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LUNG MANIFESTATIONS IN
HIGH ALTITUDE
Dr.Chandan Kumar Sheet
Post Graduate Trainee
Dept of Pulmonary Medicine
VIMSAR,Burla,Odisha,India
Altitude medicine
High altitude - above 10000 feet(3000m) of sea level
typically focus on people above 2500m- 8000m
 Subdivision of altitude-
- High
[8000-12000 feet]
- Very high
[12,000-18,000 feet]
- Extreme high-
[>18,000 feet]
 UPTO 10,000 feet
-safe zone to rapid ascent
-classically defines high
altitude
 At 18,000 feet
-upper limit of permanent
human inhabitation
 ABOVE 20,000 feet
-Life is endangered with out
supplemental O2
 From 40,000 feet
-Ozone layer starts
Altitude medicine(cont..)
 Study is important for
1] Mountaineering
2] Aviation & space flight
3] Permanent human settlement at highlands
4] Military & Security
Basic concepts
 Barometric pressure & Height have inverse relationship
 According to Daltons law, total air pressure is equal to
sum of partial pressure of gases it contains.
 P = pO2 + pN2 + pCO2 +PH2O
 pH2O & PCO2 does not depends upon altitude
 pO2 & pN2 decrease with increase in height
Basic concepts
 Atmospheric composition of air remains almost
constant [up to 30,000 feet]but PO2 decreases
with increase altitude
 PAO2 = FiO2 [ Patm - pH20 ] - paCO2/RER
 RER= respiratory exchange ratio =0.8
 The French physiologist PAUL BERT first recognised that
the harmful effects of high altitude are caused by low
oxygen tension
Altitude PRESSURE
FEET Mm of Hg ATMOSPHERIC UNIT
0 760 1
18,000
[~ 5,500 m]
380 1/2
34,000
[~ 10,500 m]
190 1/4
48,000
[~ 14,650 m]
95 1/8
63,000
[~ 19,000 m]
47 1/16
Basic concepts- Hypoxia at High Altitude
 Human body is designed specifically in such a way that it
delivers adequate O2 to the tissue only when O2 pressure
close to the sea level
 high altitude hypoxic hypoxia tissue oxygenation
suffers physiological derangements.
 “Connecting 24 volt motor with a 6 volt battery” - perfect
comparison by J.S.Miledge
Degree of hypoxic effects depends upon
Level of the altitude
Rate of ascent
Duration at high altitude
Altitude
 Mount Everest
 8848 M
 Atm. pressure = 255 mm Hg
 Inspired PO2= 21% * [255-47]=44 mm Hg
-Unacclimatized person
- unconscious within 45 sec
- Dead with in 4-5 min
Contributing factor for illness
 Altitude related exposure to
o Cold,
o Extreme exercise,
o Trauma,
o Infection,
o UV rays
Exposure and time course
 ACUTE
Immediate to 3-5 days
 SUBACUTE
Over weeks-leading towards acclimatization
 CHRONIC
Years, and life long residence
Effects of High Altitude on Human Body
Sea level 160 97% No Effect
5000-10,000 110 90 % Rapid ascent upto 10,000 feet
is safe zone of ascent
10,000-15,000 98 80% Moderate hypoxia with CVS &
Resp symp
15,000-20,000 70 <70% Hypoxia aggrasvates,
Unconsciousness, seizure,
muscle twitching
Critical survival altitude
More than 20,000 <60% Severe hypoxia even with o2
therapy
Level
(feet)
PO2
(mmHg)
Hb- Sat
(%)
Effects
Effect of High Altitude
 Effect of Hypoxia
 Effect of expansion of gas
 Effect of fall in temperature
 Effect of UV rays
Effect of Hypoxia
 ACUTE RESPONSE
- accommodation
- Reflex adjustment of respiration and CVS to hypoxia
 LONG TERM RESPONSE
- acclimatization
- Change in body tissue in response to long-term
hypoxia
Accommodation
 On Respiratory System
o Hyperventilation
o Decreased PO2
or
increased Pco2
chemoreceptor reflex
increase rate & depth of
breathing
On CVS
o Increase HR,
o force of contraction of
heart,
o Increase CO,
o Increase BP
o Due to reflex stimulation
of cardiac and vasomotor
centres
Accommodation..(cont)
Effects on Blood
o Increase RBC count
Due to increased secretion of
erythropoietin from JGA of
kidney
o Increases 2,3-DPG
(Within hours)
 Mechanism
Altitude
Hyperventilation
Decrease PACO2/PaCO2
Decrease [ H+]
Concomitantly increase 2,3 DPG
Reduction in PaCO2 & H+
Increase Hb affinity & decrease release
&
increased 2,3 DPG decrease affinity and
increase release
Loading & unloading of O2 depends
upon the balance between these factors
Effect on Oxy-Hb dissociation curve
 During initial ascend
&
at moderate altitude
- the curve shift to right
- under the influence of
2,3 DPG
 At extreme altitude or
long stay
- it shifts to left
- due to less CO2 in blood
High Altitude & O2 –Hb Saturation
 Above 10,000 feet, the arterial O2 saturation falls rapidly
 Due to increased 2,3 DPG concentration in RBC
 It is slightly less than 70% at 20,000 feet and much less at
higher altitudes
 When haemoglobin saturation falls bellow 60% serious cellular
dysfunction occurs,
and if prolonged, can cause death
Accommodation..(cont)
 On digestive system
o loss of appetite
o Nausea, vomiting
 On kidney
o Alkaline urine due to
increased
erythropoietin
secretion
 On CNS
o Depression,
o Apathy,
o Talkative,
o Disorientation,
o Loss of power of
judgement
o Impaired memory,
o Fatigue,
o Lack of cordination
o Sudden LOC
High Altitude & Cellular metabolism
High altitude
Low partial pressure of O2
Decrease PAo2
Decrease PaO2
Decrease oxidative phosphorylation
Decrease ATP
Effect of expansion of gases
 According to Boyle’s law , as the atmospheric pressure
decreases with altitude, volume of gases increase
proportionately
 On GIT
Painful distension of stomach and intestine
 On lungs
Expansion of gases may destroy alveoli
 Rapid ascent may cause Decompression sickness
Effect of fall in Temperature
 Atmospheric temperature falls by 2°C for every 1000 ft
increase in altitude
 EFFECTS
- Cutaneous vasoconstriction
- Prolonged and severe vasoconstriction may lead to
tissue damage known as frost bite
Effect of UV rays
Manifestations
 Skin irritation
 Photokeratitis
 Photoconjunctivitis
Recomendations
- Sunscreen (atleast30 SPF)
- Sunglass
(polycarbonate or CR-39
LENS)
For every 1000 ft
- 4-8% more UVB exposure
So, at8000 ft-
>30% more exposure
Clinical Syndromes In High Altitude
 Acute high altitude headache (HAH)
With hurried assent many (80%) will report -
transient headache
 Acute Mountain Sickness (AMS)
 High Altitude Cerebral Edema (HACE)
 High Altitude Pulmonary Edema (HAPE)
 Chronic Mountain Sickness (CMS)
 RVH,Low birth wt,cong heart disease-Present in some
resident
Acute Mountain Sickness
 Symptom complex
 Occurs in an individual who residing at sea level, when he ascends to
high altitude over a period of 1-2 days for first time.
 The symptoms develops 8-24 hours after arrival at high altitude
 Last for 4-8 days
Lake Louise symptom Score
symptoms severity pointssymptoms severity points
Headache No Headache 0
Mild Headache 1
Moderate Headache 2
Severe Headache 3
Gastrointestinal No GI symptoms 0
Poor appetite/nausea 1
Moderate nausea/vomiting 2
Severe nausea/incapacitating 3
Fatigue /Weakness No 0
Mild 1
Moderate 2
Severe 3
Symptoms Severity Points
Dizziness/Light headedness No 0
Mild 1
Moderate 2
Severe 3
Difficulty of Sleeping Slept as well as Usual 0
Sleep as well as usual 1
Woke up many times, poor
night’s sleep 2
Unable to sleep 3
o Self report score
o Diagnosis of AMS based on recent rise in altitude, presence of headache, with at
least one of the other symptom
o Total score >3 with no other of symptoms
Treatment
 Most patients- symptoms abate in 2-3 days without specific
treatment
 Mild to Moderate AMS-
o O2 therapy
o Large dose of glucocorticoids to decrease cerebral oedema
o Acetazolamide-Decrease alkalosis by H+ excretion through
kidney by inhibiting carbonic anhydrase enzyme
o Descent
 Severe symptoms/HACE- Transport to lower altitudes
 Those who develop AMS- usually have a recurrence with future ascents
unless they take preventive measures
 AMS rarely cause death, unless evacuation of rare patients
who have HACE to lower altitude
High altitude pulmonary oedema
 Occurs due to
- rapid ascend
- Heavy physical work during first 3-4 days after rapid
ascent to high altitude
 Mechanism
Increased sympathetic activity
Vasoconstriction
Increase pulmonary capillary hydrostatic pressure
Drives the fluid out of pulmonary capillary
Pulmonary oedema
 Treatment
- O2 therapy
- Ca Channel blocker –nifidipine
- PDE inhibitor-Tadalafil (may worsen headache of AMS)
High altitude cerebral oedema
 Considered as ‘end stage‘ or severe AMS .
 AMS with either change in mental status or ataxia or both
 Mechanism - low PO2 arteriolar dilation
normally compensated by cerebral auto-regulation
reached the level of auto-regulation
increase capillary pressure
increase transudation CE
 Treatment - large dose of glucocorticoids
Chronic mountain sickness
 Monge’s disease
 Occurs in long term residents
 EFFECTS
-Extreme polycythemia
-PAH
-RVH
-CHF
-Peripheral arterial pulse begins to fall
 These individual must be removed to a lower altitude to
prevent rapid development of pulmonary oedema
Acclimatization
 Definition
Change in body tissue in response to long-term exposure to high
altitude hypoxia for a long time
 When there is a fall in O2 following acclimatization occurs
1) Pressure during O2 transfer
2) O2 carrying capacity of blood
3) Ability of tissue to utilise O2
Acclimatzation of respiratory system
Prolonged hyper ventilation
CO2 washout
respiratory alkalosis
renal compensation
alkaline urine
normalisation of blood & CSF PH
withdrawal of central chemo-mediated respiratory depression
increase in resting pulmonary vasodilation (by 5 fold),primarily due to
increase in TV
Sustained
hyperventilation
Other respiratory changes
 Increase TLC
[In high landers for generation]
- evidenced by barrel shaped chest
- leads to increase ventilatory capacity
 Increase diffusing capacity of lung-
hypoxic pulmonary vasoconstriction
pulmonary hypertension
increase no of pulmonary capillaries
 Vascularity of the tissues
More capillary opens up in tissue than at sea level
(normal ~25% open at rest others at reserved)
 This combined with systemic vasodilation(also a hypoxic response)
More O2 delivery to tissues
Change in Body
 CVS
HR,BP,CO
Blood flow to vital organs
like- heart, brain, muscle
Change in Body
 Blood
 Increase haematocrit
to60%
 Increase Hb concentration
to about 20%
 Due to erythropoietin
secretion
 Tissue
 Increased quantities of
oxidative enzymes
involved in metabolism
 Increased number of
mitochondria in cells
 Increase myoglobin
(O2 storing pigment)
Physiological polycythemia
Hypoxia induced Erythropoiesis
Increased Hb & RBC
Expansion of Blood volume Increased amount of Hb
Haemodynamics is kept within
normal limit inspite of increased
vascularity of tissue
Inspite of decrease saturation,O2 carrying
capacity is maintained at normal limit
Conditions aggravated by high altitude
 Hypertension
 Obstructive airway disease
 CCF
 SCD,2,3 DPG deficiency
 Sleep apnoea
 Cardiovascular ds
 Seizure disorders
 Such individuals should be cautious or completely abstain
from visit to high altitude
 ALL visitors to the hight of 5000 m or more should consult
pulmonologist
 Older age (>50) mildly protective against altitude
sickness
 Women higher risk
O2 REQUIREMENT
 SPO2 >95% - OK
 SPO2 <92% - O2 needed
 SPO2 (92-95%)
- If concurrent heart & lung disease-give O2
Recommendations
If history of AMS/ Travel above 2500 m(8000 ft)
 Acetazolamide 250 mg BID
- 24 Hours before & 48 hours into stay
 first night sleep at less than 9000 ft
 Rest for 2-4 days
- Vigorous exercise may cause AMI
 Gradual activity increase over week
 Alcohol, tranquilizers –avoid 2-7 says
 Avoid salty food-increase BP
 Carbohydrate - best fuel for high altitude
(helps anaerobic &aerobic metabolism)
Above 3500m(11,500 ft)
 Acetazolamide
 Dexamethasone
 O2
Contraindications Travel above 2000m
 PULMONARY DISEASE
- PAH
- Severe COPD
(GOLD3&4)
- CO2 retention
- Poorly controlled
asthma
 CVS
- With in 3 months of
AMI,CVA,ICD Implantation
- UA,
- Before planned coronary
intervention
- Heart Failure,NYHA> II
- Congenital heart disease
(Cyanotic & acyanotic)
Travel to 2000-3000 m permissible
 PULMONARY DISEASE
- Stable COPD
- Stable asthma under
medical treatment
 CVS
- Asymptomatic CAD
- Stable CAD
- Normal performance
capacity
- Good BP controL
- No illness affecting gas
exchange
Pediatrics for hypoxia &altitude sickness
 Children <8 yrs - 4 fold risk Increase
 Teens - twice risk increase
Recommendations
 absolutely no child above 35,00m (11,500ft)
 young child not above 3000 m (10000 ft)
 teen acclimatize above 3000m but take care
Gamow bag Revolutionary invention in
the treatment of high
altitude illness
 Carried in most Himalayan
expeditions
 A sealed chamber with a
pump (6.3 kg)
 The person is placed inside
the bag
 It is then fully inflated by
pumping
 Effectively increase O2
concentration of
O2molecule
Gamow bag
 Stimulate a descent to lower
altitude
 In 10 min, it can create an
atmosphere that can
corresponds to that at 3,000-
5,000 feet lower)
 After 1-2 hours in the bag,
persons body chemistry will
have “reset "to lower altitude
 Last for 12 hours outside the
bag
 Enough time to walk them
down to a lower altitude
 Allow for further
acclimatization
Thank You…

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Lung Manifestations at High Altitude

  • 1. LUNG MANIFESTATIONS IN HIGH ALTITUDE Dr.Chandan Kumar Sheet Post Graduate Trainee Dept of Pulmonary Medicine VIMSAR,Burla,Odisha,India
  • 2. Altitude medicine High altitude - above 10000 feet(3000m) of sea level typically focus on people above 2500m- 8000m  Subdivision of altitude- - High [8000-12000 feet] - Very high [12,000-18,000 feet] - Extreme high- [>18,000 feet]  UPTO 10,000 feet -safe zone to rapid ascent -classically defines high altitude  At 18,000 feet -upper limit of permanent human inhabitation  ABOVE 20,000 feet -Life is endangered with out supplemental O2  From 40,000 feet -Ozone layer starts
  • 3. Altitude medicine(cont..)  Study is important for 1] Mountaineering 2] Aviation & space flight 3] Permanent human settlement at highlands 4] Military & Security
  • 4. Basic concepts  Barometric pressure & Height have inverse relationship  According to Daltons law, total air pressure is equal to sum of partial pressure of gases it contains.  P = pO2 + pN2 + pCO2 +PH2O  pH2O & PCO2 does not depends upon altitude  pO2 & pN2 decrease with increase in height
  • 5. Basic concepts  Atmospheric composition of air remains almost constant [up to 30,000 feet]but PO2 decreases with increase altitude  PAO2 = FiO2 [ Patm - pH20 ] - paCO2/RER  RER= respiratory exchange ratio =0.8
  • 6.  The French physiologist PAUL BERT first recognised that the harmful effects of high altitude are caused by low oxygen tension Altitude PRESSURE FEET Mm of Hg ATMOSPHERIC UNIT 0 760 1 18,000 [~ 5,500 m] 380 1/2 34,000 [~ 10,500 m] 190 1/4 48,000 [~ 14,650 m] 95 1/8 63,000 [~ 19,000 m] 47 1/16
  • 7. Basic concepts- Hypoxia at High Altitude  Human body is designed specifically in such a way that it delivers adequate O2 to the tissue only when O2 pressure close to the sea level  high altitude hypoxic hypoxia tissue oxygenation suffers physiological derangements.  “Connecting 24 volt motor with a 6 volt battery” - perfect comparison by J.S.Miledge
  • 8. Degree of hypoxic effects depends upon Level of the altitude Rate of ascent Duration at high altitude
  • 9. Altitude  Mount Everest  8848 M  Atm. pressure = 255 mm Hg  Inspired PO2= 21% * [255-47]=44 mm Hg -Unacclimatized person - unconscious within 45 sec - Dead with in 4-5 min
  • 10. Contributing factor for illness  Altitude related exposure to o Cold, o Extreme exercise, o Trauma, o Infection, o UV rays
  • 11. Exposure and time course  ACUTE Immediate to 3-5 days  SUBACUTE Over weeks-leading towards acclimatization  CHRONIC Years, and life long residence
  • 12. Effects of High Altitude on Human Body Sea level 160 97% No Effect 5000-10,000 110 90 % Rapid ascent upto 10,000 feet is safe zone of ascent 10,000-15,000 98 80% Moderate hypoxia with CVS & Resp symp 15,000-20,000 70 <70% Hypoxia aggrasvates, Unconsciousness, seizure, muscle twitching Critical survival altitude More than 20,000 <60% Severe hypoxia even with o2 therapy Level (feet) PO2 (mmHg) Hb- Sat (%) Effects
  • 13. Effect of High Altitude  Effect of Hypoxia  Effect of expansion of gas  Effect of fall in temperature  Effect of UV rays
  • 14. Effect of Hypoxia  ACUTE RESPONSE - accommodation - Reflex adjustment of respiration and CVS to hypoxia  LONG TERM RESPONSE - acclimatization - Change in body tissue in response to long-term hypoxia
  • 15. Accommodation  On Respiratory System o Hyperventilation o Decreased PO2 or increased Pco2 chemoreceptor reflex increase rate & depth of breathing On CVS o Increase HR, o force of contraction of heart, o Increase CO, o Increase BP o Due to reflex stimulation of cardiac and vasomotor centres
  • 16. Accommodation..(cont) Effects on Blood o Increase RBC count Due to increased secretion of erythropoietin from JGA of kidney o Increases 2,3-DPG (Within hours)  Mechanism Altitude Hyperventilation Decrease PACO2/PaCO2 Decrease [ H+] Concomitantly increase 2,3 DPG Reduction in PaCO2 & H+ Increase Hb affinity & decrease release & increased 2,3 DPG decrease affinity and increase release Loading & unloading of O2 depends upon the balance between these factors
  • 17. Effect on Oxy-Hb dissociation curve  During initial ascend & at moderate altitude - the curve shift to right - under the influence of 2,3 DPG  At extreme altitude or long stay - it shifts to left - due to less CO2 in blood
  • 18. High Altitude & O2 –Hb Saturation  Above 10,000 feet, the arterial O2 saturation falls rapidly  Due to increased 2,3 DPG concentration in RBC  It is slightly less than 70% at 20,000 feet and much less at higher altitudes  When haemoglobin saturation falls bellow 60% serious cellular dysfunction occurs, and if prolonged, can cause death
  • 19. Accommodation..(cont)  On digestive system o loss of appetite o Nausea, vomiting  On kidney o Alkaline urine due to increased erythropoietin secretion  On CNS o Depression, o Apathy, o Talkative, o Disorientation, o Loss of power of judgement o Impaired memory, o Fatigue, o Lack of cordination o Sudden LOC
  • 20. High Altitude & Cellular metabolism High altitude Low partial pressure of O2 Decrease PAo2 Decrease PaO2 Decrease oxidative phosphorylation Decrease ATP
  • 21. Effect of expansion of gases  According to Boyle’s law , as the atmospheric pressure decreases with altitude, volume of gases increase proportionately  On GIT Painful distension of stomach and intestine  On lungs Expansion of gases may destroy alveoli  Rapid ascent may cause Decompression sickness
  • 22. Effect of fall in Temperature  Atmospheric temperature falls by 2°C for every 1000 ft increase in altitude  EFFECTS - Cutaneous vasoconstriction - Prolonged and severe vasoconstriction may lead to tissue damage known as frost bite
  • 23. Effect of UV rays Manifestations  Skin irritation  Photokeratitis  Photoconjunctivitis Recomendations - Sunscreen (atleast30 SPF) - Sunglass (polycarbonate or CR-39 LENS) For every 1000 ft - 4-8% more UVB exposure So, at8000 ft- >30% more exposure
  • 24. Clinical Syndromes In High Altitude  Acute high altitude headache (HAH) With hurried assent many (80%) will report - transient headache  Acute Mountain Sickness (AMS)  High Altitude Cerebral Edema (HACE)  High Altitude Pulmonary Edema (HAPE)  Chronic Mountain Sickness (CMS)  RVH,Low birth wt,cong heart disease-Present in some resident
  • 25. Acute Mountain Sickness  Symptom complex  Occurs in an individual who residing at sea level, when he ascends to high altitude over a period of 1-2 days for first time.  The symptoms develops 8-24 hours after arrival at high altitude  Last for 4-8 days
  • 26. Lake Louise symptom Score symptoms severity pointssymptoms severity points Headache No Headache 0 Mild Headache 1 Moderate Headache 2 Severe Headache 3 Gastrointestinal No GI symptoms 0 Poor appetite/nausea 1 Moderate nausea/vomiting 2 Severe nausea/incapacitating 3 Fatigue /Weakness No 0 Mild 1 Moderate 2 Severe 3
  • 27. Symptoms Severity Points Dizziness/Light headedness No 0 Mild 1 Moderate 2 Severe 3 Difficulty of Sleeping Slept as well as Usual 0 Sleep as well as usual 1 Woke up many times, poor night’s sleep 2 Unable to sleep 3 o Self report score o Diagnosis of AMS based on recent rise in altitude, presence of headache, with at least one of the other symptom o Total score >3 with no other of symptoms
  • 28. Treatment  Most patients- symptoms abate in 2-3 days without specific treatment  Mild to Moderate AMS- o O2 therapy o Large dose of glucocorticoids to decrease cerebral oedema o Acetazolamide-Decrease alkalosis by H+ excretion through kidney by inhibiting carbonic anhydrase enzyme o Descent  Severe symptoms/HACE- Transport to lower altitudes  Those who develop AMS- usually have a recurrence with future ascents unless they take preventive measures  AMS rarely cause death, unless evacuation of rare patients who have HACE to lower altitude
  • 29. High altitude pulmonary oedema  Occurs due to - rapid ascend - Heavy physical work during first 3-4 days after rapid ascent to high altitude  Mechanism Increased sympathetic activity Vasoconstriction Increase pulmonary capillary hydrostatic pressure Drives the fluid out of pulmonary capillary Pulmonary oedema  Treatment - O2 therapy - Ca Channel blocker –nifidipine - PDE inhibitor-Tadalafil (may worsen headache of AMS)
  • 30. High altitude cerebral oedema  Considered as ‘end stage‘ or severe AMS .  AMS with either change in mental status or ataxia or both  Mechanism - low PO2 arteriolar dilation normally compensated by cerebral auto-regulation reached the level of auto-regulation increase capillary pressure increase transudation CE  Treatment - large dose of glucocorticoids
  • 31. Chronic mountain sickness  Monge’s disease  Occurs in long term residents  EFFECTS -Extreme polycythemia -PAH -RVH -CHF -Peripheral arterial pulse begins to fall  These individual must be removed to a lower altitude to prevent rapid development of pulmonary oedema
  • 32. Acclimatization  Definition Change in body tissue in response to long-term exposure to high altitude hypoxia for a long time  When there is a fall in O2 following acclimatization occurs 1) Pressure during O2 transfer 2) O2 carrying capacity of blood 3) Ability of tissue to utilise O2
  • 33. Acclimatzation of respiratory system Prolonged hyper ventilation CO2 washout respiratory alkalosis renal compensation alkaline urine normalisation of blood & CSF PH withdrawal of central chemo-mediated respiratory depression increase in resting pulmonary vasodilation (by 5 fold),primarily due to increase in TV Sustained hyperventilation
  • 34. Other respiratory changes  Increase TLC [In high landers for generation] - evidenced by barrel shaped chest - leads to increase ventilatory capacity  Increase diffusing capacity of lung- hypoxic pulmonary vasoconstriction pulmonary hypertension increase no of pulmonary capillaries  Vascularity of the tissues More capillary opens up in tissue than at sea level (normal ~25% open at rest others at reserved)  This combined with systemic vasodilation(also a hypoxic response) More O2 delivery to tissues
  • 35. Change in Body  CVS HR,BP,CO Blood flow to vital organs like- heart, brain, muscle
  • 36. Change in Body  Blood  Increase haematocrit to60%  Increase Hb concentration to about 20%  Due to erythropoietin secretion  Tissue  Increased quantities of oxidative enzymes involved in metabolism  Increased number of mitochondria in cells  Increase myoglobin (O2 storing pigment)
  • 37. Physiological polycythemia Hypoxia induced Erythropoiesis Increased Hb & RBC Expansion of Blood volume Increased amount of Hb Haemodynamics is kept within normal limit inspite of increased vascularity of tissue Inspite of decrease saturation,O2 carrying capacity is maintained at normal limit
  • 38. Conditions aggravated by high altitude  Hypertension  Obstructive airway disease  CCF  SCD,2,3 DPG deficiency  Sleep apnoea  Cardiovascular ds  Seizure disorders  Such individuals should be cautious or completely abstain from visit to high altitude  ALL visitors to the hight of 5000 m or more should consult pulmonologist
  • 39.  Older age (>50) mildly protective against altitude sickness  Women higher risk O2 REQUIREMENT  SPO2 >95% - OK  SPO2 <92% - O2 needed  SPO2 (92-95%) - If concurrent heart & lung disease-give O2
  • 40. Recommendations If history of AMS/ Travel above 2500 m(8000 ft)  Acetazolamide 250 mg BID - 24 Hours before & 48 hours into stay  first night sleep at less than 9000 ft  Rest for 2-4 days - Vigorous exercise may cause AMI  Gradual activity increase over week  Alcohol, tranquilizers –avoid 2-7 says  Avoid salty food-increase BP  Carbohydrate - best fuel for high altitude (helps anaerobic &aerobic metabolism) Above 3500m(11,500 ft)  Acetazolamide  Dexamethasone  O2
  • 41. Contraindications Travel above 2000m  PULMONARY DISEASE - PAH - Severe COPD (GOLD3&4) - CO2 retention - Poorly controlled asthma  CVS - With in 3 months of AMI,CVA,ICD Implantation - UA, - Before planned coronary intervention - Heart Failure,NYHA> II - Congenital heart disease (Cyanotic & acyanotic)
  • 42. Travel to 2000-3000 m permissible  PULMONARY DISEASE - Stable COPD - Stable asthma under medical treatment  CVS - Asymptomatic CAD - Stable CAD - Normal performance capacity - Good BP controL - No illness affecting gas exchange
  • 43. Pediatrics for hypoxia &altitude sickness  Children <8 yrs - 4 fold risk Increase  Teens - twice risk increase Recommendations  absolutely no child above 35,00m (11,500ft)  young child not above 3000 m (10000 ft)  teen acclimatize above 3000m but take care
  • 44. Gamow bag Revolutionary invention in the treatment of high altitude illness  Carried in most Himalayan expeditions  A sealed chamber with a pump (6.3 kg)  The person is placed inside the bag  It is then fully inflated by pumping  Effectively increase O2 concentration of O2molecule
  • 45. Gamow bag  Stimulate a descent to lower altitude  In 10 min, it can create an atmosphere that can corresponds to that at 3,000- 5,000 feet lower)  After 1-2 hours in the bag, persons body chemistry will have “reset "to lower altitude  Last for 12 hours outside the bag  Enough time to walk them down to a lower altitude  Allow for further acclimatization