GAS EXCHANGE & ABGs
Q: A patient with acute bronchospasm has increased work of breathing and low SpO₂. Which part of gas exchange is primarily impaired: ventilation, diffusion, or perfusion, and why?
A: What is ventilation, because narrowed airways increase airway resistance and limit air movement into and out of the lungs?
A: What is ventilation, because narrowed airways increase airway resistance and limit air movement into and out of the lungs?
Q: During an acute asthma exacerbation, which phase of breathing is typically most prolonged, and what does this indicate about airway resistance?
A: What is expiration, indicating increased airway resistance due to bronchospasm and airway narrowing.
A: What is expiration, indicating increased airway resistance due to bronchospasm and airway narrowing.
Q: In chronic bronchitis‑predominant COPD, explain how excess mucus and impaired ciliary function contribute to repeated exacerbations.
A: What is that thick mucus and poor mucociliary clearance promote bacterial colonization and infection, triggering frequent exacerbations.
Q: You find a dyspneic patient with COPD lying flat in bed. Name one immediate positioning change and explain the rationale based on mechanics of breathing.
A: What is placing them in high Fowler’s or tripod position to maximize diaphragmatic movement, reduce abdominal pressure on the lungs, and decrease work of breathing.
Q: Damage to alveoli and loss of surface area for gas exchange is a hallmark of this condition.
A: What is emphysema?
Q: Name two pathophysiologic mechanisms from your slides that primarily cause diffusion problems at the alveolar‑capillary membrane.
A: What are alveolar destruction (e.g., emphysema) and thickened alveolar‑capillary membrane (e.g., pulmonary edema)?
Q: A patient’s peak expiratory flow (PEF) drops from their personal best of 500 L/min to 250 L/min. Using typical zone‑based action plans, which “zone” is this, and what does it imply about airway status?
A: What is the yellow–red border (about 50% of personal best), implying significant airway narrowing and a need for urgent escalation of treatment according to the action plan.
Q: A patient with emphysema develops a “barrel chest.” Describe the underlying mechanical change in the lungs that causes this.
A: What is loss of elastic recoil and air trapping leading to chronically hyperinflated lungs and increased anteroposterior chest diameter.
Q: During an asthma exacerbation, which is a more urgent finding: increasing respiratory rate with loud wheezes, or decreasing respiratory rate with reduced effort and diminished sounds, and why?
A: What is the latter, because falling RR and effort with diminished sounds suggest fatigue and impending respiratory failure, even if the patient seems “quieter.”
Q: This severe, life‑threatening asthma exacerbation is resistant to usual treatment like repeated SABAs.
A: What is status asthmaticus?
Q: An ABG shows pH 7.31, PaCO₂ 58 mmHg, PaO₂ 58 mmHg, HCO₃⁻ 26 mmol/L in a patient with a severe asthma attack. Interpret the acid–base status and relate it to gas exchange.
A: What is acute respiratory acidosis with hypoxemia, caused by inadequate alveolar ventilation (CO₂ retention) and impaired O₂ diffusion due to severe bronchospasm and airway obstruction?
A: What is acute respiratory acidosis with hypoxemia, caused by inadequate alveolar ventilation (CO₂ retention) and impaired O₂ diffusion due to severe bronchospasm and airway obstruction?
Q: Explain why a “silent chest” in a patient with severe asthma and increasing fatigue is more concerning than loud expiratory wheezes.
A: What is that silent chest suggests critically reduced air movement due to severe bronchospasm, mucus plugging, and impending respiratory failure, whereas wheezing requires at least some airflow.
Q: Explain how long‑standing hypoxemia in COPD can lead to cor pulmonale.
A: What is chronic hypoxemia causing pulmonary vasoconstriction and pulmonary hypertension, which increases right ventricular afterload and eventually leads to right‑sided heart failure (cor pulmonale).
Q: For an Indigenous child with asthma living in overcrowded housing, identify two nursing actions that address social determinants of health while remaining culturally safe.
A: What are any two of:
Q: In asthma, spirometry usually shows these two changes: FEV₁ and FEV₁/FVC (increased or decreased?).
A: What are decreased FEV₁ and decreased FEV₁/FVC ratio?
Q: In COPD, destruction of capillary beds and damaged alveoli lead to this specific type of gas exchange problem, and it contributes to which two classic ABG abnormalities over time?
A: What is V/Q mismatch leading to chronic hypoxemia and hypercapnia (chronic respiratory acidosis)?
Q: Distinguish the early (acute) asthmatic response from the late asthmatic response in terms of timing, main cellular players, and clinical implications for nursing care.
A: What is:
Q: A patient with COPD is started on high‑flow oxygen and becomes increasingly drowsy with rising PaCO₂. Explain the pathophysiology behind this clinical deterioration.
A: What is that in some COPD patients with chronic CO₂ retention, high FiO₂ can reduce hypoxic drive and worsen V/Q mismatch, leading to decreased ventilatory drive, further CO₂ retention (CO₂ narcosis), and decreased LOC.
Q: A COPD patient is severely dyspneic and anxious. Besides medications and positioning, identify two non‑pharmacologic nursing strategies to both improve gas exchange and reduce anxiety.
A: What are any two of: coaching pursed‑lip breathing, using calm, reassuring communication, pacing activities/rest periods, using relaxation strategies, staying with the patient to reduce fear, and coordinating care to minimize energy expenditure.
Q: Salbutamol and fluticasone are both prescribed. Which should be taken first and why?
A: What is salbutamol first, then fluticasone, because bronchodilation helps the steroid reach deeper airways.
Q: A patient with severe COPD shows a near‑normal pH with elevated PaCO₂ and elevated HCO₃⁻ on ABG. Explain the underlying gas exchange and compensatory mechanisms at work.
A: What is chronic impaired ventilation (CO₂ retention) causing respiratory acidosis with renal metabolic compensation via increased bicarbonate reabsorption, resulting in a near‑normal pH?
Q: A patient with asthma has normal FEV₁ and FEV₁/FVC at today’s visit, but reports frequent night‑time symptoms and often uses their SABA inhaler. What does this tell you about their asthma control, and what should you focus on as the nurse?
A: What is that the patient’s asthma is not well controlled even though today’s spirometry looks normal, and the priority is to ask more about symptom patterns (especially at night and with activity) and teach them to use their controller (preventer) medication every day and follow their asthma action plan, instead of relying only on the “normal” test result?
Q: Differentiate how airflow limitation in asthma vs COPD appears on spirometry after bronchodilator administration, and how this informs diagnosis.
A: What is that asthma typically shows significant reversibility (marked improvement in FEV₁ and FEV₁/FVC after bronchodilator), while COPD shows persistent airflow limitation with minimal reversibility, helping distinguish reversible vs chronic, non‑fully‑reversible obstruction.
Q: A patient with both asthma and COPD (“asthma–COPD overlap”) is admitted with worsening dyspnea. From a nursing perspective, explain why careful assessment of their baseline function and current status is critical before titrating oxygen or bronchodilators.
A: What is that overlap patients may have features of both reversible bronchospasm and chronic CO₂ retention; understanding their usual SpO₂/functional level and differentiating acute from chronic changes is essential to safely titrate oxygen (avoiding CO₂ narcosis) and to evaluate response to bronchodilators, preventing under‑ or overtreatment.
A 58‑year‑old man with known COPD (chronic bronchitis type) presents with increased dyspnea, productive cough, and wheezing. He has a 30‑pack‑year smoking history. His SpO₂ is 86% on room air; RR 30/min, using accessory muscles.
a) Identify two priority nursing interventions in the first 15–30 minutes and justify each using pathophysiology of COPD.
b) Identify one assessment finding over the next hour that would indicate clinical deterioration despite treatment.
a) Any two of:
b) Any one of: