title: "Week 3: Respiratory"
Week 3: Respiratory
1. The Dyspnoeic Patient
Terminology
| Term | Definition |
|---|---|
| Dyspnoea | Subjective sensation of air hunger |
| Tachypnoea | Fast respiratory rate (>20/min in adults) |
| Respiratory distress | ↑RR + accessory muscle use + tripod posture |
Normal adult respiratory rate: 12–16 breaths/min
Normal inspiratory flow: ~30 L/min at rest (can exceed 150 L/min in respiratory distress).
ABC Differential Diagnosis
| Category | Causes |
|---|---|
| A – Airway | Foreign body, epiglottitis, retropharyngeal abscess, anaphylaxis |
| B – Breathing | Pneumothorax, asthma, COPD (Chronic Obstructive Pulmonary Disease), pneumonia, ARDS (Acute Respiratory Distress Syndrome) |
| C – Circulation | PE (Pulmonary Embolism), pulmonary oedema, tamponade, MI (Myocardial Infarction), arrhythmias |
Most dyspnoea presentations are cardiorespiratory — think worst-first in the critically unwell patient.
Top 5 Life-Threatening Causes
Life Threats to Never Miss:
- Tension pneumothorax
- Severe asthma
- Massive PE (Pulmonary Embolism)
- Acute pulmonary oedema (APO)
- Cardiac tamponade
2. Tension Pneumothorax
See also: Pneumothorax for a more comprehensive overview.
Clinical Features
| Examination | Findings |
|---|---|
| Inspection | Unwell, pale, sweaty, distressed, asymmetric chest, distended neck veins |
| Palpation | Trachea deviated AWAY from affected side |
| Percussion | Hyper-resonant on affected side |
| Auscultation | Absent breath sounds on affected side |
| Vitals | Hypotension, tachycardia |
Pathophysiology:
One-way valve → air enters pleural space but can't exit → progressive accumulation → mediastinal shift → IVC kinking → obstructive shock
Management
- Immediate decompression (temporising):
- Use a long, large-bore cannula (ideally ~8 cm, 12–14G)
- Options: 2nd ICS (Inhaled Corticosteroid) at/just lateral to the mid-clavicular line, or 4th/5th ICS (Inhaled Corticosteroid) just anterior to the mid-axillary line
- Definitive: Intercostal catheter (ICC/chest drain)
Ultrasound Signs:
- Normal: "Lung sliding" at pleural line, "seashore" on M-mode
- Pneumothorax: Static pleural line, "barcode" sign on M-mode
3. Acute Severe Asthma
Classification
| Mild–moderate | Severe | Life-threatening | |
|---|---|---|---|
| Speech | Whole sentences | Only a few words | Cannot speak |
| RR | <25 | ≥25 | Bradypnoea (exhaustion) |
| HR | <110 | ≥110 | Arrhythmia or bradycardia |
| SpO₂ (Peripheral Oxygen Saturation) (room air) | >96% | 92–96% | <92% or cyanosis |
| Work of breathing | Not severe | Accessory muscles / severe distress | Poor effort / paradoxical movement |
| Chest auscultation | Wheeze or normal | N/A | Silent chest or reduced air entry |
| Consciousness | Alert | N/A | Drowsy/confused/agitated/unconscious |
| FEV1/PEF | >50% predicted/personal best | ≤50% predicted/personal best | Not feasible |
Signs of Imminent Arrest:
- Silent chest (no wheeze)
- Bradycardia
- Paradoxical chest/abdominal movement
- Rising/normalising PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) (should be LOW if compensating!)
In acute severe asthma, the most worrying ABG (Arterial Blood Gas) finding is a normal or rising PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) (a compensating asthmatic should have a low PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) ~25–30).
Management
| Therapy | Drug/Dose | Notes |
|---|---|---|
| Bronchodilators | Salbutamol (spacer 4–12 puffs or neb 5 mg) + ipratropium 500 mcg | Repeat every 20 min for the first hour if needed; continuous nebs in life-threatening asthma |
| Oxygen | Titrate to SpO₂ (Peripheral Oxygen Saturation) 92–96% | Use 88–92% target if at risk of hypercapnoea |
| IV (Intravenous) magnesium sulfate | 2 g over 20 min | Bronchodilator (consider in severe/life-threatening asthma) |
| Steroids | Hydrocortisone 100–200 mg IV (Intravenous) | Or Pred 50 mg PO (Per Os (by mouth)) |
| Adrenaline | 0.5 mg IM (Intramuscular) (1:1000) | Not routine; consider if suspected anaphylaxis or poor inhaled delivery; senior/ICU (Intensive Care Unit) guidance for infusion |
| NIV (Non-Invasive Ventilation) | BiPAP (Bilevel Positive Airway Pressure) | May help |
| Intubation | RSI (Rapid Sequence Intubation) | LAST resort |
First-line bronchodilators: salbutamol 4-12 puffs (spacer) or 5 mg nebulised plus ipratropium 500 mcg.
Source: Australian Asthma Handbook; local ED asthma pathway.
In severe/life-threatening asthma, give IV magnesium sulfate 2 g over 20 min.
Source: Australian Asthma Handbook; local ED asthma pathway.
Steroids in acute severe asthma: hydrocortisone 100-200 mg IV or prednisolone 50 mg PO.
Source: Australian Asthma Handbook; local ED asthma pathway.
What is the next medication to add?
Source: Australian Asthma Handbook; ASCIA Guidelines.
Intubating severe asthma is high-risk.
Sedation/paralysis → loss of compensatory hyperventilation → rapid CO₂ rise → arrest. Avoid intubation unless absolutely necessary.
4. Massive Pulmonary Embolism
See also: Pulmonary Embolism for comprehensive overview.
Definitions
| Category | Definition |
|---|---|
| Massive PE (Pulmonary Embolism) | PE (Pulmonary Embolism) + haemodynamic instability (SBP (Systolic Blood Pressure) under 90) or cardiac arrest |
| Submassive PE (Pulmonary Embolism) | PE (Pulmonary Embolism) + right heart strain (echo/ECG (Electrocardiogram)/troponin) but stable BP (Blood Pressure) |
| Low-risk PE (Pulmonary Embolism) | PE (Pulmonary Embolism) with no RV (Right Ventricle) strain, stable |
Clinical Features
- Dyspnoea, pleuritic chest pain, haemoptysis
- Tachycardia, tachypnoea
- Clear chest on auscultation (key distinguishing feature!)
- If massive: hypotension, distended JVP (Jugular Venous Pressure)
Investigations
| Investigation | Findings |
|---|---|
| ECG (Electrocardiogram) | Sinus tachycardia (most common), S1Q3T3 (20%), T-wave inversion V1–V4 (most specific) |
| D-dimer | High sensitivity (95–98%), use to rule OUT |
| CTPA | Gold standard – visualises clot |
Management
| Severity | Treatment |
|---|---|
| Massive (arrest) | Alteplase 50 mg IV (Intravenous) stat (during CPR (Cardiopulmonary Resuscitation)) |
| Massive (shocked) | Alteplase 100 mg IV (Intravenous) over 2 hours |
| Submassive | Anticoagulation; consider thrombolysis |
| Low-risk | Therapeutic anticoagulation (LMWH/DOAC) |
5. Acute Pulmonary Oedema (APO)
APO creates a vicious cycle: trigger → ↑LV filling pressure → pulmonary congestion → hypoxia → sympathetic activation → vasoconstriction → ↑afterload → worsening LV failure.
CXR (Chest X-Ray) Features
- A - Alveolar oedema (bat-wing distribution)
- B - Kerley B lines (interstitial oedema)
- C - Cardiomegaly
- D - Diversion (upper lobe vascular)
- E - Effusions (pleural)
Management
| Intervention | Mechanism |
|---|---|
| NIV (Non-Invasive Ventilation) (CPAP (Continuous Positive Airway Pressure)) | ↑intrathoracic pressure → ↓preload + ↓afterload → ↑CO (Cardiac Output) |
| GTN infusion | Venodilation → ↓preload; arterial dilation → ↓afterload |
| Frusemide | Diuresis (slower onset) |
In APO, CPAP (Continuous Positive Airway Pressure) reduces mortality.
Avoid GTN in:
- Hypotensive patients
- Right ventricular infarction (preload-dependent)
CXR Pattern Examples (Quick Look)
6. Respiratory Failure
Respiratory Failure: Lung gas exchange inadequate to meet tissue demands for O₂ delivery and CO₂ removal.
Classification
| Type | Primary Problem | Typical Causes |
|---|---|---|
| Type 1 (Hypoxaemic) | Low PaO₂ (Partial Pressure of Arterial Oxygen), normal/low PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) | Pneumonia, PE (Pulmonary Embolism), ARDS (Acute Respiratory Distress Syndrome), pulmonary oedema |
| Type 2 (Hypercapnic) | High PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) ± low PaO₂ (Partial Pressure of Arterial Oxygen) | COPD (Chronic Obstructive Pulmonary Disease), neuromuscular disease, drug overdose |
Hypoxaemia = low O₂ in blood (low PaO₂ (Partial Pressure of Arterial Oxygen)).
Hypoxia = low O₂ in tissues; can occur even with normal PaO₂ (Partial Pressure of Arterial Oxygen) (anaemia, low CO (Cardiac Output), CO (Cardiac Output) poisoning).
Causes of Hypoxaemia
| Mechanism | Examples | Response to O₂ |
|---|---|---|
| Low FiO₂ (Fraction of Inspired Oxygen) | High altitude | Excellent |
| Hypoventilation | Drug overdose | Excellent |
| Diffusion impairment | Pulmonary fibrosis | Good |
| V/Q mismatch | COPD (Chronic Obstructive Pulmonary Disease), pneumonia, PE (Pulmonary Embolism) | Good |
| Shunt | ARDS (Acute Respiratory Distress Syndrome), consolidation | Poor |
Why shunt doesn't respond to O₂:
Blood passing through unventilated alveoli never contacts the high FiO₂ (Fraction of Inspired Oxygen) gas. Extra O₂ only helps ventilated areas — which are already near-saturated.
Causes of Hypercapnia
| Category | Examples |
|---|---|
| Low total ventilation | Drug overdose, obesity hypoventilation, CNS (Central Nervous System) lesion |
| Neuromuscular failure | GBS, MND, myasthenia gravis, spinal cord injury |
| Low compliance | Pulmonary fibrosis, kyphoscoliosis |
| Increased dead space | COPD (Chronic Obstructive Pulmonary Disease), PE (Pulmonary Embolism), low cardiac output |
If dead space increases (e.g., PE), minute ventilation must increase proportionally to maintain normal alveolar ventilation.
Pulse oximetry does not reliably detect hypoventilation on supplemental O₂.
SpO₂ (Peripheral Oxygen Saturation) may be normal while PaCO₂ (Partial Pressure of Arterial Carbon Dioxide) rises dangerously. Check ABG (Arterial Blood Gas)/VBG if concerned about ventilation.
7. Oxygen Delivery Devices
Low-Flow Devices
| Device | Flow Rate | FiO₂ (Fraction of Inspired Oxygen) | Notes |
|---|---|---|---|
| Nasal prongs | 1–4 L/min | 24–36% | >4 L dries mucosa |
| Hudson mask | 5–10 L/min | 35–60% | Most common ward device |
| Venturi mask | Variable | Set 24–60% | Precise FiO₂ (Fraction of Inspired Oxygen) for COPD (Chronic Obstructive Pulmonary Disease) |
| Non-rebreather | 10–15 L/min | 60–80% | Reservoir bag + one-way valves |
Low-flow devices deliver variable FiO₂ (Fraction of Inspired Oxygen).
Patient inspiratory flow (~30 L/min at rest, >150 L/min in distress) exceeds device flow → room air entrained → actual FiO₂ (Fraction of Inspired Oxygen) lower than expected. The sicker the patient, the less effective low-flow O₂ becomes.
Source: CC Bible; oxygen delivery device principles (patient inspiratory flow vs device flow).
High-Flow Nasal Cannula (HFNC)
Flow rates: 30–70 L/min (can match patient demand)
FiO₂ (Fraction of Inspired Oxygen): Up to >80% (adjustable)
Requires: Heated humidifier
Source: Local HFNC device specifications; CC Bible.
Mechanisms of benefit:
- Dead space washout – flushes nasopharyngeal CO₂
- Splints nasopharynx – reduces upper airway resistance
- Generates small CPAP (Continuous Positive Airway Pressure) (2–3 cmH₂O with mouth closed)
- Humidification – improves lung compliance
FiO₂ (Fraction of Inspired Oxygen) Ladder (lowest to highest):
Nasal prongs < Venturi < Hudson < Non-rebreather < high-flow nasal cannula (HFNC)
8. Non-Invasive Ventilation
CPAP (Continuous Positive Airway Pressure) vs BiPAP (Bilevel Positive Airway Pressure)
| CPAP (Continuous Positive Airway Pressure) | BiPAP (Bilevel Positive Airway Pressure) |
|---|---|
| Continuous positive pressure throughout cycle | Different pressures for inspiration (IPAP) and expiration (EPAP) |
| ↑End-expiratory lung volume | IPAP augments tidal volume, washes out CO₂ |
| Recruits collapsed alveoli | EPAP = PEEP (Positive End-Expiratory Pressure) |
Indications
| CPAP (Continuous Positive Airway Pressure) | BiPAP (Bilevel Positive Airway Pressure) |
|---|---|
| Acute pulmonary oedema | COPD (Chronic Obstructive Pulmonary Disease) exacerbation (Type 2 failure) |
| Obstructive sleep apnoea | Neuromuscular disease |
| Obesity hypoventilation |
Haemodynamic Effects of PEEP (Positive End-Expiratory Pressure)
| Effect | Mechanism |
|---|---|
| ↓RV (Right Ventricle) preload | Venous return impeded by ↑intrathoracic pressure |
| ↑RV (Right Ventricle) afterload | Pulmonary vessels compressed |
| ↓LV (Left Ventricle) preload | Reduced RV (Right Ventricle) output |
| ↓LV (Left Ventricle) afterload | Reduced transmural pressure gradient |
Effect on Cardiac Output depends on volume status:
- Fluid overloaded: PEEP (Positive End-Expiratory Pressure) ↑CO (Cardiac Output) (shifts Starling curve left to optimal)
- Euvolaemic/hypovolaemic: PEEP (Positive End-Expiratory Pressure) ↓CO (Cardiac Output) (reduces preload)
High levels of CPAP (Continuous Positive Airway Pressure)/PEEP (Positive End-Expiratory Pressure) can reduce cardiac output by reducing venous return (especially in hypovolaemia).
Be cautious with high PEEP (Positive End-Expiratory Pressure) in hypovolaemic patients.
NIV Settings by Condition
| Condition | Mode | Typical Settings | Rationale |
|---|---|---|---|
| APO | CPAP (Continuous Positive Airway Pressure) | 10 cmH₂O | Recruits alveoli, ↓preload and afterload |
| COPD (Chronic Obstructive Pulmonary Disease) exacerbation (Type 2) | BiPAP (Bilevel Positive Airway Pressure) | IPAP 12–20, EPAP 4–6 | Pressure support (IPAP−EPAP) augments tidal volume to wash out CO₂ |
| Obesity hypoventilation | BiPAP (Bilevel Positive Airway Pressure) | IPAP 14–24, EPAP 6–10 | Higher EPAP overcomes chest wall mass; higher IPAP augments ventilation |
| Immunocompromised with hypoxia | CPAP (Continuous Positive Airway Pressure) or BiPAP (Bilevel Positive Airway Pressure) | Titrate to SpO₂ | Avoids intubation (high mortality in this group) |
Pressure support = IPAP − EPAP. Increasing pressure support increases tidal volume and CO₂ clearance. Increasing EPAP improves oxygenation by recruiting alveoli.
NIV Contraindications
Absolute contraindications to NIV:
- Cardiac or respiratory arrest
- Inability to protect airway (GCS (Glasgow Coma Scale) less than 8)
- Facial burns, trauma, or surgery preventing mask seal
- Copious secretions or active vomiting
- Undrained pneumothorax
- Upper airway obstruction (e.g., epiglottitis)
NIV Weaning Criteria
| Parameter | Target Before Weaning |
|---|---|
| FiO₂ (Fraction of Inspired Oxygen) | ≤0.4 (40%) |
| PEEP (Positive End-Expiratory Pressure)/EPAP | ≤5–6 cmH₂O |
| Respiratory rate (Respiratory Rate) | less than 25/min |
| Conscious level | Alert, cooperative |
| Secretions | Manageable |
Wean by reducing IPAP in steps of 2 cmH₂O, monitoring for rising RR (Respiratory Rate) or falling SpO₂ (Peripheral Oxygen Saturation). If stable on minimal settings for 2+ hours, trial off NIV.
The A–a Gradient
Alveolar–arterial (A–a) gradient = PAO₂ − PaO₂
Alveolar gas equation: PAO₂ = FiO₂ × (Patm − PH₂O) − (PaCO₂ / R)
On room air: PAO₂ = 0.21 × (760 − 47) − (PaCO₂ / 0.8) ≈ 150 − (PaCO₂ × 1.25)
| A–a Gradient | Interpretation | Examples |
|---|---|---|
| Normal (less than 10–15 mmHg in young adults) | Lungs are working — problem is upstream (hypoventilation) | Drug overdose, neuromuscular disease, CNS depression |
| Elevated | Lung parenchyma or vasculature is impaired | Pneumonia, PE (Pulmonary Embolism), ARDS (Acute Respiratory Distress Syndrome), pulmonary fibrosis |
Age-adjusted normal: A–a gradient upper limit ≈ (Age / 4) + 4
What is the approximate A-a gradient and interpretation?
9. Airway Clinical Skills
Airway Adjuncts
Oropharyngeal Airway (OPA/Guedel)
| Aspect | Details |
|---|---|
| Sizing | Angle of jaw to incisors |
| Indication | Unconscious patient with no gag reflex |
| Contraindication | Conscious patient (will gag → vomit → aspiration) |
| Insertion | Insert upside-down, rotate 180° as you advance |
Nasopharyngeal Airway (NPA)
| Aspect | Details |
|---|---|
| Sizing | Tip of nose to tragus of ear |
| Indication | Semi-conscious patient, trismus, oral trauma |
| Contraindication | Base of skull fracture (relative) |
| Insertion | Lubricate, insert along floor of nose |
In semi-conscious patients, nasopharyngeal airway (NPA) is often better tolerated than OPA (less likely to trigger gag reflex).
Bag-Valve-Mask (BVM) Technique
Setup:
- Connect to oxygen (10-15 L/min)
- Attach reservoir bag
- Select appropriate mask size
C-E Grip (Two-handed):
- C = thumb and index finger form C-shape around mask, pressing down to seal
- E = remaining three fingers on mandible (not soft tissue), lifting jaw
Two-person BVM is more effective:
- One person maintains seal with both hands (C-E grip on each side)
- Second person squeezes bag
Choking (Foreign Body Airway Obstruction)
| Severity | Signs | Management |
|---|---|---|
| Mild (effective cough) | Can speak, cough, breathe | Encourage coughing, don't interfere |
| Severe (ineffective cough) | Cannot speak, silent cough, cyanosis | Conscious: back blows + chest thrusts |
| Unconscious | Unresponsive | Start CPR (Cardiopulmonary Resuscitation), check mouth before breaths |
- Assess severity - Can they cough/speak?
- Mild → Encourage coughing
- Severe + conscious → 5 back blows → 5 chest thrusts → repeat
- Severe + unconscious → Finger sweep if visible, start CPR (Cardiopulmonary Resuscitation)
Infants (under 1 year): 5 back blows + 5 chest thrusts only — NO abdominal thrusts (risk of liver/spleen injury).
10. Anaphylaxis
Definition
Anaphylaxis: Severe, life-threatening generalised hypersensitivity reaction. Defined as rash PLUS symptoms from two other organ systems (typically cardiovascular or respiratory).
Pathophysiology
| Phase | Timing | Mechanism |
|---|---|---|
| Early phase | Minutes to 5 hours | IgE-mediated mast cell degranulation → histamine, tryptase, leukotrienes |
| Late phase | 4-24+ hours | Non-IgE mediated inflammation; occurs in up to 20% of patients |
Biphasic Response: Up to 20% have a late phase (4-24+ hours after initial reaction). Patients must be observed for minimum 4 hours after treatment. If ≥2 doses of adrenaline needed, observe 8+ hours.
Source: ASCIA Guidelines.
Clinical Features - FAST Mnemonic
- F - Face (swollen lips, tongue, eyes)
- A - Airways (difficulty breathing, swallowing, speaking, wheeze)
- S - Stomach (abdominal pain, nausea, vomiting)
- T - Total body (rash, urticaria, weakness, pallor, loss of consciousness)
Common Triggers
| Category | Examples |
|---|---|
| Medications | Penicillins, NSAIDs, opioids, anaesthetics, IV (Intravenous) contrast |
| Insect venoms | Bees, wasps, ants |
| Foods | Peanuts, tree nuts, shellfish, eggs, milk |
Medications are the most common cause of anaphylaxis - not food! Penicillin allergy is often over-reported (many are adverse events, not true allergies).
Management
IM (Intramuscular) adrenaline is first-line treatment for anaphylaxis.
Do not delay for antihistamines or steroids. The vasoconstriction and bronchodilation from adrenaline is immediately life-saving.
| Treatment | Details |
|---|---|
| Adrenaline IM (Intramuscular) | 0.5 mg (0.5 mL of 1:1000) for adults; repeat every 5 min if needed |
| Position | Lie flat (or horizontal for infants) |
| Oxygen | High flow |
| IV (Intravenous) fluids | If hypotensive |
| Antihistamines | After adrenaline - helps itching/urticaria |
| Corticosteroids | Prednisolone 1 mg/kg PO (max 50 mg) or hydrocortisone 5 mg/kg IV (max 200 mg) |
Persistent wheeze in anaphylaxis: give salbutamol 8-12 puffs (100 mcg) via spacer or 5 mg nebulised.
Antihistamines are adjuncts only in anaphylaxis (itch/urticaria); they do not treat airway or cardiovascular compromise.
Avoid injectable promethazine in anaphylaxis (can worsen hypotension).
Source: CC Bible extract (anaphylaxis management section).
Refractory Anaphylaxis (Adrenaline Infusion)
If multiple IM (Intramuscular) doses are required or the reaction is severe, start an IV (Intravenous) adrenaline infusion:
- Mix 1 mL of 1:1000 adrenaline in 1000 mL normal saline
- Start at ~5 mL/kg/hour (≈ 0.1 mcg/kg/min) and titrate to response
- Continuous monitoring; avoid IV (Intravenous) bolus adrenaline due to arrhythmia risk
For persistent hypotension/shock: give normal saline 20 mL/kg rapidly, up to 50 mL/kg in the first 30 minutes. If on beta-blockers with cardiogenic shock, give glucagon 1-2 mg IV (Intravenous) bolus and consider 1-2 mg/hour infusion.
If infusion is ineffective/unavailable, adults may need selective vasoconstrictors after senior advice: metaraminol 1-20 mg or vasopressin 10-40 units.
Source: CC Bible extract (pages 021-030).
Adrenaline Dosing
Adult dose: 0.5 mg IM (Intramuscular) (= 0.5 mL of 1:1000 solution)
Weight-based paediatric: ~0.01 mg/kg (max 0.5 mg)
Route: IM (Intramuscular) into lateral thigh (NOT IV (Intravenous) unless in cardiac arrest)
Source: ASCIA Guidelines.
| Weight | Dose | Volume (1:1000) |
|---|---|---|
| 7.5-10 kg | 0.1 mg | 0.1 mL |
| 10-20 kg | 0.15 mg | 0.15 mL |
| 20-30 kg | 0.2 mg | 0.2 mL |
| 30-40 kg | 0.3 mg | 0.3 mL |
| >50 kg | 0.5 mg | 0.5 mL |
Auto-injectors:
- EpiPen Jr (150 mcg) - children 7.5-20 kg
- EpiPen (300 mcg) - children/adults >20 kg
- EpiPen (500 mcg) - available for larger adults
Blue to the sky, orange to the thigh - inject into lateral thigh through clothing if needed.
Source: ASCIA Guidelines.
Why Adrenaline First?
| Receptor | Effect | Clinical Benefit |
|---|---|---|
| α1 (vascular smooth muscle) | Vasoconstriction | ↑BP, ↓oedema |
| β1 (heart) | ↑HR, ↑contractility | ↑Cardiac output |
| β2 (bronchial smooth muscle) | Bronchodilation | Relieves wheeze |
Adrenaline has a short plasma half-life. If symptoms persist or recur, repeat IM (Intramuscular) adrenaline every 5 minutes and document times for handover.
Source: ASCIA Guidelines.
11. Practice Questions
What is the most appropriate next step?
What is the most appropriate therapy?
What is the FIRST treatment?
What is the most appropriate initial oxygen target and delivery approach?
Week 3 Study Checklist
Click to expand or view deep dives
11. Point-of-Care Ultrasound (POCUS) in Shock & Dyspnoea
POCUS answers two critical questions:
- Should I give this shocked patient fluids?
- Do they have an obstructive or cardiogenic cause?
Source: Dr. Justin Bauer lecture on SLICE protocol, North Shore Hospital Emergency Department.
The SLICE Protocol
- S - Sick patient (shocked or short of breath)
- L - Lung fields (easy to find, answers "fluid yes/no?")
- I - IVC (volume status)
- C - Cardiac (only if indicated by L or I)
- E - Extras (AAA, E-FAST - only if clinically indicated)
Q: In SLICE, why start with lungs? A: Lungs are large/easy to scan and answer the fluid question quickly; cardiac views are more complex and easy to misinterpret.
Be a doctor first, sonographer second. If you already know the answer clinically, don't do the test. Engage your brain before your machine.
Lung Ultrasound
Scanning zones: Divide each hemithorax into upper/lower, anterior/lateral/posterior (6 zones per side)
Three main patterns:
| Pattern | Appearance | Interpretation | Fluid Decision |
|---|---|---|---|
| A-lines | Horizontal lines deep to pleura, lung sliding | Normal dry lung | ✅ Yes - safe to give fluids |
| B-lines | Vertical "laser beams" from pleura to edge | Interstitial fluid or fibrosis | ⚠️ Caution - bilateral B-lines → likely APO → hold fluids |
| C-profile | Consolidated (dark chunky) lung tissue | Pneumonia or contusion | ✅ Yes (unless bilateral APO) |
B-lines = ultrasound equivalent of crackles. Bilateral diffuse B-lines = pulmonary oedema. Focal B-lines = consider pneumonia or fibrosis.
Pneumothorax detection:
- Normal: Lung sliding (shimmering at pleural line), comet-tail artifacts
- Pneumothorax: Absent lung sliding, no comet-tails, may see "lung point" (edge of pneumothorax)
Tension pneumothorax = clinical diagnosis (hypotension + respiratory distress + absent air entry). Don't wait for imaging - needle decompress immediately.
Source: Dr. Bauer SLICE lecture; international consensus on lung ultrasound.
IVC Assessment
Scanning approach: Transverse (short axis) preferred over longitudinal - easier to assess size and collapsibility
Normal IVC: ~2 cm diameter, oval shape, respiratory variation
| Finding | Size | Collapsibility | Interpretation | Action |
|---|---|---|---|---|
| Distended | Round, > 2.5 cm | Minimal respiratory variation | High CVP - likely obstructive/cardiogenic | → Scan heart |
| Collapsing | Slit-like <1 cm | Collapses significantly | Hypovolemia | ✅ Give fluids |
| Mid-range | Oval, ~2 cm | Moderate variation | Non-contributory | Clinical decision |
Distended IVC = something's backing up into the right heart. Think:
- Obstructive: tamponade, massive PE, tension pneumothorax
- Cardiogenic: right heart failure, severe LV failure
Collapsing IVC = empty tank. Give fluids.
Dry lungs + skinny IVC = not a cardiac problem. Likely hypovolemic or distributive shock. You don't need to scan the heart.
Cardiac Ultrasound (When Indicated)
Only scan if:
- IVC is distended (suggests obstructive/cardiogenic cause), OR
- Lungs show B-lines (suggests LV failure), OR
- Clinical concern for specific cardiac pathology
Three key questions:
- Is there a pericardial effusion/tamponade?
- Fluid around heart
- RV/RA collapse in diastole (chamber compression)
- Is the RV massive? (massive PE)
- RV bigger than LV (normally RV wraps around smaller LV)
- Septal bowing toward LV (D-sign)
- How's the LV squeezing?
- Grossly normal vs severely impaired (eyeball it)
Cognitive bias trap: Don't start with the heart in a patient with known poor EF. Their bad EF was bad yesterday and will be bad tomorrow - it's not the cause every time. You might miss that they're simply dehydrated.
Putting It Together: The SLICE Algorithm
Step 1: Scan the lungs (30 seconds)
- Wet (B-lines) → Don't give fluids yet
- Dry (A-lines) → Probably safe to give fluids
Step 2: Scan the IVC (30 seconds)
- Distended → High CVP → scan heart next
- Collapsing → Low CVP → Give fluids, probably skip heart
- Mid-range → Use clinical judgment
Step 3: Cardiac (if indicated)
- Tamponade? → Pericardiocentesis
- Massive PE? → Thrombolysis/ECMO
- Poor LV function? → Inotropes, diuretics
Step 4: Extras (only if clinically appropriate)
- AAA scan if relevant risk factors
- E-FAST if trauma
SLICE advantages:
- Quick - answers "can I give fluids?" in under 1 minute
- Simple - starts with easy organs (lungs, IVC), not complex ones (heart)
- Smart - rules out obstructive/cardiogenic without always needing cardiac echo
- Practical - doesn't intimidate junior doctors with complex cardiac imaging
Ultrasound is excellent at ruling OUT obstructive and cardiogenic shock. It's not as good at distinguishing hypovolemic from distributive - but that's okay, because both often get fluids initially anyway.
Source: Dr. Justin Bauer, Emergency Physician, Sydney; SLICE protocol developed at North Shore Hospital; iFIM Ultrasound SIG.