NCLEX Respiratory Review: ARDS, COPD, and Chest Tubes

Quick answer: NCLEX respiratory questions test ABG interpretation, oxygen-device selection, COPD and asthma care, pneumonia, pulmonary embolism, ARDS, chest tubes, and tracheostomy care. The core rules: airway comes first; use ROME to read ABGs; target SpO2 88–92% in known or suspected chronic hypercapnic respiratory failure without withholding oxygen; ARDS causes refractory hypoxemia that responds poorly to more oxygen — PEEP improves oxygenation and low tidal volumes protect the lung; continuous water-seal bubbling signals an air leak.

Respiratory questions reward nurses who can read an ABG in 10 seconds, pick the right oxygen delivery device for the patient’s needs, and recognize deterioration before a code is called. If you can interpret acid-base, protect the airway, and manage a chest tube without panicking, you will clear this domain.

Key takeaways

• Airway, then breathing, then circulation. A patient who cannot protect the airway always outranks a patient with low SpO2 who is still ventilating.
• Use ROME for ABGs: Respiratory Opposite, Metabolic Equal. Check the pH first, find the matching value, then look for compensation.
• Oxygenation is not ventilation. SpO2 reflects oxygen; PaCO2 reflects ventilation — a COPD patient can have a normal SpO2 and still retain CO2.
• Match the device to the need: nasal cannula for mild hypoxemia, non-rebreather for acute distress, venturi for precise titration, HFNC/NIV for moderate-to-severe failure.
• Target SpO2 88–92% in known or suspected chronic hypercapnic respiratory failure — do not withhold oxygen from a hypoxic COPD patient.
• ARDS = refractory hypoxemia. Bilateral opacities, respiratory failure not fully explained by cardiac failure or fluid overload, and a PaO2/FiO2 of 300 or less on PEEP of at least 5. It responds poorly to more FiO2 — PEEP improves oxygenation, and tidal volumes of 4–6 mL/kg of predicted body weight protect the lung.
• Chest tube rules: tidaling and gentle intermittent water-seal bubbling are normal; continuous water-seal bubbling is an air leak; never routinely clamp the tube.

How the NCLEX frames respiratory questions

Expect ABG interpretation, oxygen device selection, COPD exacerbation management, asthma teaching, pneumonia triage, pulmonary embolism recognition, ARDS recognition, and chest tube troubleshooting. NGN items often layer a respiratory scenario with labs, meds, and vital sign trends — you must identify what is new, what is worsening, and what to act on first.

Three principles anchor every answer:

• Airway before breathing before circulation. A patient who cannot protect the airway is your priority over a patient with low SpO2 who is still ventilating.
• Oxygenation is not the same as ventilation. SpO2 tells you about oxygen; PaCO2 tells you about ventilation. A COPD patient can have a normal SpO2 and still be retaining CO2.
• Position and suction come first, meds come second. Before drawing up a bronchodilator, sit the patient up, clear secretions, and apply oxygen appropriately.

ABG interpretation: ROME

Arterial blood gases look intimidating until you have a system. Use ROME — Respiratory Opposite, Metabolic Equal — and you will interpret most ABGs in under a minute.

Normal values

• pH: 7.35–7.45
• PaCO2: 35–45 mm Hg
• HCO3: 22–26 mEq/L
• PaO2: 80–100 mm Hg
• SaO2: 95–100%

The three-step read

1. Is the pH acidotic or alkalotic? Under 7.35 = acidosis. Over 7.45 = alkalosis.
2. Which value matches? If pH and CO2 move in opposite directions, it is respiratory (pH down, CO2 up = respiratory acidosis). If pH and HCO3 move in the same direction, it is metabolic (pH down, HCO3 down = metabolic acidosis).
3. Is there compensation? If the opposite system has moved out of range in the corrective direction, the body is compensating. Fully compensated means pH is back within range.

Common patterns

• Respiratory acidosis: Hypoventilation — COPD exacerbation, opioid overdose, neuromuscular weakness. pH low, CO2 high.
• Respiratory alkalosis: Hyperventilation — anxiety, pain, early PE, early sepsis. pH high, CO2 low.
• Metabolic acidosis: DKA, renal failure, severe diarrhea, lactic acidosis. pH low, HCO3 low.
• Metabolic alkalosis: Vomiting, NG suction losses, diuretic use. pH high, HCO3 high.

Clinical pearl: When you see moderate DKA (pH 7.2, HCO3 12), expect Kussmaul respirations — the lungs are compensating by blowing off CO2. Do not mistake deep, rapid breathing for respiratory distress when the metabolic picture explains it.

For a deeper walkthrough of acid-base patterns and worked examples, see the full ABG interpretation guide.

Oxygen delivery devices

Know the escalation path and the FiO2 ranges. You will be asked to choose the correct device for the scenario.

The COPD oxygen myth — updated guidance

Older teaching warned against giving oxygen to COPD patients because it could “knock out the hypoxic drive.” Current evidence-based guidance (including British Thoracic Society and GOLD) is more nuanced: target an SpO2 of 88–92% in patients with known or suspected chronic hypercapnic respiratory failure, not 94–98%. The goal is to avoid both hypoxemia and hyperoxia-induced CO2 retention. Titrate oxygen to the target, recheck ABG, and adjust — do not withhold oxygen from a hypoxic COPD patient out of fear.

Asthma vs COPD: the distinctions that matter

• Asthma: Reversible bronchoconstriction. Triggers (allergens, exercise, cold). Normal FEV1 between attacks. Treatment: short-acting beta-agonist (albuterol) for rescue, inhaled corticosteroid (fluticasone, budesonide) for control. Peak flow monitoring is central — green zone 80–100%, yellow 50–79% (use rescue), red under 50% (emergency).
• COPD: Progressive, irreversible airflow limitation. Chronic bronchitis (productive cough) and emphysema (air trapping, barrel chest). Pursed-lip breathing is a compensatory pattern; teach it intentionally. Smoking cessation is the single intervention that alters the disease course.

Inhaler teaching checkpoints

• Shake the metered-dose inhaler before use.
• Use a spacer if available — it improves deposition and reduces oral thrush.
• After inhaled corticosteroids, rinse the mouth to prevent candidiasis.
• If using a short-acting beta-agonist and a corticosteroid, give the beta-agonist first to open the airway.
• Rescue inhaler use more than twice a week suggests poor control — notify the provider.

Pneumonia

• Community-acquired pneumonia (CAP): Most common bacterial cause is Streptococcus pneumoniae. Fever, productive cough, pleuritic chest pain, crackles, possibly consolidation on chest X-ray.
• Hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP): higher risk of resistant organisms. Prevention is testable — HOB 30–45 degrees for intubated patients, oral care with chlorhexidine per protocol (the 2022 SHEA/IDSA update recommends oral care with toothbrushing but advises against routine chlorhexidine after data showed no VAP benefit and a possible mortality signal; exam items still list it in the VAP bundle), daily sedation interruption, DVT and peptic ulcer prophylaxis.
• Obtain cultures before antibiotics when possible, but do not delay antibiotics in a septic patient.
• To prevent postoperative pneumonia, CDC guidance encourages deep breathing and early ambulation, plus incentive spirometry for high-risk patients; adequate hydration, unless contraindicated, helps thin secretions.

Pulmonary embolism

Classic presentation: sudden dyspnea, pleuritic chest pain, tachycardia, possibly hemoptysis. Hypoxia and respiratory alkalosis on ABG. Risk factors mirror Virchow’s triad (stasis, endothelial injury, hypercoagulability) — recent surgery, immobility, malignancy, oral contraceptives, pregnancy, DVT history.

• ECG: Sinus tachycardia is most common. The classic S1Q3T3 pattern is specific but uncommon — do not wait to see it before acting.
• Labs/imaging: D-dimer (sensitive, not specific), CT pulmonary angiography is the definitive test.
• Treatment: Anticoagulation — heparin drip, enoxaparin, or a DOAC. Massive PE with hemodynamic compromise: thrombolytics or embolectomy.
• Prevention: Early ambulation, sequential compression devices, prophylactic anticoagulation in at-risk inpatients.

Acute Respiratory Distress Syndrome (ARDS)

ARDS is diffuse alveolar injury from an insult somewhere else in the body — sepsis, aspiration, pancreatitis, trauma, near-drowning, massive transfusion, inhalation injury. The alveolar-capillary membrane becomes leaky, protein-rich fluid floods the alveoli, surfactant is destroyed, and the lung stiffens. The result is intrapulmonary shunt: blood flows past alveoli that are full of fluid and never picks up oxygen. That single pathophysiologic fact explains every ARDS question you will see.

The Berlin Definition

The Berlin Definition (ARDS Definition Task Force, JAMA 2012) is what the NCLEX tests. All four criteria must be present. Newer consensus criteria exist that extend the definition to high-flow nasal cannula and to settings without arterial blood gases, but Berlin remains the standard for exam purposes.

• Timing: Onset within 1 week of a known clinical insult, or new or worsening respiratory symptoms.
• Chest imaging: Bilateral opacities not fully explained by pleural effusions, lobar or lung collapse, or nodules.
• Origin of edema: Respiratory failure not fully explained by cardiac failure or fluid overload. If no ARDS risk factor is apparent, objective assessment such as echocardiography is needed to exclude hydrostatic edema.
• Oxygenation: PaO2/FiO2 ratio of 300 mm Hg or less, measured with PEEP or CPAP of at least 5 cm H2O.

Calculating the ratio is straightforward: divide the PaO2 by the FiO2 expressed as a decimal. A PaO2 of 70 on 60% oxygen is 70 ÷ 0.60 = 117 — moderate ARDS. For the ABG mechanics behind the ratio, see the full ABG interpretation guide.

The hallmark: refractory hypoxemia

This is the single most-tested finding in ARDS. The patient’s hypoxemia does not improve when you increase the FiO2. You turn a nasal cannula up to a non-rebreather at 15 L/min and the SpO2 barely moves. That is shunt physiology — supplemental oxygen cannot reach alveoli that are filled with fluid, so raising the concentration of inspired oxygen accomplishes very little. Only opening the alveoli, with PEEP, changes the picture.

When a stem gives you a patient with a known insult 24–72 hours ago, new bilateral infiltrates, and an SpO2 that will not come up despite escalating oxygen, the answer is ARDS. If you see a question asking what the hallmark of ARDS is, refractory hypoxemia is almost always the intended answer.

ARDS versus cardiogenic pulmonary edema

Both present with dyspnea, crackles, and bilateral infiltrates on chest X-ray. The exam expects you to separate them on the surrounding evidence, not the lung exam.

One caveat worth knowing: the Berlin Definition removed the hard wedge-pressure cutoff and replaced it with clinical judgment, because ARDS and heart failure can coexist. Nursing exams still use the wedge pressure, JVD, and cardiomegaly contrast, so learn it — just understand that in practice it is a pattern, not a switch.

The ABG in ARDS

• Early, spontaneously breathing ARDS gives respiratory alkalosis. The patient is tachypneic and blowing off CO2, so the PaCO2 is low while the PaO2 stays low — for example pH 7.50, PaCO2 30, PaO2 55.
• A rising or normalizing PaCO2 in a tachypneic ARDS patient means fatigue and impending respiratory failure — a red flag, not improvement.
• Once the patient is on lung-protective ventilation the picture flips: permissive hypercapnia is expected and accepted.

For the acid-base patterns behind these gases, work through the ABG interpretation guide.

Management: lung-protective ventilation

You cannot fix the leaky membrane. Everything you do is supportive — keep the lung open, avoid injuring it further, and treat what caused it.

• Low tidal volume ventilation, 4–6 mL/kg of PREDICTED body weight. This is the trap. Predicted body weight is calculated from height and sex, not from the number on the scale — lung size tracks height, not adiposity. Setting a tidal volume from a 140 kg patient’s actual weight delivers a volume the lungs cannot hold. The ARDSNet (ARMA) protocol starts at 6 mL/kg predicted body weight and steps down toward 4 mL/kg if the plateau pressure stays too high.
• Plateau pressure under 30 cm H2O. Plateau pressure reflects alveolar distention. Above 30, you are producing volutrauma and barotrauma. If plateau pressure exceeds 30, the tidal volume comes down.
• PEEP for alveolar recruitment. PEEP holds alveoli open at end-expiration, recruits collapsed lung, and improves oxygenation so FiO2 can be reduced. Watch for the two complications: barotrauma (sudden hypotension with absent breath sounds and tracheal deviation is tension pneumothorax — an emergency) and decreased venous return causing hypotension.
• Permissive hypercapnia. Small tidal volumes mean CO2 rises and pH falls. This is tolerated deliberately. Do not expect a normal PaCO2 on a ventilated ARDS patient’s gas.
• Prone positioning for moderate-to-severe ARDS (PaO2/FiO2 under 150). The PROSEVA trial (NEJM 2013) enrolled patients with a PaO2/FiO2 under 150 while on an FiO2 of at least 0.6 and PEEP of at least 5, and used prone sessions of at least 16 consecutive hours, begun within 36 hours of intubation, reducing 28-day mortality (16.0% vs 32.8%). Proning redistributes ventilation to dorsal lung regions and improves ventilation-perfusion matching.
• Treat the underlying cause. Antibiotics and source control for sepsis, and conservative fluid management once the patient is no longer in shock. ARDS does not resolve until its trigger does.

Nursing priorities

• Monitor oxygenation continuously and trend the PaO2/FiO2 ratio, not just the SpO2. A stable SpO2 achieved on a rising FiO2 is a patient who is getting worse.
• Head of bed 30–45 degrees, oral care per protocol, daily sedation interruption and spontaneous breathing trial assessment, DVT and stress ulcer prophylaxis — the VAP bundle applies to every ventilated ARDS patient.
• Prone positioning is a team maneuver. Minimum of three to five staff. Secure the airway first and assign one person to the endotracheal tube. Protect pressure points (face, chest, iliac crests, knees), reposition the head every two hours, and pad generously. Unplanned extubation and facial pressure injury are the complications you are accountable for.
• Cluster care and minimize suctioning. Disconnecting the circuit drops PEEP and derecruits the lung; use in-line closed suction and suction only when indicated.
• Assess for the deterioration signs: rising peak pressures, falling SpO2, new asymmetric breath sounds, subcutaneous emphysema, sudden hypotension. Any of these can be pneumothorax.
• Support the family. ARDS carries substantial mortality and long ICU stays; these patients are frequently sedated and paralyzed, and communication with families is a nursing responsibility the exam does test.

Chest tubes: the troubleshooting rules

Chest tubes evacuate air, fluid, or blood from the pleural space. You will be asked to recognize normal function, troubleshoot a problem, and know when to act.

What is normal

• Tidaling (fluctuation in the water seal chamber with respirations) is expected and reassuring — it means the system is patent and the lung has not fully reexpanded.
• Gentle, intermittent bubbling in the water seal chamber during forced exhalation or coughing can be normal immediately after insertion.
• Continuous bubbling in the suction chamber is normal if suction is applied.

What is a problem

• Continuous bubbling in the water seal chamber indicates an air leak — check connections first, then the patient’s insertion site.
• No tidaling can mean the lung has fully reexpanded (good) or the tubing is kinked/occluded (bad). Assess the patient first.
• Sudden cessation of drainage may indicate a clot — notify the provider; do not milk or strip the tubing routinely.
• Subcutaneous emphysema (crepitus around the site) suggests air leaking into tissue — assess the site and notify the provider.

Rules you do not break

• Keep the collection system below chest level.
• Never clamp a chest tube unless changing the drainage system, per provider order, or for a brief few-second diagnostic clamp to localize an air leak — sustained clamping can cause a tension pneumothorax.
• If the tube is dislodged from the patient: cover the site with a sterile gauze dressing taped on three sides (flutter valve effect).
• If the tube is disconnected from the system: submerge the end in sterile water or saline (until a new system is available).
• Keep a bottle of sterile water and padded clamps at the bedside.

For step-by-step setup, troubleshooting, and emergency interventions, work through the dedicated chest tube management guide.

Tracheostomy and airway management

• Keep an obturator and a spare trach tube (same size and one size smaller) at the bedside.
• Suction only when indicated — not on a schedule. Hyperoxygenate before suctioning; suction no longer than 10 seconds per pass.
• If a trach is dislodged within 7 days of placement: this is an emergency — cover the stoma, call for help, and prepare for emergent reintubation. After the tract has matured (7+ days), reinsertion is often possible at the bedside.
• Humidification is required — dry air damages the mucosa and thickens secretions.

Putting it together on test day

Run this sequence on respiratory questions:

1. Can the patient protect the airway? If not, that is your priority intervention.
2. What is the oxygenation and ventilation status? Check SpO2, RR, effort, and ABG if given.
3. Match the device to the need. Nasal cannula for mild hypoxemia, non-rebreather for acute distress, venturi for precise titration, HFNC/NIV for moderate-to-severe failure.
4. Anticipate complications. Pneumonia → sepsis. COPD → respiratory failure. Post-op → atelectasis and PE. Chest tube → leak, obstruction, dislodgement.

Pair this review with your lab values sheet (ABG, D-dimer, WBC) and pharmacology review (bronchodilators, steroids, anticoagulants). For a broader map of nursing review topics, see all NCLEX resources.

Frequently Asked Questions

What is the ROME method for interpreting ABGs?

ROME stands for Respiratory Opposite, Metabolic Equal. After deciding whether the pH is acidotic (under 7.35) or alkalotic (over 7.45), check which value matches the disturbance. If the pH and CO2 move in opposite directions, the problem is respiratory; if the pH and HCO3 move in the same direction, the problem is metabolic. Then look at the opposite system to judge whether the body is compensating.

What SpO2 should you target in a COPD patient?

In patients with known or suspected chronic hypercapnic respiratory failure, target an SpO2 of 88–92% rather than 94–98%. This avoids both hypoxemia and hyperoxia-induced CO2 retention. The key point for the NCLEX is that you should never withhold oxygen from a hypoxic COPD patient out of fear of the hypoxic drive — you titrate oxygen to the target and recheck the ABG.

When is bubbling in a chest tube system normal versus a problem?

Tidaling (fluctuation in the water seal chamber with respirations) is normal and reassuring, and gentle intermittent bubbling in the water seal chamber during coughing or forced exhalation can be normal right after insertion. Continuous bubbling in the suction chamber is normal when suction is applied. However, continuous bubbling in the water seal chamber signals an air leak — check the connections first, then the insertion site.

Why should you avoid clamping a chest tube?

Sustained clamping of a chest tube can trap air in the pleural space and cause a tension pneumothorax. Clamp only when changing the drainage system, when specifically ordered, or for a brief few-second clamp to locate an air leak per agency policy. Routine stripping or milking of the tubing is also discouraged because it raises intrapleural pressure and can damage tissue.

How do you choose the right oxygen delivery device?

Match the device to the patient’s need. A nasal cannula (1–6 L/min, FiO2 24–44%) is for mild hypoxemia, a non-rebreather (10–15 L/min, up to 90%+ FiO2) is for acute respiratory distress, a venturi mask delivers precise FiO2 when exact titration matters such as in COPD, and high-flow nasal cannula or non-invasive ventilation supports moderate-to-severe respiratory failure. Always confirm the patient can protect the airway before relying on a mask or non-invasive ventilation.