Hypoxic pulmonary vasoconstriction US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Hypoxic pulmonary vasoconstriction. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Hypoxic pulmonary vasoconstriction US Medical PG Question 1: A 21-year-old man presents to his physician because he has been feeling increasingly tired and short of breath at work. He has previously had these symptoms but cannot recall the diagnosis he was given. Chart review reveals the following results:
Oxygen tension in inspired air = 150 mmHg
Alveolar carbon dioxide tension = 50 mmHg
Arterial oxygen tension = 71 mmHg
Respiratory exchange ratio = 0.80
Diffusion studies reveal normal diffusion distance. The patient is administered 100% oxygen but the patient's blood oxygen concentration does not improve. Which of the following conditions would best explain this patient's findings?
- A. Septal defect since birth (Correct Answer)
- B. Use of opioid medications
- C. Pulmonary fibrosis
- D. Pulmonary embolism
- E. Vacation at the top of a mountain
Hypoxic pulmonary vasoconstriction Explanation: ***Septal defect since birth***
- A congenital heart disease like a **septal defect** causes a right-to-left **shunt**, meaning deoxygenated blood bypasses the lungs and mixes with oxygenated blood.
- This type of shunt leads to **hypoxemia that is refractory to 100% oxygen** because the shunted blood will never pick up oxygen from the lungs.
*Use of opioid medications*
- Opioid use causes **respiratory depression**, leading to **hypoventilation** and increased arterial CO2 with decreased arterial O2.
- However, the hypoxemia from hypoventilation would typically improve significantly with **100% oxygen administration**, unlike in this case.
*Pulmonary fibrosis*
- **Pulmonary fibrosis** causes thickening of the alveolar-capillary membrane, leading to impaired gas exchange and **diffusion limitation**.
- While it causes hypoxemia, the diffusion studies are stated to be **normal**, and hypoxemia due to diffusion limitation often improves with supplemental oxygen.
*Pulmonary embolism*
- A **pulmonary embolism** leads to V/Q mismatch by blocking blood flow to a portion of the lung, causing ventilation with no perfusion.
- Hypoxemia from V/Q mismatch generally **responds well to supplemental oxygen**, as the non-affected lung areas can compensate, unlike the scenario described.
*Vacation at the top of a mountain*
- Being at a high altitude causes **hypobaric hypoxia**, meaning there is a reduced partial pressure of oxygen in the inspired air.
- This type of hypoxemia typically **improves with supplemental oxygen** as it increases the inspired oxygen tension, which is contrary to the patient's findings.
Hypoxic pulmonary vasoconstriction US Medical PG Question 2: Which of the following physiologic changes decreases pulmonary vascular resistance (PVR)?
- A. Inhaling the inspiratory reserve volume (IRV)
- B. Exhaling the entire vital capacity (VC)
- C. Exhaling the expiratory reserve volume (ERV)
- D. Breath holding maneuver at functional residual capacity (FRC)
- E. Inhaling the entire vital capacity (VC) (Correct Answer)
Hypoxic pulmonary vasoconstriction Explanation: ***Inhaling the entire vital capacity (VC)***
- As lung volume increases from FRC to TLC (which includes inhaling the entire VC), alveolar vessels are **stretched open**, and extra-alveolar vessels are **pulled open** by the increased radial traction, leading to a decrease in PVR.
- This **maximizes the cross-sectional area** of the pulmonary vascular bed, lowering resistance.
*Inhaling the inspiratory reserve volume (IRV)*
- While inhaling IRV increases lung volume, it's not the maximal inspiration of the entire VC where **PVR is typically at its lowest**.
- PVR continues to decrease as lung volume approaches total lung capacity (TLC).
*Exhaling the entire vital capacity (VC)*
- Exhaling the entire vital capacity leads to very low lung volumes, where PVR significantly **increases**.
- At low lung volumes, **alveolar vessels become compressed** and extra-alveolar vessels **narrow**, increasing resistance.
*Exhaling the expiratory reserve volume (ERV)*
- Exhaling the ERV results in a lung volume below FRC, which causes a **marked increase in PVR**.
- This is due to the **compression of alveolar vessels** and decreased radial traction on extra-alveolar vessels.
*Breath holding maneuver at functional residual capacity (FRC)*
- At FRC, the PVR is at an **intermediate level**, not its lowest.
- This is the point where the opposing forces affecting alveolar and extra-alveolar vessels are somewhat balanced, but not optimized for minimal resistance.
Hypoxic pulmonary vasoconstriction US Medical PG Question 3: A 30-year-old patient presents to clinic for pulmonary function testing. With body plethysmography, the patient's functional residual capacity is 3 L, tidal volume is 650 mL, expiratory reserve volume is 1.5 L, total lung capacity is 8 L, and dead space is 150 mL. Respiratory rate is 15 breaths per minute. What is the alveolar ventilation?
- A. 7.5 L/min (Correct Answer)
- B. 7 L/min
- C. 8.5 L/min
- D. 8 L/min
- E. 6.5 L/min
Hypoxic pulmonary vasoconstriction Explanation: ***7.5 L/min***
- Alveolar ventilation (VA) is calculated as (**tidal volume** - **dead space**) x **respiratory rate**.
- In this case, (650 mL - 150 mL) x 15 breaths/min = 500 mL x 15 = 7500 mL/min, which is 7.5 L/min.
*7 L/min*
- This answer would be obtained if the **dead space** was incorrectly subtracted from the **tidal volume** as 200 mL instead of 150 mL, or if there was a calculation error.
- The correct calculation requires accurate use of the provided tidal volume and dead space.
*8.5 L/min*
- This value is not consistent with the correct formula for alveolar ventilation using the given parameters.
- It does not arise from a common miscalculation of **tidal volume**, **dead space**, or **respiratory rate**.
*8 L/min*
- This result might occur from an incorrect addition or subtraction of volumes, or misapplication of the formula for total minute ventilation instead of alveolar ventilation.
- The formula for **total minute ventilation** is **tidal volume** x **respiratory rate**, which would be 0.65 L x 15 = 9.75 L/min, further demonstrating this option is incorrect for alveolar ventilation.
*6.5 L/min*
- This result would be obtained if the **dead space** was incorrectly assumed to be a larger value or if the calculation for subtraction from **tidal volume** was flawed.
- The correct alveolar ventilation calculation precisely accounts for the wasted ventilation in the dead space.
Hypoxic pulmonary vasoconstriction US Medical PG Question 4: A 72-year-old man with coronary artery disease comes to the emergency department because of chest pain and shortness of breath for the past 3 hours. Troponin levels are elevated and an ECG shows ST-elevations in the precordial leads. Revascularization with percutaneous coronary intervention is performed, and a stent is successfully placed in the left anterior descending artery. Two days later, he complains of worsening shortness of breath. Pulse oximetry on 3L of nasal cannula shows an oxygen saturation of 89%. An x-ray of the chest shows distended pulmonary veins, small horizontal lines at the lung bases, and blunting of the costophrenic angles bilaterally. Which of the following findings would be most likely on a ventilation-perfusion scan of this patient?
- A. Matched ventilation and perfusion bilaterally
- B. Normal ventilation with multiple, bilateral perfusion defects
- C. Normal perfusion with bilateral ventilation defects (Correct Answer)
- D. Normal perfusion with decreased ventilation at the right base
- E. Increased apical ventilation with normal perfusion bilaterally
Hypoxic pulmonary vasoconstriction Explanation: ***Normal perfusion with bilateral ventilation defects***
- The patient's presentation with **worsening shortness of breath** after an acute coronary event, along with chest x-ray findings of **distended pulmonary veins, Kerley B lines (small horizontal lines at the lung bases), and blunting of the costophrenic angles**, is highly suggestive of **pulmonary edema** due to heart failure.
- In pulmonary edema, the alveoli fill with fluid, impeding gas exchange. This leads to **impaired ventilation** in the affected areas, while **pulmonary blood flow (perfusion) remains intact**. This results in **ventilation-perfusion (V/Q) mismatch** with impaired ventilation.
*Matched ventilation and perfusion bilaterally*
- This pattern would indicate a **normal ventilation-perfusion scan**, which is inconsistent with the patient's severe shortness of breath, hypoxemia, and radiographic signs of pulmonary edema.
- A matched V/Q scan suggests **healthy lung function** and gas exchange.
*Normal ventilation with multiple, bilateral perfusion defects*
- This pattern is characteristic of **pulmonary embolism**, where blood clots obstruct pulmonary arteries, leading to areas of the lung being ventilated but not perfused.
- The clinical picture and chest x-ray findings in this patient are not consistent with pulmonary embolism.
*Normal perfusion with decreased ventilation at the right base*
- While a focal ventilation defect could occur, the patient's symptoms and chest x-ray findings (distended pulmonary veins, Kerley B lines, bilateral blunting of costophrenic angles) suggest **generalized rather than localized pulmonary edema**.
- This option describes a unilateral and focal issue, whereas heart failure typically causes bilateral findings.
*Increased apical ventilation with normal perfusion bilaterally*
- This finding is not typical in any common pulmonary pathology. Increased apical ventilation is not a characteristic of pulmonary edema or other V/Q mismatch disorders.
- This scenario does not align with the patient's symptoms or imaging findings.
Hypoxic pulmonary vasoconstriction US Medical PG Question 5: A 64-year-old man presents to his primary care physician for follow-up of a severe, unrelenting, productive cough of 2 years duration. The medical history includes type 2 diabetes mellitus, which is well-controlled with insulin. He has a 25-pack-year smoking history and is an active smoker. The blood pressure is 135/88 mm Hg, the pulse is 94/min, the temperature is 36.9°C (98.5°F), and the respiratory rate is 18/min. Bilateral wheezes and crackles are heard on auscultation. A chest X-ray reveals cardiomegaly, increased lung markings, and a flattened diaphragm. Which of the following is most likely in this patient?
- A. Increased pH of the arterial blood
- B. Increased cerebral vascular resistance
- C. Increased pulmonary arterial resistance (Correct Answer)
- D. Decreased carbon dioxide content of the arterial blood
- E. Increased right ventricle compliance
Hypoxic pulmonary vasoconstriction Explanation: ***Increased pulmonary arterial resistance***
- This patient's long-standing **smoking history**, chronic productive cough, **wheezes**, and **crackles** suggest **Chronic Obstructive Pulmonary Disease (COPD)**, likely including chronic bronchitis and emphysema.
- **COPD** often leads to **hypoxia**, causing **pulmonary vasoconstriction** and subsequent increase in **pulmonary arterial resistance**, eventually leading to **pulmonary hypertension** and **cor pulmonale** (right-sided heart failure).
*Increased pH of the arterial blood*
- Patients with severe COPD and chronic respiratory insufficiency often develop **chronic hypercapnia** (increased **PaCO2**), leading to **respiratory acidosis** and a tendency towards a **decreased pH** or a normal pH with compensation.
- An **increased pH** (alkalosis) would be less likely in the context of chronic ventilatory compromise.
*Increased cerebral vascular resistance*
- In chronic hypercapnia and hypoxia, **cerebral blood vessels** typically **dilate** to maintain cerebral perfusion, leading to **decreased cerebral vascular resistance**, not increased.
- This vasodilation can contribute to symptoms like headaches and altered mental status in severe cases.
*Decreased carbon dioxide content of the arterial blood*
- Patients with chronic obstructive lung disease often have impaired gas exchange, leading to **CO2 retention** (**hypercapnia**).
- Therefore, the **arterial carbon dioxide content** would typically be **increased**, not decreased.
*Increased right ventricle compliance*
- In the setting of chronic **pulmonary hypertension**, the right ventricle is subjected to increased pressure overload, leading to **ventricular hypertrophy** and eventually **decreased compliance** and **ventricular dysfunction**.
- **Increased compliance** (meaning the ventricle stretches more easily) is contrary to the expected response in chronic pressure overload.
Hypoxic pulmonary vasoconstriction US Medical PG Question 6: A 17-year-old boy comes to the physician for a follow-up examination. Two months ago, he suffered a spinal fracture after a fall from the roof. He feels well. His father has multiple endocrine neoplasia type 1. Vital signs are within normal limits. Examination shows no abnormalities. Laboratory studies show:
Hemoglobin 13.7 g/dL
Serum
Creatinine 0.7 mg/dL
Proteins
Total 7.0 g/dL
Albumin 4.1 g/dL
Calcium 11.4 mg/dL
Phosphorus 5.3 mg/dL
Alkaline phosphatase 100 U/L
Which of the following is the most likely cause of these findings?
- A. Immobilization (Correct Answer)
- B. Parathyroid adenoma
- C. Paraneoplastic syndrome
- D. Sarcoidosis
- E. Pseudohypercalcemia
Hypoxic pulmonary vasoconstriction Explanation: ***Immobilization***
- Prolonged **immobilization**, especially after a spinal fracture, leads to **bone resorption**, releasing calcium and phosphorus into the bloodstream, causing **hypercalcemia** and **hyperphosphatemia**.
- Though calcium and phosphorus are elevated, the **alkaline phosphatase** is normal, which is consistent with immobilization-induced bone resorption rather than primary bone disease.
*Parathyroid adenoma*
- A **parathyroid adenoma** causes primary **hyperparathyroidism**, characterized by **hypercalcemia** and **hypophosphatemia** (due to increased renal phosphate excretion), which contradicts the elevated phosphorus level seen here.
- Although the father has MEN1, a personal history of parathyroid adenoma is not indicated by the lab results.
*Paraneoplastic syndrome*
- **Paraneoplastic syndrome** causing hypercalcemia is typically due to ectopic production of **parathyroid hormone-related peptide (PTHrP)**, leading to **hypercalcemia** with **low PTH** and generally **low phosphorus** levels.
- This condition most commonly occurs with malignancies, such as squamous cell carcinoma, which is not indicated in this healthy-appearing young man with a recent fracture.
*Sarcoidosis*
- **Sarcoidosis** causes hypercalcemia due to increased synthesis of **1,25-dihydroxyvitamin D** by activated macrophages, leading to increased intestinal calcium absorption.
- This typically results in **hypercalcemia** with **normal or low PTH** and **normal or low phosphorus** levels; it is not associated with elevated phosphorus.
*Pseudohypercalcemia*
- **Pseudohypercalcemia** is an artifactual elevation of total calcium, usually due to **severe dehydration** or **elevated protein** levels, particularly **albumin** or **immunoglobulins**.
- In this case, the albumin and total protein levels are within the normal range, making pseudohypercalcemia unlikely.
Hypoxic pulmonary vasoconstriction US Medical PG Question 7: A 34-year-old woman comes to a physician for a routine health maintenance examination. She moved to Denver 1 week ago after having lived in New York City all her life. She has no history of serious illness and takes no medications. Which of the following sets of changes is most likely on analysis of a blood sample obtained now compared to prior to her move?
Erythropoietin level | O2 saturation | Plasma volume
- A. ↑ unchanged unchanged
- B. ↑ ↓ ↓ (Correct Answer)
- C. Unchanged ↓ unchanged
- D. ↓ unchanged ↑
- E. Unchanged unchanged ↓
Hypoxic pulmonary vasoconstriction Explanation: ***↑ ↓ ↓***
- Moving to a high altitude like Denver (from sea level NYC) leads to **hypoxia**, which triggers increased **erythropoietin (EPO)** production to stimulate red blood cell formation.
- The immediate physiological response to high altitude is a **decrease in arterial PO2** and thus **oxygen saturation**, along with a **reduction in plasma volume** due to increased diuresis and fluid shifts.
*↑ unchanged unchanged*
- While **erythropoietin** would increase due to hypoxia at higher altitudes, **oxygen saturation** would decrease, not remain unchanged.
- **Plasma volume** also tends to decrease acutely at high altitudes, rather than staying unchanged.
*Unchanged ↓ unchanged*
- **Erythropoietin** would be expected to increase, not remain unchanged, as a compensatory mechanism to hypoxia.
- While **oxygen saturation** would decrease, **plasma volume** typically decreases acutely, not remaining unchanged.
*↓ unchanged ↑*
- **Erythropoietin** would increase, not decrease, in response to the lower atmospheric oxygen.
- Both **oxygen saturation** and **plasma volume** would decrease, not remain unchanged or increase, respectively.
*Unchanged unchanged ↓*
- **Erythropoietin** would increase, not remain unchanged, to stimulate red blood cell production in response to hypoxia.
- **Oxygen saturation** would decrease, not remain unchanged, at higher altitudes.
Hypoxic pulmonary vasoconstriction US Medical PG Question 8: A 62-year-old man is brought to the emergency department with a 2-day history of cough productive of yellowish sputum. He has had fever, chills, and worsening shortness of breath over this time. He has a 10-year history of hypertension and hyperlipidemia. He does not drink alcohol or smoke cigarettes. His current medications include atorvastatin, amlodipine, and metoprolol. His temperature is 38.9°C (102.0°F), pulse is 105/min, respirations are 27/min, and blood pressure is 110/70 mm Hg. He appears in mild distress. He has rales over the left lower lung field. The remainder of the examination shows no abnormalities. Leukocyte count is 15,000/mm3 (87% segmented neutrophils). Arterial blood gas analysis on room air shows:
pH 7.44
pO2 68 mm Hg
pCO2 28 mm Hg
HCO3- 24 mEq/L
O2 saturation 91%
An x-ray of the chest shows a consolidation in the left lower lobe. Asking the patient to lie down in the left lateral decubitus position would most likely result in which of the following?
- A. Decreased ventilation of the left lung
- B. Worsen the hypocapnia
- C. Increase in A-a gradient (Correct Answer)
- D. Increased perfusion of right lung
- E. Improve the hypoxemia
Hypoxic pulmonary vasoconstriction Explanation: ***Increase in A-a gradient***
- Placing the patient in the **left lateral decubitus position** would worsen V/Q mismatch because the **diseased left lung** (with consolidation) would receive increased perfusion due to gravity.
- This increased perfusion to a poorly ventilated area would further impair gas exchange, leading to a larger **alveolar-arterial (A-a) gradient**.
*Decreased ventilation of the left lung*
- While lying on the left side might slightly restrict the expansion of the left lung, the primary issue is the **consolidation** itself, which already severely impairs ventilation.
- The main problem with positioning is not a further decrease in ventilation but rather the **redistribution of blood flow** to an already compromised lung.
*Worsen the hypocapnia*
- The patient has **hypocapnia (pCO2 28 mm Hg)** due to tachypnea as compensation for hypoxemia, indicating increased minute ventilation.
- While worsening the V/Q mismatch will worsen hypoxemia, it's unlikely to directly worsen hypocapnia further; the body would still try to compensate through increased respiratory drive unless the respiratory muscles become fatigued.
*Increased perfusion of right lung*
- In the left lateral decubitus position, **perfusion due to gravity** would increase in the dependent (left) lung, not the non-dependent (right) lung.
- The right lung would experience relatively decreased perfusion compared to the left lung in this position.
*Improve the hypoxemia*
- Lying on the side of the **diseased lung** (left) typically **worsens hypoxemia** because gravity directs more blood flow to the poorly ventilated, consolidated lung.
- To improve hypoxemia, the patient should be positioned with the **healthy lung dependent** (e.g., right lateral decubitus or semi-Fowler's with the right lung lower) to optimize V/Q matching.
Hypoxic pulmonary vasoconstriction US Medical PG Question 9: A 52-year-old woman presents to the emergency department with breathlessness for the past 6 hours. She denies cough, nasal congestion or discharge, sneezing, blood in sputum, or palpitation. There is no past history of chronic respiratory or cardiovascular medical conditions, but she mentions that she has been experiencing frequent cramps in her left leg for the past 5 days. She is post-menopausal and has been on hormone replacement therapy for a year now. Her temperature is 38.3°C (100.9°F), the pulse is 116/min, the blood pressure is 136/84 mm Hg, and the respiratory rate is 24/min. Edema and tenderness are present in her left calf region. Auscultation of the chest reveals rales over the left infrascapular and scapular region. The heart sounds are normal and there are no murmurs. Which of the following mechanisms most likely contributed to the pathophysiology of this patient’s condition?
- A. Secretion of vasodilating neurohumoral substances in pulmonary vascular bed
- B. Increased right ventricular preload (Correct Answer)
- C. Decreased physiologic dead space
- D. Alveolar hyperventilation
- E. Decreased alveolar-arterial oxygen tension gradient
Hypoxic pulmonary vasoconstriction Explanation: ***Increased right ventricular preload***
- The patient's presentation (acute breathlessness, unilateral leg cramps, calf tenderness and edema, rales) combined with risk factors (post-menopausal, hormone replacement therapy) strongly suggests **pulmonary embolism (PE)** from deep vein thrombosis (DVT).
- In PE, thrombus occludes pulmonary vasculature causing **increased pulmonary vascular resistance**, which increases **right ventricular afterload** (the resistance the RV must overcome to eject blood).
- **Note:** While this option states "preload," the primary mechanism is actually increased RV **afterload**. However, this is the most appropriate answer among the given options, as the increased resistance does lead to RV strain and potential backup of blood that can secondarily affect preload.
*Secretion of vasodilating neurohumoral substances in pulmonary vascular bed*
- The primary vascular response in PE is **vasoconstriction**, not vasodilation.
- Hypoxia and mediator release cause **pulmonary vasoconstriction** distal to the embolus, further increasing pulmonary vascular resistance.
*Decreased physiologic dead space*
- In PE, there is **ventilation-perfusion (V/Q) mismatch** where lung regions are ventilated but not perfused due to embolic obstruction.
- This actually **increases physiologic dead space** because these areas are ventilated but cannot participate in gas exchange.
*Alveolar hyperventilation*
- Patients with PE often develop **tachypnea and hyperventilation** due to hypoxia, anxiety, and chest discomfort.
- However, this is a **compensatory response** to hypoxemia, not the primary pathophysiological mechanism causing the condition.
*Decreased alveolar-arterial oxygen tension gradient*
- The **A-a gradient is increased in PE** due to V/Q mismatch and shunting, reflecting impaired gas exchange.
- A decreased A-a gradient would indicate efficient gas exchange, which contradicts the hypoxia and breathlessness seen in PE.
Hypoxic pulmonary vasoconstriction US Medical PG Question 10: A 22-year-old man volunteers for a research study on lung function. He has no history of lung disease or allergies and does not smoke. His pulmonary blood flow is measured in the various labeled segments of the lungs while standing. Then the volunteer, still standing, is given very low continuous positive airway pressure and the blood flow measured again. Which of the following sets of findings are most likely to be present in the second measurements relative to the first?
- A. Increased blood flow in zone 2
- B. Reduced blood flow in zone 3
- C. Reduced blood flow in zone 1
- D. Increased blood flow in zone 3
- E. Increased blood flow in zone 1 (Correct Answer)
Hypoxic pulmonary vasoconstriction Explanation: ***Increased blood flow in zone 1***
- In healthy standing subjects, **Zone 1** may not exist or is minimal at the apex where alveolar pressure (PA) can exceed arterial pressure (Pa).
- **Very low CPAP** increases alveolar pressure, but when applied at very low levels, it may **recruit collapsed or under-perfused alveoli** by preventing alveolar collapse and improving the pressure gradient.
- The net effect with **very low CPAP** can paradoxically **improve perfusion** in Zone 1 by optimizing alveolar mechanics and reducing vascular resistance through **alveolar recruitment**, particularly in previously under-ventilated apical regions.
*Increased blood flow in zone 2*
- In Zone 2, arterial pressure exceeds alveolar pressure, which exceeds venous pressure (**Pa > PA > Pv**), creating a waterfall effect.
- While CPAP increases alveolar pressure (PA), this would increase the downstream resistance and typically **reduce** the arterial-alveolar pressure gradient (Pa - PA), decreasing flow rather than increasing it.
*Increased blood flow in zone 3*
- **Zone 3** (lung base) normally has the **highest blood flow** where both arterial and venous pressures exceed alveolar pressure (**Pa > Pv > PA**).
- CPAP increases alveolar pressure (PA), which would compress capillaries and **reduce** the pressure gradient, typically decreasing rather than increasing blood flow in this zone.
*Reduced blood flow in zone 1*
- While increasing alveolar pressure with CPAP might be expected to **reduce** Zone 1 perfusion by compressing capillaries, **very low levels of CPAP** can have the opposite effect through **alveolar recruitment** and optimization of lung mechanics.
- The question specifies **very low** CPAP, which is the key—this level improves alveolar patency without significantly compressing capillaries.
*Reduced blood flow in zone 3*
- Zone 3 typically has the highest blood flow due to favorable pressure gradients from gravity.
- CPAP increases PA, which could compress capillaries and reduce the (Pa - PA) gradient, but the **very low level** specified means this effect is minimal and Zone 3 generally maintains adequate perfusion.
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