Environmental Physiology

(Hypo & Hyperbaric) Conditions

HPHS 112
Dr Lindokuhle Mabuza-Mashaba ([email protected])

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 Introduction
 Earth’s Atmosphere

 20.95% Oxygen

 78.0 % Nitrogen

 0.038 % Carbon Dioxide

 Trace elements

 Oxygen – Produced by photolysis, photosynthesis

 Carbon dioxide – Produced by oceans, animal respiration, plant decay, burning of fossil fuels

 All aerobic life is dependent on the presence of oxygen for metabolic energy

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 Introduction
 Variations in gas concentrations from that normally found in the atmosphere at sea
level can have significant influences on human physiology as evidenced primarily
as changes in:
 Pulmonary function

 Metabolism

 Neurologic

 These physiological changes have relevance to the use of respiratory protective

devices (RPDs)
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 Gaseous Exchange
 Gas exchange in humans occurs in the lungs

 Inhaled air is conducted via the airways to the alveoli

 Alveoli are in close proximity to blood capillaries – gas exchange between alveoli and capillaries
is driven by diffusion gradients
 Oxygen is transported by diffusion from the alveoli to the blood and is transported by the
hemoglobin in red blood cells
 Carbon Dioxide – produced metabolically – is carried from the blood to the alveoli where it is
exhaled to the atmosphere

 The exchange is rapid and normally occurs regardless of the level of physical activity

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The Alveoli-Capillary Relationship

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 Central and Peripheral Chemoreceptors
Detect changes in pH, PaO2, and PaCO2 in the blood resulting in a ventilatory
response

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 Hypercarbia
 Hypercarbia is an increase in CO2 in the bloodstream.

 CO2 is a by-product of aerobic metabolism.

 Increased CO2 in the body results in important physiological responses throughout the body.

 CO2 is a potent stimulus of pulmonary minute ventilation

 Acts by stimulating chemoreceptors in the carotid bodies and respiratory control centers in the
brain and brainstem

 Changes in ventilation in response to CO2 production keeps alveolar PCO2 produced CO2 in
dynamic equilibrium

 CO2 is also a potent stimulus of cerebral vasodilation and blood flow

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 Hypercarbia
 Hypercarbia can result from:

 Hypoventilation: low breathing rate allows build-up of CO2 (e.g., deliberate

“skip-breathing” by SCUBA divers).

 Malfunctioning respirator can lead to increased re-breathing of CO 2.

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 Hypercarbia – Summary of Physiological
Effects
 CO2 can induce:

 Visual disturbances
 Headache
 Reduction in reasoning ability
 A sense of “air hunger” or dyspnea

 CO2 can act as an anesthetic and can cause unconsciousness

 CO2 can alter the intracellular pH thus having effects on metabolism (also probable mechanism for

inert gas narcotic effect)

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 Hypercarbia – Summary of
Exposure/Activity Limits
At Rest Very, very high work rate
(65 W·m 2) (400 W·m 2)
Average %CO Exposure Potential effects Exposure
( Displacement 2 Limit and/or Limitations Limit
of Oxygen in ( time ) ( time )
air)
1.5 No restrictions on Indefinite Increase in ventilation unknown
activity exposure
2.5 Increase in ventilation unknown Increase in ventilation 2 hours
3.0 Increase in ventilation 15 hours Increase in ventilation 30 min
No restrictions within the
exposure limit
5.0 Increase in ventilation 8 hours Increase in ventilation 5 min
No restrictions within the Collapse /
exposure limit unconsciousness
7.0 Increase in ventilation <30 min Collapse / n/a
Severe limitations on unconsciousness
activity
10.0 Increased heart rate <2.0 min Collapse / n/a
Collapse / unconsciousness
unconsciousness

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 Respiratory & Metabolic Acidosis and Alkalosis
 Respiratory acidosis:
 Metabolic Acidosis:
 pH decreases
 pH decreases
 Increased arterial PCO2
 No change in PCO2
 Compensation: excretion of H+ ion and retention of
 Compensation: Hyperventilation remove CO 2 which deceases PCO2.
HCO3- ions by kidneys


 Compensation: excretion of H+ ion and retention of HCO3- ions by
Respiratory alkalosis:
kidneys.
 pH increases
 Metabolic Alkalosis:
 Decreased arterial PCO2
 pH increases
 Compensation: retention of H ion and excretion of
+

HCO3- ions by kidneys  No change in PCO2

 Compensation: hypoventilation retains CO2 , which increases PCO2.

 Compensation: retention of H+ ion and excretion of HCO3- ions by kidneys.

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Respiratory & Metabolic Acidosis and Alkalosis

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Physical Activity at High
Altitude

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Categorization For Descriptive Convenience

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 Physiologically critical altitudes:
 Up to 10,000 ft (3,000 m) “safe zone of rapid ascent” classically defines
‘high altitude’

 At 18,000 ft (5,500 m) upper limit of permanent human inhabitation

 Above 20,000 ft (6,000 m) life is endangered without supplemental oxygen

 At 25,000 to 30,000 ft O2 supplement has to be started. Called Critical Survival

Altitude.

 From 40,000 ft(12,000 m) Ozone layer starts

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 Altitude
 Mount Everest

 29,028 ft (8848mt) (previously 8840m)

 Atmospheric Pr = 255mmHg

 PO2= 53mmHg

 Inspired PO2 = 44mmHg

 Unacclimatized person

 Unconscious in 45 seconds

 Dead in 4 to 6 minutes

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Physiological responses to high altitude hypoxia:

 Divided into following two

1. Acute responses (accommodation)
2. Long term responses (acclimatization)
Accommodation
 Refers to immediate reflex adjustments of respiratory and
cardiovascular system to hypoxia
Acclimatization
 Refers to changes in body tissues in response to long term exposure
to hypoxia
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 Accommodation At High Altitude
 Immediate reflex responses of the body to acute hypoxic exposure.

A) Hyperventilation:

 Decrease arterial PO2 stimulation of peripheral chemo receptors increased rate & depth of
breathing.

B) Tachycardia:

 Also stimulate peripheral chemo receptors increase Cardiac Output increase oxygen delivery to the
tissues.

C) Increased 2,3-DPG concentration in RBC:

Within hours, ↑deoxy-Hb conc. locally ↑pH  ↑2,3-DPG ↓oxygen affinity of Hb tissue O2
tension maintained at higher than normal level.

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D) Neurological :
 Considered as “warning signs”
 Depression of CNS feels lazy, sleepy, headache
 ‘Release Phenomena’ like effect of alcohol, lack of coordination, slurred
speech, slowed reflexes, overconfidence
 At further height cognitive impairment, poor judgment, twitching,
convulsion & finally unconsciousness

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 Acclimatization at high altitude:
 Various physiological readjustments and compensatory mechanisms in body that
reduces the effects of hypoxia in permanent residents at high altitude.
 It is done by:
 A great increase in pulmonary ventilation
 Increase diffusion capacity of lung
 Increased ability of the tissue cells to use O2
 Increased vital capacity

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 Respiratory alkalosis
 Cheyne-Stokes Respirations

 Increased erythropoietin
 Increased no of RBC
 Increased blood volume
 Increased Cardiac output
 Increased vascularity of the peripheral tissues
 Alkaline urine

Cellular Acclimatization
 Increased mitochondria
 Increased Cytochrome Oxidase
 Increased Myoglobin
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 1. Sustained Hyperventilation

 Prolonged hyperventilation  CO2 wash-out  respiratory alkalosis renal compensation

alkaline urine normalization of pH of blood & CSF withdrawal of central chemo- mediated
respiratory depression  net result is ↑resting pulmonary ventilation (by ~5 folds ) primarily due to
↑ in TV (upto 50% of VC)
 Such powerful ventilatory drive is also possible as
 ↑sensitivity of chemo receptor to PO2 & PCO2

 ↓ in work of breathing  make hyperventilation easy & less tiring

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 2. Other Respiratory Changes
 ↑ TLC: Especially in high-landers evidenced by relatively
enlarged (barrel-shaped) chest↑ventilatory capacity in relation to
body mass.

 ↑ Diffusing capacity of lungs: due to hypoxic pulmonary

vasoconstriction  Pulmonary Hypertension  ↑ no. of
pulmonary capillaries.
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 3. Increase Vascularity of the Tissues
 More capillaries open up in tissues than at sea-level (normal ~25 %
open & rest—remaining as ‘reserve’).
 Growth of new circulatory capillaries in non pulmonary tissues
(angiogenesis).
 This combined with systemic vasodilatation (also a hypoxic response)
will result into more O2 delivery to tissues.

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 4. Cellular level changes

↑ intracellular mitochondrial density

↑ conc. of cellular oxidative enzymes

↑ synthesis of Mb (O2-storing pigment)

→ all aimed to improve O2 utilization.

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 CVS Changes

 Cardiac output often increases as much as 30% immediately, then

gradually return to normal in one to two weeks as the blood
hematocrit increases.
 Capillary density in right ventricle muscle increases because of the
combined effects of hypoxia and excess workload on the right ventricle
caused by pulmonary hypertension at high altitude.

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 Cheyne-Stokes Respirations
 Above 10,000 ft (3,000 m) most people experience a periodic breathing during sleep. Repeated
sequence of gradual onset of apnoea followed by gradual restoration of respiration.

 Respirations may cease entirely for a few secs & then shallow breaths begin again. During period of
breathing-arrest, person often becomes restless & may wake with a sudden feeling of suffocation.

 Can disturb sleeping patterns exhausting the climber. Acetazolamide is helpful in

relieving this.

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Respiratory Responses at High Altitude

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Clinical syndromes caused by high altitude
(Hazard of rapid ascent)
 High altitude pulmonary oedema (HAPO)
 Acute mountain sickness.
 Chronic mountain sickness.

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 High altitude pulmonary edema (HAPO)
 Above 10000 ft.
 75-80% in persons doing heavy physical work in first 3-4 days
 Persons who acclimatized to high altitude, stay at sea levels for > 2 weeks and again rapidly re-
ascend.
 Characteristics

 Life-threatening form of non-cardiogenic pulmonary edema due to aggravation of hypoxia

 Not develop in gradual ascent & on avoidance of physical exertion during first 3-4 days of
exposure.

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 HAPO Manifestations
 Earliest indications are ↓exercise tolerance & slow recovery from exercise. The
person feels fatigue, weakness & exertional dyspnoea .

 Condition typically worsens at night & tachycardia and tachypnea occur at rest.

 Symptoms: Cough, frothy sputum, cyanosis, rales & dyspnea progressing to

severe respiratory distress

 Other common features-- low-grade fever, respiratory alkalosis, &

leucocytosis

 In severe cases- an altered mental status, hypotension, and ultimately death may
result.

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Mechanism of development of HAPO
Sympathetic activation by physical work is over &
above sympathetic stimulation by hypoxia & cold.

Vasoconstriction

Increase in pulmonary capillary hydrostatic pressure

(10 – 25mmHg).

Increase in capillary pressure drives the fluid out of

pulmonary capillaries.

Develops pulmonary oedema

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 Treatment of HAPO
 Standard & most to descend to lower altitude as quickly as possible( preferably by at least 1000
meters) & to take rest.

 Oxygen should also be given (if possible).

 Symptoms tend to quickly improve with descent, but less severe symptoms may continue for
several days.

 The standard drug treatments for which there is strong clinical evidence are dexamethasone & CCB’s
(like nifedipine).

 PDE inhibitors (e.g. tadalafil) are also effective.

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 Acute mountain sickness
 Occurs when person from sea level ascend to high altitude within 1-2 days for the
first time
 Develop within 8-24 hrs & lasts for 4-8 days.

 More likely if :
 Rapid ascent
 Lack of acclimatization

 Symptoms- nausea, vomiting, headache, dizziness ,irritability, insomnia &

breathlessness.
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 Cause exactly not known. Appears to be associated with Cerebral oedema (↓pO2 --
arteriolar dilatation- limit of cerebral

 Autoregulatory mechanisms are crossed ↑capillary pressure ↑fluid passage

through capillaries into brain tissue) or Alkalosis

 In the minority, more serious sequelae – high-altitude pulmonary edema and high-
altitude cerebral oedema develop.
 If remain untreated , it may cause: Ataxia, Disorientation, coma & Finally Death
(due to tentorial herniation of the brain-tissue)

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 Definition
 Hyperbaric Oxygen Therapy is the administration of
oxygen at pressure greater than sea level.
 Patient is placed in a chamber and pressurized
 100% oxygen
 Room air with oxygen via a hood
 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.

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 Clinical Uses and Therapeutic Effects of
Hyperbaric Oxygen
 Hyperoxygenation of tissues
 Mechanical Bubble Crunching
 Bactericidal / Bacteriostatic Effects
 Potent Vasoconstriction

 Hyperoxygenation of Tissues

 Plasma diffuses through tissue, supplying oxygen downstream from an occlusion

 Helps ischemic tissues meet metabolic needs during the wound healing process

 Increased breakdown of old bone

 Forms new capillaries in wound areas

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 Hyperoxygenation is a temporary measure maintaining tissue viability until
corrective measures are implemented or new blood supply is established

 Exceptional Blood Loss Anemia

 The Role of Hyperbaric Oxygen Therapy.

 Two organs at risk: heart and brain.

 Corrects accumulating oxygen debt in patients who cannot receive or refuse

transfusion.

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 RISKS ASSOCIATED
 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.
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 Summary
 Whereas oxygen is necessary for life and vital for aerobic metabolism, and
 Carbon dioxide is a normal product of aerobic metabolism and is an important
regulator of physiological function
 High levels of oxygen, especially under hyperbaric conditions is toxic and can be
fatal
 Low levels of oxygen at sea level or at altitude can result in asphyxia and death
 High levels of carbon dioxide can result in asphyxia and death

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“All things are poison and nothing is without
poison, only the dose makes something not a
poison”
Paracelsus (1493-1541)

Swiss Physician and Alchemist

Thank You…
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