Effect of hypobaric & hyperbaric environment and its preventive measures and leading to various diseases.

1. BY
MEENALI MISHRA
EFFECTS OF HYPOBARIC &
HYPERBARIC ENVIRONMENT & ITS
PREVENTIVE MEASURES..
CAISSON DISEASE...

2. HYPOBARIC ENVIRONMENT
 Altitude presents a hypobaric
environment.
 Ascending to higher altitudes
in aviation, mountain
climbing & space vehicles the
effects of altitude & low gas
pressures have greater effect
on human body.
 Hypoxia-lack of oxygen
content within body tissues &
vital human organs.
 Decrease in barometric
pressure(760mm Hg) is the
basic cause of all hypoxia
problems in high altitude
physiology.

3. Hypobaric hypoxia is a condition when body is
deprived of sufficient supply of oxygen from air to body
tissues in quantity or molecular condition.
 This condition is more likely to happen when the
person ascends to higher altitudes.
Density of air reduces upon climbing to high altitude
causing a lack of oxygen being transferred from lungs
to the blood stream. Not enough blood reaches the
brain, as a consequence the body is not able to function
efficiently.
Tends to affect most people above 10,000ft.
Above this height supplementary oxygen is needed.
In people who are stressed, ill or fatigued, symptoms
can occur as low as 8,000ft.

4. Effects of Acute Exposure to low Atmospheric
Pressures on Alveolar Gas Concentrations &
Arterial Oxygen Saturation:
BREAT HING AIR
ALTITUDE
(ft)
BAROMETRIC
PRESSURE
(mm Hg)
Po2 in
Air
(mm Hg)
PCO2 in
Alveoli
(mm Hg)
PO2 in
Alveoli
(mm Hg)
Arterial
Oxygen
Saturatio
n (%)
0 760 159 40(40) 104(104) 97(97)
10,000 523 110 36(23) 67(77) 90(92)
20,000 349 73 24(10) 40(53) 73(85)
30,000 226 47 24(7) 18(30) 24(38)
40,000 141 29
50,000 87 18

6. EFFECTS OF HYPOBARIC
ENVIRONMENT

7. Effects of Hypobaric Environment

8. Important acute effects due to hypobaric environment
in person breathing air, beginning at an altitude of
about 12,000ft are drowsiness, lassitude, mental &
muscle fatigue, sometimes headache, occasionally
nausea, sometimes euphoria.
These effects progress to a stage of twitching or
seizures above 18,000ft & end in coma above 23,000ft
followed shortly thereafter by death.
Other important effects of high altitude on physiology
of the body are as follows:
 REDUCED WORK CAPACITY
 ACUTE CEREBRAL EDEMA (HAPE)
 ACUTE PULMONARY EDEMA (HAPE)
 ACUTE MOUNTAIN SICKNESS (AMS)

9. REDUCED WORK
CAPACITY:
 Work capacity of all
muscles greatly
increased in hypoxia
including skeletal &
cardiac muscles.
 Work capacity is
reduced in direct
proportion to decrease
in maximum rate of
oxygen uptake that the
body can achieve.

10. ACUTE CEREBRAL
EDEMA (HACE):
 Local vasodilation of the
cerebral blood vessels.
 Dilation of arterioles
increases blood flow into
the capillaries thus
increasing capillary
pressure causing fluid to
leak into the cerebral
tissue.
 Cerebral edema lead to
severe disorientation &
other effects related to
cerebral dysfunction.

11. ACUTE PULMONARY
EDEMA (HAPE):
 Pulmonary arterioles
constrict potently, but
constriction is some parts of
the lungs is greater & more
flow is forced through still
unconstricted pulmonary
vessels.
 Capillary pressure in these
areas of the lungs becomes
especially high & local
edema occurs & extension
of this process causes
severe pulmonary
dysfunction that can be
lethal.

12. ACUTE MOUNTAIN
SICKNESS (AMS):
 Presence of headache.
 Gastrointestinal(anorexia,
nausea, vomiting)
 Fatigue or weakness.
 Dizziness, difficulty sleeping.

14. RESPIRATORY RESPONSE TO ALTITUDE
 Hyperventilation occurs &
pulmonary ventilation
increases.
 Hyperventilation causes
decrease in PCO2 &
respiratory alkalosis (RA)
occurs.
 Renal bicarbonate(HCO3-)
excretion is increased &
RA is resolved (via
increased excretion of CSF
HCO3-).

16. Acute & Chronic Response to Altitude:
ACUTE RESPONSE CHRONIC RESPONSE
RESPIRATORY •Increased breathing
rate.
•Decreased pulmonary
diffusion.
•Decreased
haemoglobin
saturation.
•Increased ventilation
remains stabilised.
•Pulmonary diffusion
remains stabilised.
•Haemoglobin saturation
remains decreased.
CARDIOVASCULAR •Increased sub maximal
heart rate.
•Increased sub maximal
cardiac output.
•Decreased maximal
stroke volume.
•Decreased maximal
heart rate.
•Sub maximal heart rate
remains elevated.
•Decreased sub maximal
cardiac output to below sea
level.
•Maximal stroke volume
remains decreased.
•Maximal heart rate
remains decreased.

17. ACUTE RESPONSE CHRONIC RESPONSE
HEMATOLOGIC •Decreased plasma
volume.
•Increased hematocrit.
•Increased viscosity.
• Plasma volume remains
decreased but increases from
acute stage.
•Hematocrit elevated.
•No change or less viscous.
METABOLIC •Increased lactate
concentration at a given
sub maximal work load.
•Decreased maximal
lactate concentration at
maximal workload.
•Decreased sub maximal
lactate concentration
compared to acute stage.
•Decreased maximal lactate
concentration compared to
acute stage.
LOCAL TISSUE •Increased capillary density in
blood.
•Increased number of
mitochondria in blood.
•Increased aerobic enzymes.
PERFORMANCE •Decreased VO2 max. •Decreased VO2 max although
may improve in some groups.

18. PREVENTIVE MEASURES FOR HYPOBARIC
EFFECTS:
Slow the ascent rate.
Drink plenty of water &
remain hydrated.
Avoid drinking alcohol as
alcohol has tendency to
dehydrate the body.
Physically & mentally fit.
No smoking.
Avoid using sedatives.
Carry oxygen masks.

19. HYPERBARIC ENVIRONMENT
When human beings descend beneath the sea the
pressure around them increases tremendously.
Hyperbarism is a condition when blood in lungs is
exposed to extremely high alveolar gas pressure.
Beyond certain limits, these high pressures can cause
tremendous alteration in the body physiology & can be
lethal.
Another important effect of depth is compression of
gases to smaller volumes.
Volume of compressed gas is inversely proportional to
the pressure (Boyle’s Law).

20.  Exposure to elevated ambient pressure (hyperbaric
conditions) occurs most commonly in underwater
diving, during which respired gas density & partial
pressures, work of breathing & physiological dead
space are all increased, tendency towards
hypercapnia. There is reduced responsiveness of
respiratory controller to rising arterial CO2, leading to
hypoventilation & CO2 retention. Elevated arterial
PO2, inert gas narcosis are contributing factors.

21. Nitrogen, oxygen & carbon dioxide cause significant physiologic
effects at high pressures on the body.
NITROGEN NARCOSIS:
 Four fifths of air is nitrogen, at high pressures cause varying
degrees of narcosis.
 Nitrogen narcosis has characteristics similar to those of alcohol
toxication, known as “raptures of the depths”.
 Nitrogen dissolves in neuronal membranes, reduces neuronal
excitability.
120 feet First symptom of mild narcosis occurs. Diver
begins to exhibit joviality & lose many of his or
her cares.
150-200 feet Diver becomes drowsy
200-250 feet Diver becomes too clumsy to perform the
required work.
>250 feet Diver becomes useless due to nitrogen
narcosis

22.  OXYGEN TOXICITY:
Extreme oxygen
poisoning
 Extremely high tissue PO2
occurs when oxygen is
breathed at very high alveolar
oxygen pressure can be
detrimental to many of body
tissues. Breathing oxygen at 4
atmospheres pressure will
cause brain seizures followed
by coma (30-60min). Nausea,
muscle twitching, dizziness,
disturbances of vision,
irritability & disorientation
are other symptoms.

23. “OXIDIZING FREE RADICALS”
 Molecular oxygen (O2) has little capability of oxidizing other
chemical compounds, converted to several forms of active
oxygen called “oxygen free radicals”.
 Superoxide free radical & peroxide radical is important.
 Tissue contain multiple enzymes that rapidly removes these free
radicals such as peroxidases, catalases & superoxide dismutases.
 Above critical alveolar PO2(>2 atmospheres PO2), buffering
mechanism fails, tissue PO2 rises & oxidising free radicals
swamp the enzyme system designed to remove them & cause
serious destructive & lethal effects on the cells:
 Oxidises polyunsaturated fatty acids that are essential
component of many cell membranes.
 Nervous system are susceptible because of their high
lipid content & most of acute oxygen toxicity are caused
by brain dysfunction.

24. Chronic oxygen poisoning causes pulmonary
disability:
 due to longer duration to exposure( say 12 hours) of 1
atmosphere oxygen lung passageway congestion,
pulmonary edema & atelactasis caused by damage to
the linings of the lungs begins to develop. The reason
for this effect in lungs & not in the tissues is that air
spaces of the lungs are directly exposed to high oxygen
pressure.

25.  CARBON DIOXIDE TOXICITY:
 Beyond 80mm Hg alveolar PCO2 the situation becomes
intolerable & respiratory centers are depressed rather than
excited because of negative tissue metabolic effects of high PO2.
Respiratory acidosis develops with varying degrees of lethargy,
narcosis & even anesthesia.
“HYPERCAPNIA”
 Excessive CO2 in the body fluids.
 Occurs in association with hypoxia only when hypoxia is caused
by hypoventilation or circulatory deficiency.
 Hypoventilation is when CO2 transfer between the alveoli &
atmosphere is affected.
 In circulatory deficiency CO2 removal from tissues is decreased.
 If PCO2 rises to 80-100mm Hg person becomes lethargic & even
semi comatose. At 120-150mm Hg anaesthesia & death results.

27. DEPTH
METERS
DEPTH
FEET SIGNS & SYMPTOMS
0 to 10 0 to 33 Too small to notice
10 to 30 33 to 100 Mild difficulties with unpractised motor skills.
Mildly impaired reasoning.
Mild euphoria.
30 to 50 100 to 65 Delayed response to visual & auditory stimuli.
Calculation errors & wrong choices.
Anxiety (common in cold Murphy water ).
50 to 70 165 to 230 Sleepiness.
Impaired judgement.
Hallucinations.
70 to 50 230 to 300 Poor concentration & mental confusion.
Loss of memory & increase excitability.
90+ 300+ A sense of levitation.
Disorganisation of sense of time.
Death.

28. PREVENTIVE MEASURES FOR
HYPERBARIC EFFECTS:
Use of breathing
apparatus- gives gas to
breathe & either dissolves
CO2 (close circuits) or
bubbles out in water(open
circuit).
SCUBA DIVING(self-
contained underwater
breathing apparatus.

29. CAISSON DISEASE
HISTORY:
“During the building of James Ead’s St. Louis Bridge,
several construction workers digging the river bed
inside the caisson fell ill. An alarmed Eads reduced his
men’s working hours & called his personal worker
doctor on the scene, still some of the workers died, they
were victims of caisson disease”

30.  Decompression sickness (DCS) also known as diver’s
disease, the bends or caisson disease.
 Occurs when body is exposed to sudden drop in
surrounding pressure & occurs most frequently in deep
sea diving.
 The air we breathe is mixture of two gases,
nitrogen(78%) & oxygen(21%). Unlike oxygen, nitrogen
we inhale is expelled when we exhale but some is
dissolved into blood & other tissues.
 During a dive, lungs take in more nitrogen than usual,
as surrounding water pressure > air pressure at sea
level.
 Increased pressure causes an increase in gas density &
diver takes in more nitrogen with each breath than
he/she would at sea level.

31.  Instead of being exhaled, the extra nitrogen safely
dissolves into the tissues, where it remains until the
diver begin his/her return to the surface. On way up,
decompression occurs (pressure drops) & with the
change in pressure, the extra nitrogen gradually
diffuses out of the tissues & is delivered by the blood
stream to the lungs which expels it from the body. If
the diver surfaces too quickly, potential dangerous
nitrogen bubbles form in the tissues & cause DCS.
These bubbles compress nerves, obstruct arteries,
veins& lymphatic vessels & triggers harmful reactions
in blood.

32.  SYMPTOMS:
 Bubbles in tissues cause severe pain particularly around joints &
neurological symptoms like itching.
 Bubbles in blood stream occur in more severe cases, obstruct the
arteries to brain& spinal cord. Symptoms commonly appear 30-
60min after diver surfaces.
 Abnormalities due to damage of spinal cord is most common,
major paralyses & respiratory failure also occurs.
 Bubbles in pulmonary capillaries are responsible foe dyspnoea
(“the chokes”) & bubbles in coronary arteries cause myocardial
damage.
 Less severe type of DCS is DCS1 (inflammation of muscles,
joints & tendons resulting in pain & swelling, commonly known
as “bends”.
 More severe type of DCS is DCS 2, results in serious systematic
effects including neurological symptoms such as numbness &
tingling.

34. FREQUENCY & ONSET OF DCS SYMPTOMS
SYMPTOMS FREQUENCY
Local joint pain 89%
Arm symptoms 70%
Leg symptoms 30%
Dizziness 5.3%
Paralysis 2.3%
Shortness of breath 1.6%
Extreme fatigue 1.3%
Collapse/
unconsciousness
0.5%
TIME TO
ONSET
PERCENTAGE
OF CASES
Within 1 hour 42%
Within 3 hours 60%
Within 8 hours 83%
Within 24 hours 98%
Within 48 hours 100%

35. TREATMENT:
 All cases of DCS should be treated initially with 100% oxygen
until hyperbaric oxygen therapy can be provided.
 It is beneficial to give fluids, as this helps reduce dehydration.
 Treatment of this disease is prompt recompression in a pressure
chamber, followed by slow decompression.
PREVENTION:
 Limiting the depth & duration of deep sea divers.
 Following standard diving guidelines.
 Avoiding excessive alcohol consumption for 24 hours before
diving.
 Avoiding repeated dives within a 12 hour period .

36. HYPERBARIC OXYGEN THERAPY
 Intense oxidizing properties of
high pressure oxygen
(hyperbaric oxygen) have
valuable therapeutic effect in
several clinical conditions.
 Large pressure tanks available
in which patients are placed &
treated with hyperbaric oxygen.
 Hyperbaric chamber pressure is
raised to 3-4 atmospheres so
that tissues absorb more O2.
 Used for the treatment of gas
gangrene (clostridial
organisms).
 Other treatments include
decompression sickness, arterial
gas embolism, CO poisoning,
osteomyelitis & myocardial
infarction.

37. OSTEOMYELITISGAS GANGRENE

38. THANK YOU........