NLE Respiratory Nursing — Acute Respiratory Failure & ARDSExam Answer Templates

Marks

1

Topic

Acute Respiratory Failure — Types and ABG Criteria

Difficulty

easy

Template Id

T1

Examiner Tip

For 1-mark questions on ABG criteria, always write the exact numeric threshold and the gas being measured. Examiners scan for the number first.

Model Answer

Type I (hypoxaemic) respiratory failure is defined by a PaO2 less than 60 mmHg on room air, indicating a failure of oxygenation.

Question Type

very_short_answer

Answer Structure

• State the ABG value with correct unit: PaO2 <60 mmHg on room air [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'low PaO2' without the specific threshold value of 60 mmHg — no marks awarded for vague answers
• Confusing Type I with Type II by mentioning PaCO2 instead of PaO2
• Omitting 'on room air' — the hypoxaemia must be on room air to qualify

Key Phrases To Include

• PaO2 <60 mmHg
• room air
• oxygenation failure
• Type I

Marks

1

Topic

ARDS — Hallmark Clinical Feature

Difficulty

easy

Template Id

T2

Examiner Tip

The word 'refractory' is what separates ARDS from other causes of hypoxaemia. Examiners look for this specific adjective. Never drop it.

Model Answer

The hallmark of ARDS is refractory hypoxaemia — a severe drop in PaO2 that does NOT improve with supplemental oxygen administration, due to massive intrapulmonary shunting.

Question Type

very_short_answer

Answer Structure

• Name the hallmark: refractory hypoxaemia [1 mark] — must include the key qualifier 'does not improve with supplemental oxygen'

Scoring Breakdown

Common Mark Deductions

• Writing only 'hypoxaemia' without the qualifier 'refractory' or 'does not respond to O2' — this does not distinguish ARDS from simple respiratory failure
• Listing bilateral infiltrates as the hallmark — this is a diagnostic finding, not the clinical hallmark

Key Phrases To Include

• refractory hypoxaemia
• does not improve with supplemental oxygen
• intrapulmonary shunting

Marks

2

Topic

Acute Respiratory Failure — Clinical Manifestations

Difficulty

easy

Template Id

T3

Examiner Tip

The NLE frequently tests the ability to distinguish early from late signs. Always mentally sort signs into 'early' (restlessness, tachycardia) versus 'late' (cyanosis, bradycardia, arrest) before writing.

Model Answer

Two early signs of hypoxaemia are: 1. Restlessness and agitation — the brain is among the first organs affected by decreased oxygen delivery, causing altered mentation. 2. Tachycardia and tachypnoea — compensatory responses of the cardiovascular and respiratory systems to maintain oxygen delivery.

Question Type

very_short_answer

Answer Structure

• Point 1: Name the sign with brief physiological rationale [1 mark]
• Point 2: Name a second distinct sign with brief rationale [1 mark]

Scoring Breakdown

Common Mark Deductions

• Listing cyanosis — this is a LATE sign, not early; this error costs 1 mark
• Listing two signs from the same category (e.g., restlessness AND agitation) — examiners may count these as one sign
• Omitting any physiological reason when the question asks you to 'explain' — adds context expected at NLE level

Key Phrases To Include

• restlessness
• agitation
• change in mental status
• tachycardia
• tachypnoea
• early sign
• compensatory

Marks

2

Topic

Acute Respiratory Failure — Types

Difficulty

medium

Template Id

T4

Examiner Tip

Differentiation questions are best answered in a parallel two-column or two-paragraph structure. Match each type clearly to its defect and ABG so the examiner can award marks by scanning each line.

Model Answer

Type I (hypoxaemic) respiratory failure involves a failure of OXYGENATION. ABG shows PaO2 <60 mmHg on room air with a normal or low PaCO2. Causes include pneumonia and ARDS. Type II (hypercapnic) respiratory failure involves a failure of VENTILATION — the lungs cannot remove CO2 adequately. ABG shows PaCO2 >50 mmHg with a pH <7.35 (respiratory acidosis). Causes include COPD exacerbation and drug overdose.

Question Type

short_answer

Answer Structure

• Type I: name the defect (oxygenation) + ABG value (PaO2 <60 mmHg) [1 mark]
• Type II: name the defect (ventilation) + ABG values (PaCO2 >50 mmHg, pH <7.35) [1 mark]

Scoring Breakdown

Common Mark Deductions

• Reversing the ABG values — putting PaCO2 under Type I or PaO2 under Type II
• Missing the pH criterion for Type II — PaCO2 alone without pH context is incomplete
• Using lay terms like 'not enough oxygen' instead of clinical terms like 'oxygenation failure'

Key Phrases To Include

• oxygenation failure
• ventilation failure
• PaO2 <60 mmHg
• PaCO2 >50 mmHg
• pH <7.35
• respiratory acidosis

Marks

3

Topic

Pulmonary Embolism — Nursing Management

Difficulty

medium

Template Id

T5

Examiner Tip

For any management question worth 3 marks, always write EXACTLY 3 numbered points with one clear intervention and one clear rationale per point. Do not combine multiple interventions in one bullet — each line must earn its own mark.

Model Answer

Priority nursing interventions for a patient with pulmonary embolism: 1. Administer supplemental oxygen immediately (priority: airway and oxygenation — Maslow's physiological need). Rationale: PE causes V/Q mismatch and hypoxaemia; oxygen corrects arterial desaturation and reduces hypoxic drive. 2. Elevate the head of the bed to 30–45 degrees. Rationale: Semi-Fowler's position reduces the work of breathing and promotes lung expansion by lowering diaphragmatic pressure. 3. Monitor vital signs and oxygen saturation continuously and prepare for anticoagulation therapy (heparin IV as ordered). Rationale: Anticoagulation prevents further clot propagation; continuous monitoring detects haemodynamic deterioration (drop in BP, rising tachycardia) that signals a massive PE requiring emergency thrombolytics.

Question Type

short_answer

Answer Structure

• Intervention 1: Oxygen administration + rationale [1 mark]
• Intervention 2: Positioning (HOB elevation) + rationale [1 mark]
• Intervention 3: Continuous monitoring + anticoagulation preparation + rationale [1 mark]

Scoring Breakdown

Common Mark Deductions

• Listing interventions without any rationale — for 3-mark answers on management, rationale is expected and examiners deduct for absence
• Giving interventions out of priority order without any Maslow or ABC framework explanation
• Recommending thrombolytics as first-line for all PE — thrombolytics are reserved for massive/unstable PE only

Key Phrases To Include

• supplemental oxygen
• V/Q mismatch
• head of bed 30–45 degrees
• anticoagulation
• heparin
• haemodynamic monitoring
• Maslow's physiological need
• clot propagation

Marks

3

Topic

ARDS — Mechanical Ventilation and PEEP

Difficulty

medium

Template Id

T6

Examiner Tip

Mechanism questions reward the 'define-explain-apply' structure. Define the term, explain how it works in the disease context, then apply it to nursing (monitoring or complications). This three-step structure maps perfectly to 3 marks.

Model Answer

PEEP (Positive End-Expiratory Pressure) is positive airway pressure maintained at the END of expiration during mechanical ventilation. In ARDS, the alveolar-capillary membrane is damaged, surfactant is lost, and alveoli collapse (atelectasis), causing severe intrapulmonary shunting and refractory hypoxaemia. PEEP addresses this by: 1. Keeping the alveoli OPEN at the end of expiration — preventing repetitive collapse and re-opening (atelectrauma). 2. Recruiting previously collapsed alveoli — improving the ventilation-perfusion (V/Q) ratio. 3. Improving oxygenation — by increasing the surface area available for gas exchange, PEEP raises PaO2 without requiring dangerously high FiO2. Clinical consideration: Excessive PEEP reduces venous return to the heart (decreased preload → decreased cardiac output) and increases the risk of barotrauma (pneumothorax). The nurse must monitor blood pressure and watch for signs of tension pneumothorax.

Question Type

short_answer

Answer Structure

• Define PEEP clearly [1 mark]
• Explain the ARDS pathophysiology that PEEP corrects (collapsed alveoli, shunting) [1 mark]
• Describe the mechanism of benefit AND note a key complication to monitor [1 mark]

Scoring Breakdown

Common Mark Deductions

• Describing PEEP as pressure during inspiration — this is a fundamental error; PEEP is end-expiratory
• Explaining benefits without mentioning any risks or monitoring — incomplete for a 3-mark question
• Failing to connect PEEP to the specific ARDS pathophysiology (surfactant loss, alveolar collapse)

Key Phrases To Include

• end of expiration
• alveolar recruitment
• prevents collapse
• intrapulmonary shunting
• V/Q mismatch
• oxygenation
• barotrauma
• decreased venous return

Marks

3

Topic

Pulmonary Embolism — Risk Factors

Difficulty

easy

Template Id

T7

Examiner Tip

Virchow's Triad is a classic 3-mark question precisely because it has exactly three components. Treat each component as one mark. Write the name in CAPS, then define it, then give the example. This predictable format speeds up writing and scoring.

Model Answer

Virchow's Triad describes the three conditions that predispose to thrombus formation and subsequent pulmonary embolism: 1. VENOUS STASIS — Sluggish blood flow promotes clot formation. Clinical example: A post-operative patient confined to bed rest for 3 days after a major abdominal surgery (common in Philippine government and private hospitals post-laparotomy). 2. HYPERCOAGULABILITY — An increased tendency of blood to clot. Clinical example: A pregnant patient in her third trimester or a patient taking oral contraceptive pills (OCP) — both cause hormonal elevation of clotting factors. 3. ENDOTHELIAL INJURY — Damage to the inner vessel wall exposes subendothelial collagen, activating the clotting cascade. Clinical example: A patient who sustained trauma to the lower extremity or has a femoral central venous catheter in situ.

Question Type

short_answer

Answer Structure

• Component 1: Venous stasis — definition + clinical example [1 mark]
• Component 2: Hypercoagulability — definition + clinical example [1 mark]
• Component 3: Endothelial injury — definition + clinical example [1 mark]

Scoring Breakdown

Common Mark Deductions

• Naming the three components without any clinical example — the question explicitly asks for one example each
• Using the same clinical example for two different components (e.g., surgery for both stasis and endothelial injury without distinguishing them)
• Misnaming a component — e.g., writing 'vessel damage' for the third component without the term 'endothelial injury'

Key Phrases To Include

• Virchow's Triad
• venous stasis
• hypercoagulability
• endothelial injury
• thrombus formation
• pulmonary embolism risk

Marks

5

Topic

ARDS — Pathophysiology

Difficulty

hard

Template Id

T8

Examiner Tip

For 5-mark pathophysiology questions, think in steps and number them. An examiner reads quickly and rewards students who make their reasoning obvious through structure. Aim for 5 distinct steps — each step earns one mark. Lead with a definition, end with the clinical result.

Model Answer

ACUTE RESPIRATORY DISTRESS SYNDROME (ARDS) — PATHOPHYSIOLOGY Definition: ARDS is a severe, acute, diffuse inflammatory lung injury characterized by refractory hypoxaemia, bilateral pulmonary infiltrates, and non-cardiogenic pulmonary oedema. Step 1 — Triggering Event: ARDS is initiated by a direct (pulmonary) or indirect (extrapulmonary) insult. The MOST COMMON trigger is SEPSIS (systemic infection). Other triggers include aspiration of gastric contents, severe trauma, massive blood transfusion, pancreatitis, and near-drowning. Step 2 — Diffuse Alveolar-Capillary Membrane Damage: The trigger activates an overwhelming systemic inflammatory response. Pro-inflammatory mediators (cytokines, neutrophils, oxygen free radicals) attack the alveolar-capillary membrane — the thin barrier between the air sac and the blood vessel. This barrier becomes highly permeable (leaky). Step 3 — Non-Cardiogenic Pulmonary Oedema: Because the alveolar-capillary membrane is now permeable, protein-rich fluid leaks from the capillaries into the alveolar spaces. This is NON-CARDIOGENIC pulmonary oedema — it is not caused by heart failure but by membrane injury. The pulmonary capillary wedge pressure (PCWP) remains normal, which distinguishes ARDS from cardiogenic oedema. Step 4 — Surfactant Loss and Alveolar Collapse: The fluid flooding the alveoli destroys surfactant (the substance produced by Type II pneumocytes that reduces surface tension). Without surfactant, alveoli collapse (atelectasis). Lung compliance decreases significantly — the lungs become 'stiff' and harder to ventilate. Step 5 — V/Q Mismatch and Intrapulmonary Shunting: Collapsed, fluid-filled alveoli continue to receive blood flow (perfusion) but have NO ventilation. This creates severe ventilation-perfusion (V/Q) mismatch and intrapulmonary shunting — blood passes through the lungs without being oxygenated. Step 6 — Refractory Hypoxaemia (Clinical Hallmark): Because the blood bypasses functioning alveoli (shunting), increasing the FiO2 (supplemental oxygen) does NOT correct the hypoxaemia — oxygen cannot reach the collapsed or flooded alveoli. The result is REFRACTORY HYPOXAEMIA — the defining clinical hallmark of ARDS. Nursing Priority: Based on Maslow's hierarchy, oxygenation is the highest physiological priority. The nurse must recognize ARDS early (severe dyspnoea, tachypnoea, bilateral crackles, refractory hypoxaemia) and prepare for mechanical ventilation with PEEP.

Question Type

long_answer

Answer Structure

• Introduction: Define ARDS in one sentence [1 mark]
• Triggering event: Name the most common trigger (sepsis) and 2–3 others [1 mark]
• Membrane damage and non-cardiogenic oedema: explain the leaky membrane and protein-rich fluid [1 mark]
• Surfactant loss and alveolar collapse leading to stiff lungs [1 mark]
• V/Q mismatch and intrapulmonary shunting leading to refractory hypoxaemia — explain WHY O2 doesn't help [1 mark]

Scoring Breakdown

Common Mark Deductions

• Describing ARDS oedema as cardiogenic — this is a fundamental error that shows conceptual misunderstanding
• Skipping the surfactant-loss step — this is a commonly omitted but mark-bearing step
• Not explaining WHY oxygen doesn't help (shunting) — simply saying 'it doesn't respond to O2' without the mechanism of shunting loses the reasoning mark
• Writing a list of bullet points with no sequential logical flow — pathophysiology questions reward sequential narrative
• Exceeding the scope by writing on treatment without being asked — stay within the question

Key Phrases To Include

• alveolar-capillary membrane
• non-cardiogenic pulmonary oedema
• surfactant loss
• alveolar collapse
• intrapulmonary shunting
• V/Q mismatch
• refractory hypoxaemia
• sepsis
• lung compliance
• PCWP normal

Marks

5

Topic

ARDS — Comprehensive Nursing Management

Difficulty

hard

Template Id

T9

Examiner Tip

For 5-mark management questions on mechanical ventilation, structure your answer with clear Roman numeral or numbered headings. Examiners scan for VAP bundle, PEEP, prone positioning, and alarm response — these four areas are the most commonly rewarded in ARDS ventilation questions.

Model Answer

NURSING MANAGEMENT OF ARDS ON MECHANICAL VENTILATION I. PRIORITY ASSESSMENT (Based on Maslow — Physiological) Assess airway patency, respiratory rate and effort, SpO2, mental status, and ABG results. ARDS patients deteriorate rapidly; continuous monitoring is essential. NANDA Nursing Diagnosis (Priority): • Impaired Gas Exchange related to alveolar-capillary membrane damage and intrapulmonary shunting, as evidenced by refractory hypoxaemia and bilateral infiltrates. II. VENTILATOR SETTINGS AND OXYGENATION SUPPORT 1. Mechanical ventilation with PEEP: PEEP (Positive End-Expiratory Pressure) is the cornerstone. It keeps alveoli open at end-expiration, recruits collapsed alveoli, and improves oxygenation. Monitor for complications: decreased blood pressure (reduced venous return) and signs of barotrauma (pneumothorax). 2. Lung-protective ventilation: Use LOW tidal volumes of approximately 6 mL/kg of predicted body weight. High tidal volumes cause volutrauma (overdistension injury). This is the standard of care per evidence-based practice. 3. FiO2 management: Wean FiO2 to the lowest level that maintains adequate SpO2 to prevent oxygen toxicity (pulmonary fibrosis with prolonged high FiO2). III. PRONE POSITIONING For moderate-to-severe ARDS, position the patient PRONE (face-down) for 12–16 hours per protocol. Prone positioning redistributes oedema and improves V/Q matching in dorsal lung regions. Nursing responsibilities: secure the ETT, protect pressure points (face, shoulders, knees), and maintain a patent airway throughout. IV. VAP PREVENTION BUNDLE 1. Elevate the head of the bed 30–45 degrees at all times to reduce aspiration risk. 2. Provide oral care with chlorhexidine solution every 4–6 hours. 3. Perform daily sedation interruption and assess readiness to wean from the ventilator. 4. Ensure DVT prophylaxis (compression stockings, LMWH) and stress-ulcer prophylaxis (proton pump inhibitor). V. SUCTIONING Suction only when clinically indicated (not on a fixed schedule). Hyperoxygenate with 100% FiO2 before and after suctioning. Limit each suction pass to 10–15 seconds to prevent iatrogenic hypoxaemia. VI. TREAT THE UNDERLYING CAUSE Identify and treat the precipitating trigger — if sepsis is the cause, administer antibiotics as ordered within 1 hour. Fluid management is conservative to avoid worsening pulmonary oedema. VII. ALARM RESPONSE Keep a manual resuscitation (bag-valve-mask) bag at the bedside at ALL times. If an alarm sounds: • HIGH-pressure alarm → check for secretions (suction), kinked tubing, patient biting the ETT, or bronchospasm. • LOW-pressure alarm → check for disconnection or cuff leak. If the problem cannot be resolved quickly, DISCONNECT the patient from the ventilator and manually ventilate with the bag-valve-mask. Call for physician/team immediately.

Question Type

long_answer

Answer Structure

• Priority nursing assessment and NANDA diagnosis [1 mark]
• Ventilator settings: PEEP rationale + low tidal volume (6 mL/kg) [1 mark]
• Prone positioning — indication, benefit, nursing responsibilities [1 mark]
• VAP prevention bundle (HOB 30–45°, oral care, sedation interruption, DVT/ulcer prophylaxis) [1 mark]
• Alarm response, bag-valve-mask readiness, and treating the underlying cause [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing only about oxygen and medications without any ventilator-specific content — the question specifically asks about mechanical ventilation management
• Missing the VAP bundle — a very NLE-tested topic that examiners check for explicitly
• Omitting the manual resuscitation bag — this safety measure is a high-yield NLE item
• Not stating the tidal volume in specific terms (6 mL/kg) — vague answers like 'low tidal volume' without the number may not earn the mark
• Writing general nursing care without applying it to the ARDS context

Key Phrases To Include

• Impaired Gas Exchange
• PEEP
• low tidal volume 6 mL/kg
• prone positioning
• V/Q matching
• VAP prevention bundle
• head of bed 30–45 degrees
• chlorhexidine oral care
• daily sedation interruption
• manual resuscitation bag
• high-pressure alarm
• low-pressure alarm

Marks

2

Topic

Pulmonary Embolism — Diagnostics

Difficulty

medium

Template Id

T10

Examiner Tip

The CTPA versus D-dimer distinction is a classic NLE trap. Memorize: D-dimer RULES OUT (negative = reassuring in low-risk only); CTPA CONFIRMS. Always pair D-dimer with 'low-risk patients.'

Model Answer

The gold-standard confirmatory diagnostic test for pulmonary embolism is CT Pulmonary Angiography (CTPA), which directly visualizes the pulmonary arteries and detects the clot. A NORMAL D-dimer level helps rule out PE in LOW-RISK patients, because D-dimer is highly sensitive — a negative result makes PE very unlikely. However, an elevated D-dimer is non-specific (positive in many conditions) and alone cannot confirm PE.

Question Type

very_short_answer

Answer Structure

• Name the gold-standard test: CTPA [1 mark]
• State the finding that rules out PE: normal D-dimer in low-risk patients [1 mark]

Scoring Breakdown

Common Mark Deductions

• Writing 'D-dimer' as the gold-standard test — D-dimer is a screening tool, not a confirmatory test
• Stating that an elevated D-dimer confirms PE — this is incorrect; D-dimer is only useful as a negative predictor
• Omitting the qualifier 'low-risk patients' for the D-dimer point — D-dimer is not useful for ruling out PE in high-risk patients

Key Phrases To Include

• CT pulmonary angiography
• CTPA
• gold standard
• D-dimer
• rule out
• low-risk patients
• sensitive but not specific

Marks

2

Topic

Pulmonary Embolism — Anticoagulation Pharmacology

Difficulty

medium

Template Id

T11

Examiner Tip

HIT questions almost always test two things: the emergency action (STOP the drug) and the monitoring parameter. In NLE, confusing aPTT (heparin) with PT/INR (warfarin) is one of the most common errors — engrain this distinction: Heparin → aPTT; Warfarin → PT/INR.

Model Answer

Priority action: The nurse must STOP the heparin infusion IMMEDIATELY and notify the physician, as HIT is a serious immune-mediated complication in which heparin paradoxically triggers platelet activation, causing potentially life-threatening thrombosis despite low platelet counts. Monitoring parameter for heparin therapy: The activated Partial Thromboplastin Time (aPTT) is monitored to measure heparin's anticoagulant effect. The therapeutic target is approximately 1.5–2.5 times the control value.

Question Type

short_answer

Answer Structure

• Priority action: Stop heparin + notify physician [1 mark]
• Monitoring parameter: aPTT with therapeutic target [1 mark]

Scoring Breakdown

Common Mark Deductions

• Stating 'reduce the heparin dose' instead of stopping it — HIT requires complete cessation, not dose reduction
• Writing 'PT/INR' as the monitoring parameter for heparin — PT/INR is for warfarin, not heparin
• Not mentioning physician notification — independent nursing action must be paired with appropriate reporting

Key Phrases To Include

• stop heparin immediately
• notify physician
• heparin-induced thrombocytopenia
• aPTT
• 1.5–2.5 times control
• platelet count

Marks

3

Topic

Mechanical Ventilation — Alarm Management

Difficulty

medium

Template Id

T12

Examiner Tip

Ventilator alarm questions are very NLE-practical. Memorize the alarm pair: HIGH pressure = resistance/obstruction (suction, check circuit); LOW pressure = leak/disconnect (check connections, cuff). The BVM must be mentioned for any alarm response to earn full marks.

Model Answer

Causes of a HIGH-PRESSURE alarm in a mechanically ventilated patient (the ventilator meets resistance when delivering a breath): 1. Secretion accumulation in the endotracheal tube or airways — the most common cause; increased resistance blocks airflow. 2. Kinked or occluded ventilator tubing — the circuit is physically obstructed, preventing pressure from delivering to the patient. 3. Patient biting the endotracheal tube (ETT) or bronchospasm — either compresses the airway, raising circuit resistance. Priority Nursing Response: • First, assess the patient — observe chest rise, listen to breath sounds, and check SpO2 and haemodynamics. • Inspect the ventilator circuit for kinks or disconnection. • If secretions are suspected, suction the airway (after hyperoxygenation). • Administer bronchodilator for bronchospasm as ordered. • CRITICAL SAFETY RULE: If the cause cannot be quickly identified and corrected, DISCONNECT the patient from the ventilator and manually ventilate with the BAG-VALVE-MASK (BVM). Call the physician and respiratory therapist immediately.

Question Type

short_answer

Answer Structure

• Three causes of high-pressure alarm listed [1 mark — 0.5 per cause or 1 mark for any 3 correct causes]
• Assessment and systematic circuit/patient check [0.5 mark]
• Suctioning if secretions + bag-valve-mask as safety fallback [0.5 mark — or 1 mark as whole nursing response section]

Scoring Breakdown

Common Mark Deductions

• Describing the low-pressure alarm response instead of high-pressure — confusing the two alarm types (low = leak/disconnect; high = obstruction)
• Not mentioning the bag-valve-mask as the safety fallback — this is the most critical nursing action and is frequently a specific NLE item
• Recommending increasing the ventilator pressure settings as the first response — alarm assessment must precede any setting changes

Key Phrases To Include

• high-pressure alarm
• secretions
• kinked tubing
• biting the ETT
• bronchospasm
• suction
• bag-valve-mask
• manually ventilate
• never silence without checking

Marks

2

Topic

Pulmonary Embolism — Prevention

Difficulty

easy

Template Id

T13

Examiner Tip

Prevention questions in NLE often appear deceptively simple but reward clinical specificity. Write the drug name (enoxaparin not just 'anticoagulant') and the device name (TED stockings, IPC device) to show clinical competence and earn full marks.

Model Answer

DVT/PE Prevention Interventions for a Post-Operative Patient: 1. Early ambulation — encourage the patient to walk as soon as it is medically safe post-operatively (within 24–48 hours). Ambulation activates the calf muscle pump, promoting venous return and reducing stasis. 2. Apply graduated compression stockings (TED stockings) and/or intermittent pneumatic compression (IPC) devices — these apply mechanical pressure to the lower extremities, preventing venous pooling. 3. Administer prophylactic anticoagulation as ordered — typically low-molecular-weight heparin (e.g., enoxaparin subcutaneous) for high-risk patients, as ordered by the physician and within the scope of the nurse under RA 9173. 4. Encourage adequate hydration — dehydration increases blood viscosity and hypercoagulability risk; oral or IV fluids as indicated maintain normal viscosity.

Question Type

short_answer

Answer Structure

• Two interventions with brief rationale each [1 mark]
• Two more interventions with brief rationale [1 mark]

Scoring Breakdown

Common Mark Deductions

• Listing interventions applicable to already-formed DVT treatment (e.g., thrombolytics) — the question asks for prevention, not treatment
• Repeating the same type of intervention twice (e.g., listing both elastic stockings and TED stockings as separate points without distinction)
• Giving five or six interventions — this wastes time on a 2-mark question; four clear points are enough

Key Phrases To Include

• early ambulation
• compression stockings
• intermittent pneumatic compression
• prophylactic anticoagulation
• enoxaparin
• hydration
• venous stasis prevention

Marks

5

Topic

Pulmonary Embolism — Anticoagulation Patient Education

Difficulty

hard

Template Id

T14

Examiner Tip

Patient teaching questions for 5 marks expect five clearly identifiable teaching areas. Structure them as numbered sections. Examiners in the NLE frequently award 1 mark per distinct teaching area. In warfarin teaching, the vitamin K 'consistent — not avoid' teaching point is the #1 most tested concept — it directly traps students who default to 'avoid all green vegetables.'

Model Answer

DISCHARGE TEACHING: WARFARIN THERAPY FOLLOWING PULMONARY EMBOLISM I. WHAT IS WARFARIN AND WHY IS IT PRESCRIBED? Explain to the patient and family: 'Warfarin is an oral anticoagulant (blood thinner) that prevents your blood clot from growing larger and reduces your risk of forming new clots. You will need to take it consistently as prescribed.' II. MONITORING — PT/INR 1. Regular blood monitoring is essential. Warfarin's anticoagulant effect is measured by the Prothrombin Time/International Normalized Ratio (PT/INR). 2. The TARGET INR for PE/DVT is 2.0–3.0. An INR below 2.0 means under-anticoagulation (clot risk); above 3.0 means over-anticoagulation (bleeding risk). 3. Keep all laboratory and clinic follow-up appointments — especially important in Philippine community settings where point-of-care INR monitoring may be done at barangay health centers or outpatient laboratories. 4. Take warfarin at the SAME TIME every day to maintain consistent blood levels. III. DIETARY CONSIDERATIONS (VITAMIN K) 1. Vitamin K directly opposes warfarin's anticoagulant effect. The patient does NOT need to avoid vitamin K–rich foods entirely, but must keep intake CONSISTENT from day to day. 2. Foods high in Vitamin K: green leafy vegetables (malunggay, kangkong, alugbati, camote leaves), broccoli, and green onions — commonly eaten in the Philippine diet. 3. Teach: 'You can still eat these vegetables, but eat the same amount every day. Sudden large increases will lower your INR (clot risk); sudden large decreases will raise your INR (bleeding risk).' IV. BLEEDING PRECAUTIONS (SAFETY) 1. Watch for and IMMEDIATELY report: unusual bruising, prolonged bleeding from cuts, blood in urine (pink/red urine), dark or tarry stools, coughing up blood, or severe headache (possible intracranial bleed). 2. Use a SOFT-BRISTLED toothbrush and ELECTRIC RAZOR to reduce minor trauma and cuts. 3. Avoid contact sports or activities with high injury risk. 4. Inform ALL healthcare providers (dentist, other doctors, pharmacist) that you are on warfarin — many drugs interact with warfarin (NSAIDs, antibiotics, antifungals increase bleeding risk). 5. Do not take over-the-counter pain relievers (aspirin, ibuprofen) without physician approval. V. ANTIDOTE AND EMERGENCY The antidote for warfarin overdose is VITAMIN K (phytonadione). In emergencies, fresh frozen plasma (FFP) is given for immediate reversal. Teach the patient to carry a medical identification card or bracelet stating 'On anticoagulant therapy.' VI. FOLLOW-UP Regularly attend INR monitoring. In the Philippine context, the patient may follow up at the Outpatient Department (OPD) of their PhilHealth-accredited facility for INR checks and dose adjustment as prescribed by the physician.

Question Type

long_answer

Answer Structure

• Explain purpose of warfarin to patient in understandable terms [1 mark]
• PT/INR monitoring: target range 2.0–3.0, consistency of dosing time, clinic follow-up [1 mark]
• Vitamin K dietary guidance: consistent intake, Philippine food examples [1 mark]
• Bleeding precautions: signs to report, soft toothbrush/electric razor, drug interactions [1 mark]
• Antidote (Vitamin K), emergency identification, and Philippine follow-up context [1 mark]

Scoring Breakdown

Common Mark Deductions

• Telling the patient to AVOID all green vegetables — the correct teaching is consistent intake, not avoidance
• Confusing the antidote — writing 'protamine sulfate' (heparin's antidote) instead of 'vitamin K' for warfarin
• Failing to mention any drug interactions — warfarin has many interactions and omitting this is a significant teaching gap
• Writing the answer from the nurse's clinical perspective rather than in the patient-teaching format the question requires
• Not mentioning the INR target numerical range — vague references to 'therapeutic levels' are incomplete

Key Phrases To Include

• PT/INR
• target INR 2.0–3.0
• consistent vitamin K intake
• soft toothbrush
• electric razor
• report unusual bleeding
• vitamin K antidote
• drug interactions
• same time daily
• medical identification

Marks

2

Topic

ARDS — ABG Interpretation

Difficulty

medium

Template Id

T15

Examiner Tip

ABG interpretation in ARDS follows a predictable trajectory: the patient starts by blowing off CO2 (alkalosis) then eventually cannot maintain it (acidosis). This is the same trajectory as any severe respiratory condition. Understanding the WHY behind each pattern prevents memorization errors.

Model Answer

Early ARDS ABG Pattern — Respiratory Alkalosis: In the early stage, the patient hyperventilates in response to hypoxaemia and dyspnoea. This blows off excess CO2, resulting in: decreased PaCO2 (<35 mmHg), increased pH (>7.45), and low PaO2 (<60 mmHg). ABG pattern: respiratory alkalosis with hypoxaemia. Late ARDS ABG Pattern — Respiratory Acidosis: As respiratory muscles fatigue and the lungs become increasingly non-compliant and flooded, the patient can no longer maintain adequate ventilation. CO2 accumulates: increased PaCO2 (>45–50 mmHg), decreased pH (<7.35), and worsening severe hypoxaemia. ABG pattern: respiratory acidosis with severe, refractory hypoxaemia. This late pattern signals impending respiratory failure and urgent need for intubation.

Question Type

short_answer

Answer Structure

• Early ARDS: respiratory alkalosis (low PaCO2, high pH) with hypoxaemia [1 mark]
• Late ARDS: respiratory acidosis (high PaCO2, low pH) with severe refractory hypoxaemia [1 mark]

Scoring Breakdown

Common Mark Deductions

• Reversing the patterns — stating late ARDS shows alkalosis or early ARDS shows acidosis
• Not explaining the physiological reason for the pattern change (hyperventilation early; muscle fatigue late)
• Ignoring the pH value and only mentioning PaCO2 — incomplete ABG interpretation

Key Phrases To Include

• respiratory alkalosis
• hyperventilation
• low PaCO2
• respiratory acidosis
• muscle fatigue
• elevated PaCO2
• pH <7.35
• refractory hypoxaemia