NLE Respiratory Nursing — Chronic Obstructive & Restrictive Pulmonary DisordersRevision Notes

Formulas

Exam Tips

• The NLE question will often give a scenario with a 'smoker with barrel chest and pursed-lip breathing' — think EMPHYSEMA (pink puffer). 'Cyanotic patient with oedema and productive cough' — think CHRONIC BRONCHITIS (blue bloater).
• If the question says 'SpO2 88%' in a known COPD patient and asks what to do: DO NOT automatically increase O2. Assess the patient; if they are comfortable and alert, 88–92% is the ACCEPTABLE target range for COPD.
• Spirometry in COPD: FEV1/FVC < 70% post-bronchodilator = COPD. Remember 'COPD cannot be corrected' — irreversibility is the key.
• ABG in COPD: high CO2, high HCO3 (kidneys compensate by retaining bicarb), low PaO2, near-normal pH = CHRONIC respiratory acidosis with metabolic compensation.
• For NLE SATA/priority questions: the FIRST nursing action for a COPD patient in respiratory distress is to position in high-Fowler's or tripod position AND apply controlled low-flow oxygen with SpO2 monitoring.

Key Points

• COPD is a progressive, largely IRREVERSIBLE airflow limitation caused primarily by cigarette smoking. In the Philippine setting, biomass/cooking-fuel smoke (kalan, uling) and occupational dust/fume exposure are also significant causes.
• COPD is an umbrella term: most patients have a combination of chronic bronchitis AND emphysema.
• Chronic Bronchitis is defined CLINICALLY: productive cough for at least 3 months in 2 consecutive years, not explained by another condition.
• Emphysema is defined PATHOLOGICALLY: permanent destruction of alveolar walls (acini) with loss of elastic recoil, creating enlarged air spaces (bullae) and air trapping.
• Alpha-1 antitrypsin (AAT) deficiency is a genetic cause of emphysema in younger, non-smoking patients — watch for this in NLE scenarios involving a young adult with no smoking history.
• Spirometry confirming COPD: FEV1/FVC ratio < 70% that is NOT fully reversible after bronchodilator administration. This irreversibility distinguishes COPD from asthma.
• ABG pattern in COPD: chronic respiratory acidosis WITH metabolic (renal) compensation — elevated PaCO2, elevated HCO3, near-normal pH, and low PaO2.
• Chronic complications of COPD include: cor pulmonale (right-sided heart failure from pulmonary hypertension), secondary polycythaemia (bone marrow increases RBC production to compensate for chronic hypoxaemia), and spontaneous pneumothorax from ruptured bullae.

Definitions

Section Title

COPD: Overview, Pathophysiology, and Classification

Common Mistakes

• Confusing the 'blue bloater' (chronic bronchitis) with 'pink puffer' (emphysema) — remember: Blue Bloater = Bronchitis; Pink Puffer = emphysema (Pursed-lip, Puffer).
• Giving HIGH-FLOW oxygen to a COPD patient without SpO2 monitoring — this can suppress the hypoxic drive and cause CO2 narcosis. Always titrate to SpO2 88–92%.
• Thinking COPD spirometry is reversible — it is NOT. Reversibility post-bronchodilator = asthma, not COPD.
• Forgetting that cor pulmonale is RIGHT-sided heart failure (not left). Chronic hypoxaemia → pulmonary vasoconstriction → pulmonary hypertension → right heart strain.
• Overlooking Philippine-specific risk factors: biomass/cooking-fuel smoke (kalan) and occupational exposures are major COPD causes in the Filipino population, not just cigarette smoking.

Exam Tips

• NLE PRIORITY QUESTION: 'Which nursing intervention is MOST important for a COPD patient with dyspnoea?' → Position in high-Fowler's/tripod AND apply controlled low-flow O2 (via Venturi mask, target SpO2 88–92%). Do NOT give high-flow O2.
• Remember the sequence of COPD medications: SABA (salbutamol) for rescue/relief → LABA or LAMA (tiotropium) for maintenance → ICS added for frequent exacerbators.
• For any question about patient teaching in COPD: pursed-lip breathing, small frequent meals, smoking cessation, vaccination, and early reporting of exacerbation signs (change in sputum, increased dyspnoea) are all correct answers.
• Theophylline toxicity triad: tachycardia + nausea + seizures. Therapeutic range = 10–20 mcg/mL. This is a classic NLE pharmacology question.
• A patient with COPD who becomes suddenly confused and drowsy after receiving oxygen — think CO2 narcosis (oxygen suppressed hypoxic drive). Immediately reduce the FiO2 and monitor ABGs.

Key Points

• PRIORITY NURSING DIAGNOSIS for COPD: Impaired Gas Exchange related to alveolar-capillary membrane changes (emphysema) or excessive secretions (bronchitis), as evidenced by abnormal ABGs, hypoxaemia, and altered LOC. This maps to Maslow's Physiological (Level 1) needs.
• Second priority: Ineffective Airway Clearance related to excessive, tenacious mucus and bronchospasm.
• Third priority: Activity Intolerance related to imbalance between oxygen supply and demand.
• POSITIONING: High-Fowler's (60–90°) or tripod position (leaning forward on overbed table) — maximises diaphragmatic excursion and reduces work of breathing.
• PURSED-LIP BREATHING: Inhale through the nose for 2 counts, exhale slowly through pursed lips for 4 counts. This creates back-pressure (positive end-expiratory pressure) that keeps small airways open, reduces air trapping, and slows the respiratory rate — the patient controls it themselves.
• DIAPHRAGMATIC (ABDOMINAL) BREATHING: Patient places hand on abdomen; belly rises on inhalation, falls on exhalation. Strengthens the diaphragm and reduces use of accessory muscles.
• CONTROLLED COUGHING: Deep breath → hold 2 seconds → short, sharp coughs (not forced violent coughing, which collapses airways). Huff coughing is an alternative.
• NUTRITION: Small, frequent, HIGH-CALORIE meals (6 small meals rather than 3 large). Large meals raise the diaphragm, compress the lungs, and worsen dyspnoea. Emphysema patients are often malnourished and cachectic. High-protein, high-calorie diet is needed.
• HYDRATION: 2–3 litres per day (unless contraindicated by cor pulmonale/heart failure) to thin secretions.
• VACCINATIONS: Annual influenza vaccine AND pneumococcal vaccine — respiratory infections are the most common cause of COPD exacerbations and death.
• SMOKING CESSATION: The SINGLE MOST EFFECTIVE intervention to slow COPD progression. Nurses must reinforce this at every patient contact. In the Philippine setting, also address indoor biomass/cooking-smoke (pagiging malapit sa kalan).
• THEOPHYLLINE: Narrow therapeutic window — therapeutic range is 10–20 mcg/mL. Toxicity signs: tachycardia, nausea/vomiting, tremors, and seizures. Rarely used now but still tested on NLE.
• Inhaled corticosteroids (ICS): Teach patient to RINSE MOUTH after use to prevent oral candidiasis (bukhaw/oral thrush). Shake the MDI, exhale first, inhale slowly, hold 10 seconds.
• Energy conservation: Plan activities around periods of least dyspnoea (usually mornings after bronchodilator use), pace activities, use energy-saving techniques (sit while bathing/cooking, use long-handled tools).

Definitions

Section Title

COPD: Nursing Management, Pharmacology, and Patient Teaching

Common Mistakes

• Teaching the patient to eat 3 large meals — this is WRONG for COPD. Large meals raise the diaphragm and worsen dyspnoea. Correct teaching: 6 small, frequent, high-calorie meals.
• Forgetting to teach patients to RINSE MOUTH after using inhaled corticosteroids — failure leads to oral candidiasis.
• Administering oxygen at 5–6 L/min (simple face mask) to a COPD patient without titrating — this risks CO2 narcosis. Always use a Venturi mask or low-flow nasal cannula with SpO2 monitoring, targeting 88–92%.
• Prescribing LABAs (long-acting beta-2 agonists) alone in asthma — LABAs must ALWAYS be combined with ICS in asthma management, never as monotherapy. (This is an asthma rule, but tested in comparison questions.)
• Stopping systemic corticosteroids abruptly after prolonged use — this causes adrenal insufficiency. Always taper. Teach patients NEVER to suddenly stop prednisone.

Exam Tips

• NLE will test the 'silent chest' concept: a scenario describes an asthmatic patient with NO wheeze but is in severe distress, cyanotic, and using accessory muscles. The correct interpretation: this is an EMERGENCY — severe obstruction, not improvement.
• Differentiating asthma from COPD on NLE: REVERSIBLE = asthma; IRREVERSIBLE = COPD. Post-bronchodilator spirometry: asthma FEV1/FVC returns to ≥70%; COPD stays < 70%.
• Green-Yellow-Red zone PEFR: Green > 80% (continue routine); Yellow 50–80% (use reliever, call doctor if no improvement); Red < 50% (use reliever immediately, seek emergency care).
• For the NLE scenario of a patient with BOTH wheezing and cyanosis: oxygen first, then bronchodilator nebulisation. Oxygenation is always the first priority.
• IV Magnesium Sulfate is used for SEVERE, refractory asthma unresponsive to other treatments. It acts as a bronchodilator and muscle relaxant. Monitor for toxicity: loss of knee-jerk reflex, respiratory depression, and hypotension.

Key Points

• Asthma is a CHRONIC INFLAMMATORY airway disorder characterised by REVERSIBLE bronchospasm, mucosal oedema, and mucus plugging — this reversibility distinguishes it from COPD.
• Triggers: allergens (dust mites — alikabok, animal dander, pollen), exercise, cold air, smoke, respiratory infections, NSAIDs (aspirin-sensitive asthma), emotional stress, and strong smells.
• Classic triad of asthma symptoms: EXPIRATORY WHEEZE, COUGH, CHEST TIGHTNESS — worse at night and early morning.
• Prolonged expiratory phase is characteristic: air gets in but has difficulty getting out due to bronchospasm.
• SILENT CHEST: An asthmatic patient who is in severe distress but has NO audible wheeze — this is OMINOUS and indicates near-total obstruction. The patient is too exhausted and too obstructed to move enough air to produce a wheeze. This is a PRE-ARREST sign.
• STATUS ASTHMATICUS: A severe, prolonged asthma attack that does NOT respond to standard bronchodilator therapy (2–3 doses of salbutamol). Medical emergency requiring hospitalisation, IV corticosteroids, possible IV magnesium sulfate, and ICU-level monitoring.
• Reliever (rescue) medications: SHORT-ACTING BETA-2 AGONISTS (SABA) — Salbutamol/albuterol. Give first during acute attacks. Side effects: tachycardia, tremors, jitteriness.
• Controller (preventer) medications: INHALED CORTICOSTEROIDS (ICS) — taken DAILY even when feeling well. Beclomethasone, budesonide, fluticasone. Must rinse mouth after each dose.
• LABA (e.g., salmeterol, formoterol) is ONLY used IN COMBINATION with ICS — NEVER as monotherapy in asthma (risk of fatal attack if used alone).
• Leukotriene modifiers (montelukast): oral controller, useful for exercise-induced and aspirin-sensitive asthma.
• PEFR (Peak Expiratory Flow Rate) monitoring: Green zone (>80% personal best) = good control; Yellow zone (50–80%) = caution, step up treatment; Red zone (<50%) = emergency, use reliever and seek care.
• Severe acute asthma management: O2, nebulised salbutamol + ipratropium, systemic corticosteroids, IV magnesium sulfate for severe/refractory cases.
• Correct spacer use: attach spacer to MDI, exhale, seal lips around spacer mouthpiece, activate MDI, inhale SLOWLY and DEEPLY, hold breath for 10 seconds.

Definitions

Section Title

Chronic Asthma

Common Mistakes

• Confusing RELIEVER (salbutamol — use when needed, rescue) with CONTROLLER (ICS — use DAILY, prevention). NLE will specifically ask which one is 'taken daily' or 'used for acute attack.'
• Forgetting that a SILENT CHEST in a distressed asthma patient = EMERGENCY (not improvement). Students sometimes think 'no wheeze = getting better' — the opposite is true in a distressed patient.
• Using LABAs alone (without ICS) in asthma management — this is contraindicated and has been associated with fatal outcomes. LABAs are add-on therapy combined with ICS.
• Thinking that rising PaCO2 in an asthmatic is normal — in EARLY asthma, hyperventilation causes LOW CO2 (respiratory alkalosis). A NORMAL or RISING CO2 in an asthmatic patient means they are TIRING and heading toward respiratory failure — prepare for intubation.
• Forgetting to teach patients to rinse their mouth after ICS use — this leads to oral candidiasis.

Exam Tips

• If the NLE scenario describes: 'large amounts of foul-smelling, purulent sputum, haemoptysis, clubbing, and a history of TB' — think BRONCHIECTASIS.
• Priority nursing action for bronchiectasis = airway clearance (postural drainage + CPT). This addresses the Maslow Level 1 need (oxygenation/airway).
• Gold standard DIAGNOSIS of bronchiectasis = HRCT chest. This will be tested in diagnostic priority questions.
• Postural drainage timing: BEFORE meals or 1–2 hours AFTER. This is a specific NLE pharmacology/procedure fact.
• Three-layer sputum is PATHOGNOMONIC of bronchiectasis — if the NLE describes sputum that separates into 3 layers on standing, the answer is bronchiectasis.

Key Points

• Bronchiectasis is the PERMANENT, abnormal, irreversible dilation of the bronchi caused by destruction of the bronchial wall from chronic infection and inflammation.
• In the Philippine setting, TUBERCULOSIS (TB) is a major cause of bronchiectasis — this is a highly relevant Philippine context point for NLE. Other causes include recurrent pneumonia, cystic fibrosis, and severe pertussis.
• HALLMARK SYMPTOM: Chronic cough producing LARGE AMOUNTS of thick, purulent, FOUL-SMELLING sputum (because infected, stagnant mucus in dilated airways becomes colonised with bacteria).
• Classic 'THREE-LAYER SPUTUM' on standing: top layer = frothy mucus; middle layer = turbid (cloudy) sputum; bottom layer = thick, purulent sediment.
• Other manifestations: haemoptysis (blood in sputum — from inflamed, vascular bronchial walls), DIGITAL CLUBBING, coarse crackles on auscultation, and recurrent lower respiratory infections (frequent pneumonias).
• DIAGNOSIS: High-Resolution CT (HRCT) of the chest is the GOLD STANDARD diagnostic test for bronchiectasis — it visualises the dilated bronchi clearly.
• PRIORITY NURSING DIAGNOSIS: Ineffective Airway Clearance related to excessive, tenacious, purulent secretions as evidenced by productive cough, abnormal breath sounds, and dyspnoea.
• PRIORITY INTERVENTION: POSTURAL DRAINAGE AND CHEST PHYSIOTHERAPY — position the patient so the affected lobe drains by gravity; use percussion (cupped hand tapping) and vibration to loosen secretions; then have the patient cough.
• Timing of postural drainage: best performed on an EMPTY STOMACH (30–60 minutes before meals or 1–2 hours after) to prevent aspiration and nausea.
• Adequate hydration (2–3 L/day) and mucolytics/nebulised saline to thin secretions.
• Antibiotics for acute exacerbations (based on culture and sensitivity; common organisms: Pseudomonas aeruginosa, Haemophilus influenzae).
• Vaccinations: annual influenza and pneumococcal to reduce risk of respiratory infections.
• Bronchodilators for associated bronchospasm.
• Surgical resection may be considered for localised disease unresponsive to medical management.

Definitions

Section Title

Bronchiectasis

Common Mistakes

• Performing postural drainage immediately AFTER a meal — this causes nausea, vomiting, and aspiration risk. Always perform on an EMPTY STOMACH (before meals or 1–2 hours after).
• Confusing bronchiectasis with asthma or COPD — bronchiectasis produces copious, PURULENT, FOUL-SMELLING sputum in large quantities. The smell is distinctive and the amount is large.
• Forgetting that HRCT is the gold standard diagnostic (not chest X-ray or spirometry) for bronchiectasis.
• Not recognising TB as a major cause of bronchiectasis in the Philippine context — NLE questions may give a history of previous TB.

Exam Tips

• Restrictive vs Obstructive SPIROMETRY: Restrictive = FVC LOW, FEV1/FVC NORMAL or HIGH. Obstructive (COPD) = FEV1/FVC LOW (<70%), FVC may be normal or low.
• If NLE describes 'fine crackling sounds at the lung bases, like Velcro, in a patient with progressive dyspnoea and dry cough' — think PULMONARY FIBROSIS (restrictive).
• Occupational causes of restrictive disease relevant to NLE: silicosis (quarry/construction), asbestosis (old buildings), coal dust. Community health nursing role = occupational hazard surveillance and PPE education.
• NLE may ask about management: for IPF, antifibrotic drugs (pirfenidone/nintedanib) SLOW progression but do NOT cure. O2 therapy and pulmonary rehab are supportive measures.
• For a SATA question on restrictive disease signs: select reduced lung volumes, dry non-productive cough, fine crackles, exertional dyspnoea, digital clubbing, and reduced FVC. Do NOT select wheeze or large amounts of sputum.

Key Points

• In RESTRICTIVE disorders, the problem is REDUCED LUNG EXPANSION (the lung cannot fill adequately), not airflow limitation. Think of the lung being 'stiff' or the chest wall being unable to expand.
• CONTRAST with obstructive disease: Obstructive = difficulty blowing AIR OUT; Restrictive = difficulty getting air IN.
• Spirometry pattern: REDUCED FVC (total lung volume is reduced) with a NORMAL or INCREASED FEV1/FVC ratio. This is the OPPOSITE of obstructive disease (which has reduced FEV1/FVC).
• Causes — INTRINSIC (lung parenchyma): Idiopathic Pulmonary Fibrosis (IPF), pneumoconioses (silicosis from quarry/construction work — common in Philippine occupational settings; asbestosis; coal worker's pneumoconiosis), sarcoidosis, and radiation pneumonitis.
• Causes — EXTRINSIC (outside the lung): kyphoscoliosis (severe spinal deformity), morbid obesity (restricts diaphragm movement), pleural effusion, severe pneumonia, and neuromuscular diseases (Guillain-Barré syndrome, muscular dystrophy).
• Classic symptoms of IPF/pulmonary fibrosis: PROGRESSIVE EXERTIONAL DYSPNOEA (gradual, insidious onset), DRY, NON-PRODUCTIVE COUGH, and FINE 'VELCRO' CRACKLES on auscultation (the hallmark sound — like tearing Velcro at the lung bases).
• Digital clubbing and cyanosis in advanced disease.
• Prognosis of IPF is POOR — median survival 3–5 years after diagnosis. Advance-care planning and palliative care discussion are integral nursing roles.
• Management: treat underlying cause, supplemental O2 for hypoxaemia, pulmonary rehabilitation, antifibrotic agents (pirfenidone, nintedanib) for IPF, and lung transplantation in selected patients.
• Occupational exposure prevention is CRITICAL in the Philippine context: silicosis from quarrying (Rizal, Bulacan — common areas); asbestosis from old building materials. Health education on PPE use (N95 masks, respirators) is a key community health nursing role under RA 9173.

Definitions

Section Title

Restrictive Pulmonary Disorders

Common Mistakes

• Confusing restrictive and obstructive spirometry patterns. Memorise: COPD/Obstructive = LOW FEV1/FVC (<70%); Restrictive = LOW FVC but NORMAL or HIGH FEV1/FVC ratio.
• Thinking 'no wheeze = no problem' in restrictive disease — restrictive disease presents with crackles (Velcro), NOT wheezes. Wheeze = obstructive.
• Forgetting that the PRIMARY symptom of IPF is progressive EXERTIONAL dyspnoea with a DRY cough — not productive cough (that's bronchitis/bronchiectasis).
• Not incorporating advance-care planning in IPF nursing care — because of poor prognosis, nurses must initiate sensitive conversations about code status, palliation, and end-of-life preferences.

Exam Tips

• NLE EMERGENCY SCENARIO: Patient with chest trauma, absent breath sounds on the LEFT, tracheal deviation to the RIGHT, JVD, hypotension. Answer: TENSION PNEUMOTHORAX — Priority action: prepare for/assist with needle decompression at 2nd ICS, midclavicular line of the AFFECTED (left) side.
• Tracheal deviation direction: always toward the UNAFFECTED (normal) side. Easy memory: the trachea RUNS AWAY from the pressure (away from the tension side).
• Open chest wound → 3-sided dressing = flutter valve. 4-sided dressing = danger (tension). This is a recurring NLE question.
• Chest tube water-seal chamber: continuous bubbling = air leak (problem). Tidalling = normal lung movement with breathing. No fluctuation in a fresh post-op patient = possible tube kink or occlusion (check the tube).
• In simple spontaneous pneumothorax in a young healthy patient (non-COPD): administer HIGH-FLOW O2 (accelerates nitrogen reabsorption and lung re-expansion). Do NOT restrict oxygen here.

Key Points

• Pneumothorax = air in the pleural space. Normally, the pleural space is a potential space with negative pressure that keeps the lung expanded. When air enters, this negative pressure is lost and the lung collapses.
• THREE TYPES: (1) Spontaneous — rupture of a bleb/bulla; classically in TALL, THIN, YOUNG MEN (primary spontaneous) or from ruptured bullae in COPD (secondary spontaneous). (2) Traumatic — penetrating (stab wound, gunshot) or blunt chest trauma; open wound allows air into pleural space. (3) Tension pneumothorax — a one-way valve mechanism lets air IN but not OUT with each breath, causing progressive pressure build-up.
• TENSION PNEUMOTHORAX is a LIFE-THREATENING EMERGENCY that causes mediastinal shift, compressed great vessels, and cardiac arrest if untreated.
• Signs of SIMPLE pneumothorax: sudden sharp PLEURITIC chest pain (worse with breathing/movement), dyspnoea, tachypnoea, DECREASED or ABSENT breath sounds on the AFFECTED side, HYPERRESONANCE to percussion on affected side (air instead of lung tissue), and reduced chest expansion on affected side.
• TENSION PNEUMOTHORAX RED FLAGS (memorise ALL 5): (1) Tracheal deviation TOWARD the UNAFFECTED side, (2) Absent breath sounds on affected side, (3) Severe hypotension (obstructive shock), (4) Distended neck veins (JVD), (5) Profound cyanosis and respiratory distress. This is the 'D-A-N-G-E-R' presentation.
• IMMEDIATE TREATMENT of tension pneumothorax: NEEDLE DECOMPRESSION — insert a large-bore needle (14G) at the 2nd intercostal space (ICS), midclavicular line on the affected side. A hiss of air confirms the diagnosis. This is a LIFE-SAVING emergency procedure followed immediately by chest tube insertion.
• OPEN (SUCKING) CHEST WOUND: Air enters the pleural space through the chest wall wound with each inspiration. Treatment: apply an OCCLUSIVE DRESSING TAPED ON THREE SIDES ONLY. This creates a flutter valve — allows air to escape on exhalation (through the untaped side) but prevents air from entering on inhalation.
• WARNING: Taping an occlusive dressing on ALL FOUR SIDES on an open chest wound can convert it to a TENSION PNEUMOTHORAX — a fatal error.
• Chest tube insertion (thoracentesis/thoracostomy) with water-seal drainage system is the definitive treatment for larger pneumothoraces.
• WATER-SEAL DRAINAGE: Normal finding = tidalling (water level fluctuates with breathing). ABNORMAL = continuous bubbling in water-seal chamber (indicates an air leak from the lung or tubing); NO tidalling (tube is kinked, clotted, or lung is fully re-expanded).
• For pneumothorax WITHOUT CO2 retention (unlike COPD): give HIGH-FLOW oxygen — it speeds up reabsorption of pleural air by replacing nitrogen with oxygen (nitrogen reabsorption effect).
• Nursing: maintain the drainage system below the level of the chest; never clamp the tube without a physician's order (unless tube accidentally dislodges); encourage deep breathing to promote lung re-expansion; assess for subcutaneous emphysema (crepitus under the skin).

Definitions

Section Title

Pneumothorax: Types, Assessment, and Emergency Management

Common Mistakes

• Stating that tracheal deviation is TOWARD the affected side — it is AWAY from (toward the UNAFFECTED side) in tension pneumothorax. The trachea moves away from the high-pressure side.
• Applying a 4-sided occlusive dressing to an open chest wound — this converts it to tension pneumothorax. ALWAYS tape only 3 sides.
• Giving low-flow oxygen (88–92% target) to a pneumothorax patient who does NOT have COPD — the 88–92% target is ONLY for CO2-retaining COPD patients. A non-COPD pneumothorax patient should receive HIGH-FLOW O2.
• Placing the chest drainage system ABOVE the chest — it must be BELOW the chest level at all times to prevent siphoning fluid back into the pleural space.
• Clamping a chest tube routinely — this should not be done as it can cause tension pneumothorax if there is an ongoing air leak.