4.1 Respiratory Failure Pathologies (ARDS, Asthma, COPD)

Respiratory Failure Pathologies (ARDS, Asthma, COPD)

Introduction to Acute Respiratory Failure

In the critical care transport environment, acute respiratory failure is classified as either Type I (hypoxemic, PaO2 < 60 mmHg with normal or low PaCO2) or Type II (hypercapnic, PaCO2 > 50 mmHg with pH < 7.35). Managing these patients requires a deep understanding of lung compliance, airway resistance, and the physiological consequences of mechanical ventilation.

Acute Respiratory Distress Syndrome (ARDS)

ARDS is a form of non-cardiogenic pulmonary edema characterized by diffuse alveolar damage, inflammatory cytokine release, and disruption of the alveolar-capillary membrane. This leads to protein-rich fluid accumulation in the alveoli, surfactant inactivation, and severe intrapulmonary shunting.

Diagnostic Criteria

The Berlin Criteria are utilized to diagnose ARDS:

1. Acute Onset: Within one week of a known clinical insult or new/worsening respiratory symptoms.
2. Bilateral Opacities: Present on chest radiograph or CT scan, not fully explained by effusions, lobar/lung collapse, or nodules.
3. Non-Cardiogenic Origin: Respiratory failure not fully explained by cardiac failure or fluid overload. An objective assessment (e.g., echocardiogram) is required if no risk factor is present.
4. Oxygenation Impairment: Categorized by the PaO2/FiO2 (P/F) ratio on a minimum PEEP of 5 cmH2O:
   • Mild ARDS: P/F ratio 200–300 mmHg.
   • Moderate ARDS: P/F ratio 100–200 mmHg.
   • Severe ARDS: P/F ratio <= 100 mmHg.

ARDSnet Lung-Protective Ventilation Strategy

To prevent Ventilator-Induced Lung Injury (VILI), specifically volutrauma, barotrauma, and atelectrauma, the ARDS Clinical Trials Network (ARDSnet) recommends a protocol focused on low tidal volumes and limiting alveolar pressures:

• Tidal Volume (Vt): Target 4–8 mL/kg of Predicted Body Weight (PBW). The initial setting should be 6 mL/kg PBW. PBW must be calculated based on height and biological sex, as actual body weight overestimates lung size due to adipose tissue.
  • Male PBW: 50 + 2.3 * (Height in inches - 60)
  • Female PBW: 45.5 + 2.3 * (Height in inches - 60)
• Plateau Pressure (Pplat): Measured during an expiratory or inspiratory hold. Maintain Pplat < 30 cmH2O. If Pplat exceeds 30 cmH2O, tidal volume should be down-titrated in 0.5–1 mL/kg steps (minimum of 4 mL/kg).
• PEEP and FiO2 Titration: Titrate PEEP and FiO2 concurrently using a high-PEEP or low-PEEP strategy to maintain oxygenation targets while avoiding oxygen toxicity. The target PaO2 is 55–80 mmHg, and SpO2 is 88–95%.
• Driving Pressure (ΔP): Defined as Pplat - PEEP. Maintaining a driving pressure < 15 cmH2O is strongly associated with decreased mortality in ARDS, representing the strain on functional lung tissue.
• Permissive Hypercapnia: Allowing PaCO2 to rise (and pH to drop to 7.25, or even 7.20 in severe cases) is acceptable to maintain low tidal volumes and plateau pressures. This is contraindicated in patients with acute brain injury (due to cerebral vasodilation and increased ICP), severe pulmonary hypertension, or life-threatening cardiac arrhythmias.

Compliance vs. Resistance

• Compliance refers to the change in volume for a given change in pressure (C = ΔV/ΔP). ARDS is characterized by decreased lung compliance ('stiff' lungs), which dramatically elevates plateau pressure.
• Resistance refers to the pressure difference required to drive gas through the airways (R = ΔP/Flow). Asthma and COPD are characterized by elevated airway resistance, which increases peak inspiratory pressure (PIP) but leaves plateau pressure relatively normal unless significant auto-PEEP has developed.
• PIP vs. Pplat: A high PIP with a normal Pplat indicates an airway resistance problem (e.g., bronchospasm, tube kink, secretions), whereas a high PIP with a high Pplat indicates a lung compliance problem (e.g., ARDS, pneumothorax, mainstem intubation, pulmonary edema).

Obstructive Airway Disease: Asthma and COPD

Unlike the restrictive pathology of ARDS, asthma and COPD represent obstructive airway diseases characterized by increased airway resistance and prolonged expiratory times.

Severe Status Asthmaticus

Asthma involves bronchoconstriction, airway inflammation, and thick mucous plugging. In mechanical ventilation, the primary risk is dynamic hyperinflation, which leads to auto-PEEP (air trapping). Auto-PEEP increases intrathoracic pressure, compressing the vena cava, reducing venous return (preload), and potentially causing obstructive shock and cardiovascular collapse.

• Ventilator Strategy: The goal is to maximize expiratory time to allow complete exhalation.
  • Respiratory Rate (RR): Low, typically 6–10 breaths per minute.
  • Tidal Volume: 6–8 mL/kg PBW to minimize peak pressures.
  • Inspiratory Flow Rate: High, 80–100 L/min. A faster inspiratory flow delivers the breath quickly, leaving more time for exhalation and generating an I:E ratio of 1:4 or 1:5.
  • Applied PEEP: Titrated carefully. It should match approximately 80% of the patient’s intrinsic auto-PEEP (typically 5 cmH2O) to splint the airways open and reduce the work of breathing required to trigger a breath, without worsening air trapping.
  • Permissive Hypercapnia: Standard strategy. Keep pH > 7.20.
  • Measuring auto-PEEP: Perform an expiratory hold at the end of exhalation to measure the total PEEP. Subtract set PEEP to determine intrinsic auto-PEEP. If hemodynamics deteriorate due to gas trapping, immediately disconnect the circuit and manually compress the chest.
• Transport Pharmacotherapy:
  • Ketamine: Preferred induction agent for RSI due to catecholamine release causing beta-2 mediated bronchodilation (1–2 mg/kg IV).
  • Magnesium Sulfate: Smooth muscle relaxant. Administer 2 g IV over 15–20 minutes.
  • Epinephrine: 0.3 mg IM (1:1,000) or continuous IV infusion (0.1–0.5 mcg/kg/min) for refractory bronchospasm.

COPD Exacerbation

COPD features alveolar destruction (emphysema) and chronic bronchitis. These patients have chronic CO2 retention, causing their respiratory drive to rely on oxygen levels rather than carbon dioxide (hypoxic drive).

• Target SpO2: 88–92%. Providing excessive oxygen can abolish their hypoxic drive and worsen ventilation/perfusion (V/Q) mismatch via the Haldane effect (unloading CO2 from hemoglobin into the blood).
• Non-Invasive Positive Pressure Ventilation (NIPPV): BiPAP is the first-line therapy during transport to avoid the high risk of intubation.
  • IPAP: Initial 10–12 cmH2O, titrated to assist ventilation and reduce PaCO2.
  • EPAP: Initial 4–5 cmH2O, titrated to recruit alveoli and overcome intrinsic PEEP.
  • Delta P (IPAP - EPAP): Represents the level of pressure support; increase this difference to increase tidal volume and clear CO2.

Ventilator Parameters Comparison Table