LPN exams respiratory practice questions set 9

Correct answer:

Mixed expired PCO2 (PECO2) reflects CO2 in exhaled air, diluted by dead space ventilation. Given dead space (VD) is one-third of tidal volume (VT), VD/VT = 1/3. The Bohr equation relates physiological dead space to CO2: VD/VT = (PaCO2 - PECO2) / PaCO2, where PaCO2 (arterial PCO2) is 45 mmHg. Substituting: 1/3 = (45 - PECO2) / 45. Solving: 45 / 3 = 45 - PECO2, so 15 = 45 - PECO2, and PECO2 = 45 - 15 = 30 mmHg. This assumes physiological dead space equals anatomic here, as no alveolar dead space is specified. Intuitively, if one-third of each breath doesn't participate in gas exchange (PCO2 ~0 mmHg in inspired air), the expired CO2 is diluted from arterial levels (45 mmHg) to two-thirds strength (30 mmHg), matching the calculation. Options like 45 mmHg imply no dead space effect, while 20 mmHg overestimates dilution. Thus, 30 mmHg aligns with the given ratio and respiratory physiology principles.

Correct answer:

Pulmonary fibrosis, a restrictive disease, stiffens lungs with interstitial scarring. The FEV1/FVC ratio is normal or high (≥80%) because both FEV1 and FVC decrease proportionally, unlike obstructive diseases. Increased pulmonary vascular resistance occurs as fibrosis compresses capillaries, raising resistance. Peak expiratory flow (PEF), when corrected for reduced lung volume, can remain normal or above, as airflow isn't obstructed, just limited by volume. However, residual volume (RV) decreases in pulmonary fibrosis (e.g., from 1.5 L to <1 L) due to stiff lungs limiting all volumes, contrasting with obstructive diseases (e.g., COPD) where RV increases from air trapping. Increased RV doesn't fit fibrosis's restrictive pattern, where reduced elasticity shrinks residual air, not expands it, making this the inconsistent value among the set, reflecting the disease's impact on lung mechanics.

Correct answer:

The 2009 H1N1 influenza virus was a reassortant strain with genes from pig (swine flu viruses), bird (avian influenza), and human sources, reflecting its zoonotic origins. Pigs act as ‘mixing vessels,' allowing genetic exchange between flu strains from different species, which occurred here, creating a novel virus that jumped to humans. Bird genes contributed via prior avian flu strains, while human genes enabled efficient human-to-human transmission, fueling the pandemic. Cat-derived flu genes aren't documented in H1N1's makeup felines aren't typical influenza reservoirs. Pig genes alone don't tell the full story; it's the combination that matters. The nurse educates on this multi-species origin to highlight how influenza evolves, emphasizing vigilance for zoonotic threats, a key infection control lesson from H1N1's global spread, informing strategies like surveillance and vaccination.

Correct answer:

Asking if the infant is having trouble breathing best determines acuity because respiratory distress in a 6-month-old with flu-like symptoms signals a potentially life-threatening condition, like bronchiolitis or pneumonia, requiring immediate evaluation. Infants have small airways and immature lungs, making breathing difficulty a red flag symptoms like rapid breathing or grunting indicate severity. Temperature matters, but fever alone doesn't assess urgency as precisely. Nasal drainage is common in flu but not inherently acute. Symptom onset helps timeline illness but doesn't pinpoint critical status. The nurse prioritizes breathing difficulty because, in infants under six months (too young for flu shots), respiratory compromise is a leading cause of flu-related hospitalization, guiding the parent to seek care if this symptom is present, ensuring timely intervention for the vulnerable child.

Correct answer:

Most CO₂ diffusing into blood in systemic capillaries converts to bicarbonate ions in red blood cells (RBCs), making choice C correct. Only about 5-10% remains dissolved as CO₂ (choice A) due to low solubility. Around 20-25% forms carbamino compounds (choice B) by binding to hemoglobin's amino groups, but this is less dominant. The majority (65-70%) enters RBCs, where carbonic anhydrase catalyzes its reaction with H₂O to form carbonic acid (H₂CO₃), which dissociates into H⁺ and HCO₃⁻ (bicarbonate). ' CO₂ doesn't combine directly with hemoglobin significantly carbamino formation is specific. Choice E occurs minimally in plasma (slow without enzyme) compared to RBCs. Bicarbonate then exits RBCs via the chloride shift, maintaining pH balance. This process's efficiency in RBCs, driven by enzymatic speed and volume, ensures C is the primary fate of CO₂ in systemic capillaries.

Correct answer:

Decreased wheezing in a child with asthma during an acute exacerbation can signal worsening, not improvement. Asthma, a chronic inflammatory airway disease, causes bronchoconstriction, typically producing wheezing as air squeezes through narrowed passages. If wheezing diminishes without treatment resolving the attack, it may indicate a 'silent chest' severe airflow obstruction where air movement is too restricted to produce sound, risking respiratory failure. Warm, dry skin suggests improvement, as exacerbations often cause diaphoresis. A pulse of 90 beats/minute (normal: 70-110 for a 10-year-old) and respirations of 18 breaths/minute (normal: 16-20) are within expected ranges and not alarming. Monitoring for decreased wheezing is critical, as it prompts urgent intervention like bronchodilators to restore airflow, a key nursing priority in asthma management to prevent hypoxia and escalation.

Correct answer:

Decreased wheezing in a child with asthma during an acute exacerbation can signal worsening, not improvement. Asthma, a chronic inflammatory airway disease, causes bronchoconstriction, typically producing wheezing as air squeezes through narrowed passages. If wheezing diminishes without treatment resolving the attack, it may indicate a 'silent chest' severe airflow obstruction where air movement is too restricted to produce sound, risking respiratory failure. Warm, dry skin suggests improvement, as exacerbations often cause diaphoresis. A pulse of 90 beats/minute (normal: 70-110 for a 10-year-old) and respirations of 18 breaths/minute (normal: 16-20) are within expected ranges and not alarming. Monitoring for decreased wheezing is critical, as it prompts urgent intervention like bronchodilators to restore airflow, a key nursing priority in asthma management to prevent hypoxia and escalation.

Correct answer:

Pulmonary fibrosis, a restrictive disease, stiffens lungs with interstitial scarring. The FEV1/FVC ratio is normal or high (≥80%) because both FEV1 and FVC decrease proportionally, unlike obstructive diseases. Increased pulmonary vascular resistance occurs as fibrosis compresses capillaries, raising resistance. Peak expiratory flow (PEF), when corrected for reduced lung volume, can remain normal or above, as airflow isn't obstructed, just limited by volume. However, residual volume (RV) decreases in pulmonary fibrosis (e.g., from 1.5 L to <1 L) due to stiff lungs limiting all volumes, contrasting with obstructive diseases (e.g., COPD) where RV increases from air trapping. Increased RV doesn't fit fibrosis's restrictive pattern, where reduced elasticity shrinks residual air, not expands it, making this the inconsistent value among the set, reflecting the disease's impact on lung mechanics.

Correct answer:

The 2009 H1N1 influenza virus was a reassortant strain with genes from pig (swine flu viruses), bird (avian influenza), and human sources, reflecting its zoonotic origins. Pigs act as ‘mixing vessels,' allowing genetic exchange between flu strains from different species, which occurred here, creating a novel virus that jumped to humans. Bird genes contributed via prior avian flu strains, while human genes enabled efficient human-to-human transmission, fueling the pandemic. Cat-derived flu genes aren't documented in H1N1's makeup felines aren't typical influenza reservoirs. Pig genes alone don't tell the full story; it's the combination that matters. The nurse educates on this multi-species origin to highlight how influenza evolves, emphasizing vigilance for zoonotic threats, a key infection control lesson from H1N1's global spread, informing strategies like surveillance and vaccination.

Correct answer:

Severe respiratory muscle weakness (e.g., in myasthenia gravis) impairs ventilation by weakening inspiratory and expiratory muscles. Tidal volume (VT, ~500 ml normally) decreases due to limited inspiratory force, reducing breath size. Vital capacity (VC, ~4-5 L) drops as maximal inhalation and exhalation are compromised. Oxyhemoglobin saturation falls (e.g., from 95-100% to <90%) as hypoventilation lowers PaO2, causing hypoxemia. Arterial pH may decrease (acidosis) if CO2 retention raises PCO2, but this isn't specified as above normal. However, PCO2 itself (normal 35-45 mmHg) rises above normal (e.g., 50-60 mmHg) due to inadequate CO2 expulsion, a direct result of weak ventilation. Though not listed, if B intended PCO2 (a common mix-up), it fits; otherwise, none are above normal' assuming intent, PCO2's rise is the key abnormality, reflecting ventilatory failure's impact on gas exchange.