventilator setting are not adjusted to compensate
for the higher dead space a raise in paco2 will occur.

49. Delivery of anaesthesia at incresed ambient
pressure
• Ross & associates discussed the challenges of
anaesthesia upto 35 ATA in order to provide care for
injured divers while in saturation diving system.
• They suggested using intravenous agents for general
anaesthesia rather than gaseous anaesthetics because
of the problems of the pollution of the chamber
environment. IV anaesthetics unlikely to be affected
within the range of ambient pressure
• Regional anaesthesia recommended whenever possible
• Muscle relaxants should be titrated to effect because of
some degree of pressure reversal at around 10ATA has
been reported

50. NITROUS OXIDE
• At increased ambient pressure N2O to be used at
partial pressure exceeding the MAC value
• Potential problem associated with N2O at increased
pressure is the possibility that tissues could become
super saturated during compression allowing N2O
bubbles to form during decompression
• Neurological symptoms were reported after N2O
anaesthetic after spontaneous resolution of
decompression illness

51. VOLATILE ANAESTHETICS
• The effect of volatile anaesthetic on a patient is
proportional not to the alveolar concentration but to
the partial pressure of the anaesthetic. Vaporiser
deliver a variable concentration but fixed partial
pressure
• Ex- effect of 1% halothane at 1ATA will be equivalent
to 0.5% concentration @ 2ATA (with same partial
pressure). So there is no need to adjust vaporizer
settings when delivering anaesthesia @ hyperbaric or
@ altitude.

52. REGIONAL ANAESTHESIA
• A number of special problems peculiar to hyperbaric
environment arise when regional anaesthesia used
1) Care must be taken that no air is injected. Entrapped
air could expand some 30 times on decompression
2) Bottles containing local drugs should be opened
prior to compression to prevent implosion & to allow
some equilibration of dissolved gases in solution with
the environment.
3) Avoid contamination of the drugs because of
additional risk of sepsis in these conditions

53. CONTRAINDICATIONS
Absolute:
• Pneumothorax
• Pressure converts to tension pneumothorax
Circulatory disruption and collapse
• So all patients get screening for CXR
Relative:
• Claustrophobia
• COPD
• Seizure disorders
• Upper respiratory infection

54. • Hyperthermia
• Malignant tumours
• Anxiety
• Gas emboli
• Pregnancy
• Inner ear infection/tympanic membrane rupture
• Sinus conditions
• Optic neuritis

55. OXYGEN TOXICITY
A condition of oxygen overdosage that can result
in pathological tissue changes
It leads to
• pulmonary toxicity
• Retrolental fibroplasia in neonates
• Hypoventilation
• CNS oxygen toxicity

56. PULMONARY TOXICITY
• Lorrain Smith (1899) carried out the effects of
increased oxygen tension on lungs of animals
• 0.7 – 3.0ATA oxygen pressure lung damage is
predominant
• In man rate of development and degree of damage of
lung is proportional to the dosage of oxygen and
duration of the exposure.

57. SIGNS AND SYMPTOMS OF OXYGEN TOXICITY
• Dry cough, hiccups, seizures, substernal chest pain,
sweating, pallor, anxiety
• Shortness of breath, bronchitis
• Tinnitus, vertigo, visual changes, hallucinations,
pulmonary edema, muscle twitching, decreased
level of consciousness.

59. HISTOPATHOLOGICAL CHANGES
Using electron microscopy – the oxygen concentration
between 90 – 100% at 1 AT.A changes seen are
Swelling of endothelial cells, increase in interstitial
tissue fluid- seen after few hrs t0 3 days.
4th day- destruction of alveolar type 1 cells
increase in thickness of air and blood barrier
7th day – hyperplasia of type 2 cells, complete
destruction of type 1 cells
12th day- proliferative changes in granular pneumocytes
and reduction in alveolar spaces.

60. PROPOSED MECHANISM OF OXYGEN TOXICITY
• 1. Absorption collapse- capillary congestion progress
into alveolar exudation and damage leading to
atelectasis.
• 2. lung surfactants- collapse is prevented by
surfactant, it decreases the surface tension , HBO
reduces surfactant activity.
• 3. metabolic upset-
o inactivation of sulphydral group by HBO
o enzymes invoved in TCA cycle
o enzymes involved in glycolysis and in ETC chain.

61. • 4. myocardial failure- myocardial metabolism is
depressed by HBO
• 5.Endocrine system-
thyroxine and thyroid extract hastens the onset of
convulsions and pulmonary oxygen damage
- Sympathomimetic agents augment onset of
pulmonary oxygen damage, sympatholytics delay the
developments.

62. CNS TOXICITY
• Born Stein and Stronik (1912) reported muscle spasms in legs with
exercise after exposure for 50mins to oxygen at 3AT.A
• Convulsions usually are not preceded by muscle twitchings of eyes,
mouth or forehead.
• With increase in time. There is loss of consciousness and spread of
excitation occurs, rigid tonic phase of convulsions begins which last for
30 seconds.
• Symptoms- lip twitchings, nausea, vertigo and convulsions.
• Diagnosis- sudden onset of convulsions EEG shows hyperirritability
• EMG of lip muscles to detect the muscle twitchings.
• Treatment – withdrawing of HBO and patient is allowed to breathe
room air.

63. Conclusion
˗ HBOT was started as a treatment modality for management of
decompression sickness and with passage of time scope has greatly increased.
˗ There is good evidence to support HBOT in diabetic ulcers,necrotizing soft
tissue infections,gas gangrene,decompression sickness and CO poisoning.
˗ Complications include barotrauma and oxygen toxicity, although they are not
common,there is limited evidence on the cost effectiveness of HBO for major
areas of application.
˗ In view of lack of strong evidence of the effectiveness of HBO for many
clinical conditions as well as high capital and operating costs it is
recommended that to be considered for a centre of excellence or specialized
regional centre.

64. Thank you