Partial Pressure Environmental Factors

Blood Gases: Altitude and Diving

• Atmospheric Pressure Basics: As altitude increases, the total atmospheric pressure ($P_{ATM}$) decreases because there is less weight of air pressing down on the person.

  • Sea Level: At sea level ($0\,ft$), $P_{ATM} = 760\,mm\,Hg$.

  • 10,000 Feet: At this altitude, $P_{ATM} = 523\,mm\,Hg$.

  • 30,000 Feet (Mount Everest): At this extreme altitude, $P_{ATM} = 226\,mm\,Hg$.

• Gas Composition Consistency: The percentage (%) of individual gases in the air (e.g., Oxygen, Nitrogen) does not change significantly as altitude increases. Therefore, the partial pressure of oxygen ($P_{O_2}$) remains approximately $20\%$ of the total $P_{ATM}$.

• Partial Pressures of Oxygen at Various Altitudes:

  • $0\,ft$ (Sea Level):

    • $P_{ATM} = 760\,mm\,Hg$

    • $P_{O_2}$ of Air: $159\,mm\,Hg$

    • $P_{O_2}$ in Alveoli: $104\,mm\,Hg$

  • $10,000\,ft$:

    • $P_{ATM} = 523\,mm\,Hg$

    • $P_{O_2}$ of Air: $110\,mm\,Hg$

    • $P_{O_2}$ in Alveoli: $67\,mm\,Hg$. At this point, the lungs are functioning at their functional residual capacity.

  • $30,000\,ft$:

    • $P_{ATM} = 226\,mm\,Hg$

    • $P_{O_2}$ of Air: $47\,mm\,Hg$

    • $P_{O_2}$ in Alveoli: $18\,mm\,Hg$

  • Drop in alveolar PO2 as altitude increases will alter Hb saturation

Hemoglobin ($Hb$) Saturation and Supplemental Oxygen

• The Impact of Altitude on Alveolar $P_{O_2}$: The drop in alveolar $P_{O_2}$ directly affects hemoglobin saturation ($Hb\,SAT$).

• Breathing Ambient Air:

  • Sea Level:$Hb\,SAT$: $97\%$.

  • $10,000\,ft$:$Hb\,SAT$: $90\%$.

  • $30,000\,ft$: $Hb\,SAT$: $24\%$.

• Breathing $100\%$ Oxygen ($O_2$):

  • Sea Level:$Hb\,SAT$: $100\%$ .

  • $10,000\,ft$ : $Hb\,SAT$: $100\%$.

  • $30,000\,ft$: $Hb\,SAT$: $99\%$.

• Safety Thresholds: Breathing regular air up to $10,000\,ft$ keeps hemoglobin saturation in the safe range (greater than $90\%$). However, breathing supplemental pure oxygen can keep $Hb$ almost fully saturated even at altitudes as high as $30,000\,ft$.

Acute Physiological Response to High Altitude

• Initial Arterial Drop: Upon reaching higher altitude, the arterial $P_{O_2}$ drops immediately (e.g., from a normal arterial $P_{O_2}$ of $~95\,mm\,Hg$ down to $~60\,mm\,Hg$ at $10,000\,ft$).

• Chemoreceptor Activation: This drop in arterial oxygen is sensed by peripheral chemoreceptors, specifically the carotid and aortic bodies.

  • Respiratory Response: These receptors cause an increase in Respiratory Rate and Tidal Volume (deeper breaths).

  • Goal: This increases Minute Ventilation of the Alveoli, attempting to make alveolar air look more like the air being breathed.

  • Limitation: Despite these efforts, only modest increases in alveolar $P_{O_2}$ are achieved initially.

• Acute Hypoxia Symptoms: These effects typically begin above $12,000\,ft$ and include:

  1. Drowsiness.

  2. Mental Fatigue.

  3. Muscle Fatigue (which is noted as being particularly dangerous for pilots).

  4. Headache.

  5. Nausea.

  6. Euphoria.

Acclimatization Processes

• Overview: If an individual remains at high altitude for days to weeks, the body undergoes acclimatization to maintain homeostasis.

• Key Changes During Acclimatization:

  1. Increased Pulmonary Ventilation: Significant increase in the volume of air moved.

  2. Increased Red Blood Cell Count and Hemoglobin ($Hb$): Enhances oxygen carrying capacity.

  3. Increased Diffusing Capacity of the Lungs: Improves the efficiency of gas exchange.

  4. Increased Vascularity of Peripheral Tissues: More blood vessels reaching the cells.

  5. Increased Efficiency of Oxygen Utilization: Cells (mitochondria) adapt to operate at lower oxygen needs.

• Blood Gas Data: Acute vs. Acclimatized states:

  • Alt $0\,ft$: $P_{CO_2}$: $40\,mm\,Hg$; $P_{O_2}$: $104\,mm\,Hg$; $Hb\,SAT$: $97\%$.

  • Alt $10,000\,ft$ (Acute): $P_{CO_2}$: $36\,mm\,Hg$; $P_{O_2}$: $67\,mm\,Hg$; $Hb\,SAT$: $90\%$

  • Alt $10,000\,ft$ (Acclimatized): $P_{CO_2}$ drops to $23\,mm\,Hg$; $P_{O_2}$ increases to $77\,mm\,Hg$; $Hb\,SAT$: $92\%$

  • Alt $30,000\,ft$ (Acute): $P_{CO_2}$: $24\,mm\,Hg$; $O_{O_2}$: $18\,mm\,Hg$; $Hb\,SAT$: $24\%$

  • Alt $30,000\,ft$ (Acclimatized): $P_{CO_2}$: $10\,mm\,Hg$; $P_{O_2}$: $30\,mm\,Hg$; $Hb\,SAT$: $~38\%$

• Summary of Blood Gas Shifts: Acclimatization produces small increases in $P_{O_2}$ but large decreases in $P_{CO_2}$. The severe drop in $P_{CO_2}$ results in Respiratory Alkalosis (increased blood pH).

Mechanisms of Acclimatization

• Pulmonary Ventilation Changes:

  • Immediate (Seconds): Decreased arterial $O_2$ stimulates carotid/aortic bodies, increasing alveolar ventilation to $1.65\times$ normal.

  • The Respiratory Brake: Hyperventilation lowers $P_{CO_2}$. This is sensed by central chemoreceptors in the medulla. Because low $CO_2$ (alkalosis) inhibits breathing, the central chemos limit the initial ventilation increase to that $1.65\times$ level.

  • Kidney Compensation: Over several days, the kidneys secrete bicarbonate ($HCO_3^-$) and retain fewer hydrogen ions ($H^+$), making urine less acidic and returning blood pH back toward $7.4$.

  • Full Acclimatization (Several Days): Once the pH is adjusted, the central chemoreceptors "reset" to a lower level of $P_{CO_2}$. This removes the respiratory brake, allowing ventilation to increase to $5\times$ normal.

• Red Blood Cells and Hemoglobin:

  • Mechanism: Hypoxia for several weeks triggers the kidneys to produce the hormone Erythropoietin.

  • Target: Erythropoietin stimulates hematopoietic stem cells in the bone marrow.

  • Result: Red blood cell production increases. Hematocrit rises from a normal range of $40$ to $45\%$ up to $60\%$. Total blood volume also increases by $20$ to $30\%$. Combined, this leads to a total $Hb$ increase of approximately $50\%$.

    • Increased O2 transport

• Increased Diffusing Capacity:

  • Oxygen's ability to cross from the alveoli into the blood can increase by $3$-fold.

  • Capillary Volume: Increased capillary blood volume in the lungs provides more surface area for gas exchange.

  • Alveolar Volume: Increased volume of alveoli leads to a larger surface area for diffusion, often manifesting as a "barrel chest."

  • Pulmonary Hypertension: Increased pulmonary blood pressure forces blood into underperfused (usually upper) alveoli, increasing overall efficiency.

  • Risk: Elevated pulmonary pressure increases the threat of pulmonary edema and poses a greater risk of heart failure.

• Vascularity and Cellular Efficiency:

  • Cardiac Output: In the acute phase, hypoxia triggers a $~30\%$ increase in cardiac output to transport more oxygen. Over weeks, this return to normal as the Hematocrit (HCT) increases.

  • Angiogenesis: New blood vessel growth occurs over weeks due to local hypoxia. This is less effective in older individuals (as suggested by the note: "remind me to forget about Machu Picchu!").

  • Native Populations: Groups inhabiting high altitudes for generations (e.g., Sherpas, Peruvians) show increased mitochondria and electron transport proteins. Physical traits include barrel chests, small bodies, high cardiac output, large hearts, and high $Hb$/HCT.

Physiology of Diving

• Pressure Changes Under Water: For every $33\,ft$ traveled underwater, the total gas pressure increases by $1\,ATM$.

  • $0\,ft$ (Sea Level): $1\,ATM$; Gas volume = $1\,L$.

  • $33\,ft$: $2\,ATM$; Gas volume = $0.5\,L$ (compressed).

  • $66\,ft$: $3\,ATM$; Gas volume = $0.33\,L$.

  • $99\,ft$: $4\,ATM$; Gas volume = $0.25\,L$.

  • Result: Lungs gets compressed as gases are compacted under pressure.

    • As total pressure increase so do partial pressures, opposite to increase in altitude

• Gas Compression in the Body: High pressure "packs" gases like Nitrogen ($N_2$), Oxygen ($O_2$), and Carbon Dioxide ($CO_2$) into the blood, tissues, and joints.

• Decompression Sickness ("The Bends"): When ascending (arising), a diver must give Nitrogen time to escape the tissues. If the ascent is too fast, Nitrogen cannot escape into the blood and then the lungs; instead, it forms expanding bubbles in the blood, which can lead to death.

• Nitrogen Narcosis: At a depth of approximately $250\,ft$, the partial pressure of Nitrogen ($P_{N_2}$) is about $8\times$ normal. This high concentration causes effects similar to intoxication/drunkenness.

• Oxygen Poisoning: While $P_{O_2}$ levels are usually "good" as one dives down (more $O_2$ forced into solution), once pressure reaches around $4\,ATM$, the extremely high $P_{O_2}$ can cause acute oxygen poisoning, leading to disorientation, seizures, and coma. To dive deeper, divers must use gas mixtures with lower $O_2$ and $N_2$, often substituting Nitrogen with Helium.

• Breath-Holding and Diving (Amah Pearl Divers):

  • $P_{CO_2}$ increases at depth and causes the "urge to breathe."

  • Amah Whistle: Pearl divers hyperventilate at the surface to "blow off" as much $CO_2$ as possible to delay the urge to breathe while underwater. They whistle to add resistance and control the hyperventilation process.

  • Drowning Danger: If they hyperventilate too much, their $P_{O_2}$ might drop to dangerously low levels before the $P_{CO_2}$ rises enough to signal they need to breathe, leading to loss of consciousness (shallow water blackout) and potential drowning upon ascent.