Airway and Ventilation

Comprehensive Assessment, Pathophysiology, and Intervention

1. Comprehensive Respiratory Assessment

IPPA Framework & Physical Examination

A systematic respiratory assessment utilizes the IPPA framework: Inspection, Palpation, Percussion, and Auscultation.

  • Inspection: Observe for cyanosis, diaphoresis, accessory muscle use (tripoding, tracheal tug), chest wall symmetry, and frothy sputum (e.g., in drowning/APO).
  • Palpation: Feel for tracheal deviation (late sign of tension pneumothorax), subcutaneous emphysema, and tactile fremitus.
  • Percussion: Dullness suggests fluid (haemothorax, pneumonia consolidation), while hyper-resonance suggests trapped air (asthma, pneumothorax).
  • Auscultation: Listen methodically to anterior and posterior lung fields. Note the presence of wheeze (bronchospasm), crackles (fluid/oedema), stridor (upper airway obstruction), or a 'silent chest' (life-threatening lack of air movement).

QAS Respiratory Status Matrix

Utilise this matrix to rapidly differentiate normal physiology from respiratory distress or failure.

Component Normal Respiratory Distress / Altered
Conscious State Alert, calm, and quiet. Altered, anxious, struggling to breathe, exhausted.
Speech Clear, fluent, and steady. Difficult, short sentences or phrases, unable to verbalise.
Ventilatory Rate 12-18 breaths/min (Adult). Greater than 18 (Tachypnoea) or abnormally slow (Bradypnoea).
Ventilatory Rhythm Regular, even cycles. No respiratory pause, prolonged expiratory phase (Asthma/COPD).
Ventilatory Effort Minimal chest/abdominal movement. Marked chest movement, intense accessory muscle use.
Skin Pink and warm. Pale and sweaty; cyanosis is a late and serious sign.

2. Differentiating Respiratory Compromise

Integrating clinical presentations with real-world simulation cases.

Asthma Exacerbation (Special Context: Pregnancy)

  • Pathophysiology: Reversible airway obstruction due to bronchospasm, mucosal oedema, and mucus plugging. Results in prolonged expiratory phase and polyphonic wheezing.
  • Pregnancy Physiology (Sim Case): Normal PCO2 in pregnancy is 32 mmHg (due to progesterone-driven baseline hyperventilation). A PCO2 of 40 mmHg in a pregnant asthmatic is a sign of impending respiratory failure and exhaustion. Decreased diaphragmatic excursion due to the gravid uterus limits reserve.
  • Management: Stepwise approach: 1. Salbutamol (Bronchodilator), 2. Ipratropium, 3. Systemic Corticosteroids (Methylprednisolone), 4. Adjuncts (IV Magnesium Sulfate). Note: Avoid Epinephrine if possible due to concerns for uterine vasoconstriction and fetal hypoxia.

Acute Pulmonary Oedema (APO)

  • Pathophysiology: Left ventricular failure leads to increased pulmonary capillary hydrostatic pressure, forcing fluid into the alveoli. This creates a severe V/Q mismatch and hypoxemia.
  • Clinical Presentation (Sim Case): A 68yo male with a fractured hip, kept NPO with withheld cardiac meds (Furosemide), given IV fluids overnight. Presents with severe dyspnoea, diffuse bilateral crackles, hypertension (180/100), and peripheral oedema.
  • Differentiation: Differentiated from COPD by the presence of crackles, elevated JVP, orthopnoea, and history of heart failure (e.g., low Ejection Fraction).
  • Management: Reduce preload and afterload aggressively. Nitroglycerin (SL spray/IV), BiPAP/CPAP, and eventual diuresis (Furosemide).

Submersion Injury (Drowning) & ARDS

  • Pathophysiology (Sim Case): When water enters the airway, it causes surfactant washout (even with just 3-4 cc/kg of water), leading to profound atelectasis, intrapulmonary shunting, and direct cellular injury causing pulmonary oedema.
  • Clinical Presentation: Frothy foam in the airway, unconsciousness, bilateral crackles/wheeze, severe hypoxemia. May lead to hypoxia-induced bradycardia (a terminal rhythm in pediatrics).
  • Management: Prioritize ventilation. Do NOT persistently suction the "surfactant foam" (it is not physically obstructing); instead, ventilate with Positive Pressure Ventilation (PPV) directly through it.

COPD, Pneumonia, and Pulmonary Embolism (PE)

  • COPD: Chronic hypercapnia, pursed-lip breathing, barrel chest. Wheeze or diminished breath sounds. Hypoxic drive relies on carefully titrated O2 (target 88-92%).
  • Pneumonia: Febrile, productive cough, unilateral focal crackles or bronchial breath sounds, pleuritic chest pain.
  • Pulmonary Embolism (PE): Sudden onset dyspnoea, clear lung sounds, pleuritic chest pain, tachycardia. High suspicion in immobilized patients (e.g., orthopedic injuries), deep vein thrombosis, or hypercoagulable states (like pregnancy).

3. Relevant Investigations & Interpretations

Pulse Oximetry (SpO2) & Capnography (EtCO2)

Essential continuous monitoring tools:

  • SpO2: Measures oxygen saturation of haemoglobin. Can be falsely elevated in carbon monoxide poisoning or falsely low in poor peripheral perfusion.
  • EtCO2: Measures the partial pressure of carbon dioxide at the end of an exhaled breath. Normal is 35-45 mmHg.
    Waveform Interpretation: A "shark fin" waveform indicates bronchospasm (Asthma/COPD) due to uneven alveolar emptying. A sudden drop to zero indicates cardiac arrest, tube dislodgement, or massive PE.

Blood Gases (ABG / VBG)

Used to assess acid-base balance and adequacy of ventilation.

Parameter Normal Range Interpretation Example (Asthma Sim Case)
pH 7.35 - 7.45 pH 7.32 (Acidaemia)
PCO2 35 - 45 mmHg PCO2 40 mmHg (Normally this is fine, but in a pregnant patient whose baseline is 32 mmHg, 40 mmHg indicates respiratory fatigue and impending failure).
HCO3 22 - 26 mEq/L HCO3 19 (Metabolic compensation attempt or concurrent lactic acidosis).

Radiography (CXR) & Peak Flows

  • CXR: Differentiates APO (bilateral fluffy infiltrates, cardiomegaly, Kerley B lines) from Asthma (hyperinflation, clear fields). Note: Prominent vascular markings are normal in pregnancy.
  • Peak Expiratory Flow (PEF) / FEV1: Measures the maximum speed of expiration. Useful for grading asthma severity (e.g., PEF < 50% predicted indicates a severe exacerbation).

4. Optimising Gas Exchange: Ventilation Strategies

Non-Invasive Ventilation (NIV): CPAP & BiPAP

Used to prevent the need for intubation in conscious, cooperative patients failing standard oxygen therapy.

  • CPAP (Continuous Positive Airway Pressure): Provides a constant pressure throughout the respiratory cycle. Splints alveoli open (increasing functional residual capacity), pushes fluid out of the alveoli in APO, and reduces the work of breathing.
  • BiPAP (Bilevel Positive Airway Pressure): Provides a higher Inspiratory Positive Airway Pressure (IPAP) to assist ventilation/clear CO2, and a lower Expiratory Positive Airway Pressure (EPAP/PEEP) to maintain oxygenation. Indicated in severe Asthma/COPD exacerbations where ventilatory failure (hypercapnia) is occurring.

Invasive Ventilation & Post-Intubation Hypoxemia (DOPES)

When a patient is intubated (e.g., the 3yo Submersion case), sudden hypoxemia is a life-threatening crisis. Use the DOPES mnemonic to systematically troubleshoot:

  • D - Displacement: The endotracheal tube (ETT) has slipped into the right main bronchus or out into the esophagus. Check depth and confirm with EtCO2 / Direct laryngoscopy.
  • O - Obstruction: The tube is blocked by secretions, blood, or kinking. Pass a suction catheter to clear.
  • P - Pneumothorax: Positive pressure ventilation can pop a bleb, causing a tension pneumothorax. Assess for absent lung sounds and hyper-resonance.
  • E - Equipment Failure: Ventilator malfunction, empty oxygen tank, or circuit disconnect. Immediately disconnect the vent and manually bag the patient with 100% O2.
  • S - Stacking (Breath Stacking/Auto-PEEP): In asthma/bronchospasm, incomplete exhalation leads to trapped air, increasing intrathoracic pressure and crushing venous return (hypotension). Action: Disconnect the circuit and push firmly on the chest to expel trapped air.

Lung-Protective Ventilation Strategy

For patients with ARDS/Submersion injuries where lungs are non-compliant and vulnerable to barotrauma (volutrauma):

  • Use low tidal volumes: 6 - 8 cc/kg of ideal body weight.
  • Apply adequate PEEP (Positive End-Expiratory Pressure) to overcome surfactant loss and recruit collapsed alveoli.
  • Titrate FiO2 to maintain a PaO2 of 55-80 mmHg or SpO2 88-95%, avoiding oxygen toxicity.