High Altitude Physiology Quiz

Physiology Lecture: Aviation, High Altitude, and Space Physiology

• Topic: Aviation, high altitude, and space physiology
• Instructor: Glenn Nathaniel S.D. Valloso, MD, DPSP
• Academic year: 2024-2025

Physiological Challenges at High Altitudes and in Space

• Altitude Effects: Reduced atmospheric pressure lowers oxygen availability.
• Low Gas Pressure: Alters oxygen and carbon dioxide exchange, impacting body function.
• Weightlessness: Affects muscle mass, bone density, and fluid distribution.
• Acceleratory Forces: Stress cardiovascular and musculoskeletal systems.
• Significance: Enhances safety in aviation, mountain climbing, and space exploration. Supports understanding of adaptation in extreme environments.

Effects of Low Oxygen Pressure on the Body

• Barometric Pressure Variation: Sea level: 760 mm Hg, ~159 mm Hg Po2. 10,000 feet: 523 mm Hg, ~110 mm Hg Po2. 50,000 feet: 87 mm Hg, ~18 mm Hg Po2.
• Impact of Reduced Barometric Pressure: Proportional decrease in oxygen availability. Primary cause of hypoxia at high altitudes.

Table 44-1: Effects of Acute Exposure to Low Atmospheric Pressures

• Presents data on alveolar gas concentrations and arterial oxygen saturation at various altitudes.
• Data includes barometric pressure, P02 in air, P02 in alveoli, arterial oxygen and saturation at different altitudes (0, 10,000, 20,000, 30,000, 40,000, 50,000 feet).
• Acclimatized values are also included in parentheses.

Alveolar Po2 at Different Elevations

• Dilution of Alveolar Oxygen: Water vapor pressure remains constant at 47 mm Hg regardless of altitude. CO2 partial pressure (Pco2) at sea level: 40 mm Hg, high altitude: ~7 mm Hg. Acclimatized individuals have increased ventilation.
• Impact on Alveolar Po2 at 29,028 ft (Mount Everest): Barometric pressure is 253 mm Hg. Remaining pressure after accounting for water vapor and CO2 is 199 mm Hg. Alveolar Po2 is approximately 35 mm Hg in acclimatized individuals.
• Survival Considerations: Breathing pure oxygen dramatically improves oxygenation and survivability at this altitude.

Alveolar Po2 at Different Altitudes

• Alveolar Po2 decreases with altitude. At sea level: Alveolar Po2 = 104 mm Hg, 20,000 feet: unacclimatized = 40 mm Hg, acclimatized = 53 mm Hg. Difference due to increased alveolar ventilation in acclimatized individuals.

Saturation of Hemoglobin with Oxygen at Different Altitudes

• Up to 10,000 feet: Breathing air: Arterial O2 saturation is ≥ 90%.
• Above 10,000 Feet: Rapid decrease in arterial O2 saturation. At 20,000 feet, slightly below 70%. Higher altitudes: O2 saturation significantly decreases. Breathing O2 can mitigate these effects.

Effect of Breathing Pure Oxygen on Alveolar Po2 at Different Altitudes

• At 30,000 feet, alveolar Po2 increases from 18 mm Hg (air) to 139 mm Hg (pure O2).
• Arterial O2 saturation while breathing pure O2 is >90% up to 39,000 feet. Rapid decline to 50% at 47,000 feet.

The "Ceiling" When Breathing Air vs. Pure Oxygen

• Comparison of arterial O2 saturation curves: at 47,000 feet, arterial O2 saturation with pure O2 is about 50%, equivalent to saturation at 23,000 feet when breathing air.
• Ceiling altitude limits: breathing air: ≈23,000 feet; breathing pure O2: ≈47,000 feet, assuming optimal O2 equipment performance.

Acute Effects of Hypoxia in the Unacclimatized Person

• Symptoms at ~12,000 feet: drowsiness, lassitude, mental and muscle fatigue, headache, nausea, sometimes euphoria.
• Progression at higher altitudes: twitching, seizures at 18,000 feet; coma and death at 23,000 feet ("Ceiling" at breathing air)
• Impact on mental proficiency: 15,000 feet for 1 hour = 50% of normal efficiency; after 18 hours at 15,000 feet, = 20% of normal efficiency.

Acclimatization to Low Po2

• Adaptation at high altitudes: Reduced hypoxic effects over time. Enables harder physical work and ascension to higher altitudes.
• Key physiological changes: Increased pulmonary ventilation; higher red blood cell count; enhanced lung diffusing capacity; improved vascularity of peripheral tissues; enhanced cellular oxygen utilization.

Increased Pulmonary Ventilation - Role of Arterial Chemoreceptors

• Immediate response to low Po2: Arterial chemoreceptors stimulate ventilation (~1.65x normal), allowing ascent to higher altitudes.
• Prolonged high-altitude exposure (days): Ventilation increases up to 5x normal, Initial CO2 loss reduces Pco2 and increases body fluid pH, temporarily inhibiting respiratory drive. Mechanisms of adjustment over days include reduced bicarbonate in cerebrospinal fluid and brain tissues restoring respiratory center sensitivity; kidney compensation. Decreases hydrogen ion secretion, increases bicarbonate excretion, restoring plasma and cerebrospinal fluid pH toward normal.

Increase in Red Blood Cells and Hemoglobin During Acclimatization

• Hypoxia triggers red blood cell production. Hematocrit increases from 40%-45% to about 60%. Hemoglobin concentration rises from 15 g/dl to approximately 20 g/dl. Blood volume also increases by 20%-30%. Total body hemoglobin increases by 50% or more, combining effects of increased hematocrit, hemoglobin, and blood volume.

Increased Diffusing Capacity During Acclimatization

• Normal O₂ diffusing capacity: 21 ml/mm Hg/min, increases 3-fold during exercise and high altitude. Contributing factors: increased pulmonary capillary blood volume expanding capillaries, increasing diffusion surface area, increased lung air volume enlarging the alveolar-capillary interface, Higher pulmonary arterial pressure improving capillary recruitment, particularly in poorly perfused upper lung regions.

Peripheral Circulatory Changes During Acclimatization

• Initial increase in cardiac output: Rises by up to 30%, normalizing as hematocrit increases. Angiogenesis: Growth of systemic capillaries, most prominent in animals bred at high altitudes, and active tissues under chronic hypoxia. Right ventricular adaptation: Increased capillary density due to hypoxia and pulmonary hypertension.

Cellular Acclimatization to High Altitude

• Enhanced mitochondrial function: Animals at 13,000–17,000 feet have increased mitochondria and oxidative enzymes. Presumed adaptation in humans: high-altitude-acclimatized individuals likely utilize oxygen more efficiently than sea-level residents.

Hypoxia-Inducible Factors (HIFs): The Master Switch for Hypoxia Response

• Function: DNA-binding transcription factors activated by low oxygen levels.
• Activated Genes include Vascular Endothelial Growth Factor (VEGF), Erythropoietin genes, Mitochondrial genes, Glycolytic enzymes, Nitric oxide genes.
• Mechanism: HIFs are downregulated in normoxia by HIF hydroxylases. Hypoxia inactivates HIF hydroxylases, enabling HIF complex formation and gene activation.

Natural Acclimatization of High-Altitude Natives

• Population Characteristics: Live above 13,000 feet, some even at 19,000 feet. Exhibit superior acclimatization compared to lowlanders, even after decades at high altitudes.
• Key Adaptations: Increased chest size relative to body size; larger hearts; enhanced oxygen delivery; higher hemoglobin levels; greater O2 content in arterial blood despite low Po2; efficient oxygen utilization with minimal reduction in venous Po2.

Reduced Work Capacity at High Altitudes and Benefits of Acclimatization

• Work Capacity Decline: Hypoxia significantly reduces muscle work capacity (cardiac and skeletal), proportionally decreasing work capacity with maximum O₂ uptake.
• Impact of Acclimatization: Acclimatization significantly improves work capacity at high altitudes. At 17,000 feet: Naturally acclimatized natives maintain work output similar to lowlanders at sea level, while acclimatized lowlanders show improvement but cannot match native performance.

Acute Mountain Sickness and High-Altitude Pulmonary Edema

• Acute Mountain Sickness: Affects individuals who rapidly ascend to high altitudes; symptoms appear within hours to 2 days. Causes include acute cerebral edema and acute pulmonary edema.
• Causes of Acute Mountain Sickness (AMS): Local vasodilation, increasing capillary pressure, fluid leakage, swelling of brain regions. (involves inflammatory cytokines). Involvement of vascular endothelial growth factor (VEGF).
• Acute Pulmonary Edema: caused by uneven pulmonary arteriole constriction and fluid leakage/swelling in lung areas due to severe hypoxia. Increased capillary pressure in some areas causing this localized, spreading edema. Breathing oxygen can rapidly reverse symptoms.

Chronic Mountain Sickness

• Key Effects: Excessively high red blood cell mass and hematocrit; elevated pulmonary arterial pressure beyond normal acclimatization; enlargement of the right side of the heart; decreased peripheral arterial pressure. Congestive heart failure and possible death without descent to lower altitude are possible.
• Causes: Increased blood viscosity, pulmonary vasoconstriction, increased pulmonary shunt.

Effects of Acceleratory Forces on the Body

• Linear Acceleration: Felt during takeoff or launch. Deceleration: Experienced at the end of flight or landing. Centrifugal acceleration: Occurs during sharp turns or maneuvers. Body adapts to changes in velocity and direction.

Centrifugal Acceleratory Forces

• Formula: F=mv^2/r (f=Centrifugal Force, m=mass, v=velocity, r=radius of rotation). Mass, velocity and radius influence centrifugal force.
• Measurement in G-Forces: +1 G: Normal gravitational pull. +5 G: Experienced during pull-out from a dive; force is five times body weight. -1 G: Negative G when inverted; body weight counteracts seat belt restraint.

Effects of Centrifugal Acceleratory Force on the Body (Positive G) - Circulatory System

• Blood Pooling: Positive G forces push blood toward the lower body; venous pressure increases (standing: ≈450 mm Hg, sitting: ≈300 mm Hg). Impact on Cardiac Output: Blood pooling reduces the volume returning to the heart; cardiac output decreases as blood vessels in the lower body dilate.

Effects of Centrifugal Acceleratory Force on the Body (Positive G) - Blood Pressure Changes

• Blood Pressure Response: Initial drop in systolic and diastolic pressures; falls below 22 mm Hg in the upper body. Baroreceptor reflex recovery: systolic: ~55 mm Hg; diastolic: ~20 mm Hg. Critical Thresholds: +4 to +6 G causes blackout and unconsciousness; prolonged exposure can result in death.

Effects of Centrifugal Acceleratory Force on the Body - Effects on the Vertebrae

• Vertebral Risk: High acceleratory forces can cause vertebral fractures. Threshold: ≈ +20 G in a sitting position.

Effects of Centrifugal Acceleratory Force on the Body - Negative G

• Impact of Negative G: Negative G forces centrifuge blood into the head; head hyperemia: Up to -4 to -5 G causes intense head hyperemia; extreme negative G (e.g., -20G) increases cerebral blood pressure to 300-400 mm Hg.
• Risks: Brain Protection: Cerebrospinal fluid cushions brain vessels; reducing rupture risk. Redout: Eyes often experience hyperemia, leading to temporary blindness.

Protection Against Centrifugal Forces

• Protective Measures: Abdominal Compression: Tightening abdominal muscles and leaning forward delays blood pooling. Anti-G Suits: Apply positive pressure to legs and abdomen. Water Immersion: Theoretically balances G forces, but lung displacement limits safety to <10 G.

Effects of Linear Acceleratory Forces on the Body: Space Travel

• Space travel involves linear acceleration during blastoff and deceleration upon landing. Blastoff acceleration can peak at 9 G during first-stage booster, 8 G during second-stage booster. Astronauts sit in semireclining seats to withstand prolonged acceleratory forces. Deceleration at Mach 100 (interplanetary speeds) requires exponentially longer distances.

Deceleratory Forces in Parachute Jumps

• During freefall, velocity increases by 32 feet/sec per second due to gravity. Terminal velocity is reached at ≈12 seconds (109–119 mph). Parachute deployment: opening shock load up to 1200 lbs. Parachute slows descent to 20 feet/sec (1/81 of free fall impact). Trained parachutists land with bent knees, using muscles to absorb shock. Avoid fractures from extended-leg landings.

Artificial Climate in the Sealed Spacecraft

• Artificial Atmosphere: Essential for life support in space. Modern spacecraft atmosphere: oxygen (O2) to prevent suffocation; carbon dioxide (CO2) at low levels to avoid toxicity; nitrogen (N2) present in four times the concentration of O2 to reduce fire risks and prevent lung atelectasis; total pressure 760 mm Hg, similar to Earth's atmosphere.

Oxygen Recycling for Long-Duration Space Travel

• Challenges: Carrying adequate oxygen supplies is impractical for prolonged space travel. Recycling techniques: Physical methods (electrolysis of water); biological methods (algae photosynthesis using chlorophyll). No fully reliable recycling system exists yet.

Weightlessness (Microgravity) in Space

• Microgravity occurs in orbiting satellites or non-propelled spacecraft, not due to the absence of gravity, but due to equal acceleratory forces acting on the spacecraft and the person simultaneously. Results in floating within the spacecraft. Physiological Challenges include short-term issues (motion sickness, fluid translocation), and observed effects of prolonged exposure (reduced blood volume, red blood cell mass, muscle strength reduction, loss of calcium, phosphate, and bone mass).

Deconditioning During Prolonged Microgravity

• Impact on the Body: Cardiovascular system (reduced work capacity, blood volume, orthostatic tolerance, impaired baroreceptor reflexes) and muscle and bone (1% monthly bone loss, atrophy of cardiac and skeletal muscles). Challenges on return to Earth (difficulty standing upright, susceptibility to fractures from bone demineralization, weeks required to regain preflight fitness levels).

Countermeasures for Microgravity Effects

• Exercise Programs: Essential to mitigate deconditioning during space missions, requiring rigorous programs to prevent cardiovascular and musculoskeletal decline. Innovative Solutions: Artificial Gravity with intermittent centrifugal acceleration for ~1 hour daily to achieve forces of 2-3 G to mitigate the effects of microgravity.

Test your knowledge on the physiological challenges and adaptations related to high altitude exposure. This quiz covers various effects of reduced barometric pressure, arterial oxygen saturation, and acclimatization processes. Challenge yourself with questions on how the body responds to hypoxia and altitude changes.