Ventilator strategies addressing V/Q US Medical PG Practice Questions and MCQs
Practice US Medical PG questions for Ventilator strategies addressing V/Q. These multiple choice questions (MCQs) cover important concepts and help you prepare for your exams.
Ventilator strategies addressing V/Q US Medical PG Question 1: A 32-year-old woman presents with progressive shortness of breath and a dry cough. She says that her symptoms onset recently after a 12-hour flight. Past medical history is unremarkable. Current medications are oral estrogen/progesterone containing contraceptive pills. Her vital signs include: blood pressure 110/60 mm Hg, pulse 101/min, respiratory rate 22/min, oxygen saturation 88% on room air, and temperature 37.9℃ (100.2℉). Her weight is 94 kg (207.2 lb) and height is 170 cm (5 ft 7 in). On physical examination, she is acrocyanotic. There are significant swelling and warmth over the right calf. There are widespread bilateral rales present. Cardiac auscultation reveals accentuation of the pulmonic component of the second heart sound (P2) and an S3 gallop. Which of the following ventilation/perfusion (V/Q) ratios most likely corresponds to this patient’s condition?
- A. 1.3 (Correct Answer)
- B. 1
- C. 0.8
- D. 0.5
- E. 0.3
Ventilator strategies addressing V/Q Explanation: ***1.3***
- This value represents an increased V/Q ratio, or **dead space ventilation**, which is characteristic of a **pulmonary embolism (PE)**. In PE, a portion of the lung is ventilated but not perfused due to the embolism blocking blood flow, leading to wasted ventilation.
- The patient's symptoms (sudden onset dyspnea after a long flight, use of oral contraceptives, calf swelling, hypoxia, and accentuated P2) are highly suggestive of a PE, which is the most likely cause of increased V/Q mismatch.
*1*
- A V/Q ratio of 1 indicates **perfect matching** of ventilation and perfusion, which is an ideal state not typically achieved throughout the entire lung, especially in disease.
- This value would not explain the patient's severe **hypoxia** and overall clinical picture of respiratory distress.
*0.8*
- This is the **average normal V/Q ratio** for the lung as a whole, representing slightly more perfusion than ventilation.
- While it's a normal physiological state, it does not account for the significant V/Q mismatch indicated by the patient's severe hypoxemia (SpO2 88%) and clinical symptoms.
*0.5*
- This value represents a **low V/Q ratio**, indicating relatively more perfusion than ventilation, often seen in conditions like **shunt physiology** (e.g., pneumonia, atelectasis, pulmonary edema).
- While the patient has rales and an S3 gallop suggesting potential pulmonary edema or heart failure secondary to increased right heart strain, the primary pathophysiology in PE is increased V/Q due to unperfused but ventilated lung regions.
*0.3*
- This is a severely **low V/Q ratio**, approaching a **shunt**, where blood passes through the lungs without being adequately oxygenated. This is typical of conditions like **severe pneumonia, ARDS, or significant atelectasis**.
- While PE can cause some degree of bronchoconstriction leading to areas of low V/Q, the predominant and most impactful V/Q mismatch in PE is the high V/Q ratio in areas of unperfused lung.
Ventilator strategies addressing V/Q 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)
Ventilator strategies addressing V/Q 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.
Ventilator strategies addressing V/Q US Medical PG Question 3: A 25-year-old previously healthy woman is admitted to the hospital with progressively worsening shortness of breath. She reports a mild fever. Her vital signs at the admission are as follows: blood pressure 100/70 mm Hg, heart rate 111/min, respiratory rate 20/min, and temperature 38.1℃ (100.6℉); blood saturation on room air is 90%. Examination reveals a bilateral decrease of vesicular breath sounds and rales in the lower lobes. Plain chest radiograph demonstrates bilateral opacification of the lower lobes. Despite appropriate treatment, her respiratory status worsens. The patient is transferred to the intensive care unit and put on mechanical ventilation. Adjustment of which of the following ventilator settings will only affect the patient’s oxygenation?
- A. Tidal volume and respiratory rate
- B. FiO2 and PEEP (Correct Answer)
- C. Respiratory rate and PEEP
- D. Tidal volume and FiO2
- E. FiO2 and respiratory rate
Ventilator strategies addressing V/Q Explanation: ***FiO2 and PEEP***
- **FiO2 (fraction of inspired oxygen)** directly controls the oxygen concentration delivered to the patient, thus solely impacting **oxygenation**.
- **PEEP (positive end-expiratory pressure)** prevents alveolar collapse and recruits collapsed alveoli, improving the **functional residual capacity** and thus **oxygenation** without significantly altering CO2 removal (ventilation).
*Tidal volume and respiratory rate*
- **Tidal volume (Vt)** directly impacts the amount of air moved with each breath, primarily affecting **ventilation** (CO2 removal).
- **Respiratory rate (RR)** also directly determines the total minute ventilation, thus influencing **ventilation** more than oxygenation.
*Respiratory rate and PEEP*
- As mentioned, **respiratory rate** significantly affects **ventilation** by altering minute ventilation (Vt x RR).
- While **PEEP** primarily affects oxygenation, the combination with respiratory rate means it's not exclusively targeting oxygenation.
*Tidal volume and FiO2*
- **Tidal volume** is a key determinant of **ventilation** (CO2 removal), not solely oxygenation.
- **FiO2** does affect oxygenation, but its combination with tidal volume makes this option incorrect for *only* affecting oxygenation.
*FiO2 and respiratory rate*
- **FiO2** directly impacts **oxygenation**.
- **Respiratory rate** primarily affects **ventilation** (CO2 removal), thereby influencing carbonic acid levels and pH.
Ventilator strategies addressing V/Q US Medical PG Question 4: A 21-year-old man is admitted to the intensive care unit for respiratory failure requiring mechanical ventilation. His minute ventilation is calculated to be 7.0 L/min, and his alveolar ventilation is calculated to be 5.1 L/min. Which of the following is most likely to decrease the difference between minute ventilation and alveolar ventilation?
- A. Increasing the partial pressure of inhaled oxygen
- B. Decreasing the affinity of hemoglobin for oxygen
- C. Increasing the respiratory depth
- D. Decreasing the physiologic dead space (Correct Answer)
- E. Increasing the respiratory rate
Ventilator strategies addressing V/Q Explanation: ***Decreasing the physiologic dead space***
- The difference between **minute ventilation (VE)** and **alveolar ventilation (VA)** is the **dead space ventilation (VD)**, calculated as: VE - VA = VD
- In this case: 7.0 L/min - 5.1 L/min = 1.9 L/min of dead space ventilation
- Decreasing the **physiologic dead space** directly reduces this difference by allowing a greater proportion of each breath to participate in gas exchange
- This is the most direct way to narrow the gap between VE and VA
*Increasing the partial pressure of inhaled oxygen*
- This intervention primarily affects **oxygenation** by increasing the driving pressure for oxygen diffusion into the blood
- It does not directly change the volume of air participating in alveolar ventilation or reduce dead space ventilation
- The distribution of ventilation between alveolar and dead space remains unchanged
*Decreasing the affinity of hemoglobin for oxygen*
- A decrease in hemoglobin affinity for oxygen facilitates **oxygen unloading** to the tissues (rightward shift of the oxygen-hemoglobin dissociation curve)
- This effect is related to **oxygen delivery** and does not alter the proportion of minute ventilation that reaches the alveoli for gas exchange
- Dead space ventilation remains unchanged
*Increasing the respiratory depth*
- Increasing respiratory depth increases **tidal volume (VT)**, which improves the **ratio** of alveolar ventilation to minute ventilation (VA/VE efficiency)
- However, the **absolute difference** (VE - VA) in L/min depends on the **total dead space volume**, which is not changed by increasing tidal volume alone
- While this improves ventilation efficiency, it does not directly reduce the dead space ventilation measured in L/min unless physiologic dead space itself decreases
*Increasing the respiratory rate*
- While increasing respiratory rate increases **minute ventilation (VE)**, it also increases the frequency of ventilating the **dead space** with each breath
- Since dead space ventilation (VD) = respiratory rate × dead space volume, increasing rate while keeping tidal volume constant will proportionally increase both VE and VD
- This can actually widen the absolute gap between VE and VA, making it less efficient
Ventilator strategies addressing V/Q US Medical PG Question 5: A 35-year-old woman volunteers for a study on respiratory physiology. Pressure probes A and B are placed as follows:
Probe A: between the parietal and visceral pleura
Probe B: within the cavity of an alveolus
The probes provide a pressure reading relative to atmospheric pressure. To obtain a baseline reading, she is asked to sit comfortably and breathe normally. Which of the following sets of values will most likely be seen at the end of inspiration?
- A. Probe A: -6 mm Hg; Probe B: 0 mm Hg (Correct Answer)
- B. Probe A: 0 mm Hg; Probe B: -1 mm Hg
- C. Probe A: -4 mm Hg; Probe B: 0 mm Hg
- D. Probe A: -4 mm Hg; Probe B: -1 mm Hg
- E. Probe A: -6 mm Hg; Probe B: -1 mm Hg
Ventilator strategies addressing V/Q Explanation: ***Probe A: -6 mm Hg; Probe B: 0 mm Hg***
- At the **end of inspiration**, the **intrapleural pressure (Probe A)** is at its most negative, typically around -6 to -8 cm H2O (equivalent to -4 to -6 mmHg), reflecting the maximum expansion of the thoracic cavity.
- At the **end of inspiration**, just before exhalation begins, there is **no airflow**, so the **intrapulmonary pressure (Probe B)** equalizes with atmospheric pressure, resulting in a 0 mm Hg reading.
*Probe A: 0 mm Hg; Probe B: -1 mm Hg*
- An **intrapleural pressure of 0 mm Hg** would indicate a **pneumothorax** since it should always be negative to prevent lung collapse.
- An **intrapulmonary pressure of -1 mm Hg** would indicate that **inspiration is still ongoing**, as air would be flowing into the lungs.
*Probe A: -4 mm Hg; Probe B: 0 mm Hg*
- While an **intrapulmonary pressure of 0 mm Hg** is correct at the end of inspiration, an **intrapleural pressure of -4 mm Hg** is typical for the **end of expiration (Functional Residual Capacity)** during quiet breathing, not the end of inspiration.
- The **intrapleural pressure becomes more negative** during inspiration due to increased thoracic volume, so -4 mm Hg would be insufficient.
*Probe A: -4 mm Hg; Probe B: -1 mm Hg*
- An **intrapleural pressure of -4 mm Hg** is the normal pressure at the **end of expiration**, not the end of inspiration, where it becomes more negative.
- An **intrapulmonary pressure of -1 mm Hg** indicates that **inspiration is still in progress**, not at its end, as air would still be flowing into the lungs.
*Probe A: -6 mm Hg; Probe B: -1 mm Hg*
- While an **intrapleural pressure of -6 mm Hg** is consistent with the end of inspiration, an **intrapulmonary pressure of -1 mm Hg** means that **airflow is still occurring into the lungs**.
- At the **very end of inspiration**, just before the start of exhalation, airflow momentarily ceases, and intrapulmonary pressure becomes zero relative to the atmosphere.
Ventilator strategies addressing V/Q US Medical PG Question 6: 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
Ventilator strategies addressing V/Q 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.
Ventilator strategies addressing V/Q US Medical PG Question 7: 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)
Ventilator strategies addressing V/Q 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.
Ventilator strategies addressing V/Q US Medical PG Question 8: A 57-year-old man presents to the clinic for a chronic cough over the past 4 months. The patient reports a productive yellow/green cough that is worse at night. He denies any significant precipitating event prior to his symptoms. He denies fever, chest pain, palpitations, weight changes, or abdominal pain, but endorses some difficulty breathing that waxes and wanes. He denies alcohol usage but endorses a 35 pack-year smoking history. A physical examination demonstrates mild wheezes, bibasilar crackles, and mild clubbing of his fingertips. A pulmonary function test is subsequently ordered, and partial results are shown below:
Tidal volume: 500 mL
Residual volume: 1700 mL
Expiratory reserve volume: 1500 mL
Inspiratory reserve volume: 3000 mL
What is the functional residual capacity of this patient?
- A. 4500 mL
- B. 2000 mL
- C. 2200 mL
- D. 3200 mL (Correct Answer)
- E. 3500 mL
Ventilator strategies addressing V/Q Explanation: ***3200 mL***
- The **functional residual capacity (FRC)** is the volume of air remaining in the lungs after a normal expiration.
- It is calculated as the sum of the **expiratory reserve volume (ERV)** and the **residual volume (RV)**. In this case, 1500 mL (ERV) + 1700 mL (RV) = 3200 mL.
*4500 mL*
- This value represents the sum of the **inspiratory reserve volume (3000 mL)** and the **residual volume (1700 mL)**, which does not correspond to a standard lung volume or capacity.
- It does not logically relate to the definition of functional residual capacity.
*2000 mL*
- This value represents the sum of the **tidal volume (500 mL)** and the **expiratory reserve volume (1500 mL)**, which is incorrect for FRC.
- This would represent the inspiratory capacity minus the inspiratory reserve volume, which is not a standard measurement used in pulmonary function testing.
*2200 mL*
- This value could be obtained by incorrectly adding the **tidal volume (500 mL)** and the **residual volume (1700 mL)**, which is not the correct formula for FRC.
- This calculation represents a miscombination of lung volumes that does not correspond to any standard pulmonary capacity measurement.
*3500 mL*
- This value is the sum of the **tidal volume (500 mL)**, the **expiratory reserve volume (1500 mL)**, and the **residual volume (1700 mL)**.
- This would represent the FRC plus the tidal volume, which is not a standard measurement and does not represent the functional residual capacity.
Ventilator strategies addressing V/Q US Medical PG Question 9: 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
Ventilator strategies addressing V/Q 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.
Ventilator strategies addressing V/Q US Medical PG Question 10: 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
Ventilator strategies addressing V/Q 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.
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