NLE Respiratory Nursing — Acute Respiratory Failure & ARDSRevision Notes

Formulas

Exam Tips

• NLE PRIORITY TIP: If a question asks what the nurse should do FIRST for any respiratory patient — the answer is almost always POSITION THE PATIENT UPRIGHT and ENSURE AIRWAY PATENCY, then deliver appropriate oxygen.
• MEMORY TIP for Type I vs Type II: 'Type I = I cannot breathe IN enough oxygen (oxygenation)'; 'Type II = Two gases involved — too much CO2, too little ventilation'.
• EARLY signs are the KEY to prioritization: Restlessness + agitation + tachypnoea = suspect hypoxia. This is a NANDA nursing diagnosis of Impaired Gas Exchange.
• In NLE questions about COPD patients needing oxygen, the correct answer almost always involves CONTROLLED low-flow oxygen with SpO2 target 88–92%, NOT a non-rebreather mask.
• Always choose the option that addresses AIRWAY and BREATHING before circulation (unless the question context specifies a circulation problem as primary).

Key Points

• Respiratory failure = lungs can no longer maintain adequate gas exchange; defined by ABG values.
• Type I (Hypoxaemic) failure: PaO2 < 60 mmHg on room air — the OXYGENATION problem. Think: lungs cannot LOAD oxygen. Examples: pneumonia, ARDS, pulmonary oedema, PE.
• Type II (Hypercapnic) failure: PaCO2 > 50 mmHg WITH pH < 7.35 — the VENTILATION problem. Think: lungs cannot UNLOAD CO2. Examples: COPD exacerbation, opioid overdose, neuromuscular disease (e.g., Guillain-Barré), chest-wall injury.
• Four mechanisms of hypoxaemia: V/Q mismatch (most common), shunting (blood bypasses unoxygenated alveoli), diffusion impairment, and hypoventilation.
• EARLY signs of hypoxaemia: RESTLESSNESS, agitation, anxiety, tachypnoea, tachycardia, and hypertension — these are the MOST TESTED early signs. A suddenly agitated patient = suspect hypoxia until proven otherwise.
• Hypercapnia signs: headache, drowsiness, confusion, CO2 narcosis (decreased LOC), warm flushed skin, bounding pulse.
• LATE/OMINOUS signs: cyanosis, bradycardia, dysrhythmias, decreased LOC, and respiratory arrest — these indicate a critical emergency.
• ABG is the DEFINING diagnostic test. Serial ABGs track the trend of improvement or deterioration.
• PRIORITY nursing action: ensure a patent airway and deliver APPROPRIATE oxygen.
• Type I management: high-concentration oxygen (e.g., non-rebreather mask) to correct hypoxaemia.
• Type II management: CONTROLLED oxygen — target SpO2 88–92%. Why? High-flow O2 in CO2 retainers can suppress the hypoxic drive and worsen hypoventilation. Support ventilation with BiPAP or prepare for intubation if pH continues to fall.
• Always treat the UNDERLYING CAUSE alongside supportive oxygenation.
• Prepare for intubation and mechanical ventilation if the patient tires, mental status worsens, or ABG values do not improve.

Definitions

Section Title

Acute Respiratory Failure: Types, Pathophysiology, and Nursing Management

Common Mistakes

• Giving high-flow oxygen to a known CO2 retainer (e.g., COPD patient) — this removes the hypoxic drive and can cause further CO2 retention and respiratory depression. Always use CONTROLLED oxygen (SpO2 target 88–92%).
• Mistaking early hypoxaemia (restlessness, agitation) for anxiety or behavioral issues — always assess oxygen saturation and ABG before attributing mental status changes to non-physiologic causes.
• Waiting for cyanosis to appear before acting — cyanosis is a LATE sign. By the time cyanosis is visible, the patient is already in critical danger.
• Confusing Type I and Type II failure: Type I = O2 problem (PaO2 low); Type II = CO2 problem (PaCO2 high with acidosis).
• Relying solely on pulse oximetry — SpO2 can be falsely normal (e.g., in CO poisoning where oximetry reads carboxyhaemoglobin as oxyhaemoglobin). ABG is the gold standard for accurate assessment.

Formulas

Exam Tips

• ARDS HALLMARK TRIAD to remember: (1) Refractory hypoxaemia, (2) Bilateral white-out infiltrates on CXR, (3) Non-cardiogenic oedema (normal heart).
• MOST COMMON CAUSE = SEPSIS — if the NLE question mentions a patient with sepsis who suddenly develops respiratory distress and bilateral infiltrates, ARDS is the diagnosis.
• PEEP = keeps alveoli OPEN. Think of PEEP as a 'splint' for the alveoli — it stops them from collapsing at end-expiration.
• NANDA nursing diagnosis for ARDS: Impaired Gas Exchange related to alveolar-capillary membrane injury — this is the PRIORITY nursing diagnosis, highest on Maslow's physiologic hierarchy.
• CXR pattern NLE mnemonic: 'ARDS = All Regions Diffusely Snowed-in' — bilateral white-out infiltrates across both lung fields.
• If asked about early ABG changes in ARDS: RESPIRATORY ALKALOSIS first (patient hyperventilates and blows off CO2). Then progresses to respiratory acidosis as patient tires.

Key Points

• ARDS = severe, acute, diffuse INFLAMMATORY lung injury producing REFRACTORY HYPOXAEMIA. 'Refractory' means it does NOT improve with supplemental oxygen — this is the single most important feature.
• Most common trigger/cause: SEPSIS. Other triggers: aspiration of gastric contents, trauma, pancreatitis, near-drowning, massive blood transfusion.
• Pathophysiology in sequence: trigger → diffuse alveolar-capillary membrane damage → membrane becomes LEAKY → protein-rich fluid floods the alveoli (NON-CARDIOGENIC pulmonary oedema) → surfactant destroyed → alveoli COLLAPSE (atelectasis) → lung compliance falls ('stiff lungs') → severe V/Q mismatch and intrapulmonary shunting → refractory hypoxaemia.
• Key distinguishing feature from cardiogenic pulmonary oedema: the oedema is NON-CARDIOGENIC (normal pulmonary capillary wedge pressure — PCWP is normal, meaning the heart is NOT the cause).
• HALLMARK clinical signs: severe dyspnoea, tachypnoea, restlessness, use of accessory muscles, bilateral crackles — appearing rapidly within hours to a few days of the triggering event.
• Chest X-ray finding: DIFFUSE BILATERAL 'WHITE-OUT' INFILTRATES — also called 'ground-glass' appearance. Bilateral = both lungs; white-out = fluid-filled alveoli blocking normal black air spaces.
• ABG pattern: EARLY = respiratory alkalosis (patient hyperventilates, blowing off CO2). LATE = respiratory acidosis + severe refractory hypoxaemia (patient tires, cannot sustain hyperventilation).
• CORNERSTONE of ARDS treatment: mechanical ventilation with PEEP (positive end-expiratory pressure).
• PEEP = keeps alveoli open at the END of expiration, recruits collapsed alveoli, and improves oxygenation.
• Lung-protective ventilation: LOW tidal volume (~6 mL/kg of PREDICTED body weight) to prevent barotrauma and volutrauma (additional lung injury from mechanical ventilation itself).
• PRONE POSITIONING: turning the patient face-down improves V/Q matching and oxygenation in moderate-to-severe ARDS. It is a nursing-intensive intervention requiring a coordinated team.
• Treat the UNDERLYING CAUSE (e.g., antibiotics for sepsis-triggered ARDS).
• Complications: barotrauma/pneumothorax, ventilator-associated pneumonia (VAP), multi-organ dysfunction syndrome (MODS), and pulmonary fibrosis in survivors.
• Mortality remains HIGH despite best care — early recognition and trigger treatment are paramount.

Definitions

Section Title

Acute Respiratory Distress Syndrome (ARDS): Pathophysiology and Critical Care Nursing

Common Mistakes

• Confusing ARDS oedema with cardiogenic pulmonary oedema (heart failure). KEY DIFFERENTIATOR: ARDS oedema is NON-CARDIOGENIC — heart function and PCWP are normal. Cardiogenic oedema has elevated PCWP and signs of heart failure.
• Thinking that giving more oxygen will fix ARDS hypoxaemia — it will NOT, because the problem is shunting. PEEP and mechanical ventilation are needed.
• Forgetting that SEPSIS is the most common cause/trigger of ARDS — NLE questions about a septic patient who then develops bilateral infiltrates and refractory hypoxaemia = think ARDS.
• Using high tidal volumes 'to open the lungs' — this causes VOLUTRAUMA and worsens ARDS. Always use LOW tidal volumes (~6 mL/kg) for ARDS patients.
• Neglecting prone positioning as a nursing intervention — it is a significant evidence-based intervention for moderate-to-severe ARDS and is NLE-testable.

Exam Tips

• PE CLASSIC PRESENTATION memory aid: 'Sudden DPTA' — Dyspnoea, Pleuritic chest pain, Tachycardia, Anxiety (impending doom).
• PREVENTION questions: the NLE frequently tests nursing interventions to PREVENT DVT/PE in post-op patients. Correct answers include: early ambulation, compression stockings, IPC devices, prophylactic anticoagulation, and adequate hydration.
• D-Dimer rule: 'Normal D-dimer = No PE' (for low-risk patients). Elevated D-dimer = needs further workup (CTPA).
• THROMBOLYTICS = only for MASSIVE (unstable) PE. Think: 'Lyse it only if the patient is about to die from it.'
• IVC filter indication = anticoagulation is CONTRAINDICATED. Think: patient has active GI bleeding + PE = cannot anticoagulate = IVC filter.
• Virchow's Triad is the framework for EVERY PE/DVT risk factor question. If a question lists multiple risk factors, mentally check which part of the triad each one belongs to.

Key Points

• PE = obstruction of the pulmonary artery or a branch, MOST COMMONLY by a THROMBUS from a deep vein thrombosis (DVT) of the legs or pelvis.
• Less common emboli: fat (long bone fractures), air (central line insertion errors), amniotic fluid (obstetric emergency).
• RISK FACTORS follow Virchow's Triad: (1) VENOUS STASIS — immobility, prolonged bed rest, long flights/travel, post-surgical state; (2) HYPERCOAGULABILITY — cancer, pregnancy, oral contraceptives, dehydration, inherited clotting disorders; (3) ENDOTHELIAL INJURY — trauma, surgery, central venous catheters.
• CLASSIC PRESENTATION: SUDDEN ONSET of dyspnoea (most common symptom), pleuritic chest pain (sharp pain that worsens with breathing), tachypnoea, tachycardia, anxiety, and a SENSE OF IMPENDING DOOM.
• Haemoptysis (coughing up blood) and low-grade fever may also be present.
• MASSIVE PE: hypotension, syncope (fainting), cyanosis, signs of right-heart strain — this is OBSTRUCTIVE SHOCK and can progress to cardiac arrest.
• Always check for coexisting DVT signs: unilateral calf swelling, warmth, tenderness, and erythema (redness) in one leg.
• GOLD-STANDARD confirmatory test: CT Pulmonary Angiography (CTPA).
• D-Dimer: a SENSITIVE but NOT SPECIFIC blood test. A NORMAL D-dimer RULES OUT PE in low-risk patients. An elevated D-dimer does NOT confirm PE (many conditions raise D-dimer).
• ABG in PE: hypoxaemia WITH RESPIRATORY ALKALOSIS (hypocapnia from hyperventilation — patient is breathing fast, blowing off CO2).
• ECG: most common finding is sinus tachycardia. The classic 'S1Q3T3' pattern is uncommon but tested.
• PRIORITY NURSING INTERVENTIONS: (1) Administer OXYGEN immediately; (2) Elevate head of bed to ease breathing; (3) Stay with the patient and provide reassurance; (4) Monitor vital signs and SpO2 continuously; (5) Prepare for ANTICOAGULATION.
• ANTICOAGULATION is the MAINSTAY of PE treatment — it prevents further clot formation and allows the body to dissolve existing clots.
• THROMBOLYTICS (e.g., alteplase) are reserved ONLY for MASSIVE PE with haemodynamic instability (severe hypotension, shock).
• IVC (inferior vena cava) FILTER is used when anticoagulation is CONTRAINDICATED (e.g., active bleeding, recent surgery, recent haemorrhagic stroke).
• PE PREVENTION is HEAVILY TESTED in the NLE: early ambulation post-operatively, compression stockings, intermittent pneumatic compression (IPC) devices, and prophylactic anticoagulation in at-risk patients.

Definitions

Section Title

Pulmonary Embolism (PE): Recognition, Diagnosis, and Priority Nursing Care

Common Mistakes

• Giving a patient with suspected PE vigorous chest physiotherapy or deep massage to the leg — this can dislodge a clot and worsen the embolism. Keep the patient at rest initially.
• Confusing D-dimer's clinical utility: a HIGH D-dimer does NOT confirm PE; a NORMAL D-dimer RULES IT OUT in low-risk patients. Many students reverse this.
• Forgetting that the FIRST PRIORITY for PE is OXYGEN — before waiting for CTPA results or anticoagulation orders, administer oxygen and position the patient.
• Using thrombolytics for every PE — thrombolytics are ONLY indicated for MASSIVE PE with haemodynamic instability. They carry a high bleeding risk including intracranial haemorrhage.
• Neglecting DVT prevention in post-operative Filipino patients — early ambulation, compression stockings, and prophylactic anticoagulation are standard and heavily NLE-tested.

Exam Tips

• ANTICOAGULANT DRUG TABLE — memorize this: Heparin→aPTT→Protamine; Warfarin→PT/INR (target 2-3)→Vitamin K; LMWH→no routine monitor→Protamine (partial).
• HIT memory tip: 'HIT is a HIT to BOTH platelets AND blood vessels' — thrombocytopenia + thrombosis. Paradox = high-yield NLE topic.
• WARFARIN PATIENT TEACHING: the most common NLE-tested warfarin teaching points are: (1) Keep vitamin K intake CONSISTENT; (2) Monitor for bleeding signs; (3) Take medication at the SAME TIME daily; (4) Report ALL new medications to the doctor; (5) Never skip INR monitoring appointments.
• NLE ANTIDOTE QUESTION FORMAT: 'A patient on IV heparin develops severe bleeding. What will the nurse prepare?' Answer: PROTAMINE SULFATE. 'A patient on warfarin with INR of 8.5 is bleeding.' Answer: VITAMIN K (and/or FFP for immediate reversal).
• DOAC reversal: Dabigatran = Idarucizumab (specific reversal agent). This is increasingly tested in NLE as DOACs become more common in Philippine clinical practice.

Key Points

• ANTICOAGULANTS prevent NEW clot formation and stop existing clots from growing. They do NOT dissolve existing clots (thrombolytics do that).
• HEPARIN (unfractionated, IV): immediate onset. Monitor with aPTT (activated partial thromboplastin time). Target aPTT = 1.5–2.5 times the control value. Antidote: PROTAMINE SULFATE. Watch for HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) — monitor platelet count.
• HIT is paradoxical — heparin causes CLOTTING (not just thrombocytopenia). If HIT is suspected, STOP heparin immediately and switch to a NON-heparin anticoagulant.
• ENOXAPARIN (LMWH — Low Molecular Weight Heparin): subcutaneous injection, more predictable pharmacokinetics, NO routine monitoring needed (but anti-Xa levels can be checked). Partial reversal with protamine sulfate.
• WARFARIN (oral): delayed onset (takes 3–5 days to be effective). Must OVERLAP with heparin for several days when starting. Monitor with PT/INR. Target INR = 2.0–3.0 for PE/DVT. Antidote: VITAMIN K (slow reversal) or fresh frozen plasma (FFP) for immediate reversal. MANY drug and food interactions.
• Warfarin teaching: maintain CONSISTENT vitamin K intake (do not suddenly increase or decrease green leafy vegetables — consistent intake is key, not avoidance). Many medications interact with warfarin (antibiotics, NSAIDs, etc.).
• DOACs (Direct Oral Anticoagulants): rivaroxaban, apixaban (Factor Xa inhibitors), dabigatran (direct thrombin inhibitor). Fixed dosing, no routine monitoring, more predictable. Dabigatran reversal agent = IDARUCIZUMAB. Andexanet alfa reverses Factor Xa inhibitors.
• BLEEDING is the KEY adverse effect of ALL anticoagulants. Teach patients: watch for unusual bruising, bleeding gums, prolonged bleeding from cuts, blood in urine (pink/red/brown urine), black/tarry stools, and severe headache (possible intracranial bleed).
• Safety precautions for anticoagulant patients: use a SOFT toothbrush, ELECTRIC razor (not a straight razor), avoid contact sports and IM injections, and apply pressure to all puncture sites for at least 5 minutes.

Definitions

Section Title

Anticoagulation Pharmacology for PE and DVT: High-Yield Drug Knowledge

Common Mistakes

• Monitoring aPTT for warfarin or PT/INR for heparin — these are reversed! Heparin = aPTT; Warfarin = PT/INR.
• Telling warfarin patients to AVOID all green leafy vegetables — the correct advice is to keep vitamin K intake CONSISTENT, not eliminate it. Suddenly stopping or increasing greens causes INR to swing dangerously.
• Expecting HIT to cause bleeding — HIT paradoxically causes THROMBOSIS. If a patient on heparin develops new clots AND low platelets, think HIT and stop all heparin immediately.
• Thinking DOACs do not need any monitoring — while they do not require routine INR monitoring, renal and hepatic function should still be monitored because DOACs are cleared renally/hepatically.
• Forgetting that warfarin has a DELAYED onset — it takes 3–5 days. Patients transitioning from heparin to warfarin must OVERLAP both drugs until the INR is therapeutic.

Formulas

Exam Tips

• ALARM RESPONSE MEMORY GUIDE: HIGH pressure = OBSTRUCTION (something is blocked — suction, check tubing, check for biting). LOW pressure = LEAK or DISCONNECTION (something is open or not connected).
• GOLDEN RULE for ventilator emergencies: If you cannot quickly identify and fix the problem, DISCONNECT and MANUALLY VENTILATE with the bag-valve-mask. Never leave the patient without ventilation while you troubleshoot.
• VAP BUNDLE acronym: 'HEAD-COD' — H = Head of bed 30–45°; E = Evaluate/Daily sedation interruption and SBT; A = Antiseptic oral care (chlorhexidine); D = DVT prophylaxis; C = (stress ulcer/gastric) prophylaxis with COX inhibitors / PPIs; O = Oral hygiene daily; D = Daily assessment for extubation readiness.
• ETT PLACEMENT confirmation: the best IMMEDIATE bedside confirmation after intubation is CAPNOGRAPHY (ETCO2). The DEFINITIVE anatomical confirmation is CHEST X-RAY.
• ETT cuff pressure should be maintained at 20–30 cmH2O — too low allows aspiration; too high causes tracheal ischaemia and stenosis. This is tested in NLE clinical management questions.
• SUCTIONING = only when NEEDED + PRE-OXYGENATE + limit to 10–15 seconds per pass. These three points are frequently tested as correct suction technique.

Key Points

• Mechanical ventilation (MV) supports or replaces the patient's breathing when oxygenation or ventilation fails despite other measures. It requires ENDOTRACHEAL INTUBATION (ETT).
• CONFIRM ETT PLACEMENT IMMEDIATELY after intubation: bilateral breath sounds on auscultation, condensation in the tube, capnography (ETCO2 — gold standard for confirmation), and CHEST X-RAY (shows tip position above the carina, approximately 2–3 cm above the carina at the level of T2–T4).
• SECURE the ETT carefully and mark the centimetre level at the lips. Prevent accidental extubation — it is a LIFE-THREATENING emergency.
• KEEP A MANUAL RESUSCITATION BAG (bag-valve-mask, 'Ambu bag') AT THE BEDSIDE at ALL times — for accidental extubation or ventilator failure.
• PEEP: keeps alveoli open at end-expiration (improves oxygenation). Too much PEEP → reduces venous return (preload) → hypotension, and risk of barotrauma (pneumothorax).
• FiO2 (fraction of inspired oxygen): wean to the LOWEST FiO2 that keeps SpO2 adequate. Prolonged high FiO2 (> 0.60 for extended periods) causes OXYGEN TOXICITY (worsens lung injury).
• SUCTIONING: perform ONLY as needed (not on a schedule). HYPEROXYGENATE the patient (pre-oxygenate with 100% O2) BEFORE suctioning. Limit each suction pass to 10–15 SECONDS to prevent hypoxaemia and mucosal trauma.
• HIGH-PRESSURE ALARM: indicates OBSTRUCTION somewhere — check for secretions (SUCTION), KINKED tubing, patient BITING the ETT (use a bite block), BRONCHOSPASM, or the patient coughing/bucking the vent. FIRST ACTION: assess the patient, then troubleshoot.
• LOW-PRESSURE ALARM: indicates a LEAK or DISCONNECTION — check all circuit connections, check the ETT CUFF (may be leaking), and check for accidental extubation.
• If you cannot quickly identify and fix a ventilator problem: DISCONNECT the ventilator and manually ventilate with the bag-valve-mask, then call for help.
• VAP (VENTILATOR-ASSOCIATED PNEUMONIA) PREVENTION BUNDLE — all elements are NLE-tested: (1) Elevate the head of the bed 30–45°; (2) Daily sedation interruption and spontaneous breathing trial (readiness-to-wean assessment); (3) Oral care with CHLORHEXIDINE; (4) DVT prophylaxis; (5) Stress ulcer prophylaxis.
• Patient COMMUNICATION: patients with an ETT CANNOT SPEAK. Provide an alternative communication method (writing board, picture boards, alphabet board) to reduce frustration and anxiety.
• SEDATION and ANALGESIA: most intubated patients require sedation to tolerate the ETT and ventilator. Use the lightest sedation possible (daily sedation interruption). Pain control is always addressed first (analgesia-first approach).
• Monitor for COMPLICATIONS of MV: barotrauma (pneumothorax), VAP, ventilator-induced lung injury, haemodynamic compromise (PEEP reduces cardiac output), and gastric aspiration.

Definitions

Section Title

Mechanical Ventilation: Nursing Care, Alarms, and VAP Prevention

Common Mistakes

• Suctioning on a FIXED TIME SCHEDULE (e.g., every 2 hours) rather than as needed — this increases the risk of hypoxaemia and mucosal trauma without benefit. Suction ONLY when clinically indicated.
• Forgetting to pre-oxygenate before suctioning — hyperoxygenating with 100% FiO2 for 30–60 seconds before suctioning prevents procedure-induced desaturation.
• SILENCING a ventilator alarm without first ASSESSING THE PATIENT — alarms exist to signal life-threatening problems. Always assess first, then troubleshoot.
• Not keeping the head of the bed at 30–45° in ventilated patients — even a few hours in the supine position significantly increases VAP risk through aspiration of oral secretions.
• Responding to a LOW-PRESSURE alarm by only silencing it — this usually means a disconnection or ETT cuff leak. The patient may not be receiving ventilation. Assess and reconnect/fix immediately.