Out-of-Hospital Respiratory Assessment
A systematic approach is crucial for identifying the nature and severity of a respiratory complaint.
Systematic Approach (Look, Listen, Feel)
| Component | Key Areas to Assess | Potential Findings & Significance |
|---|---|---|
| Look (Inspection) | Positioning, work of breathing, skin colour, audible sounds, chest shape, symmetry. | Tripod position, accessory muscle use, pursed-lip breathing: Signs of severe respiratory distress. Cyanosis: Indicates significant hypoxemia. Audible wheeze/stridor: Suggests significant airway obstruction. Barrel chest: Associated with chronic air trapping (e.g., COPD). |
| Listen (Auscultation) | Presence and quality of breath sounds, adventitious sounds. | Wheeze: Continuous, high-pitched sound from narrowed lower airways (asthma, COPD). Crackles (Rales): Discontinuous sounds from fluid in the alveoli (pneumonia, pulmonary oedema). Stridor: High-pitched inspiratory sound from upper airway obstruction (croup, foreign body). Absent/Reduced sounds: May indicate pneumothorax, pleural effusion, or severe airway obstruction. |
| Feel (Palpation) | Chest wall tenderness, symmetry of expansion, subcutaneous emphysema. | Asymmetrical expansion: Suggests unilateral pathology (e.g., pneumothorax). Subcutaneous emphysema: Air trapped under the skin, feels like "crackling"; indicates air leak from the thoracic cavity. |
Respiratory Failure
Respiratory failure occurs when the respiratory system cannot maintain adequate gas exchange, leading to hypoxemia and/or hypercapnia.
| Type | Pathophysiology | ABG Findings | Common Causes |
|---|---|---|---|
| Type 1 (Hypoxemic) | Failure of oxygenation. Occurs due to a ventilation/perfusion (V/Q) mismatch or impaired diffusion across the alveolar-capillary membrane. The ability to remove CO₂ is often preserved or even enhanced by compensatory hyperventilation. | Low PaO₂ (<60 mmHg) Normal or Low PaCO₂ |
Pneumonia, Pulmonary Oedema, Pulmonary Embolism, ARDS. |
| Type 2 (Hypercapnic) | Failure of ventilation. Occurs due to alveolar hypoventilation, where the respiratory system cannot adequately remove CO₂. This always leads to a secondary hypoxemia. | Low PaO₂ (<60 mmHg) High PaCO₂ (>45 mmHg) |
COPD exacerbation, severe asthma, drug overdose (opioids), neuromuscular disease. |
Airway Management Techniques
Foreign Body Removal (Laryngoscopy & Forceps)
- Indication: Complete or near-complete upper airway obstruction by a visible foreign body in an unconscious or obtunded patient.
- Technique:
- Perform direct laryngoscopy to visualise the glottic opening and the foreign body.
- Use Magill forceps to grasp the object firmly.
- Remove the object under direct vision, being careful not to push it further down.
- Reassess airway patency and ventilate.
Supraglottic Airway (SGA) Insertion
- Indication: As a primary advanced airway in cardiac arrest or as a rescue airway after failed intubation.
- Technique (e.g., i-gel):
- Select the appropriate size based on patient weight.
- Lubricate the device.
- Position the patient's head and neck appropriately ("sniffing" position).
- Insert the SGA along the hard palate until a definitive "stop" is felt.
- Confirm placement by observing chest rise with ventilation, auscultation, and capnography. Secure the device.
Continuous Positive Airway Pressure (CPAP)
- Indication: Acute cardiogenic pulmonary oedema, some cases of severe respiratory distress in COPD.
- Mechanism: Delivers constant positive pressure to the airways, which stents open collapsed alveoli, reduces the work of breathing, and pushes fluid out of the alveoli back into the interstitium.
- Application:
- Ensure the patient is conscious, cooperative, and can maintain their own airway.
- Select the correct mask size and ensure a good seal.
- Start at a low pressure (e.g., 5 cmH₂O) and titrate upwards based on patient response and vital signs.
- Continuously monitor the patient's respiratory status, vital signs, and level of consciousness.
Adult Respiratory Emergencies
Asthma
Pathophysiology: A chronic inflammatory disorder characterized by bronchial hyper-responsiveness and reversible airflow obstruction. An acute exacerbation involves three key components: 1) Bronchospasm (smooth muscle contraction), 2) Mucosal oedema (airway wall swelling), and 3) Mucus plugging.
Assessment: History of asthma, known triggers, recent medication use. Assess work of breathing, ability to speak in sentences, respiratory rate, and heart rate. Auscultation reveals widespread, polyphonic expiratory wheeze. A silent chest in a distressed asthmatic is an ominous sign of severe obstruction.
Management: Focuses on reversing bronchospasm and reducing inflammation. Administer high-flow oxygen, continuous nebulised salbutamol (β₂-agonist), and ipratropium bromide (anticholinergic). For severe, life-threatening asthma, administer IM adrenaline and IV corticosteroids. Consider CPAP in severe cases.
Chronic Obstructive Pulmonary Disease (COPD)
Pathophysiology: A progressive disease characterized by persistent airflow limitation. An acute exacerbation is often triggered by infection, leading to increased airway inflammation, mucus production, and bronchospasm, worsening the baseline obstruction.
Assessment: History of smoking, chronic cough, and dyspnoea. Presentation includes increased work of breathing, wheeze, and often a productive cough. Be alert for signs of Type 2 respiratory failure (drowsiness, confusion).
Management: Titrate oxygen to a target SpO₂ of 88-92% to avoid worsening hypercapnia. Administer nebulised salbutamol and ipratropium bromide. Corticosteroids are also indicated. CPAP can be highly effective in reducing work of breathing and preventing the need for intubation.
Pneumonia
Pathophysiology: An infection of the lung parenchyma (alveoli). The inflammatory response causes the alveoli to fill with fluid, pus, and cellular debris (consolidation), impairing gas exchange and leading to a V/Q mismatch and hypoxemia.
Assessment: History of fever, productive cough (often purulent sputum), and pleuritic chest pain. On examination, the patient may be febrile and tachycardic. Auscultation often reveals focal crackles over the affected area and bronchial breath sounds.
Management: Primarily supportive. Administer oxygen to correct hypoxemia. Provide IV fluids for dehydration or signs of sepsis. Consider CPAP for severe respiratory distress or hypoxemia. Transport for antibiotic therapy.
Pulmonary Embolism (PE)
Pathophysiology: Obstruction of a pulmonary artery by an embolus (usually a thrombus from a DVT). This blocks blood flow to a section of the lung, creating a large area of alveolar dead space (ventilation without perfusion). This leads to a significant V/Q mismatch and hypoxemia. A massive PE can cause acute right ventricular failure and obstructive shock.
Assessment: High index of suspicion is key. Look for risk factors for DVT (immobility, surgery, cancer). Classic presentation is sudden onset of pleuritic chest pain and dyspnoea. Patient may be tachycardic, tachypnoeic, and hypoxic. Unilateral leg swelling may be present.
Management: High-flow oxygen is critical. For haemodynamically unstable patients (obstructive shock), provide supportive care with fluids and prepare for potential cardiac arrest. Rapid transport to a hospital with thrombolysis/embolectomy capabilities is essential.
COVID-19
Pathophysiology: A viral respiratory illness caused by SARS-CoV-2. In severe cases, it can cause widespread lung inflammation and damage to the alveolar-capillary membrane, leading to Acute Respiratory Distress Syndrome (ARDS), profound hypoxemia, and multi-organ failure.
Assessment: Symptoms include fever, cough, fatigue, and dyspnoea. A key feature can be "silent hypoxia," where patients have very low SpO₂ levels without proportional signs of respiratory distress.
Management: Follow appropriate PPE protocols. Administer oxygen to maintain target saturation. Consider CPAP for severe hypoxemic respiratory failure. Manage any associated complications like sepsis or PE.
Paediatric Respiratory Emergencies
Croup (Laryngotracheobronchitis)
Pathophysiology: A viral infection (commonly Parainfluenza virus) causing inflammation and swelling of the subglottic region (larynx, trachea, bronchi). This narrowing of the upper airway leads to the characteristic signs.
Assessment: Typically affects children aged 6 months to 6 years. Presents with a gradual onset of a distinctive "barking" cough, hoarse voice, and inspiratory stridor, often worse at night.
Management: Mild cases can be managed with reassurance and cool air. For moderate to severe croup (stridor at rest, significant work of breathing), the primary treatment is nebulised adrenaline to cause vasoconstriction and reduce subglottic swelling. Corticosteroids are also a mainstay of treatment.
Bronchiolitis
Pathophysiology: A viral infection (most commonly RSV) of the lower respiratory tract in infants and young children (<2 years). It causes inflammation, oedema, and necrosis of the epithelial cells lining the small airways (bronchioles), leading to mucus plugging and obstruction.
Assessment: Presents with initial cold-like symptoms followed by increasing respiratory distress, tachypnoea, and widespread expiratory wheeze and fine inspiratory crackles. Feeding difficulties and apnoea (in young infants) are common.
Management: Purely supportive. The mainstay of treatment is gentle nasal suctioning to clear secretions and maintain airway patency. Provide oxygen if hypoxic. Bronchodilators are generally not effective. Transport is required for infants with significant respiratory distress, hypoxia, or apnoea.