Altitude and Diving Physiology Practice Questions

Q: A 28-year-old woman undergoes rapid ascent to 4500 meters altitude. She develops headache, nausea, and dyspnea within 6 hours. Which immediate compensatory mechanism is most responsible for maintaining oxygen delivery?

Hyperventilation driven by peripheral chemoreceptors. ***Hyperventilation driven by peripheral chemoreceptors*** - High altitude causes a decrease in **alveolar PO2**, which triggers the **carotid body chemoreceptors** to increase the respiratory rate within minutes. - This **hypoxic ventilatory response** increases oxygen levels and causes **respiratory alkalosis**, the most immediate physiological adaptation to hypoxia. *Polycythemia from increased erythropoietin* - **Erythropoietin** levels begin to rise within hours, but the production of new **red blood cells** takes several days to weeks to significantly impact oxygen-carrying capacity. - This is a **chronic adaptation** mechanism rather than an immediate compensatory response to acute ascent. *Increased cardiac output from myocardial hypertrophy* - While **cardiac output** increases acutely via increased heart rate, **myocardial hypertrophy** is a long-term structural change occurring over months or years due to chronic stress. - Acute exposure relies on **sympathetic activation** to increase heart rate, not cellular growth of the heart muscle. *Increased 2,3-DPG production in RBCs* - Levels of **2,3-Bisphosphoglycerate (2,3-DPG)** increase within 12 to 24 hours to shift the **oxygen-dissociation curve** to the right. - Although relatively fast, it is not as **immediate** as the ventilatory response triggered by peripheral chemoreceptors upon arrival at high altitude.

Q: Ascent to high altitude may cause all of the following except:

Cerebral palsy. **Explanation:** The physiological changes at high altitude are primarily driven by **hypobaric hypoxia** (low partial pressure of oxygen). **Why Cerebral Palsy is the correct answer:** Cerebral palsy is a non-progressive clinical syndrome resulting from an insult to the **developing fetal or infant brain** (typically due to birth asphyxia, infection, or trauma). It is a developmental neurological disorder and is not an acute or chronic manifestation of high-altitude exposure in adults or children. **Analysis of incorrect options:** * **Cerebral Edema (HACE):** High Altitude Cerebral Edema occurs due to hypoxia-induced cerebral vasodilation and increased capillary permeability (vasogenic edema). It is a life-threatening emergency. * **Pulmonary Edema (HAPE):** Hypoxia causes **hypoxic pulmonary vasoconstriction (HPV)**. When this is uneven or severe, it leads to increased pulmonary capillary hydrostatic pressure and leakage of fluid into the alveoli. * **Venous Thrombosis:** High altitude increases the risk of thromboembolism due to a "Virchow’s triad" effect: **Hemoconcentration** (increased hematocrit due to erythropoietin release), dehydration, and relative stasis during cold-induced inactivity. **High-Yield Clinical Pearls for NEET-PG:** * **HAPE** is the most common cause of death related to high altitude. * **Acetazolamide** (a carbonic anhydrase inhibitor) is the drug of choice for prophylaxis of Acute Mountain Sickness (AMS) as it induces metabolic acidosis, stimulating ventilation. * **Nifedipine** is used for the prevention/treatment of HAPE by reducing pulmonary artery pressure. * **Dexamethasone** is the drug of choice for HACE.

Q: What is the minimum altitude above sea level that a healthy person would need to ascend to rapidly to develop an alveolar PO2 of 60 mm Hg, potentially leading to altitude illness?

3,000 meters. **Explanation:** The correct answer is **3,000 meters**. This question tests the understanding of the physiological response to hypobaric hypoxia. **1. Why 3,000 meters is correct:** As altitude increases, the barometric pressure ($P_B$) decreases, leading to a proportional drop in the partial pressure of inspired oxygen ($PiO_2$). At sea level, $P_B$ is 760 mmHg and Alveolar $PO_2$ ($P_AO_2$) is approximately 100 mmHg. At an altitude of **3,000 meters (approx. 10,000 feet)**, the $P_B$ drops to about 523 mmHg. Using the alveolar gas equation, the $P_AO_2$ at this height falls to roughly **60 mmHg**. This is a critical threshold because it corresponds to the "knee" of the oxyhemoglobin dissociation curve; below this point, arterial oxygen saturation ($SaO_2$) drops precipitously, significantly increasing the risk of Acute Mountain Sickness (AMS). **2. Why other options are incorrect:** * **2,000 meters:** At this height, $P_AO_2$ remains well above 70 mmHg. Most healthy individuals compensate easily without significant symptoms. * **4,000 - 5,000 meters:** At these altitudes, $P_AO_2$ drops significantly below 50 mmHg. While these heights certainly cause altitude illness, the *minimum* threshold for the onset of symptoms and the specific $P_AO_2$ of 60 mmHg is reached earlier, at 3,000 meters. **High-Yield Clinical Pearls for NEET-PG:** * **The 60/90 Rule:** A $P_AO_2$ of 60 mmHg roughly corresponds to an $SaO_2$ of 90%. Below this, small drops in $PO_2$ cause large drops in $O_2$ saturation. * **Immediate Response:** The first physiological response to high altitude is **hyperventilation**, mediated by peripheral chemoreceptors (carotid bodies) sensing low $PO_2$. * **Acclimatization:** Involves increased 2,3-BPG (shifting the curve to the right) and polycythemia (via erythropoietin). * **Acetazolamide:** The drug of choice for prevention of AMS; it works by causing a mild metabolic acidosis, which stimulates ventilation.

Question 1

A 25-year-old elite swimmer training at sea level travels to compete at altitude (2400 meters). After 2 days of acclimatization, she experiences decreased performance. Her arterial blood gas shows pH 7.46, PaO2 65 mmHg, PaCO2 32 mmHg, HCO3- 22 mEq/L. Analyze the limiting factor for her current exercise performance at altitude.

Accepted Answer

Inadequate time for erythropoietin-stimulated red blood cell production

Answer

Decreased plasma volume reducing stroke volume and cardiac output

Answer

Alkalosis shifting the oxygen-hemoglobin dissociation curve leftward

Answer

Incomplete respiratory compensation reducing oxygen delivery

Answer

Reduced oxidative enzyme activity in skeletal muscle mitochondria

Question 2

A 28-year-old woman undergoes rapid ascent to 4500 meters altitude. She develops headache, nausea, and dyspnea within 6 hours. Which immediate compensatory mechanism is most responsible for maintaining oxygen delivery?

Accepted Answer

Hyperventilation driven by peripheral chemoreceptors

Answer

Polycythemia from increased erythropoietin

Answer

Increased cardiac output from myocardial hypertrophy

Answer

Increased 2,3-DPG production in RBCs

Question 3

Ascent to high altitude may cause all of the following except:

Accepted Answer

Cerebral palsy

Answer

Cerebral edema

Answer

Pulmonary edema

Answer

Venous thrombosis

Question 4

What is true about ascent to high altitude?

Accepted Answer

Acetazolamide may be given prophylactically

Answer

Respiratory acidosis

Answer

Polycythemia due to dehydration

Answer

Acute mountain sickness starts to develop on the 7th day of ascent

Question 5

What is the minimum altitude above sea level that a healthy person would need to ascend to rapidly to develop an alveolar PO2 of 60 mm Hg, potentially leading to altitude illness?

Accepted Answer

3,000 meters

Answer

2,000 meters

Answer

4,000 meters

Answer

5,000 meters

Altitude and Diving Physiology — MCQs

Altitude and Diving Physiology — MCQs

On this page

Practice by Chapter

Want unlimited practice?