Acute Respiratory Distress Syndrome (ARDS) Case Study (Harding & Snyder Case Study 40): Nursing Clinical Reasoning Guide
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Get it written →Case study: Adult Respiratory Distress Syndrome
Harding, M. & Snyder, J. S. Clinical Reasoning Cases in Nursing (7th ed.). St. Louis, MO: Elsevier Mosby. Required textbook.
Adult Respiratory Distress Syndrome, Case Study 40, pages 180–185.
How to use this guide: the textbook case and its questions are copyrighted, so they are not reproduced here. Instead, this guide explains the clinical content the case tests and walks through an original practice case with model answers. Use it to study and to check your reasoning, then answer the questions in your textbook in your own words. It is not an answer key.
ARDS: what the case tests
Acute respiratory distress syndrome (ARDS), called “adult respiratory distress syndrome” in older texts, is a sudden, life-threatening form of lung injury. A direct insult (such as pneumonia, aspiration or inhalation injury) or an indirect insult (such as sepsis, major trauma, pancreatitis or massive transfusion) triggers widespread inflammation. The alveolar-capillary membrane becomes leaky, and protein-rich fluid floods the alveoli. Surfactant is lost, alveoli collapse, and the lungs become stiff (low compliance). The result is refractory hypoxemia: low oxygen that does not improve much with increasing oxygen, because blood passes through collapsed, fluid-filled alveoli without picking up oxygen (intrapulmonary shunt) (Harding et al., 2023).
Clinical reasoning cases on ARDS test early recognition of respiratory failure, arterial blood gas (ABG) interpretation, mechanical ventilation, prone positioning, prevention of ventilator complications and support for the family.
Defining ARDS
The 2012 Berlin definition requires all of the following (ARDS Definition Task Force, 2012):
- Timing: within 1 week of a known insult or new or worsening respiratory symptoms.
- Imaging: bilateral opacities on chest X-ray or CT not fully explained by effusions, collapse or nodules.
- Origin of edema: respiratory failure not fully explained by heart failure or fluid overload.
- Oxygenation (PaO2/FiO2 ratio with PEEP or CPAP of at least 5 cm H2O): mild 201–300 mm Hg, moderate 101–200 mm Hg, severe 100 mm Hg or less.
A newer global definition builds on Berlin. It includes patients on high-flow nasal oxygen of at least 30 L/min, allows an SpO2/FiO2 ratio of 315 or less (when SpO2 is 97% or below) when an ABG is not available, and accepts lung ultrasound for imaging, which makes diagnosis possible in resource-limited settings (Matthay et al., 2024).
Leaky capillaries, alveolar edema, hypoxemia (first days)
Inflammation continues, lungs stiffen (about days 7–21)
Scarring in some patients, long-term lung damage
Original practice case
Fictional case written for study. It is not the textbook case.
Mr. Marcus Bell, 48, 175 cm tall, was admitted 2 days ago with community-acquired pneumonia and sepsis. This morning he is anxious, restless and using accessory muscles. RR is 36, HR 122, BP 98/58, T 38.9°C, and SpO2 is 85% on a non-rebreather mask.
ABG on 100% oxygen: pH 7.47, PaCO2 31 mm Hg, HCO3− 22 mEq/L, PaO2 58 mm Hg. The chest X-ray shows new bilateral “white-out” infiltrates. An echocardiogram shows normal heart function. He is intubated and placed on mechanical ventilation.
Clinical reasoning questions and model answers
1. What early signs of ARDS did Mr. Bell show?
Early signs are subtle: restlessness, anxiety and confusion (from hypoxia), tachypnea, tachycardia and dyspnea, followed by accessory muscle use and falling SpO2 despite more oxygen. Crackles may develop. Restlessness and a rising respiratory rate are often the first clues, so nurses should report them promptly rather than attributing them to anxiety alone.
2. Interpret the ABG and calculate the P/F ratio.
pH 7.47 is alkalotic, and PaCO2 31 is low, so this is respiratory alkalosis from hyperventilation, with severe hypoxemia. The P/F ratio is 58 ÷ 1.0 = 58, which falls in the severe range (100 or less). As he tires, PaCO2 will rise and respiratory acidosis will follow, a sign of impending respiratory failure.
3. How is ARDS distinguished from cardiogenic pulmonary edema?
Both cause bilateral infiltrates and hypoxemia. In ARDS, the edema is caused by leaky capillaries, not high pressure in the heart. Mr. Bell’s normal echocardiogram, the absence of signs of fluid overload and a clear trigger (pneumonia and sepsis) support ARDS. In cardiogenic edema, you would expect a history of heart disease, an S3, jugular venous distension, elevated BNP and reduced heart function. See our heart failure case study for comparison.
4. What ventilator strategy is used, and why?
Lung-protective ventilation reduces further injury from overstretching the lungs:
- Low tidal volume: about 6 mL/kg of predicted body weight (PBW), not actual weight. A landmark trial showed lower tidal volumes reduced mortality (Acute Respiratory Distress Syndrome Network, 2000). For a man, PBW = 50 + 0.91 × (height in cm − 152.4). For Mr. Bell, PBW = 50 + 0.91 × 22.6 ≈ 70.6 kg, so the target tidal volume is about 424 mL.
- Plateau pressure 30 cm H2O or less to limit barotrauma.
- PEEP keeps alveoli open at the end of expiration and improves oxygenation, allowing lower FiO2.
- Permissive hypercapnia: a higher PaCO2 and mildly low pH may be accepted to protect the lungs.
The nurse monitors airway pressures, SpO2, ABGs and blood pressure. High PEEP raises intrathoracic pressure and can reduce venous return and cardiac output, causing hypotension.
5. Why is prone positioning used, and what are the nursing responsibilities?
In severe ARDS (P/F below 150), placing the patient face-down for long sessions (at least 16 hours a day in the landmark trial) improved survival (Guérin et al., 2013). Proning improves ventilation of the posterior lung, matches ventilation to blood flow and drains secretions. Nursing care includes:
- Coordinating a trained team to turn the patient safely while securing the endotracheal tube, lines and drains.
- Padding the face, chest, knees and other pressure points; repositioning the head and arms regularly (the “swimmer’s position”).
- Checking eyes, lips and facial skin for pressure injury and edema; protecting the eyes.
- Monitoring for tube displacement, hemodynamic instability and feeding intolerance.
6. The high-pressure alarm sounds. What should the nurse check?
High-pressure alarms mean resistance to airflow. Common causes are secretions (suction), the patient biting the tube or coughing (bite block, sedation), kinked tubing, fighting the ventilator, bronchospasm or pneumothorax. A sudden rise in pressure with falling SpO2, absent breath sounds on one side, tracheal deviation and hypotension suggest tension pneumothorax, an emergency requiring immediate provider notification and decompression. If the cause cannot be found quickly and the patient is deteriorating, disconnect the ventilator and ventilate with a bag-valve device while calling for help.
7. How does the nurse prevent ventilator-associated complications?
- Ventilator-associated pneumonia: head of bed at 30–45 degrees (unless prone), regular oral care, daily sedation interruption and readiness-to-wean checks, subglottic suction when available and hand hygiene.
- Venous thromboembolism: pharmacologic prophylaxis and compression devices as ordered.
- Stress ulcers: prophylaxis for high-risk patients as ordered.
- Pressure injuries and weakness: skin checks, repositioning, early mobility when stable.
- Fluid balance: after shock resolves, a conservative fluid strategy helps reduce lung edema. Monitor intake and output and daily weights.
8. How should the nurse support Mr. Bell and his family?
Provide light sedation and pain control so he is comfortable but can interact when possible, explain care even when he is sedated, and offer a way to communicate. Keep the family informed, invite them to participate in care and prepare them for a long ICU stay. Survivors often experience post-intensive care syndrome (weakness, memory problems, anxiety, depression and post-traumatic stress), so early mobility, delirium prevention, ICU diaries and follow-up services are important.
Sample nursing care plan
| Nursing problem | Goal | Key interventions |
|---|---|---|
| Impaired gas exchange | SpO2 88–95% and PaO2 55–80 mm Hg | Lung-protective ventilation; PEEP; prone positioning; ABG monitoring; suction as needed |
| Decreased cardiac output (sepsis and PEEP) | MAP at least 65 mm Hg | Hemodynamic monitoring; fluids and vasopressors as ordered |
| Risk for infection (VAP) | No new infection | VAP bundle; oral care; head-of-bed elevation; sedation interruption |
| Anxiety (patient and family) | Family verbalizes understanding of the plan | Regular updates; communication tools; involve family in care |
Frequently asked questions
Why doesn’t more oxygen fix hypoxemia in ARDS?
Much of the blood passes through collapsed or fluid-filled alveoli that receive no air (shunt), so increasing inspired oxygen does not reach it. PEEP and proning reopen alveoli.
Why use predicted rather than actual body weight?
Lung size depends on height and sex, not weight. Using actual weight in a heavy patient would deliver tidal volumes that overstretch the lungs.
What is the mortality of ARDS?
It remains high, especially in severe ARDS, and many survivors have long-term physical and psychological effects.
Clinical Reasoning Cases in Nursing: case study series
- Type 2 diabetes (Case Study 91)
- Benign prostatic hyperplasia (Case Study 70)
- IBD with small bowel involvement (Case Study 62)
- Acute respiratory distress syndrome (Case Study 40) (this guide)
- Fractured hip with postoperative complications (Case Study 46)
- Coronary artery disease and heart failure (Case Study 4)
Related reading: respiratory assessment guide, subjective vs. objective nursing data and critical appraisal for evidence-based practice.
Conclusion
ARDS cases reward nurses who notice early deterioration, interpret ABGs and P/F ratios, and understand why lung-protective ventilation, PEEP and prone positioning work. Preventing ventilator complications and supporting the family are as important as managing the ventilator itself.
References
Acute Respiratory Distress Syndrome Network. (2000). Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. New England Journal of Medicine, 342(18), 1301–1308. https://doi.org/10.1056/NEJM200005043421801
ARDS Definition Task Force. (2012). Acute respiratory distress syndrome: The Berlin definition. JAMA, 307(23), 2526–2533. https://doi.org/10.1001/jama.2012.5669
Guérin, C., Reignier, J., Richard, J.-C., Beuret, P., Gacouin, A., Boulain, T., Mercier, E., Badet, M., Mercat, A., Baudin, O., Clavel, M., Chatellier, D., Jaber, S., Rosselli, S., Mancebo, J., Sirodot, M., Hilbert, G., Bengler, C., Richecoeur, J., … Ayzac, L. (2013). Prone positioning in severe acute respiratory distress syndrome. New England Journal of Medicine, 368(23), 2159–2168. https://doi.org/10.1056/NEJMoa1214103
Harding, M. M., Kwong, J., Hagler, D., & Reinisch, C. (2023). Lewis’s medical-surgical nursing: Assessment and management of clinical problems (12th ed.). Elsevier.
Harding, M. M., & Snyder, J. S. (2019). Clinical reasoning cases in nursing (7th ed.). Elsevier Mosby.
Matthay, M. A., Arabi, Y., Arroliga, A. C., Bernard, G., Bersten, A. D., Brochard, L. J., Calfee, C. S., Combes, A., Daniel, B. M., Ferguson, N. D., Gong, M. N., Gotts, J. E., Herridge, M. S., Laffey, J. G., Liu, K. D., Machado, F. R., Martin, T. R., McAuley, D. F., Mercat, A., … Wick, K. D. (2024). A new global definition of acute respiratory distress syndrome. American Journal of Respiratory and Critical Care Medicine, 209(1), 37–47. https://doi.org/10.1164/rccm.202303-0558WS
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