Altitude and Diving Physiology — MCQs
On this page
A woman from Delhi travels to Ladakh, a high-altitude region. Soon after arrival, she develops symptoms such as breathlessness, headache, and lightheadedness. What is the primary underlying mechanism responsible for her symptoms?
A new resident to a high-altitude area develops hypoxia. What is the causative factor?
A 28-year-old mountaineer ascends rapidly to 4,500 meters altitude. Within 24 hours, he develops severe headache, nausea, and dyspnea. Arterial blood gas analysis shows pH 7.48, PaCO2 28 mmHg, PaO2 55 mmHg, and HCO3- 22 mEq/L. What is the primary physiological mechanism responsible for his acid-base disturbance?
Which of the following is seen in high altitude?
A man is climbing a mountain for trekking. Based on his physiological response to the high altitude, what is the most likely primary acid-base abnormality in his blood?
Which physiological adaptation does not happen at high altitudes?
A patient is going skiing high in the Rockies and is given acetazolamide to protect against altitude sickness. Unfortunately, the patient is also a type 1 diabetic. He is admitted to the hospital in a worsening ketoacidosis. In which of the following cells has acetazolamide inhibited a reaction that has led to the severity of the metabolic acidosis?
Which of the following is seen in high altitude climbers?
What is the primary physiological effect of positive G forces on the human body?
Compensating mechanism involved in acclimatization to altitude is:
Altitude and Diving Physiology Indian Medical PG Practice Questions and MCQs
Question 51: A woman from Delhi travels to Ladakh, a high-altitude region. Soon after arrival, she develops symptoms such as breathlessness, headache, and lightheadedness. What is the primary underlying mechanism responsible for her symptoms?
- A. Metabolic alkalosis
- B. Metabolic acidosis
- C. Respiratory acidosis
- D. Respiratory alkalosis (Correct Answer)
Explanation: ***Respiratory alkalosis***- Acute exposure to high altitude decreases the **partial pressure of inspired oxygen ($P_{I}O_2$)**, leading to **hypoxemia**, which stimulates the peripheral chemoreceptors (carotid bodies) to increase the respiratory drive (hyperventilation).- This hyperventilation causes a massive *washout* of **carbon dioxide ($ ext{CO}_2$)**, resulting in low arterial $ ext{P}_{ ext{a}} ext{CO}_2$ (hypocapnia) and an immediate increase in blood $ ext{pH}$ (alkalosis).*Respiratory acidosis*- This condition is characterized by **hypoventilation** resulting in the retention of $ ext{CO}_2$ and a resultant drop in $ ext{pH}$.- Acute high altitude exposure leads to increased ventilation (hyperventilation), making this mechanism incorrect.*Metabolic alkalosis*- This state results from excess plasma **bicarbonate ($ ext{HCO}_3^{-})$** or significant loss of $ ext{H}^{+}$ (e.g., protracted vomiting, loop diuretics).- This is not the primary acid-base disturbance leading to acute mountain sickness (AMS) symptoms.*Metabolic acidosis*- This state is the **delayed renal compensatory mechanism** for respiratory alkalosis, where the kidneys increase the excretion of $ ext{bicarbonate}$.- While it occurs, it is a secondary compensation that takes 24–48 hours and is not the *primary underlying mechanism* responsible for the immediate symptoms upon arrival.
Question 52: A new resident to a high-altitude area develops hypoxia. What is the causative factor?
- A. Low hemoglobin levels
- B. Low partial pressure of O2 (Correct Answer)
- C. Low blood lactate levels
- D. High partial pressure of CO2
Explanation: ***Low partial pressure of O2***- At high altitudes, the **barometric pressure** is significantly lower, and while the fraction of oxygen remains 21%, the resulting **partial pressure of inspired O2 (PiO2)** is reduced.- This reduction in PiO2 lowers the **alveolar PO2**, thereby decreasing the driving pressure for oxygen diffusion into the blood and causing **hypoxic hypoxia**.*Low hemoglobin levels*- The immediate cause of high-altitude illness is **hypoxic hypoxia**, where the problem is low inspired oxygen, not an issue with the carrying capacity of the blood.- Over time, the body adapts by increasing red blood cell mass and thus **hemoglobin levels** (polycythemia).*Low blood lactate levels*- Hypoxia often triggers **anaerobic metabolism**, especially under exertion, leading to an *increase* in blood lactate (lactic acidosis), not a decrease.- Lactate levels are a metabolic consequence of tissue hypoxia, not the primary cause of developing low oxygen levels at altitude.*High partial pressure of CO2*- The hypoxia stimulates peripheral chemoreceptors, leading to an **increase in ventilation** (hyperventilation).- Hyperventilation causes the body to "blow off" CO2, resulting in **decreased arterial PCO2 (hypocapnia)** and respiratory alkalosis, not high PCO2.
Question 53: A 28-year-old mountaineer ascends rapidly to 4,500 meters altitude. Within 24 hours, he develops severe headache, nausea, and dyspnea. Arterial blood gas analysis shows pH 7.48, PaCO2 28 mmHg, PaO2 55 mmHg, and HCO3- 22 mEq/L. What is the primary physiological mechanism responsible for his acid-base disturbance?
- A. Lactic acidosis from tissue hypoxia
- B. Renal bicarbonate retention causing metabolic alkalosis
- C. Hyperventilation-induced respiratory alkalosis (Correct Answer)
- D. Metabolic compensation for chronic respiratory acidosis
Explanation: ***Hyperventilation-induced respiratory alkalosis*** - At high altitude, **hypoxia** (PaO2 55 mmHg) stimulates peripheral chemoreceptors in the carotid and aortic bodies, triggering an immediate increase in respiratory rate and depth (hyperventilation). - This hyperventilation causes excessive elimination of **CO2**, resulting in **hypocapnia** (PaCO2 28 mmHg) and **respiratory alkalosis** (pH 7.48). - This is the **primary physiological mechanism** occurring within 24 hours of acute altitude exposure. *Lactic acidosis from tissue hypoxia* - While severe tissue hypoxia can lead to **anaerobic metabolism** and lactic acidosis, the ABG shows an **alkalotic pH (7.48)**, not acidotic, ruling this out as the primary mechanism. - The relatively preserved PaO2 (55 mmHg) and normal HCO3- (22 mEq/L) indicate no significant metabolic acidosis is present. *Renal bicarbonate retention causing metabolic alkalosis* - This is physiologically **incorrect** - at altitude, the kidneys actually **excrete bicarbonate** (not retain it) as a compensatory response to respiratory alkalosis. - Renal compensation involves increasing HCO3- excretion and reducing H+ secretion to normalize pH, but this process takes **2-3 days** to become significant, not 24 hours. - The nearly normal HCO3- (22 mEq/L) confirms minimal renal compensation has occurred yet. *Metabolic compensation for chronic respiratory acidosis* - There is **no respiratory acidosis** present - the patient has respiratory **alkalosis** (high pH, low PaCO2). - This option is incorrect as it misidentifies the primary acid-base disturbance entirely.
Question 54: Which of the following is seen in high altitude?
- A. Respiratory alkalosis (Correct Answer)
- B. Respiratory acidosis
- C. Metabolic acidosis
- D. Metabolic alkalosis
Explanation: ***Respiratory alkalosis*** - High altitude exposure leads to **hypoxia** (low inspired oxygen), which stimulates peripheral chemoreceptors. - This stimulation increases the **respiratory rate and depth** (hyperventilation), resulting in excessive blowing off of **carbon dioxide (CO₂)**, which causes a decrease in arterial pCO₂ and elevates the blood pH (alkalosis). *Metabolic acidosis* - This is a condition where the blood pH is low due to a low bicarbonate (HCO₃⁻) concentration, which is not the primary immediate response to high altitude. - However, in a later stage, the kidneys attempt to compensate for respiratory alkalosis by **excreting bicarbonate**, leading to a compensatory metabolic acidosis. *Metabolic alkalosis* - This condition involves a high blood pH due to an excess of bicarbonate, which is typically seen in conditions like severe vomiting or use of diuretics, not acute high altitude exposure. - It is the opposite of the renal compensation mechanism seen in response to high altitude. *Respiratory acidosis* - Characterized by reduced ventilation (hypoventilation) leading to **retention of CO₂** (increased pCO₂), resulting in a lowered blood pH. - High altitude causes hyperventilation, not hypoventilation, and therefore results in respiratory *alkalosis*.
Question 55: A man is climbing a mountain for trekking. Based on his physiological response to the high altitude, what is the most likely primary acid-base abnormality in his blood?
- A. Metabolic acidosis
- B. Respiratory alkalosis (Correct Answer)
- C. Respiratory acidosis
- D. Metabolic alkalosis
Explanation: ***Respiratory alkalosis*** - Exposure to **high altitude** causes decreased ambient partial pressure of oxygen (PO₂), leading to **hypoxemia**. - The physiological response to hypoxemia is reflex **hyperventilation** mediated by peripheral chemoreceptors, which blows off excessive **carbon dioxide (CO₂)**, causing decreased PaCO₂ and consequently elevated blood pH (alkalosis). - This is the **primary and immediate** acid-base abnormality at high altitude. *Metabolic acidosis* - This condition occurs due to the accumulation of **non-volatile acids** (e.g., lactic acid, ketoacids) or loss of bicarbonate. - While the kidney eventually compensates for the respiratory alkalosis by excreting bicarbonate (leading to compensatory **metabolic acidosis**), this is the **secondary, not the primary**, abnormality. *Metabolic alkalosis* - This abnormality is typically caused by loss of acid (e.g., severe vomiting, gastric suction) or excessive administration of alkali. - It is not related to the immediate respiratory compensatory response to **high-altitude hypoxemia**. *Respiratory acidosis* - This is caused by **hypoventilation** or impaired alveolar ventilation, leading to retention of **CO₂** and decreased pH. - At high altitude, the body actively **hyperventilates** to improve oxygen uptake, making respiratory acidosis the opposite of the expected primary response.
Question 56: Which physiological adaptation does not happen at high altitudes?
- A. Pulmonary vasoconstriction
- B. Respiratory acidosis (Correct Answer)
- C. Hypoxia
- D. Polycythemia
Explanation: ***Respiratory acidosis*** - At high altitudes, the primary physiological response to **hypoxia** is to increase ventilation, leading to a decrease in **arterial PCO2**. - This reduction in **PCO2** causes **respiratory alkalosis**, not acidosis, as the body tries to compensate for the lower oxygen levels. *Pulmonary vasoconstriction* - This is a significant physiological response to **hypoxia** at high altitudes, leading to an increase in **pulmonary artery pressure**. - Its purpose is to divert blood flow to better-ventilated areas of the lung, but it can also contribute to **pulmonary hypertension**. *Hypoxia* - Reduced **atmospheric pressure** at high altitudes directly results in a lower partial pressure of oxygen (**PO2**), leading to **hypoxia**. - This low **PO2** is the primary trigger for most other physiological adaptations seen at high altitudes. *Polycythemia* - Prolonged exposure to **hypoxia** stimulates the kidneys to release **erythropoietin (EPO)**, which in turn increases **red blood cell production**. - This adaptive increase in **red blood cell count** and **hemoglobin concentration** aims to enhance the oxygen-carrying capacity of the blood.
Question 57: A patient is going skiing high in the Rockies and is given acetazolamide to protect against altitude sickness. Unfortunately, the patient is also a type 1 diabetic. He is admitted to the hospital in a worsening ketoacidosis. In which of the following cells has acetazolamide inhibited a reaction that has led to the severity of the metabolic acidosis?
- A. Cells in the lens of the eye
- B. Liver cells
- C. Immune system cells
- D. Renal tubular cells (Correct Answer)
Explanation: ***Renal tubular cells*** - Acetazolamide is a **carbonic anhydrase inhibitor**, primarily acting in the **proximal renal tubular cells** to block the enzyme carbonic anhydrase. - This inhibition prevents **bicarbonate (HCO₃⁻) reabsorption** in the proximal tubule, causing bicarbonate wasting in urine and resulting in **metabolic acidosis** (specifically type 2 renal tubular acidosis). - In this patient already suffering from **diabetic ketoacidosis** (DKA), which is itself a metabolic acidosis with low bicarbonate, the additional bicarbonate loss from acetazolamide **worsens the severity** of the acidosis. - This represents a clinically important drug-disease interaction. *Cells in the lens of the eye* - While carbonic anhydrase is present in the eye and acetazolamide can reduce **intraocular pressure** (used therapeutically for glaucoma), this mechanism is unrelated to systemic metabolic acidosis. - Inhibition here affects aqueous humor production but does not directly or significantly contribute to **acid-base balance** in the blood. *Liver cells* - The liver is crucial for metabolism and ammonia detoxification, but acetazolamide's primary action on acid-base balance is not directly through **hepatic carbonic anhydrase**. - Liver dysfunction can impact acid-base balance, but the liver is not the direct target or primary cause of acetazolamide-induced acidosis. *Immune system cells* - Carbonic anhydrase activity in **immune cells** is involved in processes like **pH regulation within phagosomes** and T-cell activation. - However, modulation of immune cell function by acetazolamide does not significantly contribute to its effect on systemic **metabolic acidosis**.
Question 58: Which of the following is seen in high altitude climbers?
- A. Hyperventilation
- B. Pulmonary edema
- C. Decreased PaCO2
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - High altitude climbers experience **hypoxia**, which triggers several physiological responses as the body tries to compensate. - **Hyperventilation**, **pulmonary edema**, and **decreased PaCO2** are all common occurrences in individuals exposed to high altitudes. *Hyperventilation* - **Hypoxia** at high altitudes stimulates the peripheral chemoreceptors, leading to an increased respiratory rate and depth. - This increased ventilation is a compensatory mechanism to try and increase **oxygen intake**. *Pulmonary edema* - **High-altitude pulmonary edema (HAPE)** is a potentially life-threatening condition caused by exaggerated hypoxic pulmonary vasoconstriction. - This leads to increased pulmonary arterial pressure, capillary leakage, and **fluid accumulation in the lungs**. *Decreased PaCO2* - The increased respiratory rate due to **hyperventilation** causes an excessive exhalation of carbon dioxide. - This results in a **decreased partial pressure of arterial carbon dioxide (PaCO2)**, leading to respiratory alkalosis.
Question 59: What is the primary physiological effect of positive G forces on the human body?
- A. Increased cardiac output
- B. Red out
- C. Increased cerebral arterial pressure
- D. Black out (Correct Answer)
Explanation: ***Black out*** - Positive G forces cause blood to pool in the **lower extremities**, leading to reduced blood flow to the brain and eyes, resulting in a **temporary loss of vision (blackout)**. - This is a direct consequence of the body's inability to maintain **cerebral perfusion** against the increased gravitational load. *Increased cardiac output* - While the heart may initially try to compensate, prolonged or high positive G forces can actually **decrease cardiac output** due to reduced venous return. - The primary hemodynamic effect is a redistribution of blood, not an overall increase in output. *Red out* - **Red out** (or red vision) is primarily associated with **negative G forces**, where blood surges towards the head. - It results from increased pressure in the cranial vessels, leading to capillary rupture and blood pooling in the eyes. *Increased cerebral arterial pressure* - Positive G forces cause a **decrease** in cerebral arterial pressure due to the displacement of blood away from the head. - A decrease in cerebral arterial pressure is the direct cause of the **vision impairment** and potential loss of consciousness.
Question 60: Compensating mechanism involved in acclimatization to altitude is:
- A. Respiratory depression
- B. Hypoventilation
- C. Hyperventilation (Correct Answer)
- D. Respiratory acidosis
Explanation: ***Hyperventilation*** - **Hyperventilation** is the primary immediate compensatory mechanism at altitude, increasing alveolar ventilation to improve **oxygen uptake** despite lower partial pressures of oxygen. - This response is mediated by the **carotid bodies**, which sense the reduced arterial PO2 and stimulate the respiratory center. *Respiratory depression* - **Respiratory depression** would worsen hypoxia at high altitude by further reducing **oxygen intake**. - This is not a compensatory, but rather a detrimental, response in this setting. *Hypoventilation* - **Hypoventilation** decreases the amount of air reaching the alveoli, exacerbating the **hypoxia** present at high altitudes. - This would further reduce the **partial pressure of oxygen** in the blood, which is counterproductive for acclimatization. *Respiratory acidosis* - **Respiratory acidosis** results from **hypoventilation** and CO2 retention. - Acclimatization leads to **respiratory alkalosis** due to increased CO2 excretion from hyperventilation, which is then partially compensated by renal mechanisms.
Practice by Chapter
Atmospheric Pressure and Gas Laws
Practice Questions
High Altitude Acclimatization
Practice Questions
Hypoxia and Oxygen Transport
Practice Questions
Altitude Illnesses
Practice Questions
Hyperbaric Environments
Practice Questions
Decompression Theory
Practice Questions
Physiology of Breath-Hold Diving
Practice Questions
Nitrogen Narcosis
Practice Questions
Oxygen Toxicity
Practice Questions
Fitness for Altitude and Diving
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free