This document discusses respiratory physiology at high altitudes. It begins by classifying altitudes and explaining how atmospheric pressure decreases with increasing altitude. The body adapts to high altitudes through hyperventilation, polycythemia, and shifts in the oxygen-hemoglobin dissociation curve. Acute mountain sickness can occur if the ascent is too rapid and symptoms include headache, fatigue, and nausea. Other issues discussed include high altitude pulmonary and cerebral edema, chronic mountain sickness, oxygen toxicity, and respiratory changes during space flight and scuba diving.

1. RESPIRATORY PHYSIOLOGY
AT HIGH ALTITUDES
DR. DAVIS KURIAN

2.  High altitude = 1,500–3,500 metres (4,900–11,500 ft)
 Very high altitude = 3,500–5,500 metres (11,500–18,000 ft)
 Extreme altitude = above 5,500 metres (18,000 ft)
 The death zone - altitudes above a certain point where the
amount of oxygen is insufficient to sustain human life. This
point is generally tagged as 8,000 m (26,000 ft) [less than
356 millibars of atmospheric pressure]
Classification of heights

3.  Atmospheric pressure
decreases with increase in
altitude.
 At 5000m it is only half the
normal pressure –
½ X 760=380mm Hg.
 So PO2 of inspired gas =
(380-47)*0.2093 = 70mm Hg

4. HYPERVENTILATION:
 Most important mechanism
 In normal ventilation
PCO2 = 40mm Hg, respiratory exchange ratio = 1, PO2 =
3mm Hg.
 In hyperventilation – PCO2 = 8mm Hg, alveolar PO2 = 35mm
Hg.
 Mechanism – hypoxic stimulation of peripheral
chemoreceptors – decreased PCO2 and alkalosis – inhibits
hyperventilation – inhibition removed by excretion of excess
HCO3 by kidneys.
 Increased sensitivity of carotid bodies to hypoxia.
ACCLIMATIZATION AT HIGH ALTITUDES

5. POLYCYTHEMIA
 Increased RBC concentration – increased Hb concentration –
increases O2 carrying capacity.
 Mechanism : hypoxemia – stimulates erythropoietin secretion
from kidneys – stimulates bone marrow – polycythemia.
 Disadvantage – increases blood viscosity
ACCLIMATIZATION AT HIGH ALTITUDES

6. OTHER CHANGES:
 ODC –> right (at moderate heights) –d/t increased 2,3 DPG and
respiratory alkalosis – promotes O2 release.
 ODC --> left (at very high altitudes) – d/t alkalosis – Increased
O2 uptake form pulmonary capillaries.
 Number of capillaries per unit volume in peripheral tissues
increases and changes occur in the oxidative enzymes in cells.
 Increase in maximum breathing capacity because the air is less
dense, but O2 uptake declines above 4600m.
ACCLIMATIZATION AT HIGH ALTITUDES

7.  Alveolar hypoxia – pulmonary vasoconstriction – increased
pulmonary arterial pressure – increased work of right heart
– hypertrophy.
 Increased pulmonary arterial pressure – pulmonary edema –
d/t uneven arteriolar constriction and leakage from
unprotected and damaged capillaries. The fluid has
increased proteins
ACCLIMATIZATION AT HIGH ALTITUDES

8.  Usually above 8,000 feet (2,400 meters) in un-acclimatized
climbers.
 The faster you climb to a high altitude, the more likelihood of
acute mountain sickness.
 Symptoms include – nausea, vomiting, headache, fatigue,
dizziness, palpitation, loss of apetite and insomnia.
 Mechanisms postulated are cerebral edema and alkalosis due
to hypoxemia (hypoxemia – arteriolar dilatation – limit of
cerebral autoregulatory mechanisms – cerebral edema due to
fluid transudition.)
 In more severe cases – high altitude pulmonary edema and
high altitude cerebral edema develops.
ACUTE MOUNTIAN SICKNESS

9.  Symptoms – reduced by large doses glucocorticoids
(decreases cerebral edema) and acetazolamide (decreases
alkalosis –by inhibiting carbonic anhydrase).
 If not treated – may lead to ataxia, disorientation, coma and
finally death – d/t tentorial herniation of brain tissue.
 Keys to preventing acute mountain sickness include:
 Climb the mountain gradually
 Stop for a day or two of rest for every 2,000 feet (600 meters)
above 8,000 feet (2,400 meters)
 Sleep at a lower altitude when possible
 Learn how to recognize early symptoms of mountain sickness
ACUTE MOUNTIAN SICKNESS

10.  HAPE - life-threatening form of non-cardiogenic pulmonary
edema due to leaky capillaries.
 HAPE - symptoms start gradually within the first 2-4 days at
altitude.
 Earliest symptoms - shortness of breath with exercise, with
decreased exercise performance – may progress to - severe
shortness of breath even at rest, a persistent cough sometimes
with blood, chest tightness or congestion, and severe
weakness.
 If untreated - progress to coma and death.
HIGH ALTITUDE PULMONARY EDEMA

11. The Lake Louise Consensus Definition for High-Altitude Pulmonary Edema has
set widely used criteria for defining HAPE symptoms:
Symptoms: at least two of
 Difficulty in breathing (dyspnea) at rest
 Cough
 Weakness or decreased exercise performance
 Chest tightness or congestion
Signs: at least two of
 Crackles or wheezing (while breathing) in at least one lung field
 Central cyanosis (blue skin color)
 Tachypnea (rapid shallow breathing)
 Tachycardia (rapid heart rate)
Symptoms worsen at night and tachypnea and tachycardia occurs at rest.
HIGH ALTITUDE PULMONARY EDEMA

12. Suggested mechanisms include
 Increased pulmonary arterial and capillary pressures
(pulmonary hypertension) secondary to hypoxic pulmonary
vasoconstriction.
 An idiopathic non-inflammatory increase in the permeability of
the vascular endothelium.
HIGH ALTITUDE PULMONARY EDEMA

13. Treatment includes:
 Administration of oxygen, and descent to a lower altitude as
soon as possible.
 Take rest
 Dexamethasone, CCBs have also been found to be effective.
Phosphodiesterase inhibitors are also effective but can worsen
headache
HIGH ALTITUDE PULMONARY EDEMA

14.  Also called Monge’s disease.
 Seen in long term residents of high altitude
 Ill defined syndrome of polycythemia, fatigue, exercise
intolerance and hypoxemia.
 Treatment is mainly return to lower altitudes possible.
CHRONIC MOUNTAIN SICKNESS

15. OXYGEN TOXICITY

16.  Experimental studies in guinea pigs - 100% O2 at
atmospheric pressure for 48 hrs produced pulmonary
edema.
 First change that occurs in oxygen toxicity is in the
endothelium of pulmonary capillaries and alveolo-capillary
membrane similar to ARDS.
 There is evidence of impaired gas exchange after 30hrs of
inhalation of 100% O2.

17.  In normal volunteers in experimental study, 100% O2 for 24 hrs
produced substernal discomfort which is aggravated by deep
breathing and the vital capacity decreased by 500-800ml –
probably due to absorption atelectasis.
 100% O2 in premature infants – blindness d/t retrolental
fibroplasia – d/t local vasoconstriction caused by high PO2 –
avoided when arterial PO2 is kept below 140 mm Hg.

18.  Generation of free radicals – superoxide ions, activated hydroxyl
ions, singlet O2 and hydrogen peroxide.
 Free radicals react with DNA, sulfhydryl proteins and lipids.
 Normally protected by SOD, Catalase, antioxidants and free
radical scavengers.

19.  PaO2 > 60 mmHg may depress ventilation in some patients with
chronic hypercapnia.
 FiO2 > 0.5 may cause atelectasis, O2 toxicity & or ciliary or
leucocyte depression.
 PaO2 > 80 mmHg may cause retinopathy of prematurity in
premature infants (arterial O2 tension more important than
alveolar O2 tension)
 In infants with certain congenital heart ds such as hypoplastic
left heart, high PaO2 can compromise balance b/w systemic
and pulmonary blood flow and may also cause
bronchopulmonary dysplasia.
 Patients using 100% O2 for prolonged periods can have
tracheobronchitis

20.  Prolonged inhalation of 100% O2 can damage the lung – like
absorption atelectasis, depression of mucociliary functions etc.
 At high PO2 – CNS damage may result – resulting in seizures –
which may be preceded by nausea, ringing in the ears or
twitching of the face.
 At PO2 of 4 atm – convulsions occur at a frequency of 30 per
minute.
 Suggested mechanism for CNS action – is the inactivation of
certain enzymes esp dehydrogenases containing sulfhydryl
groups.

22.  Refers to CNS toxicity of O2 – d/t polymerisation of SH group
of enzymes – inactivation – cellular damage – aggravated by
stress, cold, fatigue, deficiency of trace elements – Se, Zn
(antioxidant elements)
 Muscle twitch, spasm, nausea, vomiting, dizziness, vision and
hearing difficulty, twitching of facial muscles, irritability,
confusion, sense of impending doom, trouble in breathing,
in coordination, convulsions.
PAUL BERT EFFECT

23.  Pulmonary toxicity – more than 0.5 ATA – affects pulmonary
epithelium and inactivates surfactant – intra-alveolar edema
and interstitial thickening – fibrosis and pulmonary
atelectasis – resemble paraquat poisoning
 Progresses in three phases - Tracheobronchtis ->ARDS - >
pulmonary interstitial fibrosis
LORANE SMITH EFFECT

24. ABSORPTION ATELECTASIS
When 100% O2 is breathed in
Trapped gas in alveoli – 760mm Hg
Sum of partial pressure of gases in
venous blood - <760 mm Hg.
Sum of partial pressures in alveoli
> venous blood – gas difusion into
blood – collapse of alveoli –
difficult to reopen d/t surface
tension forces

25.  When air is breathed in – the same process happens – but at a
slower rate – here the difference being the rate being limited
by rate of diffusion of N2 – slow solubility – acts as splint –
supports alveoli and delays collapse.
 Post op atelectasis is common in patients treated with high
oxygen mixtures.
 Collapse of alveoli is more common at the base of lung where
the parenchyma is less well expanded or the small airways are
closed.
ABSORPTION ATELECTASIS

26.  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
OPTIMUM O2 USE

27. RESPIRATORY CHANGES IN
SPACE FLIGHT

28.  Absence of gravity – more uniform distribution of blood flow
and hence small improvement in gas exchange.
 Absence of sedimentation – altered deposition of inhaled
aerosols.
 Thoracic blood volume – initially increases and raises
pulmonary capillary blood volume and diffusing capacity.
 Postural hypotension occurs on return to earth –
cardiovascular deconditioning.
 Decalcification of bone and muscle atrophy occurs due to
disuse and also a slight reduction in the red cell mass

29. RESPIRATORY CHANGES
DURING DIVING AND ASCEND

30.  Diving – pressure increases by 1 atmosphere for every 10m
(33ft) of descent – a non communicating gas cavity such as
lung, middle ear or intracranial sinus – pressure difference
causes compression on descent or over expansion on ascent.
 Hence scuba divers should exhale as they ascend to prevent
over inflation and possible rupture of lungs.
 Increased density at depth increases the work of breathing –
CO2 retention

31.  Diving – high partial pressure of N2 – forces poorly soluble N2
into tissues (esp fat). The diffusion is slow because of the low
solubility of N2 and equilibration takes hours.
 Ascend – N2 diffuses out from the tissues. Rapid ascend –
bubbles of N2 form – pain at the joints (bends), neurological
symptoms – deafness, impaired vision and even paralysis may
occur.
DECOMPRESSION SICKNESS

32. Management
 Recompression – reduces volume of bubbles and force them
back into circulation.
 Reduced incidence with use of He-O2 mixture – helium has one
and half times the solubility of N2 – so less dissolved in tissues &
1/7th the molecular wt of N2 – hence diffuses out more rapidly
through tissues.
 He-O2 mixture has less density hence reduces the work of
breathing.
DECOMPRESSION SICKNESS

33.  Mainly used by workers working on under water
pipeline systems.
 While not in water – they live in high pressure
chambers on the supply ship – hence avoiding
decompression sickness.
SATURATION DIVING

34.  N2 – inert gas but affects CNS at high pressures.
 At a depth of 50m (160ft) – euphoria can occur with
increased N2 concentration – further high partial
pressures – loss of coordination and coma occurs.
INERT GAS NARCOSIS

35. HYPERBARIC OXYGEN THERAPY

36.  A mode of medical treatment where the patient breathes
100% oxygen at a pressure greater than one Atmosphere
Absolute (1 ATA). Under these conditions, your lungs can
gather more oxygen than would be possible breathing
pure oxygen at normal air pressure.
 The basis is to increase the concentration of dissolved
oxygen. This helps fight bacteria and stimulate the release
of substances called growth factors and stem cells, which
promote healing.

37.  HENRY’S LAW – states that the concentration of any gas in
solution is proportional to the partial pressure.
Dissolved O2 in plasma :0.003ml / 100ml of blood / mm PO2
Breathing Air (PaO2 100mm Hg)
0.3ml / 100ml of blood
Breathing 100% O2 (PaO2 600mm Hg)
1.8ml / 100ml of blood
Breathing 100% O2 at 3 atm (PaO2 2000 mm Hg)
6.0ml / 100ml of blood

39.  Bubble reduction (Boyle’s law – P1V1=P2V2)
 Increasing the oxygen concentration of blood
 Enhanced host immune function
 Neovascularization
 Vasoconstriction
PHYSIOLOGICAL EFFECTS

40.  ACUTE CHRONIC
• Decompression sickness Radiation necrosis
• Carbon monoxide poisoning Diabetic wounds of lower limbs
• Severe crush injuries Refractory osteomyelitis
• Thermal burns
• Acute arterial insufficiency
• Clostridial gangrene
• Necrotizing soft-tissue infection
• Ischemic skin graft or flap
INDICATIONS

41.  Temporary nearsightedness (myopia) caused by temporary
eye lens changes
 Middle ear injuries, including leaking fluid and eardrum
rupture, due to increased air pressure
 Lung collapse caused by air pressure changes (barotrauma)
 Seizures as a result of too much oxygen (oxygen toxicity) in
your central nervous system
 In certain circumstances, fire — due to the oxygen-rich
environment of the treatment chamber
RISKS ASSOCIATED

42. METHODS OF DELIVERING HBOT
MONOPLACE CHAMBER MULTIPLACE CHAMBER