2025 PACUPrep BCCCP Preparatory Course COPD Exacerbation Optimizing Respiratory Support and Sedation in AECOPD
Non-Invasive and Invasive Ventilation Strategies with Targeted Sedation in AECOPD

Non-Invasive and Invasive Ventilation Strategies with Targeted Sedation in AECOPD

Learning Objective

Recommend appropriate respiratory support strategies to prevent complications and optimize outcomes in AECOPD-induced acute respiratory failure.

I. Criteria for Initiating Non-Invasive Ventilation (NIV)

Summary: Early NIV in hypercapnic AECOPD reduces intubation rates, complications, and mortality. Candidate selection relies on bedside assessment and arterial blood gases.

Clinical Indicators

  • Tachypnea >25 breaths/min with use of accessory muscles
  • Severe dyspnea signs: paradoxical abdominal movement, intercostal retractions, inability to speak full sentences
  • Agitation or diaphoresis secondary to respiratory distress

Laboratory Indicators

  • Arterial pH <7.35 and PaCO2 >45 mmHg
  • Hypoxemia not corrected by low-flow oxygen (PaO2/FiO2 <200)

Contraindications

  • Respiratory or cardiac arrest, inability to protect airway or clear secretions
  • Copious secretions, severe encephalopathy, facial trauma/deformity
  • High aspiration risk, recent upper gastrointestinal surgery
Key Pearl

Initiate NIV promptly in AECOPD with respiratory acidosis to reduce need for intubation and shorten ICU stay.

II. Non-Invasive Ventilation Strategy

Summary: Select the appropriate mode and titrate settings to alleviate work of breathing while avoiding excessive pressures.

Mode Selection

  • BiPAP in spontaneous/timed (S/T) mode or pressure support ventilation

Initial Settings

  • IPAP 10–12 cmH2O; EPAP 4–6 cmH2O
  • FiO2 titrated to SpO2 88–92%
  • Adjust IPAP to reduce PaCO2 and improve pH; increase EPAP if airway collapse is noted

Monitoring

  • ABG at baseline and 1 hr after initiation; track pH, PaCO2, PaO2
  • Respiratory rate, mask fit and leak, patient comfort, hemodynamics

Troubleshooting

  • Optimize interface fit; switch between nasal, oronasal or helmet mask
  • Add heated humidification to improve tolerance and secretion clearance
Key Pearl

An early rise in pH and decrease in respiratory rate within the first 1–2 hrs predicts NIV success.

III. Recognizing NIV Failure and Escalation

Summary: Reassess clinical and laboratory response within 1–2 hrs and prepare for IMV if criteria for failure are met.

Clinical Triggers

  • Worsening encephalopathy (confusion, somnolence), persistent accessory muscle use
  • Hemodynamic instability: hypotension, new arrhythmias
  • Inability to tolerate NIV interface

Laboratory Triggers

  • Persistent pH <7.30 or rising PaCO2 despite maximal NIV settings
  • Refractory hypoxemia (SpO2 <88% on FiO2 ≥0.6)

Time Frame

  • Reevaluate at 1–2 hrs; avoid prolonged ineffective NIV (>2 hrs without improvement)

Escalation Criteria

  • Indications for intubation: NIV intolerance, worsening acidosis/hypoxemia, cardiac or respiratory arrest, severe encephalopathy, hemodynamic compromise
Key Pearl

Delay in switching to IMV after NIV failure increases morbidity and mortality. Aim for timely escalation.

IV. Invasive Mechanical Ventilation (IMV) to Minimize Dynamic Hyperinflation

Summary: IMV settings should prioritize longer expiratory times to prevent auto-PEEP and reduce barotrauma.

Indications for Intubation

  • NIV failure, PaCO2 >60 mmHg with pH <7.25
  • Altered mental status, respiratory arrest, refractory hypoxemia, hemodynamic instability

Initial Ventilator Settings

  • Tidal volume: 6–8 mL/kg ideal body weight
  • Respiratory rate: ≤12 breaths/min to prolong exhalation
  • I:E ratio: ≥1:3
  • Inspiratory flow: 80–100 L/min
  • External PEEP: 3–5 cmH2O (to offset intrinsic PEEP)
  • FiO2: titrate to SpO2 88–92%

Monitoring Auto-PEEP

  • Inspect flow-time waveform for incomplete exhalation
  • Measure plateau pressure and adjust settings accordingly

Adjustments for Synchrony

  • Optimize trigger sensitivity and flow delivery
  • Ensure adequate sedation/analgesia to prevent dyssynchrony
Key Pearl

Minimal external PEEP helps trigger alveolar inflation without worsening hyperinflation in COPD.

V. Pharmacotherapy: Sedation and Analgesia Strategies

Summary: Light, analgesia-first sedation promotes synchrony, reduces delirium risk, and shortens ventilation duration.

Sedation Goals & Protocols

  • Target RASS –1 to 0; use an analgesia-first approach
  • Daily sedation interruption and early mobilization

Agent Selection & Profiles

Sedation and Analgesia Agents for Mechanically Ventilated AECOPD Patients
Agent Mechanism Dosing Advantages Disadvantages Monitoring
Propofol GABA-A agonist 5–50 mcg/kg/min infusion; avoid >48 hrs high-dose Rapid onset/offset, easy titration Hypotension, hypertriglyceridemia, infusion syndrome BP, triglycerides, acid-base status
Dexmedetomidine α2-adrenergic agonist 0.2–1.5 mcg/kg/hr infusion; avoid bolus Minimal respiratory depression, cooperative sedation Bradycardia, hypotension, cost HR, BP
Benzodiazepines
(Midazolam, Lorazepam)		 GABA-A agonist Midazolam 0.02–0.1 mg/kg/hr; Lorazepam 0.02–0.06 mg/kg/hr Anxiolytic, amnestic Delirium, prolonged sedation, respiratory depression. Reserve for seizures or refractory agitation. Sedation score, respiratory status
Opioids
(Fentanyl, Remifentanil)		 μ-opioid receptor agonist Fentanyl 1–3 mcg/kg/hr; Remifentanil 0.1–0.2 mcg/kg/min Potent analgesia, remifentanil for rapid weaning Tolerance, withdrawal, respiratory depression, constipation Resp rate, sedation scores, pain scores

Weaning & Early Mobilization

  • Conduct daily sedation holidays and extubation readiness trials
  • Balance sedation reduction with comfort and synchrony

Controversies

Current Debates in Sedation
  • Optimal sedative in hypercapnic COPD: propofol vs dexmedetomidine
  • Role of neuromuscular blockade in severe asynchrony
  • Impact of sedation depth on long-term cognitive outcomes
Key Pearl

Dexmedetomidine may facilitate earlier extubation due to its minimal respiratory depression and delirium-sparing profile.

References

  1. Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med. 1995;333(13):817-22.
  2. Wedzicha JA, Miravitlles M, Hurst JR, Calverley PMA, Albert RK, et al. Management of COPD exacerbations: an ERS/ATS guideline. Eur Respir J. 2017;49(1):1600791.
  3. Osadnik CR, Tee VS, Carson-Chahhoud KV, Picot J, Wedzicha JA, Smith BJ. Non-invasive ventilation for acute hypercapnic respiratory failure in AECOPD. Cochrane Database Syst Rev. 2017;7(7):CD004104.
  4. Plant PK, Owen JL, Elliott MW. Early use of non-invasive ventilation for AECOPD on general wards. Lancet. 2000;355(9219):1931-5.
  5. Lindenauer PK, Stefan MS, Shieh MS, Pekow PS, Rothberg MB, Hill NS. Outcomes associated with invasive and noninvasive ventilation in hospitalized AECOPD. JAMA Intern Med. 2014;174(12):1982-93.
  6. Conti G, Antonelli M, Navalesi P, et al. Noninvasive vs conventional mechanical ventilation after medical treatment failure in COPD. Intensive Care Med. 2002;28(12):1701-7.
  7. Siemieniuk RAC, Chu DK, Kim LH-Y, et al. Oxygen therapy for acutely ill medical patients: clinical practice guideline. BMJ. 2018;363:k4169.
  8. Austin MA, Wills KE, Blizzard L, et al. Effect of high-flow oxygen on mortality in COPD patients: randomised controlled trial. BMJ. 2010;341:c5462.
  9. Celli BR, MacNee W; ATS/ERS Task Force. Standards for diagnosis and treatment of COPD: summary. Eur Respir J. 2004;23(6):932-46.
  10. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of COPD. 2025 report. https://goldcopd.org
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