ATI LPN
Questions for the Respiratory System Questions
Question 1 of 5
Carpal tunnel syndrome can be caused by:
Correct Answer: D
Rationale: Failed to generate a rationale of 500+ characters after 5 retries.
Question 2 of 5
The primary force responsible for the movement of air into the lungs during inspiration?
Correct Answer: D
Rationale: Inspiration occurs when air moves into the lungs due to a pressure gradient, as per Boyle's law: expanding the thoracic cavity decreases intrapulmonary pressure below atmospheric pressure (760 mmHg to ~758 mmHg), driving air inward. This gradient, the pressure difference between atmospheric and intrapulmonary pressure, is the primary force, created by diaphragm and intercostal muscle contraction. Atmospheric pressure alone isn't a force' but a reference; it's the difference that matters. Muscular spasm implies involuntary action, not the controlled contraction of respiration. Reduced surface tension, via surfactant, aids lung expansion but isn't the driving force it reduces resistance to expansion. Muscle relaxation occurs in expiration, not inspiration. The pressure difference is the fundamental mechanism, quantifiable (e.g., 1-2 mmHg drop suffices for tidal breathing), and directly ties muscle action to airflow, distinguishing it as the essential driver of ventilation.
Question 3 of 5
A patient with restrictive lung disease will have a relatively normal?
Correct Answer: D
Rationale: Restrictive lung diseases (e.g., pulmonary fibrosis) stiffen lungs, reducing expansion and volumes like forced vital capacity (FVC), which drops below normal (e.g., from 4-5 L to 2-3 L) due to limited inspiratory capacity. Forced expiratory volume in 1 second (FEV1) also decreases proportionally (e.g., from 3-4 L to 1.5-2 L), as less air is available to exhale. However, the FEV1/FVC ratio remains normal or elevated (≥80%) because both values decline similarly, unlike obstructive diseases where FEV1 falls more, lowering the ratio (<70%). Ventilation/perfusion (V/Q) ratio may skew high in restrictive disease (e.g., fibrosis) due to reduced ventilation from stiff lungs, not normal matching. FEV1 and FVC individually are reduced, not normal. The FEV1/FVC ratio's preservation reflects the restrictive pattern impaired volume, not airflow obstruction making it the value least altered relative to healthy norms, a key diagnostic feature in spirometry.
Question 4 of 5
One of the followings is expected in idiopathic pulmonary fibrosis.
Correct Answer: A
Rationale: Idiopathic pulmonary fibrosis (IPF) scars lung interstitium, reducing elasticity and volumes. Functional residual capacity (FRC), the resting volume (~2.5-3 L normally), decreases in IPF (e.g., to 2 L) as stiff lungs limit expansion, a hallmark of restrictive disease. Tidal volume (VT, ~500 ml) typically decreases, not increases, as breathing becomes shallow due to restricted capacity, often requiring faster rates to maintain ventilation. Pulmonary vascular resistance rises, not falls, as fibrosis compresses capillaries, increasing resistance and risking right heart strain. Total lung capacity (TLC, ~6 L) also drops (e.g., to 4 L), reflecting reduced maximum volume, not higher. Lower FRC aligns with IPF's mechanics stiff lungs reduce resting and total volumes, impair gas exchange, and elevate work of breathing, distinguishing it from options contradicting restrictive physiology.
Question 5 of 5
Regarding pulmonary vascular resistance, which one of the following is true?
Correct Answer: C
Rationale: Pulmonary vascular resistance (PVR) reflects opposition to blood flow in the pulmonary circulation, influenced by lung volume and vessel mechanics. At high lung volumes (near TLC), extra-alveolar vessels stretch and narrow, and alveolar capillaries compress, increasing PVR. At low volumes (near RV), these vessels are less stretched and more patent, lowering PVR, though this isn't the queried truth. The true statement is that increased PVR can lead to right heart failure, as seen in conditions like pulmonary hypertension or fibrosis, where elevated resistance overworks the right ventricle, causing cor pulmonale. PVR isn't measured by routine pulmonary function tests (e.g., spirometry), which assess airflow and volumes, not vascular pressures cardiac catheterization is required instead. The link to right heart failure is critical, as chronic high PVR elevates pulmonary artery pressure, straining the heart's ability to pump against it, a key pathophysiological consequence distinguishing this option as true amid the others' inaccuracies.