Respiratory System
Educational use only. This content is intended for paramedic students and practitioners as a study aid. Always follow your service's clinical practice guidelines and protocols.
Respiratory Control
Breathing is primarily controlled by the medulla oblongata and pons. The medullary respiratory centre contains a dorsal group driving inhalation and a ventral group driving exhalation. CO₂ is the dominant driver of ventilation — central chemoreceptors in the cerebrospinal fluid detect pH changes caused by dissolved CO₂. Peripheral chemoreceptors in the carotid and aortic bodies respond primarily to falling PaO₂.
Normal Adult RR
12–20
breaths per minute
Normal Tidal Volume
500 mL
approximately 7 mL/kg
Primary Drive
CO₂
via pH / PaCO₂ at central receptors
Hypoxic Drive — COPD
In chronic hypercapnia (severe COPD), central chemoreceptors become desensitised to CO₂. Some patients rely on hypoxaemia as their primary respiratory drive. Uncontrolled high-flow oxygen can suppress this drive and cause hypercapnic respiratory failure. Target SpO₂ 88–92% in known chronic CO₂ retainers.
Alveolar Ventilation and Dead Space
Formula
V̇A = (VT − VD) × RR
- →Anatomical dead space ~150 mL — conducting airways; no gas exchange occurs here
- →Physiological dead space — includes alveoli that are ventilated but not perfused
Clinical Implications
- !Rapid, shallow breathing reduces V̇A disproportionately — dead space ventilation is fixed
- !Increased dead space (PE, emphysema) reduces effective alveolar ventilation
- ✓Hypercapnia = inadequate alveolar ventilation relative to CO₂ production
V/Q Mismatch
High V/Q — Dead Space
- →Ventilated but not perfused
- →Wasted ventilation — gas exchange cannot occur
- →Causes: pulmonary embolism, emphysema
Low V/Q — Shunt
- !Perfused but not ventilated
- !Blood bypasses gas exchange — returns deoxygenated to systemic circulation
- !Causes: pneumonia, atelectasis, pulmonary oedema
Clinical Rule
Hypoxaemia from V/Q mismatch generally responds to supplemental oxygen. True shunt (severe pneumonia, ARDS) does not correct well with O₂ alone — perfused but non-ventilated alveoli cannot be oxygenated regardless of inspired FiO₂.
Hypoxia — Four Types
| Type | Mechanism | Common Causes | SpO₂ |
|---|---|---|---|
| Hypoxic | Low PaO₂ — inadequate oxygenation of blood | Hypoventilation, V/Q mismatch, shunt, altitude | Low |
| Anaemic | Reduced O₂-carrying capacity of blood | Haemorrhage, anaemia, carbon monoxide poisoning | Normal* |
| Ischaemic | Inadequate cardiac output — impaired O₂ delivery | Cardiogenic shock, cardiac arrest | Normal* |
| Histotoxic | Cells unable to utilise delivered O₂ | Cyanide poisoning, severe sepsis | Normal* |
Carbon Monoxide — SpO₂ Pitfall
CO binds haemoglobin with 250× the affinity of O₂. Pulse oximetry cannot differentiate oxyhaemoglobin from carboxyhaemoglobin — SpO₂ reads falsely normal. Always suspect CO poisoning in enclosed-space exposures regardless of SpO₂ reading.
Abnormal Breathing Patterns
| Pattern | Description | Clinical Associations |
|---|---|---|
| Tachypnoea | RR > 20 bpm | Hypoxia, fever, anxiety, metabolic acidosis, pain |
| Bradypnoea | RR < 12 bpm | Opioid toxicity, raised ICP, CNS depression |
| Hyperventilation | Increased rate and depth → excess CO₂ removal → respiratory alkalosis | Anxiety/panic, pain, metabolic acidosis (compensatory) |
| Kussmaul | Deep, laboured breathing — compensatory CO₂ expulsion | Diabetic ketoacidosis, severe metabolic acidosis |
| Cheyne-Stokes | Cyclic crescendo–decrescendo breathing with apnoeic episodes | Left heart failure, stroke, brainstem injury |
| Agonal | Slow, gasping, irregular — no effective ventilation | Cardiac arrest — do not confuse with normal breathing. Begin CPR |
Overview
Dyspnoea is the subjective awareness that an abnormal amount of effort is required for breathing. It is not synonymous with hypoxia — a patient may be severely hypoxic without reporting breathlessness (e.g. altered consciousness), and vice versa. It is a common reason for hospital presentation. Most common causes presenting to emergency: decompensated heart failure, pneumonia, COPD exacerbation, PE, and asthma.
Severity Recognition — Red Flags
Imminent Respiratory Arrest
- !Depressed or rapidly deteriorating mental status
- !Inability to maintain respiratory effort
- !Central cyanosis
- !Agonal or absent breathing
Severe Respiratory Distress
- !Significant accessory muscle use
- !Speaking in words only — word dyspnoea
- !Tachypnoea > 30 bpm
- !Agitation, marked distress, unable to lie supine
- !Audible stridor or wheeze
Differential Diagnosis by Onset
| Onset | Likely Causes |
|---|---|
| Seconds–minutes | Tension pneumothorax, anaphylaxis, upper airway obstruction (foreign body, angioedema), acute arrhythmia |
| Hours | Acute asthma, pulmonary oedema, pulmonary embolism, COPD exacerbation, pneumothorax |
| Days | Pneumonia, pleural effusion, decompensated cardiac failure |
| Weeks–months | Interstitial lung disease, lung carcinoma, progressive COPD, chronic pleural effusion |
Emergency Stabilisation
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1Primary survey — identify red flags. Assess mental status, work of breathing, cyanosis. Determine need for immediate airway intervention.
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2Optimise oxygenation. Supplemental oxygen titrated to SpO₂ 94–98% (88–92% in known COPD). Position of comfort — upright or tripod.
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3Monitoring and access. Continuous SpO₂, cardiac monitoring, 12-lead ECG, IV access.
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4Identify cause and treat. Targeted history and examination. Initiate condition-specific management — bronchodilators, decompression, fluid, etc.
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5Transport decision. Determine appropriate destination and priority. Consider escalating to advanced care support or early notification for deteriorating patients.
Pathophysiology
Asthma is a chronic inflammatory disorder of the airways characterised by bronchial hyper-responsiveness to triggers. On allergen exposure, IgE-sensitised mast cells degranulate, releasing histamine, leukotrienes and cytokines. The primary inflammatory cell is the eosinophil.
Pathological Changes
- →Bronchospasm — smooth muscle contraction
- →Mucosal oedema — increased capillary permeability
- →Mucus plugging — thick secretion production
- →Airway remodelling — chronic wall thickening
Net Effect
- !Obstruction primarily affects expiration — air trapping, dynamic hyperinflation
- !Increased work of breathing, elevated intrinsic PEEP
- ✓Obstruction is largely reversible — distinguishes asthma from COPD
Risk Factors and Triggers
Risk Factors
- →Atopy — strongest risk factor; genetic tendency to IgE sensitisation
- →Family history of asthma or atopy
- →Premature birth, childhood viral respiratory infections
- →Urban living, air pollution, cigarette smoking
- →Occupational exposures (bakers, painters, healthcare workers)
Common Triggers
- !Allergens: dust mites, pollen, pet dander, mould
- !Irritants: cold air, smoke, exercise, chemical fumes
- !Viral upper respiratory infections
- !NSAIDs and aspirin in sensitive patients
- !Emotional stress and anxiety
Severity Classification
| Severity | SpO₂ | Speech | Clinical Features |
|---|---|---|---|
| Mild | ≥ 95% | Full sentences | Mild wheeze, RR normal or slightly raised, no accessory muscle use |
| Moderate | 92–95% | Phrases | Moderate wheeze, RR 20–30, accessory muscle use, elevated HR |
| Severe | < 92% | Words only | Loud wheeze, RR > 30, marked accessory muscle use, tachycardia, agitation, pulsus paradoxus |
| Life-Threatening | < 92% | Unable to speak | Silent chest (absent wheeze), cyanosis, bradycardia, exhaustion, altered consciousness — impending arrest |
Silent Chest = Impending Arrest
Absence of wheeze in a known asthmatic with significant distress is a critical finding. Airflow is too low to generate audible wheeze. This indicates near-complete obstruction — do not be falsely reassured.
Prehospital Management
| Intervention | Detail |
|---|---|
| Position | Upright or tripod — never force the patient supine |
| Oxygen | Titrate to SpO₂ 94–98% via appropriate delivery device |
| Salbutamol | Nebulised, often first-line bronchodilator; commonly repeated as required |
| Ipratropium bromide | Nebulised — commonly combined with salbutamol for moderate–severe exacerbations |
| Hydrocortisone | Given IV — reduces airway inflammation. Effect delayed; not a rescue drug |
| Magnesium sulphate | Given IV — commonly used for life-threatening or refractory exacerbation |
| Adrenaline | IM adrenaline is commonly used when bronchospasm is a component of anaphylaxis, and may be considered in severe refractory attacks |
| IPPV / BVM | Reserve for respiratory arrest. Use a slow rate with prolonged expiratory phase to prevent dynamic hyperinflation |
Asthma in Cardiac Arrest
Modified Approach Required
Ventilate with prolonged expiratory phase to prevent auto-PEEP and dynamic hyperinflation. Tension pneumothorax is a reversible cause — consider bilateral needle decompression.
- →High-dose salbutamol via ETT or nebuliser during CPR
- !Consider bilateral needle decompression — tension pneumothorax is a reversible cause in asthma arrest
- →Magnesium sulphate 2 g IV during resuscitation
- !If no-flow suspected from air trapping — briefly disconnect circuit to allow trapped gas to escape
Asthma vs. COPD
Asthma
- ✓Largely reversible obstruction
- →Eosinophil — primary inflammatory cell
- →Allergen and irritant-driven
- →Any age; atopic predisposition
- →Clubbing not associated
COPD
- !Obstruction not fully reversible
- !Neutrophil — primary inflammatory cell
- !Noxious gas — smoking primary cause
- !Typically > 40 years; significant smoking history
- !Clubbing not typical — if present, suspect malignancy
Pathophysiology — Two Syndromes
Emphysema
- →Permanent destruction of alveolar walls and capillary beds
- →Loss of elastic recoil → air trapping → barrel chest
- →Reduced surface area for gas exchange — V/Q inequality
- →Pursed-lip breathing to maintain intrinsic PEEP
Chronic Bronchitis
- →Productive cough ≥ 3 months/year for ≥ 2 consecutive years
- →Goblet cell hypertrophy → excess thick mucus production
- →Airway inflammation with neutrophil infiltration
- →Progressive narrowing — expiratory obstruction
Clinical Features
Inspection Findings
- →Barrel chest (increased AP diameter)
- →Pursed-lip breathing
- →Tripod positioning, accessory muscle use
- →Intercostal recession, tracheal tug
- →Central cyanosis in advanced disease
Other Signs
- !Flapping tremor (asterixis) — severe CO₂ retention
- !P pulmonale on ECG — tall peaked P waves from RV strain
- →Chronic productive cough — worse in mornings
- →Wheeze and prolonged expiration on auscultation
ECG — P Pulmonale
Lead II — tall, peaked P waves (> 2.5 mm)
Right atrial enlargement (cor pulmonale). The P wave becomes tall and peaked (> 2.5 mm in the inferior leads) while its width stays normal (< 120 ms) — it is the height, not the width, that changes, distinguishing it from the broad, bifid P of left atrial enlargement (P mitrale). A rightward P axis also flattens or inverts the P in leads I and aVL. Model-generated at 25 mm/s, 10 mm/mV.
Acute Exacerbation of COPD (AECOPD)
Defined as acute worsening beyond normal day-to-day variation in one or more of: dyspnoea, cough severity/frequency, or sputum volume/character. Most commonly triggered by respiratory infections. Frequency of exacerbations increases with disease severity.
| Intervention | Detail |
|---|---|
| Controlled O₂ | Target SpO₂ 88–92%. Avoid uncontrolled high-flow — risk of hypercapnic respiratory failure |
| Salbutamol | Nebulised, often first-line bronchodilator |
| Ipratropium bromide | Nebulised — commonly combined with salbutamol; not used as monotherapy |
| Hydrocortisone | Given IV — reduces severity and shortens recovery |
| CPAP / NIV | Consider for hypercapnic respiratory failure or severe exacerbation unresponsive to pharmacotherapy |
COPDX Management Framework
A Structured Approach to Ongoing COPD Care
- CCase finding and confirm diagnosis — spirometry, thorough history; smoking is the primary risk factor
- OOptimise function — pharmacotherapy, pulmonary rehabilitation, inhaler technique
- PPrevent deterioration — smoking cessation, vaccinations, long-term O₂ therapy
- DDevelop a care plan — self-management, COPD action plan, community support
- XManage eXacerbations — early recognition, bronchodilators, corticosteroids, antibiotics if infective
Classification
Spontaneous
- →Primary: No underlying lung disease. Typically tall, thin young males. Ruptured subpleural blebs
- !Secondary: Underlying lung disease (COPD, asthma, CF, TB). Higher risk of tension due to reduced lung reserve
Traumatic
- →Non-iatrogenic: Blunt or penetrating chest trauma
- →Iatrogenic: Central line insertion, pleural tap, positive pressure ventilation
Clinical Features
Simple Pneumothorax
- →Sudden-onset pleuritic chest pain — ipsilateral
- →Dyspnoea — often out of proportion to size
- →Reduced or absent breath sounds ipsilaterally
- →Hyperresonant percussion on affected side
- →Reduced chest expansion on affected side
Tension — Additional Signs
- !Haemodynamic compromise — hypotension, tachycardia
- !Tracheal deviation away from affected side (late sign)
- !Jugular venous distension
- !Progressive hypoxia despite oxygen
- !Cardiovascular collapse — pulseless arrest
Tension Pneumothorax — Management
Clinical Diagnosis — Do Not Wait for Imaging
Tension pneumothorax is a clinical diagnosis. Haemodynamic compromise + absent ipsilateral breath sounds + suspected mechanism = immediate needle decompression. Delay is fatal.
| Step | Detail |
|---|---|
| Needle decompression | 2nd ICS, mid-clavicular line — or 4th–5th ICS, anterior axillary line. 14 G cannula. Positive result = rush of air |
| Finger thoracostomy | 4th–5th ICS, anterior axillary line. Preferred in intubated patients or when needle decompression fails |
| Definitive treatment | Chest tube in hospital. Needle decompression is temporary — tension can re-accumulate |
Virchow's Triad — Pathophysiology
VTE arises from one or more components of Virchow's Triad. A thrombus — most commonly from deep veins of the legs or pelvis — embolises to the pulmonary circulation, obstructing arterial flow and increasing dead space ventilation. Massive PE causes acute right heart failure.
Stasis
Altered flow
Immobility, long travel, bed rest, cardiac failure
Endothelial Injury
Vessel damage
Surgery, trauma, indwelling catheters
Hypercoagulability
Altered blood
Malignancy, pregnancy, OCP, thrombophilia
Clinical Features
Symptoms
- →Sudden-onset dyspnoea — most common
- →Pleuritic chest pain
- →Cough — may be blood-stained (haemoptysis)
- →Calf or thigh pain and swelling (DVT source)
- !Syncope or pre-syncope in massive PE
Signs
- →Tachycardia — most common sign
- →Tachypnoea
- !Hypoxaemia with clear lung fields — key clinical clue
- !Hypotension and shock in massive PE
- →ECG: right heart strain — S1Q3T3, sinus tachycardia, RBBB
Wells Criteria
Wells criteria stratifies pre-test probability of PE. Hypoxaemia with clear lung fields in a tachycardic patient should always raise PE as a differential, particularly with relevant risk factors from Virchow's Triad.
Prehospital Management
- →Supplemental oxygen titrated to SpO₂ ≥ 94%
- →IV access, cardiac monitoring, 12-lead ECG
- !Fluid resuscitation cautiously — avoid excessive preload in right ventricular failure
- →Adrenaline if haemodynamic collapse
- !Rapid transport — massive PE may require thrombolysis or surgical embolectomy
ECG — S1Q3T3 & Right Heart Strain
Model-generated 12-lead (25 mm/s, 10 mm/mV). Sinus tachycardia — the most common finding — with the classic S1Q3T3 pattern — a deep S wave in lead I, a Q wave and inverted T wave in lead III — plus right ventricular strain: T-wave inversions across V1–V4 and the inferior leads (their simultaneous appearance is the most specific ECG sign of PE), an incomplete RBBB with a dominant R′ in V1, and right axis deviation. S1Q3T3 appears in only ~20% of PE and is neither sensitive nor specific alone. Scroll horizontally on narrow screens.
Pathophysiology and Risk Factors
Pneumonia results from bacterial, viral, fungal or protozoal infection of the alveoli and terminal airways. Infectious debris and exudate fill bronchioles, causing V/Q inequality and hypoxaemia. Immune mediator release produces systemic inflammatory features.
Risk Factors
- →Extremes of age (< 2 and > 65 years)
- →Immunosuppression — HIV, steroids, chemotherapy
- →Smoking and excess alcohol use
- →Recent viral upper respiratory infection
- →Aspiration risk — reduced GCS, dysphagia
- →Malnutrition and chronic illness
Clinical Features
- !Fever, rigors, malaise
- →Productive cough — purulent (yellow/green) sputum
- →Pleuritic chest pain
- →Dyspnoea and tachypnoea
- →Inspiratory crackles, dullness to percussion over consolidation
- !Hypoxaemia — may be disproportionate to apparent severity
Prehospital Management
- →Supplemental oxygen titrated to SpO₂ ≥ 94%
- →IV access, fluid resuscitation if septic (MAP < 65 mmHg)
- !Consider sepsis protocol — pneumonia is a leading cause of sepsis. Early hospital notification
- →Appropriate infection control precautions — PPE, masking
- !Notify hospital of suspected TB — isolation precautions required
Pleural Effusion
Classification
- →Transudative — low protein. Raised hydrostatic pressure or reduced oncotic pressure. Causes: cardiac failure, hypoalbuminaemia, renal failure
- !Exudative — high protein. Pleural inflammation or impaired lymphatics. Causes: infection, malignancy, PE, pancreatitis
Clinical Features
- →Stony dull to percussion at the base
- →Reduced or absent breath sounds over effusion
- →Tracheal deviation away if large
- →Dyspnoea proportional to size and lung reserve
Anaphylaxis — Respiratory Component
IM Adrenaline Immediately
Anaphylaxis causes airway compromise via upper airway oedema (stridor) and bronchospasm (wheeze). Both typically require IM adrenaline as first-line. In severe upper airway oedema — prepare for surgical airway; intubation may be impossible.
Upper Airway — Stridor
- !Laryngeal and tongue oedema — rapidly progressive
- →IM adrenaline — α₁ effect reduces mucosal oedema
- !Prepare for surgical airway — early
Lower Airway — Wheeze
- !Bronchospasm — diffuse wheeze
- →IM adrenaline — β₂ effect causes bronchodilation
- →Nebulised salbutamol as adjunct if bronchospasm persists
Smoke Inhalation and Carbon Monoxide
Airway Signs
- !Singed nasal or facial hair
- !Carbonaceous (sooty) sputum
- !Stridor, hoarseness, oropharyngeal oedema
- !Burns swell progressively — consider early intubation before airway closes
Carbon Monoxide
- !SpO₂ falsely normal — pulse oximetry cannot detect COHb
- →Headache, dizziness, nausea, confusion
- →Reduced GCS, ataxia in severe poisoning
- ✓High-flow O₂ via NRB — reduces CO half-life from ~5 hrs to ~1 hr
Awareness Conditions
| Condition | Key Features | Prehospital Priorities |
|---|---|---|
| Tuberculosis | Chronic productive cough (weeks–months), haemoptysis, night sweats, weight loss, fever. Risk groups: immigrants, immunosuppressed, homeless | N95, full PPE, hospital notification, isolation. Do not delay transport |
| Lung Carcinoma | Chronic cough, haemoptysis, weight loss, hoarseness, clubbing, recurrent infections | Manage acute complications (PE, effusion, haemoptysis). Urgent referral |
| Croup | Paediatric — viral subglottic inflammation. Seal-bark cough, inspiratory stridor, low-grade fever, worse at night | Nebulised adrenaline and dexamethasone are commonly used, with cool air. Position of comfort — do not agitate |
| Epiglottitis | Rapidly progressive upper airway obstruction. High fever, muffled voice, drooling, tripod, stridor. Historically H. influenzae (rare post-vaccination) | Do not examine throat. Immediate ALS and anaesthetics — surgical airway standby. Minimise distress |
Cough Duration Classification
Acute
< 3 weeks
Viral URTI, acute bronchitis, pneumonia, asthma exacerbation
Subacute
3–8 weeks
Post-infectious cough, pertussis (whooping cough), resolving pneumonia
Chronic
> 8 weeks
Asthma, COPD, GORD, upper airway syndrome, ACE inhibitor use, lung carcinoma
Cough Character — Differential Diagnosis
| Character | Consider |
|---|---|
| Dry, irritating | Viral URTI, early ILD, ACE inhibitor-induced, asthma, lung carcinoma |
| Productive — clear | Asthma, viral bronchitis |
| Productive — purulent (yellow/green) | Bacterial pneumonia, COPD exacerbation, bronchiectasis |
| Large volume purulent | Bronchiectasis, lung abscess |
| Pink, frothy | Pulmonary oedema — not true sputum, emanates from trachea |
| Barking / seal-bark | Croup — subglottic inflammation |
| Bovine (muffled, no explosive onset) | Vocal cord paralysis — recurrent laryngeal nerve compression; suspect lung carcinoma |
| Paroxysmal, inspiratory whoop | Pertussis (whooping cough) |
Haemoptysis
Always Investigate — Sinister Sign
Haemoptysis must be distinguished from haematemesis (vomiting blood — darker, may contain food debris) and nasopharyngeal bleeding. True haemoptysis is bright red and frothy, coughed not vomited.
Common Causes
- →Bronchitis and URTI — most common, minor
- →Pneumonia
- →Pulmonary embolism (infarction)
- →Lung carcinoma
Severe / Massive Haemoptysis
- !Lung carcinoma
- !Tuberculosis
- !Bronchiectasis
- !Cystic fibrosis
Scope & Guidelines
This pharmacology is general educational information. Indications, dosing and routes vary between services — always follow your own scope of practice and current clinical guidelines.
Salbutamol
Short-Acting Beta-2 Adrenergic Agonist (SABA)
Often First-Line
Mechanism of Action
Selective β₂ agonist → stimulates adenylyl cyclase → ↑ cAMP → bronchial smooth muscle relaxation and bronchodilation. Also inhibits mast cell mediator release at therapeutic doses.
Caution
Tachycardia is a class effect — assess HR before and after each dose. Use with caution in known cardiac disease and elderly patients.
Ipratropium Bromide
Short-Acting Muscarinic Antagonist (SAMA)
Adjunct
Mechanism of Action
Competitive antagonism at muscarinic receptors (M1, M3) → inhibits bronchoconstriction and reduces airway secretion production. Complementary mechanism to salbutamol.
Hydrocortisone
Corticosteroid — Glucocorticoid
Anti-Inflammatory
Mechanism of Action
Suppresses inflammatory mediator synthesis (leukotrienes, prostaglandins, cytokines) → reduces airway oedema, mucus production and bronchial hyper-responsiveness over hours.
Magnesium Sulphate
Bronchodilator — Smooth Muscle Relaxant
Refractory / Life-Threatening
Mechanism of Action
Calcium antagonism → inhibits smooth muscle contraction → bronchodilation. Also inhibits acetylcholine release and reduces mast cell degranulation.
Adrenaline (Epinephrine)
Catecholamine — α₁, β₁, β₂ Agonist
Critical
Mechanism of Action
β₂ → bronchodilation. α₁ → vasoconstriction, reduces mucosal oedema in upper airway, reverses anaphylactic vasodilation. β₁ → increased HR and contractility.
Oxygen Delivery Devices
| Device | FiO₂ (approx.) | Flow Rate | Indication |
|---|---|---|---|
| Nasal Cannula | 24–44% | 1–6 L/min | Mild hypoxia, patient comfort, known COPD |
| Simple Face Mask | 35–55% | 5–10 L/min | Moderate hypoxia |
| Non-Rebreather Mask | 60–90% | 10–15 L/min | Severe hypoxia, CO poisoning |
| BVM with O₂ reservoir | Up to 100% | 15 L/min | Respiratory failure, cardiac arrest |
Titrate — Do Not Free-Flow
Target SpO₂ 94–98% for most patients. Target 88–92% for known COPD. Hyperoxia causes vasoconstriction, increases mortality in MI and stroke, and can suppress hypoxic drive. Always titrate.