315.1 🎓 醫孞生版

315.1.0.1 📌 䞀頁重點

315.1.0.1.1 Respiratory Failure
315.1.0.1.1.1 Categories

Type I (Hypoxemic): - PaO2 < 60 mmHg - A-a gradient ↑ - V/Q mismatch or shunt - Examples: pneumonia, pulmonary edema, ARDS, PE, atelectasis

Type II (Hypercapnic): - PaCO2 > 45 mmHg - Alveolar hypoventilation - Examples: COPD, neuromuscular, drug overdose, OHS

Type III (Perioperative): - Atelectasis post-op - Often resolves with PEEP, mobilization

Type IV (Shock): - Hypoperfusion + hypoxemia

315.1.0.1.1.2 Acute vs Chronic
  • Acute: sudden onset, no time for compensation
  • Chronic: gradual, kidney compensates HCO3
  • Acute on chronic: severe decompensation
315.1.0.1.2 Acute Respiratory Distress Syndrome (ARDS)
315.1.0.1.2.1 Definition — Berlin Criteria (2012)

4 Criteria: 1. Timing: within 1 week of known clinical insult 2. Imaging: bilateral opacities not fully explained by effusion, atelectasis, nodules 3. Origin: respiratory failure not fully explained by cardiac or volume overload (objective assessment if needed) 4. Oxygenation: PaO2/FiO2 < 300 with PEEP ≥ 5 cm H2O

315.1.0.1.2.2 Severity (by PaO2/FiO2 with PEEP ≥ 5)
  • Mild ARDS: 200-300
  • Moderate ARDS: 100-200
  • Severe ARDS: ≀ 100
315.1.0.1.2.3 2023 Global Definition Update (Proposed)
  • Includes high-flow nasal cannula
  • Includes ultrasound criteria
  • Resource-limited settings
315.1.0.1.2.4 Etiology

Direct Lung Injury: - Pneumonia (most common) - Aspiration - Pulmonary contusion - Inhalation injury - Near-drowning - Reperfusion injury

Indirect Lung Injury: - Sepsis (most common indirect) - Trauma - Pancreatitis - Transfusion (TRALI) - Cardiopulmonary bypass - Drug overdose - Fat embolism

315.1.0.1.2.5 Pathophysiology

Three Phases:

  1. Exudative (0-7 days):
    • Epithelial + endothelial injury
    • Increased permeability → protein-rich edema
    • Hyaline membranes
    • Inflammation, cytokines (TNF, IL-1, IL-6, IL-8)
    • Surfactant dysfunction
    • V/Q mismatch + shunt
  2. Proliferative (7-21 days):
    • Type II pneumocyte proliferation
    • Fibroblast invasion
    • Beginning of repair
  3. Fibrotic (≥ 14-21 days):
    • Collagen deposition
    • Long-term fibrosis (variable)
315.1.0.1.2.6 Clinical Presentation
  • Dyspnea, tachypnea, cyanosis
  • Hypoxemia refractory to supplemental O2
  • Bilateral lung crackles
  • Decreased compliance
  • Often septic / inflammatory state
315.1.0.1.3 Management of ARDS
315.1.0.1.3.1 Lung-Protective Ventilation (ARMA / ARDSnet 2000)

Tidal Volume 6 mL/kg of Predicted Body Weight (PBW): - Lower than traditional (10-12 mL/kg) - ↓ Ventilator-induced lung injury (VILI) - ↓ Mortality 9% - Foundation of modern ARDS care

Plateau Pressure < 30 cm H2O: - Limits stretch - Reduces VILI - Permissive hypercapnia OK (target pH > 7.20)

PEEP: - Higher PEEP for moderate-severe ARDS - ALVEOLI, ExPress, LOVS trials - PEEP-FiO2 table guidance - Recruit alveoli, reduce shunt

Driving Pressure (Plateau - PEEP) < 15 cm H2O: - Most predictive of mortality (Amato 2015) - Reduce by lowering Vt or increasing PEEP

315.1.0.1.3.2 Prone Positioning (PROSEVA 2013)
  • Severe ARDS (PaO2/FiO2 < 150)
  • ≥ 16 hours/day in prone position
  • ↓ Mortality 16% (relative reduction 50%)
  • Mechanisms: improves V/Q, reduces atelectasis, optimal lung mechanics
  • Standard of care for severe ARDS
315.1.0.1.3.3 Neuromuscular Blockade (NMB)

ACURASYS (2010): cisatracurium × 48 hours improved survival ROSE (2019): more careful sedation + early NMB no benefit Current Practice: NMB for refractory hypoxemia + ventilator dyssynchrony

315.1.0.1.3.4 Fluid Management

FACTT Trial (2006): - Conservative fluid management ↑ ventilator-free days - No difference in mortality - Practice: diurese to euvolemia if hemodynamically stable

315.1.0.1.3.5 ECMO (Extracorporeal Membrane Oxygenation)

Indications: - Refractory hypoxemia (PaO2/FiO2 < 80, pH < 7.20) - Severe ARDS not improving with conventional therapy

Types: - VV-ECMO: blood from vena cava → oxygenator → return to RA/SVC - VA-ECMO: also adds cardiac support

Evidence: - CESAR (2009): ECMO referral improved survival - EOLIA (2018): borderline; crossover issues; benefit suggested - EOLIA + Bayesian Analysis (2018): probably beneficial

Complications: - Bleeding (anticoagulation) - Hemolysis - Limb ischemia (cannula) - Stroke - Infection - Cost + resource intensive

315.1.0.1.3.6 Supportive Care
  • Adequate sedation: minimize, target light sedation when possible (SBT/SAT trials)
  • DVT prophylaxis
  • PUD prophylaxis
  • Nutrition: enteral preferred; not too early aggressive (EDEN)
  • Glucose control: avoid hypoglycemia
  • Steroids: see below
315.1.0.1.3.7 Steroids in ARDS

Pre-COVID Era: - Meduri (1998, 2007): methylprednisolone in early ARDS — improved outcomes (single-center) - DEXA-ARDS (2020): dexamethasone in non-COVID ARDS — improved outcomes - Practice: methylprednisolone 1 mg/kg/d × 14 days then taper, started within 7 days - Or dexamethasone

COVID-ARDS Era: - RECOVERY (2020): dexamethasone 6 mg × 10 days reduced mortality in COVID-19 requiring oxygen or ventilation (28%) - REMAP-CAP (2021): tocilizumab improved survival in severe COVID - REMAP-CAP + EMPACTA: baricitinib also effective - Foundation of COVID-19 ARDS treatment

315.1.0.1.3.8 Subphenotypes (Calfee, ARDS Network)

Hyperinflammatory: - ↑ IL-6, IL-8, TNF - Shock, lactic acidosis - Worse outcomes - Different treatment response (PEEP, fluids, anti-inflammatory)

Hypoinflammatory: - Less severe physiology - Better outcomes

Personalized medicine emerging in ARDS

315.1.0.1.4 Other ARDS Therapies (Investigational / Adjunctive)
  • Inhaled nitric oxide (iNO): improves oxygenation but not mortality (INSPIRE)
  • Inhaled prostacyclin: similar
  • Inhaled GM-CSF: trial
  • HFOV (high-frequency oscillatory ventilation): harmful in adult ARDS (OSCILLATE)
  • Vitamin C, thiamine, steroids (“HAT”): CITRIS-ALI negative
315.1.0.1.5 COVID-19 ARDS — Lessons (2020-2024)
315.1.0.1.5.1 Unique Features
  • Hypercoagulability + thromboembolism
  • More variable lung phenotypes (L vs H)
  • Steroid + anti-IL-6 effective
  • Awake prone positioning (selected)
315.1.0.1.5.2 Treatment
  • Dexamethasone 6 mg/d × 10 days (RECOVERY)
  • Tocilizumab or baricitinib (REMAP-CAP, EMPACTA, COV-BARRIER)
  • Awake proning (consider)
  • Anticoagulation strategy
  • Standard ARDS care (lung-protective, prone if intubated)
315.1.0.1.6 Type II Respiratory Failure (Hypercapnic)
315.1.0.1.6.1 Common Causes
  • COPD exacerbation (Ch304)
  • OHS (Ch312)
  • Neuromuscular disorders (ALS, GBS, MG, MD)
  • Drug overdose (opioids, sedatives)
  • Severe asthma (late stage)
  • Chest wall disorders
  • Severe obesity
315.1.0.1.6.2 Management

Address Underlying Cause: - Reverse drug overdose (naloxone) - Bronchodilators + steroids for COPD/asthma - Treat NM disease (IVIG, plasmapheresis, etc.) - Drain effusion / pneumothorax

Non-Invasive Ventilation (NIV): - First-line for COPD exacerbation (pH < 7.35) - Effective for OHS, cardiogenic pulmonary edema - Helpful in select neuromuscular disease

Invasive Mechanical Ventilation: - NIV failure - Severe respiratory acidosis - Altered mental status - Hemodynamic instability

315.1.0.2 🩺 床邊速查

  • ARDS Berlin Criteria: within 1 wk + bilateral opacities + not solely cardiac + PaO2/FiO2 < 300 with PEEP ≥ 5
  • Severity: mild 200-300, moderate 100-200, severe ≀ 100
  • Lung-protective ventilation: 6 mL/kg PBW, plateau < 30, driving pressure < 15
  • PROSEVA: prone for severe ARDS (PaO2/FiO2 < 150) ↓ mortality 16%
  • NMB: ACURASYS positive, ROSE neutral; use for refractory dyssynchrony
  • ECMO: refractory (PaO2/FiO2 < 80, pH < 7.20)
  • COVID-19 ARDS: dexamethasone + tocilizumab + awake prone
  • Type II RF: NIV for COPD exacerbation (pH < 7.35) + OHS