NLE Respiratory Nursing — Acute Respiratory Failure & ARDSCheat Sheet

Formulas

Common values

Important facts

• Restlessness and CHANGE IN MENTAL STATUS are the EARLIEST signs of hypoxaemia — NOT cyanosis, NOT bradycardia
• Early hypoxaemia: restlessness, agitation, anxiety, tachypnoea, tachycardia, hypertension
• Hypercapnia: headache, drowsiness, confusion, CO2 narcosis (decreased LOC), warm flushed skin, bounding pulse
• Late/ominous signs: cyanosis, bradycardia, dysrhythmias, severe decreased LOC, respiratory arrest
• ABG is the DEFINING diagnostic test — must be serial to track trend
• Type I → oxygen INCREASES oxygenation (not shunt-based); Type II → oxygen is cautious in CO2 retainers (risk of removing hypoxic drive)

Key definitions

Diagrams to know

• ABG interpretation algorithm (acute vs chronic; respiratory vs metabolic)
• Mechanisms of hypoxaemia (hypoventilation, diffusion impairment, V/Q mismatch, shunt, low FiO2)
• Breathing pattern changes in respiratory failure (early tachypnoea → late bradypnoea)

Common values

Important facts

• Most common ARDS trigger: SEPSIS (followed by aspiration, trauma, pancreatitis, near-drowning, massive transfusion, transfusion-related acute lung injury — TRALI)
• Hallmark: REFRACTORY HYPOXAEMIA — does NOT improve with supplemental O2 (because it is shunt, not V/Q mismatch)
• Pathophysiology: Trigger → diffuse alveolar–capillary damage → protein-rich oedema floods alveoli → surfactant loss → atelectasis → V/Q mismatch + shunt
• Onset: rapidly progressive over HOURS to a few DAYS after the inciting event
• Chest X-ray: bilateral diffuse 'white-out' infiltrates, 'ground-glass' appearance (NOT focal, NOT unilateral)
• ABG: early respiratory alkalosis (hyperventilation) → progresses to respiratory acidosis as patient tires
• Oedema is NON-CARDIOGENIC — normal PCWP (< 18 mmHg) on Swan-Ganz catheter distinguishes from cardiogenic pulmonary oedema
• ARDS is a clinical diagnosis; no specific laboratory test confirms it (ABG, CXR, clinical context)

Key definitions

Diagrams to know

• ARDS pathophysiology cascade: trigger → endothelial damage → increased permeability → protein-rich oedema → surfactant loss → atelectasis → hypoxaemia
• Difference between ARDS (non-cardiogenic) and cardiogenic pulmonary oedema (PCWP, CXR pattern, treatment)

Common values

Important facts

• Nearly ALL ARDS patients require mechanical ventilation with PEEP — spontaneous breathing cannot maintain oxygenation
• PEEP is the cornerstone of ARDS ventilation — keeps alveoli open at end-expiration, recruits collapsed alveoli, improves shunt
• Excessive PEEP → decreases venous return → ↓ cardiac output → hypotension (monitor haemodynamics)
• Lung-protective ventilation reduces mortality in ARDS — lower tidal volumes, lower plateau pressure (< 30 cm H2O)
• Prone positioning improves oxygenation in moderate-to-severe ARDS by redistributing perfusion and improving V/Q matching; consider early
• Wean PEEP gradually as oxygenation improves — do not reduce too rapidly (risk of alveolar collapse)
• ARDS is progressive — compliance often worsens before improving; expect plateau pressures to increase despite lung-protective strategy
• Treat the UNDERLYING CAUSE** (e.g., antibiotics for sepsis, source control) — mechanical ventilation buys time

Key definitions

Diagrams to know

• PEEP effect: alveolar recruitment curve (low PEEP = some alveoli closed; optimal PEEP = recruitment; excessive PEEP = overdistension)
• ARDSNet lung-protective ventilation protocol flowchart

Common values

Important facts

• Classic presentation: sudden-onset dyspnoea, pleuritic chest pain, tachycardia, tachypnoea, anxiety, sense of IMPENDING DOOM
• Risk factors: Virchow's Triad — stasis (immobility, post-op, prolonged travel), hypercoagulability (cancer, pregnancy, OCP, dehydration), endothelial injury (trauma, surgery, central lines)
• Most common source of PE: DVT from legs/pelvis; also fat embolism (trauma), air embolism, amniotic fluid
• Gold-standard diagnostic test: CT pulmonary angiography (CTPA)
• D-dimer: HIGH = non-specific (many causes); NORMAL = helps RULE OUT PE in low-risk patients
• ABG: usually hypoxaemia + respiratory alkalosis (low CO2 from hyperventilation)
• ECG findings: typically sinus tachycardia; classic 'S1Q3T3' (tall S wave in I, Q wave in III, T-wave inversion in III) is UNCOMMON
• Haemoptysis, low-grade fever may occur (infarction if distal PE)
• Look for coexisting DVT (unilateral calf swelling, warmth, tenderness, positive Homan's/Wells score)

Key definitions

Diagrams to know

• PE risk assessment: Virchow's Triad + clinical presentation → CTPA/D-dimer
• Haemodynamic classification of PE: massive (unstable) vs submassive vs low-risk

Important facts

• PE priority: OXYGEN + elevate head of bed + reassurance + anticoagulation
• Anticoagulation is the mainstay — prevents clot propagation and allows natural fibrinolysis
• Thrombolytics ONLY for massive (unstable) PE — haemodynamic instability (hypotension, shock), right-heart strain, high mortality risk
• Prevention is heavily tested: early ambulation, compression stockings, intermittent pneumatic compression (IPC), prophylactic anticoagulation in at-risk patients
• Post-operative PE prophylaxis: mechanical (early ambulation, compression) + pharmacological (enoxaparin, fondaparinux) depending on risk
• Watch for pulmonary infarction: distal PE may cause infarction → pleuritic pain, haemoptysis, pleural effusion (days later)

Key definitions

Diagrams to know

• PE treatment algorithm: massiveUnstable (thrombolytics) vs submassive/low-risk (anticoagulation)
• DVT/PE prophylaxis protocol by risk category

Common values

Important facts

• Heparin (UFH & LMWH): watch for HIT — monitor platelets (baseline, Day 3–5, Day 10); platelet drop of > 50% or absolute < 100K is suspicious
• Heparin antidote: Protamine sulfate (1 mg per 100 U heparin IV slow); gives within 15 min of last heparin dose
• Warfarin: SLOW onset (2–5 days) — overlap with heparin for ≥5 days AND until INR 2.0–3.0 for ≥24 hours
• Warfarin interactions: alcohol, NSAIDs, antibiotics, statins, azole antifungals ↑ INR; vitamin K, barbiturates ↓ INR
• Warfarin patient teaching: maintain CONSISTENT vitamin-K intake (green leafy vegetables), avoid binge drinking, many drug interactions, monthly INR checks
• Warfarin antidote: Vitamin K (10 mg IV slow over 1–2 hours, or oral if minor bleeding); also fresh frozen plasma (FFP) or prothrombin complex concentrate (PCC) for major bleeding
• DOACs: fixed dosing, no monitoring, but NO antidote (except dabigatran → idarucizumab); easier for patient compliance
• BLEEDING is the key adverse effect of ALL anticoagulants — teach signs (bruising, bleeding gums, blood in urine/stool), use soft toothbrush, electric razor, avoid trauma

Key definitions

Diagrams to know

• Anticoagulant choice flowchart (UFH vs LMWH vs warfarin vs DOAC based on indication, renal function, compliance)
• HIT timeline: days 3–10 after heparin start; platelet count drops; stop heparin; switch to DTI

Common values

Important facts

• Confirm & secure the endotracheal tube: bilateral equal breath sounds, capnography (ETCO2 detection), chest X-ray (tip above carina, ~2 cm from entrance to trachea)
• Keep manual resuscitation (bag-valve-mask) bag at the bedside — ready for accidental extubation or ventilator failure
• Suction ONLY as needed (not routine schedule); hyperoxygenate before suctioning (100% O2 × 30 sec); limit pass to 10–15 seconds
• VAP (Ventilator-Associated Pneumonia) prevention bundle:
• — Elevate head of bed 30–45° (prevent gastric reflux and aspiration)
• — Daily sedation interruption + readiness-to-wean assessment (spontaneous breathing trial, extubation criteria)
• — Oral care with chlorhexidine 0.12% rinse twice daily
• — DVT prophylaxis (compression, early ambulation, prophylactic anticoagulation)
• — Stress-ulcer prophylaxis (H2 blocker or PPI)
• High-pressure alarm: suggests OBSTRUCTION — check for secretions (suction), kinked tubing, patient biting tube, or bronchospasm; may need sedation or neuromuscular blockade
• Low-pressure alarm: suggests LEAK or DISCONNECTION — check tubing circuit, cuff, connections; if unsure, manually ventilate with bag-valve-mask and call for help
• NEVER ignore an alarm — always assess the patient first, then the machine
• Wean O2 first, then pressure/volume, then rate; gradual weaning prevents rebound hypoxaemia and respiratory muscle fatigue
• Patient cannot speak with ETT; provide communication method (writing pad, eye blink, yes/no cards); involve family

Key definitions

Diagrams to know

• ETT placement verification: bilateral breath sounds, capnography, chest X-ray
• Ventilator alarm response flowchart (high pressure vs low pressure → troubleshooting steps)
• Weaning protocol: daily spontaneous breathing trial, extubation readiness criteria

Common values

Important facts

• Priority Maslow assessment: Airway → Breathing → Circulation
• RESTLESSNESS is the FIRST sign of hypoxaemia — assess mental status (change = hypoxaemia until proven otherwise)
• Use SBAR handover: Situation (what happened), Background (relevant hx), Assessment (your impression), Recommendation (action needed)
• Positioning: upright (Fowler's 45–90°) for all respiratory patients; allows gravity to assist breathing, improves V/Q matching
• Oxygen therapy: titrate to achieve SpO2 ≥ 94% in most patients; exceptions: Type II (CO2 retainer) target 88–92%; avoid removing hypoxic drive
• Monitor vital signs continuously: RR (↑ early sign of distress), HR (↑ with hypoxaemia), BP (↓ in shock/tension pneumothorax), SpO2 (≥ 94%, ≤ 88–92% in CO2 retainers)
• Frequent ABG draws in acute failure: initial, after intervention, q1–2h if unstable; always assess for trends, not isolated values
• Protect the airway: keep NPO if intubation expected; suction mouth regularly; maintain ETT cuff (20–30 cm H2O to prevent aspiration and tube erosion)
• Prepare for intubation: have airway equipment ready (laryngoscope, blades, ETTs of various sizes, stylet, manual resuscitation bag), know the indication (hypoxaemia not responding to O2, inability to protect airway, RR < 8 or > 35, exhaustion)

Key definitions

Diagrams to know

• Respiratory distress assessment: RR, use of accessory muscles, stridor, ability to speak full sentences, mental status
• Intubation readiness: indication, equipment, patient position, post-intubation care

Important facts

• Anticoagulant safety teaching (for PE/DVT patients):
• — Report unusual bleeding (nosebleeds, bleeding gums, blood in urine/stool, large bruises)
• — Take dose at the same time daily (especially warfarin for consistency)
• — Keep INR monitoring appointments (warfarin every 2–4 weeks, then monthly)
• — Maintain CONSISTENT vitamin-K intake (avoid binge eating/avoiding green vegetables)
• — Avoid NSAIDs and alcohol unless approved by provider
• — Wear medical alert bracelet (on anticoagulant)
• DVT/PE prevention for patient:
• — Stay mobile; do NOT sit for long periods (> 2 hours without movement)
• — Ankle pumping exercises on long flights/car rides (10 reps, q30 min)
• — Stay hydrated (8–10 glasses water/day)
• — Wear prescribed compression stockings correctly (put on before getting out of bed)
• — Elevate legs when resting
• Ventilated patient communication: explain the tube (cannot speak but can hear), importance of sedation/analgesia, that family can visit/talk, expected duration

Key definitions

Diagrams to know

• PE risk stratification: Wells score, revised Geneva score (for clinical assessment of PE probability)