LPN exams respiratory practice questions set 5

Correct answer:

Infant respiratory distress syndrome (IRDS) in premature babies stems from inadequate surfactant production, critical for reducing alveolar surface tension (T). Without surfactant, T increases, causing alveoli to collapse due to high water-induced tension, unlike normal low-tension stability. This elevates the pressure needed to expand lungs, decreasing lung compliance (C), as stiff lungs resist inflation a hallmark of IRDS. Collapsed alveoli impair gas exchange, reducing arterial PO2 (PaO2) from normal (75-100 mmHg) to hypoxic levels (e.g., 50-60 mmHg), driving respiratory distress. Option B (T increases, C decreases, PaO2 decreases) matches this pathophysiology: high T from surfactant lack, low C from rigidity, and low PaO2 from poor oxygenation. Other options fail e.g., C increasing contradicts stiffness, PaO2 equal ignores hypoxemia. This triad reflects IRDS's core mechanism, where surfactant deficiency cascades into ventilatory and oxygenation failure.

Correct answer:

Choice C is false. Pulmonary resistance decreases as lung volume increases because extra-alveolar vessels (arteries and veins) are pulled open by radial traction, reducing resistance, not increasing it. Choice A is true; increased pulmonary arterial pressure recruits and distends vessels, lowering resistance. ' pulmonary resistance is about 1/10 of systemic due to shorter, wider vessels. Choice D is true; acetylcholine, via parasympathetic stimulation, relaxes bronchiolar smooth muscle, though its effect is less pronounced than adrenaline's. Choice E is also true; at large lung volumes, pulmonary capillaries are compressed, increasing resistance. The error in C stems from misunderstanding lung volume effects: as lungs expand, airway resistance drops (bronchioles widen), and extra-alveolar vessel resistance decreases due to mechanical stretching, not increases. This aligns with physiological principles of pulmonary circulation, making C the false statement.

Correct answer:

Choice C is false. Pulmonary resistance decreases as lung volume increases because extra-alveolar vessels (arteries and veins) are pulled open by radial traction, reducing resistance, not increasing it. Choice A is true; increased pulmonary arterial pressure recruits and distends vessels, lowering resistance. ' pulmonary resistance is about 1/10 of systemic due to shorter, wider vessels. Choice D is true; acetylcholine, via parasympathetic stimulation, relaxes bronchiolar smooth muscle, though its effect is less pronounced than adrenaline's. Choice E is also true; at large lung volumes, pulmonary capillaries are compressed, increasing resistance. The error in C stems from misunderstanding lung volume effects: as lungs expand, airway resistance drops (bronchioles widen), and extra-alveolar vessel resistance decreases due to mechanical stretching, not increases. This aligns with physiological principles of pulmonary circulation, making C the false statement.

Correct answer:

Shallow respirations in an older client with flu suggest difficulty oxygenating effectively, often due to mucus buildup or fatigue. Elevating the head of the bed helps by using gravity to open the airways, reducing pressure on the diaphragm and improving lung expansion, which is especially beneficial for older adults with weakened respiratory muscles. A humidifier adds moisture to the air, loosening mucus and easing breathing, which is critical when flu causes thick secretions. Antipyretics reduce fever but don't directly address shallow breathing, though fever management supports overall comfort. Analgesics might relieve pain but not respiratory effort. A face mask could worsen breathing by restricting airflow unless oxygen is medically indicated. The nurse's advice focuses on non-invasive, practical measures to enhance airflow and comfort, tailored to the client's age and flu-related respiratory challenges, ensuring better oxygenation and reduced strain.

Correct answer:

Shallow respirations in an older client with flu suggest difficulty oxygenating effectively, often due to mucus buildup or fatigue. Elevating the head of the bed helps by using gravity to open the airways, reducing pressure on the diaphragm and improving lung expansion, which is especially beneficial for older adults with weakened respiratory muscles. A humidifier adds moisture to the air, loosening mucus and easing breathing, which is critical when flu causes thick secretions. Antipyretics reduce fever but don't directly address shallow breathing, though fever management supports overall comfort. Analgesics might relieve pain but not respiratory effort. A face mask could worsen breathing by restricting airflow unless oxygen is medically indicated. The nurse's advice focuses on non-invasive, practical measures to enhance airflow and comfort, tailored to the client's age and flu-related respiratory challenges, ensuring better oxygenation and reduced strain.

Correct answer:

Physiological dead space (VD) is the portion of tidal volume (VT) not participating in gas exchange, calculated using the Bohr equation: VD/VT = (PaCO2 - PECO2) / PaCO2, where PaCO2 is arterial PCO2 (40 mmHg) and PECO2 is mixed expired PCO2 (28 mmHg). Plugging in the values: VD/VT = (40 - 28) / 40 = 12 / 40 = 0.3. Since VT is 600 ml, VD = 0.3 × 600 = 180 ml. To verify, alveolar ventilation (VA) is given as 4.3 L/min, and total ventilation (VE) is respiratory rate (RR) × VT. VA = VE - (VD × RR), but we can also derive VD from VA: VA = (VT - VD) × RR. Converting 4.3 L/min to 4300 ml/min and assuming RR from context (e.g., 10 breaths/min aligns with typical resting rates), VT - VD = 4300 / 10 = 430 ml, so VD = 600 - 430 = 170 ml, close to 180 ml, adjusting for rounding. The 180 ml option fits the Bohr calculation directly, confirming it as the physiological dead space, reflecting both anatomical and alveolar components not contributing to CO2 elimination.

Correct answer:

The percentage of CO2 in a structure reflects its PCO2, tied to metabolic production and gas exchange. Pulmonary arteries carry deoxygenated blood from the right heart to the lungs, with a PCO2 of ~45-46 mmHg (venous blood), the highest among options, as it's loaded with CO2 from systemic tissues. Alveolar air has a PCO2 of ~40 mmHg, equilibrated with arterial blood after CO2 diffuses out during respiration. Pulmonary veins, post-gas exchange, carry oxygenated blood with a PCO2 of ~40 mmHg, matching arterial levels. Interstitial fluid's PCO2 varies but approximates venous blood (~45 mmHg) or slightly less, depending on local metabolism, though it's not a standard respiratory measure. Systemic arteries, not listed, also have ~40 mmHg. Pulmonary arteries stand out with the highest CO2 due to their role in transporting metabolically produced CO2 to the lungs for excretion, before alveolar ventilation lowers it, making them the site of peak CO2 concentration.

Correct answer:

In a healthy upright individual, regional ventilation varies due to gravity and pleural pressure gradients. At rest, intrapleural pressure (IPP) is more negative at the apex (~-10 cm H2O) than the base (~-2.5 cm H2O) due to lung weight, making apices less compliant (stiffer) and bases more compliant (easier to expand). During quiet breathing (VT = 400 ml, RR = 12/min), the diaphragm's downward pull preferentially ventilates the lower zones, where compliance is higher and initial volume lower, allowing greater volume change (ΔV). Studies (e.g., West) show lower lobes receive ~4 times more ventilation per unit volume than apices. Thus, ventilation is greatest in the lower zones, followed by middle, then upper (Lower > Middle > Upper). Equal ventilation ignores gravity's effect, and Upper > Middle > Lower reverses the gradient. For this boy, VA = (400 - ~120 ml VD) × 12 = ~3.36 L/min, distributed predominantly to the base, making this the best description.

Correct answer:

Intrapleural pressure (IPP) is the pressure in the pleural cavity, normally negative relative to atmospheric pressure (760 mmHg) due to the opposing recoils of the lung (inward) and chest wall (outward). At rest (FRC), IPP is ~756 mmHg (-4 mmHg); during inspiration, it drops further (e.g., -6 mmHg) as the thoracic cavity expands, and during expiration, it rises slightly but remains negative. It's always less than atmospheric pressure in a healthy lung, even during forced maneuvers, unless the pleural space is breached (e.g., pneumothorax), equalizing it to 760 mmHg. It's not just low during inspiration it's consistently subatmospheric. Respiratory muscles create the gradient but don't equalize IPP to atmospheric pressure. IPP isn't the alveolar-pleural difference (that's transpulmonary pressure); it's the absolute pressure in the pleural space. The constant negativity maintains lung expansion, making this the true statement reflecting pleural mechanics.

Correct answer:

Intrapleural pressure (IPP) is the pressure in the pleural cavity, normally negative relative to atmospheric pressure (760 mmHg) due to the opposing recoils of the lung (inward) and chest wall (outward). At rest (FRC), IPP is ~756 mmHg (-4 mmHg); during inspiration, it drops further (e.g., -6 mmHg) as the thoracic cavity expands, and during expiration, it rises slightly but remains negative. It's always less than atmospheric pressure in a healthy lung, even during forced maneuvers, unless the pleural space is breached (e.g., pneumothorax), equalizing it to 760 mmHg. It's not just low during inspiration it's consistently subatmospheric. Respiratory muscles create the gradient but don't equalize IPP to atmospheric pressure. IPP isn't the alveolar-pleural difference (that's transpulmonary pressure); it's the absolute pressure in the pleural space. The constant negativity maintains lung expansion, making this the true statement reflecting pleural mechanics.