Shortness Of Breath

Shortness of breath, or dyspnea, is the subjective sensation of difficulty or discomfort in breathing, arising from cardiovascular, pulmonary, neuromuscular, or psychogenic causes that increase ventilatory demand or impair gas exchange.

Definition

Shortness of breath (SOB), medically termed dyspnoea, is defined as the unexpected awareness of breathing or a subjective experience of breathing discomfort ^[1]^[2]^[3]. Let's break the word down: "dys" = difficulty/abnormal (Greek), "pnoea" = breathing. So literally, "difficult breathing."

It is a symptom, not a diagnosis — it is the patient's perception that their current ventilatory effort is inadequate for their physiological demand. The key mechanism is the sensation of increased effort by respiratory muscles when the current ventilatory rate is insufficient to meet the physiological drive to breathe ^[1]^[2]^[3].

Core Concept

Dyspnoea is fundamentally a mismatch between ventilatory demand and ventilatory capacity. Anything that increases demand (e.g. metabolic acidosis, exercise), decreases capacity (e.g. muscle weakness, airflow obstruction), or increases the work of breathing (e.g. stiff lungs, fluid-filled alveoli) can cause it.

Since dyspnoea is a symptom, risk factors relate to the underlying conditions:

Category	Risk Factors	Relevant Conditions
Cardiac	Hypertension, diabetes, smoking, dyslipidaemia, obesity, CAD family history, prior MI	Heart failure, ACS, valvular disease
Respiratory	Smoking (>85% of COPD), occupational dust/fume exposure, indoor biomass combustion, atopy, childhood respiratory infections	COPD, asthma, ILD, lung cancer
Thromboembolic	Immobilisation, recent surgery, malignancy, OCP/HRT, inherited thrombophilia (Factor V Leiden, Protein C/S deficiency, antithrombin III deficiency), pregnancy, obesity, prior VTE	PE/DVT ^[6]^[7]
Anaemia	Chronic disease, iron deficiency, GI blood loss, heavy menses, haemolysis	Severe anaemia
Neuromuscular	Autoimmune conditions, genetic (e.g. DMD)	Myasthenia gravis, GBS, motor neuron disease
Metabolic	Diabetes (DKA), renal failure, liver failure	Metabolic acidosis
Obesity	BMI > 30 kg/m²	Obesity-hypoventilation syndrome, OSA
Psychogenic	Anxiety disorders, panic disorder, depression	Hyperventilation syndrome

Anatomy and Physiology of Breathing

To understand dyspnoea, you must understand the anatomy of the respiratory system and the mechanics of ventilation.

Etiology (Hong Kong Focus)

The causes of dyspnoea are best organized by system and acuity (acute vs. chronic). This framework is clinically essential ^[1]^[2]^[3]^[8].

A. Acute Dyspnoea

Mechanism	Causes
Depressed consciousness	Drug overdose, stroke, post-ictal
Intraluminal	Secretions, blood, vomitus; foreign body aspiration
Mural	Infections (tonsillitis, peritonsillar/retropharyngeal abscess, epiglottitis, croup); trauma; tumour; oedema (anaphylaxis, angioedema, post-operative); laryngospasm
Extramural	Penetrating neck injury; tumour; oesophageal foreign body

Pathophysiology: Physical obstruction → turbulent airflow → ↑airway resistance → stridor (inspiratory noise) → ↑work of breathing → dyspnoea. Stridor is inspiratory because the upper airway is an extrathoracic structure — during inspiration, intraluminal pressure drops below atmospheric, tending to collapse a narrowed airway.

Category	Causes	Key Features
Lower airway obstruction (wheezing)	Acute COPD exacerbation; Acute asthma	Bronchospasm + inflammation → ↑airway resistance
Alveolar congestion (crepitations)	Acute heart failure; Pneumonia; ARDS	Fluid in alveoli → ↓gas exchange + ↓compliance
Other lung pathologies	Pneumothorax/haemothorax; Pulmonary embolism; Massive pleural effusion; Pulmonary contusion	Various mechanisms (see below)

B. Chronic Dyspnoea

Condition	Pathophysiology of Dyspnoea
Congestive heart failure	Chronic ↑LV filling pressures → pulmonary venous congestion → ↓lung compliance → ↑work of breathing
Myocardial ischaemia	Ischaemia → transient LV dysfunction → ↑LVEDP → pulmonary congestion (angina equivalent)
Valvular heart disease (esp. mitral stenosis, aortic stenosis)	MS: obstruction at mitral valve → ↑LA pressure → pulmonary congestion; AS: ↑afterload → LVH → diastolic dysfunction
Hypertrophic cardiomyopathy	Diastolic dysfunction → ↓diastolic filling → ↑LV end-diastolic pressure → ↑pulmonary venous pressure → accounts for exertional dyspnoea ^[10]; also LVOT obstruction → ↑afterload → ↑demand + ↓CO → myocardial ischaemia and SAM → mitral regurgitation → ↑pulmonary venous pressure → dyspnoea, orthopnoea ^[10]
Pulmonary hypertension	↑PAP → RV strain → ↓CO → ↓tissue O₂ delivery
Pericardial disease	Constriction/effusion → ↓filling → ↓CO

Condition	Pathophysiology of Dyspnoea
COPD	Small airway disease (inflammation, fibrosis, narrowing) + emphysema (parenchymal destruction, loss of elastic recoil) → airflow obstruction → air trapping → hyperinflation → ↓diaphragm efficiency → ↑work of breathing ^[4]
Chronic asthma	Chronic airway inflammation → bronchial hyper-responsiveness → variable airflow obstruction → ↑work of breathing ^[5]
Interstitial lung disease (ILD)	Fibrosis → ↓compliance → ↑elastic work of breathing + ↓diffusion capacity → hypoxaemia on exertion
Bronchiectasis	Chronic infection → airway destruction → mucus plugging → V/Q mismatch
Lung cancer (CA bronchus)	Endobronchial obstruction, pleural effusion, lymphangitis carcinomatosa, phrenic nerve palsy
Pleural effusion	Fluid compresses lung → atelectasis → ↓ventilated lung volume + diaphragm displacement
Obesity-hypoventilation syndrome (OHS)	Excess adipose tissue → ↑chest wall load + ↓diaphragm excursion → chronic hypoventilation → hypercapnia ^[11]
Obstructive sleep apnoea (OSA)	Anatomical abnormalities predispose to functional obstruction: micrognathia, macroglossia, enlarged tonsils/adenoids, redundant pharyngeal tissues from fatty infiltration → upper airway collapses during inspiration → snoring (mild) and apnoea (severe) → arousal response ^[12]. Daytime somnolence, but can present with exertional dyspnoea

Condition	Pathophysiology of Dyspnoea
Severe anaemia	↓Hb → ↓O₂ carrying capacity → compensatory ↑CO and ↑ventilation → exertional dyspnoea ^[2]
Deconditioning / lack of fitness	Poor cardiovascular fitness → early lactic acidosis during exertion → ↑ventilatory demand ^[2]
Neuromuscular weakness (e.g. MG, motor neuron disease)	Respiratory muscle weakness → ↓vital capacity → ↑respiratory rate → exertional then resting dyspnoea ^[2]^[13]
Thoracic abnormality (e.g. kyphoscoliosis)	Chest wall deformity → ↓chest expansion → restrictive ventilatory defect → ↑work of breathing ^[2]
Obesity	↑metabolic demand + ↓chest wall compliance + ↓FRC → ↑work of breathing ^[11]
Thyrotoxicosis	↑metabolic rate → ↑O₂ demand → ↑ventilatory demand; can also precipitate AF → heart failure

Classification

Dyspnoea can be classified in multiple clinically useful ways:

Acute (minutes to hours)	Subacute (days to weeks)	Chronic (weeks to months)
PE, pneumothorax, acute asthma, ADHF, anaphylaxis, foreign body, MI	Pneumonia, pleural effusion, lung cancer, anaemia, pericardial disease	COPD, chronic HF, ILD, pulmonary HTN, anaemia, deconditioning

Cardiac	Respiratory	Other
HF (acute/chronic), ACS, valvular disease, HCMP, pulmonary HTN, tamponade, arrhythmia	Obstructive (asthma, COPD), restrictive (ILD, effusion), vascular (PE), infection (pneumonia), airway (obstruction, tumour)	Anaemia, metabolic acidosis, obesity, neuromuscular, psychogenic, thyrotoxicosis, deconditioning

Mechanism	Examples
↑Airway resistance	Asthma, COPD, upper airway obstruction, tumour
↓Lung compliance	Pulmonary oedema, ILD, ARDS, pleural effusion
↓Chest wall compliance	Obesity, kyphoscoliosis, ascites
V/Q mismatch	PE, COPD, asthma
Shunt	Pneumonia, ARDS, AVM
↓Diffusion	ILD, emphysema
↓O₂ carrying capacity	Anaemia, CO poisoning, methaemoglobinaemia
↓Cardiac output	HF, tamponade, arrhythmia
↑Ventilatory demand	Metabolic acidosis, thyrotoxicosis, fever
↓Ventilatory pump	Neuromuscular disease, diaphragm paralysis
Central drive abnormality	Brainstem lesion, drugs
Psychogenic	Hyperventilation syndrome, panic disorder

Type 1	Type 2
↓pO₂ < 60 mmHg + ↓/normal pCO₂ ≤ 50 mmHg	↓pO₂ < 60 mmHg + ↑pCO₂ > 50 mmHg
Mechanism: V/Q mismatch, shunt, diffusion impairment	Mechanism: ↓respiratory drive, neuromuscular weakness, chest wall disorder, global lung hypoventilation
Examples: PE, pneumonia, ARDS, ILD	Examples: COPD (decompensated), sedative OD, GBS, OHS, kyphoscoliosis

Grade	Description
0	Breathless only with strenuous exercise
1	Breathless when hurrying on the level or walking up a slight hill
2	Walks slower than contemporaries on the level due to breathlessness, or has to stop when walking at own pace
3	Stops for breath after walking ~100 m or after a few minutes on the level
4	Too breathless to leave the house, or breathless when dressing/undressing

Class	Description
I	No limitation of physical activity
II	Slight limitation — comfortable at rest, ordinary activity causes dyspnoea
III	Marked limitation — comfortable at rest, less than ordinary activity causes dyspnoea
IV	Unable to carry out any physical activity without discomfort — dyspnoea at rest

Clinical Features

Symptoms

The history is the most important tool in evaluating dyspnoea. Here is a systematic approach with pathophysiological explanations:

Feature	Significance	Pathophysiological Basis
Sudden onset, maximal at onset	Pneumothorax, PE, anaphylaxis	Sudden mechanical or vascular event — no time for compensation
Rapid onset over minutes	Asthma attack, ADHF, foreign body	Acute bronchospasm, acute pulmonary oedema, acute obstruction
Gradual onset over hours-days	Pneumonia, pleural effusion, AECOPD	Progressive inflammation/fluid accumulation
Chronic, progressive over months	COPD, ILD, chronic HF, anaemia	Slow structural or functional decline

Feature	Significance	Pathophysiological Basis
Orthopnoea (dyspnoea on lying flat)	Characteristic of cardiac dyspnoea ^[1]^[2]; also occurs in bilateral diaphragm paralysis	Supine → ↑venous return → ↑preload on failing LV → ↑pulmonary congestion; also abdominal contents push diaphragm cephalad → ↓FRC
PND (paroxysmal nocturnal dyspnoea)	Characteristic of cardiac dyspnoea ^[1]^[2]; virtually absent in respiratory causes	During sleep → ↑venous return from LL + ↓sympathetic tone → gradual pulmonary congestion → wakes patient 1–2 hours after falling asleep gasping for air; takes 20–30 min to resolve (cf. orthopnoea which resolves quickly on sitting up)
Orthopnoea in COPD	COPD can present with orthopnoea as cranial displacement of diaphragm by abdominal content at supine position pressing onto the lung, exacerbating airflow obstruction ^[1]^[2]	Hyperinflated lungs + supine → already flattened diaphragm further displaced → very inefficient ventilation
Platypnoea (dyspnoea on sitting up, relieved by lying flat)	Hepatopulmonary syndrome, intracardiac shunt (ASD/PFO)	Upright position → ↑shunting through basal lung AVMs (hepatopulmonary) or redistribution of blood through defect
Trepopnoea (dyspnoea in one lateral decubitus position)	Large unilateral pleural effusion, unilateral lung disease	Lying on the diseased side compresses it further; lying on the good side allows it to ventilate maximally

Symptom	Suggests	Why?
Angina, palpitation	Cardiac dyspnoea ^[1]^[2]	Ischaemia or arrhythmia → ↓CO → pulmonary congestion
Cough, sputum, wheezing	Respiratory dyspnoea ^[1]^[2]	Airway inflammation/obstruction → ↑mucus production, bronchospasm
Haemoptysis	PE (occurs late with infarction), lung cancer, TB, bronchiectasis	Pulmonary infarction → necrosis of lung tissue → bleeding; tumour erosion into vessels
Chest pain — pleuritic (sharp, worse on inspiration)	PE, pneumothorax, pneumonia, pleurisy	Inflamed/stretched parietal pleura (which has pain fibres — visceral pleura does not) moves with breathing
Chest pain — central/crushing	ACS, massive PE	Myocardial ischaemia; massive PE → acute RV dilatation → RV ischaemia
Fever	Pneumonia, TB, empyema	Infection → cytokine release → hypothalamic set-point ↑
Weight loss	Malignancy, TB, chronic HF (cardiac cachexia), thyrotoxicosis	Catabolic state, ↑metabolic demand, anorexia
Leg swelling (bilateral)	Heart failure, cor pulmonale	↑venous pressure → fluid extravasation into interstitium
Leg swelling (unilateral) + preceding pleuritic CP	DVT → PE	Venous thrombosis → embolism to pulmonary vasculature ^[6]^[7]
Stridor (inspiratory noise)	Upper airway obstruction	Turbulent flow through narrowed extrathoracic airway
Pink frothy sputum	Acute pulmonary oedema	Fluid transudation into alveoli + ruptured capillaries → blood-tinged foam
Wheeze	Asthma, COPD, "cardiac asthma"	Narrowed intrathoracic airways → turbulent expiratory flow. "Cardiac asthma" = bronchial oedema from LVF
Syncope/presyncope with exertion	Massive PE, HCMP, severe AS, pulmonary HTN	↓CO during exertion due to fixed obstruction or ↑LVOT gradient ^[10]
Perioral tingling, carpopedal spasm	Hyperventilation syndrome	Respiratory alkalosis → ↓ionised Ca²⁺ → neuromuscular excitability
Daytime somnolence, snoring	OSA	Upper airway collapses during inspiration → fragmented sleep → daytime sleepiness ^[12]
Episodic flushing + diarrhoea + wheezing	Carcinoid syndrome	Bronchospasm (10-20%): wheezing and dyspnoea often during flushing episodes due to histamine and other mediators released by NETs ^[15]

Cardiac vs. Respiratory Dyspnoea

Feature	Cardiac	Respiratory
Mechanism	HF → pulmonary congestion → ↓compliance + airway obstruction	Pathology → ↑work of breathing; ↓ventilation → hypoxaemia, hypercapnia
PND	Characteristic	Nil
Orthopnoea	Characteristic	May be present (in COPD)
Oedema	Often present	Present if cor pulmonale
Associated with	Angina, palpitation	Cough, sputum, wheezing
Signs	Oedema, ↑JVP, cardiomegaly, basal creps, tachycardia	Inflated chest, wheezing

^[1]^[2]^[3]

Signs

Sign	Significance	Pathophysiological Basis
Respiratory rate (tachypnoea > 20/min)	Almost universal in significant dyspnoea	Compensatory mechanism to maintain minute ventilation
Use of accessory muscles (SCM, scalenes, abdominals)	Severe dyspnoea / respiratory distress ^[14]	Normal muscles insufficient → recruit accessory muscles to generate greater transpulmonary pressures
Paradoxical breathing (abdominal paradox)	Diaphragmatic fatigue: chest wall and abdominal movements out of phase ^[14]	Fatigued diaphragm gets sucked upward during inspiration by negative intrathoracic pressure → abdomen moves inward (opposite to normal) — sign of impending respiratory arrest
Pursed lip breathing	COPD	Self-generated PEEP → prevents small airway collapse during expiration → ↓air trapping
Tripod position (sitting forward, hands on knees)	Severe dyspnoea (COPD, asthma)	Fixes shoulder girdle → optimises accessory muscle mechanics
Central cyanosis (tongue, lips)	Hypoxaemia ^[14]	≥5 g/dL deoxygenated Hb → bluish discolouration. Note: anaemic patients may not become cyanotic even when profoundly hypoxic (insufficient Hb to produce visible cyanosis)
Peripheral cyanosis (fingers, toes)	↓peripheral perfusion	Slow blood flow → ↑O₂ extraction → ↓SaO₂ in capillaries
Inability to speak in full sentences	Life-threatening airway/breathing compromise ^[8]	Severely ↑work of breathing → must use all respiratory effort for breathing, none left for speech
Cachexia	Chronic disease (cancer, COPD, HF)	Chronic catabolic state
Obesity	OHS, OSA, ↑cardiac risk	↑chest wall load, ↓FRC, metabolic syndrome
Anxiety, agitation	Hypoxia, hyperventilation, PE	Sympathetic activation from hypoxaemia or fear

Sign	Condition	Pathophysiological Basis
Stridor (inspiratory)	Upper airway obstruction	Turbulent flow through narrowed extrathoracic airway
Wheeze (expiratory)	Asthma, COPD, cardiac asthma	Narrowed intrathoracic airways collapse further during expiration
Inflated (barrel) chest	COPD ^[1]^[2]	Chronic air trapping → ↑AP diameter
↓Air entry	Effusion, pneumothorax, consolidation, collapse	Fluid/air/consolidation attenuates or abolishes breath sounds
Bronchial breathing	Consolidation	Solid lung transmits tracheal sounds to periphery
Crackles/crepitations (fine)	Pulmonary oedema, ILD	Fine crackles = reopening of collapsed small airways/alveoli during inspiration (fibrotic or fluid-filled)
Crackles (coarse)	Bronchiectasis, pneumonia	Air bubbling through secretions in large airways
↓Tactile vocal fremitus + stony dull percussion	Pleural effusion	Fluid between lung and chest wall attenuates sound transmission
Hyperresonant percussion + absent breath sounds	Pneumothorax	Air in pleural space → hyperresonance; lung collapses away from chest wall → no breath sounds
Tracheal deviation	Tension pneumothorax (away), collapse (towards)	Tension PTX: ↑pressure pushes mediastinum away. Collapse: loss of volume pulls mediastinum towards

Sign	Condition	Pathophysiological Basis
↑JVP	Right heart failure, cor pulmonale, PE, tamponade ^[1]^[2]	↑RA pressure → back-pressure into jugular veins
Displaced apex beat (laterally)	LV dilatation (dilated cardiomyopathy, chronic MR)	Enlarged LV shifts apex laterally
Heaving apex beat	LVH (HTN, AS)	Sustained powerful impulse from thickened LV wall
Parasternal heave	RV hypertrophy (pulmonary HTN, cor pulmonale)	RV enlarged and hypertrophied, lifts sternum
S3 gallop	LV failure, volume overload	Rapid ventricular filling into a dilated, compliant ventricle
S4	Diastolic dysfunction, LVH	Atrial contraction against stiff ventricle
Murmurs	Valvular disease	Turbulent flow across abnormal valve
Basal crepitations	Left heart failure ^[1]^[2]	Pulmonary oedema — fluid in alveoli at bases (gravity-dependent)
Peripheral oedema	Right/biventricular HF ^[1]^[2]	↑venous pressure → fluid extravasation. Why bilateral and pitting? Because hydrostatic pressure elevation is symmetric and pushes fluid into interstitium
Tachycardia	Compensatory in shock, PE, HF, hypoxia	Sympathetic activation → ↑HR to maintain CO
↓BP, narrow pulse pressure	Cardiogenic shock, tamponade, massive PE	↓CO → ↓SBP; compensatory vasoconstriction → ↑DBP (narrowing pulse pressure)
Pulsus paradoxus (>10 mmHg drop in SBP on inspiration)	Tamponade, severe asthma	Tamponade: inspiration → ↑venous return to RV → RV distends into LV (interventricular septum shifts left) → ↓LV filling → ↓CO on inspiration. Severe asthma: massive negative intrathoracic pressure swings

Sign	Suggests	Pathophysiological Basis
Pallor	Anaemia	↓Hb → pale skin and mucous membranes
Clubbing	ILD, bronchiectasis, lung cancer, cyanotic heart disease, infective endocarditis	Mechanism not fully understood — likely due to platelet clumps/megakaryocytes bypassing pulmonary capillary filter → lodge in distal digits → release PDGF/VEGF → soft tissue hypertrophy
Xanthomas/xanthelasma	Hyperlipidaemia (CAD risk factor)	Lipid deposition in skin/tendons
Stigmata of chronic liver disease + ascites	Cirrhosis → hepatopulmonary syndrome, or ascites causing diaphragmatic splinting ^[16]	Shortness of breath due to pressure on diaphragm from ascites ^[16]
Thyroid signs (goitre, lid lag, tremor, tachycardia)	Thyrotoxicosis	↑metabolic rate → ↑O₂ consumption → ↑ventilatory demand
Calf swelling, warmth, tenderness (unilateral)	DVT → PE risk ^[6]^[7]	Unilateral leg swelling, pain, heat — venous thrombosis → potential source of pulmonary embolism
Homans' sign	DVT (unreliable) ^[7]	Calf pain on passive dorsiflexion of foot — stretches thrombosed vein. Unreliable because sensitivity is only ~50%

Important Examination Findings in Acute SOB

When examining a patient with acute SOB ^[8], look specifically for:

Stridor → upper airway obstruction (potentially life-threatening)
Unilateral absent breath sounds → pneumothorax or massive effusion
Tracheal deviation → tension pneumothorax (emergency)
Wheeze → bronchospasm (asthma or COPD)
Basal crepitations + ↑JVP + peripheral oedema → heart failure
Unilateral leg swelling → DVT → PE
Urticarial rash + angioedema + wheeze → anaphylaxis

Always do a rapid ABCDE assessment before a detailed examination.

Specific Pathophysiology Deep-Dives

Respiratory failure = failure of the lungs to meet the metabolic demands of the body ^[14].

Type 1 RF (hypoxaemic):

Causes: V/Q mismatch (COPD, asthma, PE), shunting (pneumonia, ARDS, pulmonary oedema), diffusion impairment (ILD)
Why is CO₂ normal/low? Because CO₂ is much more diffusible than O₂ (20× more), so even with significant lung disease, CO₂ can be eliminated as long as the patient can increase ventilation. The ↓PaO₂ drives ↑ventilation → CO₂ is actually washed out → normal or low PaCO₂.

Type 2 RF (hypercapnic):

Causes: ↓respiratory drive (sedatives, brainstem lesion), neuromuscular failure (GBS, MG, spinal cord injury), thoracic cage disorder (kyphoscoliosis, flail chest, OHS), decompensated airway disease (severe COPD, severe asthma)
Why is CO₂ high? Because the patient cannot increase minute ventilation adequately — either the drive is reduced, the pump is failing, or the load is overwhelming.

Clinical features ^[14]:

General (T1 + T2RF)	Hypercapnia (T2RF only)
↑respiratory effort: tachypnoea, use of accessory respiratory muscles	CO₂ retention: headache (from vasodilation), altered mentation, flushing, papilloedema, HTN, flapping tremor
Diaphragmatic fatigue: paradoxical breathing of abdomen	Acidosis: air hunger, Kussmaul breathing, gasping
↑SN discharge: ↑HR, ↑BP, sweating, agitation
Hypoxaemia: central cyanosis, confusion

Why does CO₂ retention cause headache?

CO₂ is a potent cerebral vasodilator. ↑PaCO₂ → ↑cerebral blood flow → ↑intracranial pressure → headache. This is also why patients with hypercapnia can develop papilloedema (↑ICP pushes on the optic nerve sheath) and flushing (peripheral vasodilation).

Carboxyhaemoglobin (COHb): Hb bound to CO → pinkish appearance → ↓O₂ carrying capacity + left-shifts the curve (remaining Hb holds onto O₂ more tightly → ↓tissue O₂ release)
- Sources: fire, suicide (burning charcoal, vehicular exhaust) — very relevant in HK where charcoal burning is a common suicide method
- Treatment: supplemental O₂ (speeds up CO dissociation; half-life of COHb in room air = 4–5 hours, in 100% O₂ = 50–60 min, hyperbaric O₂ = 22–23 min)
Methaemoglobin (MetHb): Hb with oxidised Fe³⁺ → brownish appearance → cannot bind O₂
- Acquired causes: oxidising agents (nitrates, nitrites, aniline dye) or drugs (dapsone, benzocaine, lidocaine, chloroquine, primaquine, sulphonamides)
- Treatment: supplementary O₂ + IV 1% methylene blue (methylene blue acts as electron carrier → reduces Fe³⁺ back to Fe²⁺ via NADPH-dependent pathway)

High Yield Summary

Dyspnoea = unexpected awareness of breathing due to mismatch between ventilatory demand and capacity
Mechanism: sensation of ↑effort by respiratory muscles when ventilatory rate is insufficient to meet physiological drive; driven by chemoreceptors (hypoxia, hypercapnia, acidosis) and mechanoreceptors (J-receptors, stretch receptors)
Cardiac vs. Respiratory dyspnoea: Key discriminators are PND (cardiac), orthopnoea (cardiac > respiratory), associated symptoms (angina/palpitation vs. cough/sputum/wheeze), signs (↑JVP/oedema/basal creps vs. inflated chest/wheeze)
Acute causes: Upper airway obstruction, asthma, AECOPD, ADHF, pneumonia, PE, pneumothorax, ARDS, tamponade, metabolic acidosis, anaphylaxis
Chronic causes: COPD, chronic HF, ILD, chronic asthma, pulmonary HTN, anaemia, obesity/OHS, neuromuscular disease, deconditioning
Respiratory failure: Type 1 (hypoxaemic, normal/low CO₂) vs. Type 2 (hypoxaemic + hypercapnic). CO₂ is easier to eliminate than O₂, so T2RF means the ventilatory pump is truly failing
Inability to speak = life-threatening — immediate ABCDE approach
Paradoxical breathing = impending respiratory arrest — diaphragmatic fatigue
PE: patients die from RV failure (cardiogenic shock) rather than hypoxaemia
CO poisoning: particularly relevant in HK (charcoal burning suicide); cherry-pink skin, treat with high-flow O₂
Always ABCDE first in acute dyspnoea, then systematic history and examination to differentiate cardiac vs. respiratory vs. other causes

Active Recall - Shortness of Breath (Definition, Epidemiology, Etiology, Pathophysiology, Classification, Clinical Features)

Differential Diagnosis of Shortness of Breath

The differential diagnosis of dyspnoea is one of the broadest in medicine — because breathing depends on so many systems working in concert (airways, lungs, chest wall, respiratory muscles, cardiovascular system, haemoglobin, metabolic milieu, central drive), failure at any level produces the same subjective symptom. Your job as a clinician is to systematically narrow down which system is failing, using the history, examination, and targeted investigations.

The approach below organises differentials by system, then by acuity, then provides a clinical reasoning framework to help you discriminate between them at the bedside.

A. Respiratory Causes

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Acute asthma	Acute	Widespread polyphonic wheeze ^[4], episodic, triggers (allergens, exercise, cold air), diurnal variation, personal/family history of atopy, reversible airflow obstruction	Bronchospasm + mucosal oedema + mucus hypersecretion → ↑airway resistance → ↑work of breathing
Acute exacerbation of COPD	Acute-on-chronic	Increasing cough, SOB, wheeziness ^[5]; chronic smoker ( > 20 pack-years), baseline exertional dyspnoea, barrel chest, pursed-lip breathing, NO clubbing	Acute infection/pollution on top of chronic airflow limitation → further ↑airway resistance + mucus plugging → V/Q mismatch
Chronic asthma	Chronic	Variable symptoms, nocturnal worsening, trigger-related, atopic background	Chronic airway inflammation → bronchial hyper-responsiveness → variable obstruction ^[4]
COPD	Chronic	Small airway disease + emphysema → persistent and often progressive airflow limitation ^[6]; usually smoker > 40y, ↓DLCO in emphysema	Loss of elastic recoil + small airway narrowing → air trapping → hyperinflation → diaphragm flattening → ↓mechanical efficiency → ↑work of breathing
Upper airway obstruction	Acute	Stridor (inspiratory), depressed consciousness, foreign body, infections (epiglottitis, croup), anaphylaxis, angioedema, tumour ^[3]	Physical narrowing of extrathoracic airway → ↑resistance → turbulent flow → ↑work of breathing

D/dx tip — Asthma vs. COPD: Both present with wheeze and dyspnoea. Asthma is episodic with diurnal variation and significant reversibility; COPD is persistent with baseline symptoms in a smoker and incomplete reversibility. They can coexist (asthma-COPD overlap) ^[4]^[6].

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Pneumonia	Acute	Fever, productive cough (purulent sputum), pleuritic chest pain, bronchial breathing, crackles over consolidation, ↑WCC/CRP	Alveolar flooding with inflammatory exudate → shunt (perfused but not ventilated) → hypoxaemia + ↓compliance
ARDS	Acute	Bilateral infiltrates on CXR, PaO₂/FiO₂ ≤ 300, within 1 week of clinical insult, NOT fully explained by cardiac failure	Diffuse alveolar damage → ↑capillary permeability → non-cardiogenic pulmonary oedema → severe shunt + ↓compliance
Interstitial lung disease (ILD)	Chronic	Progressive exertional dyspnoea + dry cough, fine end-inspiratory crackles (Velcro crackles), clubbing, restrictive PFT with ↓DLCO	Fibrosis → ↓compliance → ↑elastic work of breathing + thickened alveolar-capillary membrane → diffusion impairment → exertional hypoxaemia
Lung cancer (CA bronchus)	Subacute-chronic	Smoker, haemoptysis, weight loss, clubbing, Horner syndrome, SVC obstruction, recurrent pneumonia in same lobe	Endobronchial obstruction → atelectasis; lymphangitis carcinomatosa → ↓compliance; pleural effusion → ↓lung volume; phrenic nerve invasion → diaphragm paralysis ^[2]

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Pneumothorax	Acute	Sudden onset, max at onset ^[7]^[8]; pleuritic chest pain, unilateral ↓breath sounds, hyperresonance, tracheal deviation away if tension; tall thin young male (primary spontaneous) or underlying lung disease (secondary)	Air in pleural space → lung collapse → ↓ventilated lung volume → V/Q mismatch. Tension PTX: one-way valve → progressive ↑intrapleural pressure → mediastinal shift → ↓venous return → ↓CO → cardiovascular collapse
Pleural effusion	Subacute-chronic	Stony dull percussion, ↓breath sounds, ↓tactile vocal fremitus; causes include HF (transudate), infection/malignancy (exudate)	Fluid compresses underlying lung → atelectasis → ↓ventilated volume + diaphragm displacement → ↓tidal volume

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Pulmonary embolism (PE)	Acute	Acute onset of pleuritic chest pain, dyspnoea, haemoptysis (occurs late with infarction) if small/medium; collapse/syncope, crushing central chest pain, shock, sudden death if massive ^[9]; sinus tachycardia on ECG with right heart strain pattern (RBBB, S1Q3T3) if massive ^[9]; risk factors (immobilisation, surgery, malignancy, OCP, thrombophilia); unilateral leg swelling suggesting DVT	Thrombus in pulmonary artery → ↑dead space (V/Q = ∞) + release of vasoactive mediators → V/Q mismatch; if massive → acute RV failure → ↓CO → shock. Patients with PE usually die from right heart failure rather than hypoxaemia ^[10]
Pulmonary hypertension	Chronic	Progressive exertional dyspnoea, exertional syncope, loud P2, RV heave, peripheral oedema, TR murmur	↑PAP → ↑RV afterload → RV failure → ↓CO → inadequate tissue O₂ delivery → ↑ventilatory drive

PE is the Great Mimic

PE can present as virtually anything — acute pleuritic chest pain, unexplained tachycardia, syncope, haemoptysis, or even just "not feeling right." It is the quintessential "don't miss" diagnosis. Always ask about risk factors (recent surgery, immobilisation, cancer, OCP, prior VTE, long-haul travel) and look for unilateral leg swelling. A normal CXR with unexplained hypoxia should raise immediate suspicion ^[9]^[10].

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Acute decompensated heart failure (ADHF) / Acute pulmonary oedema	Acute	Orthopnoea, PND, pink frothy sputum, bilateral basal creps, ↑JVP, S3 gallop, peripheral oedema, ↑BNP	LV failure → ↑LVEDP → ↑pulmonary capillary pressure → transudation into alveoli → ↓compliance + shunt + J-receptor stimulation ^[1]^[2]
Acute MI (as precipitant of ADHF or angina equivalent)	Acute	Central crushing chest pain radiating to jaw/arm, diaphoresis, nausea; BUT dyspnoea can be the sole presenting symptom ("angina equivalent") especially in elderly and diabetics	Acute myocardial ischaemia/necrosis → sudden ↓LV function → acute pulmonary congestion
Chronic heart failure	Chronic	Progressive SOBOE, orthopnoea, PND, ankle oedema, displaced apex, hepatomegaly, ↑JVP	Chronic ↑filling pressures → pulmonary venous congestion → ↓lung compliance → ↑work of breathing ^[1]^[2]
Valvular heart disease (esp. MS, AS, MR, AR)	Chronic (acute if decompensated)	Murmurs on auscultation; MS: mid-diastolic rumble, opening snap; AS: ejection systolic murmur radiating to carotids	MS: ↑LA pressure → pulmonary congestion. AS: ↑afterload → LVH → diastolic dysfunction → ↑LVEDP → pulmonary congestion
Hypertrophic cardiomyopathy (HCMP)	Chronic	SOBOE ( > 90%) ± orthopnoea, PND; angina (70-80%); exertional syncope; sudden cardiac death; ejection systolic murmur that ↑with Valsalva ^[11]	Diastolic dysfunction → ↓diastolic filling → ↑LV end-diastolic pressure → ↑pulmonary venous pressure → exertional dyspnoea; LVOT obstruction → ↑afterload → ↑demand + ↓CO; SAM → MR → ↑pulmonary venous pressure ^[11]
Cardiac tamponade	Acute	Beck's triad (hypotension, ↑JVP, muffled heart sounds), pulsus paradoxus, tachycardia	Pericardial fluid compresses cardiac chambers → ↓filling → ↓CO → compensatory ↑HR and ↑RR
Arrhythmia (esp. AF with rapid ventricular response, SVT, VT)	Acute or chronic	Palpitations, irregular pulse (AF), ECG findings	↓Diastolic filling time (fast rate) or loss of atrial kick (AF) → ↓CO → may precipitate HF in susceptible patients
Constrictive pericarditis	Chronic	Kussmaul sign (↑JVP on inspiration), pericardial knock, calcified pericardium on CXR	Thickened, non-compliant pericardium → ↓diastolic filling → ↓CO

Murtagh's Diagnostic Strategies for Chest Pain ^[7]^[8] — this is a high-yield lecture slide framework:

Probability diagnosis: Musculoskeletal (chest wall) incl. costochondritis; Psychogenic; Angina

Serious disorders not to be missed:

Cardiovascular: myocardial infarction/unstable angina, aortic dissection, pulmonary embolism/infarction

Neoplasia: lung cancer, tumours of spinal cord and meninges

Infection: pneumonia/pleuritis, mediastinitis, pericarditis, myocarditis

Pneumothorax

Pitfalls (often missed): Mitral valve prolapse, oesophageal spasm, gastro-oesophageal reflux, biliary colic, peptic ulcer, herpes zoster, fractured rib, spinal dysfunction, precordial catch

Rarities: pancreatitis, Bornholm disease (pleurodynia), cocaine inhalation, hypertrophic cardiomyopathy

Masquerades checklist: Depression, Anaemia, Spinal dysfunction

Is the patient trying to tell me something? Consider functional causes, especially anxiety with hyperventilation, opioid dependency ^[7]^[8]

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Severe anaemia	Usually chronic (acute if GI bleed)	Pallor, tachycardia, flow murmur, fatigue; check Hb; anaemia is an important d/dx in chronic SOB ^[6]	↓Hb → ↓O₂ carrying capacity → ↓O₂ delivery → compensatory ↑CO and ↑ventilation → exertional then resting dyspnoea
CO poisoning	Acute	Cherry-pink/pinkish appearance, headache, confusion, exposure history (fire, charcoal burning — relevant in HK suicide attempts); SpO₂ falsely normal	CO binds Hb with 240× affinity → ↓O₂ carrying capacity + left-shifts O-Hb curve → tissue hypoxia despite normal PaO₂ ^[12]
Methaemoglobinaemia	Acute	Brownish appearance, cyanosis unresponsive to O₂, drug/toxin exposure (dapsone, nitrites, benzocaine); "chocolate-coloured blood"	Fe³⁺ in MetHb cannot bind O₂ → ↓O₂ carrying capacity; also left-shifts curve → impaired O₂ offloading ^[12]

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Diabetic ketoacidosis (DKA)	Acute	Kussmaul's respiration (deep, sighing), fruity breath, polyuria, polydipsia, acute abdomen, dehydration; glucose ≥ 11 mmol/L, pH < 7.3, ketonaemia ^[13]	Acute insulin deficiency → unrestrained lipolysis → ↑↑blood ketones → metabolic acidosis → ↑H⁺ stimulates peripheral chemoreceptors → compensatory hyperventilation
Metabolic acidosis (uraemia, lactic acidosis, salicylate OD)	Acute	Kussmaul breathing, check ABG (↓pH, ↓HCO₃⁻, ↑AG or normal AG), check anion gap	Acidosis → peripheral and central chemoreceptor stimulation → ↑ventilatory drive
Salicylate overdose	Acute	Tinnitus, nausea, confusion; initially respiratory alkalosis then mixed picture	Direct stimulation of medullary respiratory centre → primary respiratory alkalosis; also causes metabolic acidosis from uncoupling of oxidative phosphorylation ^[3]
Thyrotoxicosis	Subacute-chronic	Weight loss, tremor, heat intolerance, palpitations (AF), goitre, thyroid eye disease; compressive symptoms: dyspnoea, dysphagia, dysphonia; high output HF: dyspnoea, effort tolerance ^[14]	↑Metabolic rate → ↑O₂ consumption → ↑ventilatory demand; can precipitate AF → HF → pulmonary congestion
Adrenal crisis	Acute	Circulatory shock out of proportion to illness, severe hypotension, hypoNa, hyperK, hypoglycaemia ^[15]	Severe cardiovascular collapse → ↓tissue perfusion → tissue hypoxia + metabolic acidosis → ↑respiratory drive

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Myasthenia gravis (MG)	Subacute-chronic	Fatigable weakness (worse on repeated use, better with rest), ptosis, diplopia, bulbar symptoms, respiratory muscles → respiratory arrest ^[16]	Autoimmune destruction of nicotinic AChR → ↓neuromuscular transmission → respiratory muscle weakness → ↓tidal volume → ↑RR → respiratory failure
Guillain-Barré syndrome (GBS)	Acute-subacute	Ascending weakness, areflexia, preceding viral illness, rapid progression; monitor FVC	Demyelination of peripheral nerves → respiratory muscle paralysis → ↓vital capacity → Type 2 RF
Motor neuron disease	Chronic	Progressive weakness, fasciculations, upper + lower motor neuron signs, no sensory loss	Anterior horn cell degeneration → diaphragm + intercostal weakness → chronic hypoventilation
Kyphoscoliosis	Chronic	Visible spinal deformity, restrictive PFT	Chest wall deformity → ↓chest expansion → ↑elastic work of breathing
Obesity / Obesity-hypoventilation syndrome (OHS)	Chronic	BMI > 30, daytime hypercapnia (PaCO₂ > 45 mmHg) in absence of other cause	↑Chest wall load + ↓diaphragm excursion + ↓FRC → chronic hypoventilation → hypercapnia ^[17]
Obstructive sleep apnoea (OSA)	Chronic	Loud and habitual snoring, choking and waking up with SOB, daytime sleepiness, morning headache, nocturia ^[18]	Upper airway collapses during inspiration → repetitive apnoeas → arousals → fragmented sleep → daytime somnolence; can present with exertional dyspnoea due to cardiovascular sequelae
Ascites (any cause)	Subacute-chronic	Abdominal distension, shifting dullness; causes include cirrhosis, malignancy, cardiac failure ^[19]	Shortness of breath due to pressure on diaphragm → ↓diaphragmatic excursion → ↓tidal volume ^[19]

Condition	Acuity	Key Discriminating Features	Why It Causes Dyspnoea
Psychogenic hyperventilation	Acute or recurrent	Subjective feeling of 'inability to take a deep breath', frequent sighing/erratic ventilation at rest, digital/perioral paraesthesiae, light-headedness, central chest discomfort, occurs at rest, rarely disturbs sleep ^[2]^[20]	Anxiety → ↑central respiratory drive out of proportion to metabolic demand → respiratory alkalosis → ↓ionised Ca²⁺ → perioral tingling, carpopedal spasm
Panic disorder	Acute (recurrent episodes)	Recurrent unexpected panic attacks a/w palpitations, sweating, trembling, sensations of SOB or smothering, chest pain, dizziness, paraesthesias, fear of dying; ≥1 month of persistent worry about further attacks ^[21]^[22]; diagnosis of exclusion — must rule out organic causes	Catecholamine surge → ↑HR, ↑RR, ↑minute ventilation → sensation of breathlessness despite adequate oxygenation; the somatic symptoms themselves may prompt further anxiety (positive feedback loop)
Somatic symptom disorder / Somatoform disorders	Chronic	≥1 somatic symptom a/w distress/functional impairment; excessive thoughts about symptoms; persistent ≥ 6 months; no adequate physical explanation ^[23]^[24]	No organic pathology — central misprocessing of normal body sensations; heightened interoceptive awareness

Psychogenic Dyspnoea is a Diagnosis of Exclusion

Never diagnose psychogenic hyperventilation or panic disorder as the cause of dyspnoea without first ruling out life-threatening organic causes (PE, pneumothorax, asthma, ACS). Young patients with anxiety can still have PE. The presence of digital/perioral paraesthesiae and sighing at rest that rarely disturbs sleep are useful positive discriminators for psychogenic causes ^[2]^[20], but they must be used alongside negative workup for organic disease. Murtagh reminds us: "Is the patient trying to tell me something? Consider functional causes, especially anxiety with hyperventilation" ^[7] — but only after the dangerous causes are excluded.

Feature	Most likely diagnosis	Why
PND	Cardiac dyspnoea (HF)	Reabsorption of dependent oedema during sleep → ↑preload → pulmonary congestion ^[1]^[2]
Orthopnoea + PND + peripheral oedema	Heart failure	↑Venous return supine → pulmonary congestion ^[1]^[2]
Sudden onset, max at onset + pleuritic pain	Pneumothorax, PE, aortic dissection ^[7]^[8]	Sudden mechanical/vascular event
Wheeze + episodic + atopy	Asthma	Bronchial hyper-responsiveness + variable obstruction ^[4]
Chronic smoker + persistent wheeze	COPD	Fixed airflow obstruction from smoking-related damage ^[6]
Fever + productive cough + crackles	Pneumonia	Infection → alveolar consolidation
Unilateral leg swelling + pleuritic CP	DVT → PE	Venous thromboembolism ^[9]^[10]
Pink frothy sputum	Acute pulmonary oedema	Transudation + capillary rupture
Fine Velcro crackles + clubbing	ILD	Fibrosis → ↓compliance
Kussmaul breathing + fruity breath	DKA	Metabolic acidosis from ketones ^[13]
Cherry-pink skin	CO poisoning	COHb ^[12]
Chocolate-brown blood	Methaemoglobinaemia	Oxidised Hb ^[12]
Fatigable weakness + ptosis	MG	AChR autoantibodies ^[16]
Sighing at rest + perioral tingling	Hyperventilation syndrome	Respiratory alkalosis → ↓ionised Ca²⁺ ^[2]^[20]
Snoring + daytime somnolence + obesity	OSA	Upper airway collapse during sleep ^[18]
Recurrent unexpected panic + fear of dying	Panic disorder	Catecholamine-driven hyperventilation ^[21]^[22]

These are the conditions that must be actively excluded in every patient with acute dyspnoea before considering benign diagnoses:

Condition	Why It Kills	Rapid Bedside Clue
Tension pneumothorax	↑Intrapleural pressure → ↓venous return → cardiovascular collapse	Tracheal deviation + absent breath sounds + hyperresonance + haemodynamic instability
Massive PE	Acute RV failure → obstructive shock	Sudden collapse + ↑JVP + clear lungs + hypotension + tachycardia + unilateral leg swelling
Acute MI (esp. with ADHF)	Acute LV failure → cardiogenic shock / pulmonary oedema	Chest pain + diaphoresis + ECG changes (ST elevation/depression) + ↑troponin
Cardiac tamponade	↓Cardiac filling → obstructive shock	Beck's triad + pulsus paradoxus
Anaphylaxis	Upper airway oedema + bronchospasm + distributive shock	Urticaria + angioedema + wheeze + hypotension + allergen exposure
Severe asthma (near-fatal)	Respiratory muscle fatigue → respiratory arrest	Unable to complete sentences, silent chest (ominous — no airflow to produce wheeze), ↓consciousness ^[5]
Epiglottitis	Complete upper airway obstruction	Drooling, tripod position, muffled voice, stridor, fever

The 'Silent Chest' in Asthma

A wheezy asthmatic who suddenly stops wheezing is NOT getting better — they are getting worse. A "silent chest" means airflow is so severely reduced that there is insufficient flow to generate a wheeze. This is a pre-arrest sign requiring immediate escalation (IV magnesium, ICU, consider intubation) ^[5].

In a patient with known systemic sclerosis presenting with dyspnoea, the differential includes ^[27]:

ILD (most common cause of death in SSc) → restrictive pattern, ↓DLCO, ground-glass opacities progressing to fibrosis (NSIP pattern most common)
Pulmonary arterial hypertension (esp. in limited cutaneous SSc / CREST) → isolated ↓DLCO without restriction
Aspiration pneumonia (from oesophageal dysmotility → GORD → microaspiration)
Cardiac involvement (myocardial fibrosis → HF, pericardial effusion)

High Yield Summary

Organise differentials by system (Respiratory, Cardiac, Haematological, Metabolic, Neuromuscular/Psychogenic) and by acuity (Acute vs. Chronic)
Life-threatening "don't miss" diagnoses: Tension PTX, massive PE, acute MI, tamponade, anaphylaxis, near-fatal asthma, epiglottitis
Cardiac vs. Respiratory: PND + orthopnoea + oedema = cardiac; Wheeze + cough + sputum = respiratory
PE is the great mimic — always consider in acute dyspnoea with risk factors; patients die from RV failure, not hypoxaemia
Silent chest in asthma = pre-arrest sign — ominous loss of wheeze means negligible airflow
Kussmaul breathing = metabolic acidosis — DKA, uraemia, lactic acidosis, salicylate OD
CO poisoning: cherry-pink, SpO₂ falsely normal, treat with O₂; MetHb: chocolate blood, treat with methylene blue
Psychogenic hyperventilation — sighing at rest, perioral tingling, rarely disturbs sleep — but is a diagnosis of exclusion
Murtagh's framework: Probability diagnosis (MSK, psychogenic, angina) → Serious not to miss (MI, dissection, PE, PTX) → Pitfalls (GORD, biliary, MVP) → Masquerades (depression, anaemia, spinal) → Functional causes
Always ABCDE first in acute presentations

Active Recall - Differential Diagnosis of Shortness of Breath

References

^[1] Senior notes: Ryan Ho Cardiology.pdf (p59 — Dyspnoea section) ^[2] Senior notes: Ryan Ho Fundamentals.pdf (p204, p222–223 — Dyspnoea sections) ^[3] Senior notes: Ryan Ho Critical Care.pdf (p6 — Acute SOB and Airway Management) ^[4] Senior notes: Ryan Ho Respiratory.pdf (p95, p98 — Asthma section) ^[5] Senior notes: Ryan Ho Critical Care.pdf (p13 — Management of Selected Lower Airway Emergencies) ^[6] Senior notes: Ryan Ho Respiratory.pdf (p108–110 — COPD section) ^[7] Lecture slides: murtagh merge.pdf (p25 — Chest pain in adults) ^[8] Lecture slides: murtagh merge.pdf (p26 — Chest pain in adults, continued) ^[9] Senior notes: Ryan Ho Haemtology.pdf (p131 — VTE spectrum and clinical features) ^[10] Senior notes: felixlai.md (DVT and PE section) ^[11] Senior notes: Ryan Ho Cardiology.pdf (p167 — Hypertrophic Cardiomyopathy) ^[12] Senior notes: Ryan Ho Chemical Path.pdf (p38 — COHb and MetHb) ^[13] Senior notes: Ryan Ho Endocrine.pdf (p91 — Diabetic Ketoacidosis) ^[14] Senior notes: Ryan Ho Endocrine.pdf (p18 — Thyroid lump approach, compressive symptoms) ^[15] Senior notes: Ryan Ho Endocrine.pdf (p71 — Adrenal insufficiency) ^[16] Senior notes: Ryan Ho Neurology.pdf (p188 — Myasthenia Gravis) ^[17] Senior notes: Ryan Ho Endocrine.pdf (p117 — Complications of Obesity) ^[18] Senior notes: Ryan Ho Psychiatry.pdf (p229 — Sleep Apnoea) ^[19] Senior notes: Ryan Ho GI.pdf (p316 — Ascites) ^[20] Senior notes: Ryan Ho Respiratory.pdf (p20 — Features of psychogenic hyperventilation) ^[21] Senior notes: Ryan Ho Psychiatry.pdf (p178–179 — Panic Disorder) ^[22] Senior notes: Ryan Ho Psychiatry.pdf (p170 — Approach to Anxiety) ^[23] Senior notes: Ryan Ho Psychiatry.pdf (p199, p203 — Somatoform Disorders) ^[24] Senior notes: Ryan Ho Psychiatry.pdf (p173–174 — GAD and somatic features) ^[25] Senior notes: felixlai.md (Differential diagnosis of DVT) ^[26] Senior notes: Ryan Ho Urogenital.pdf (p67 — Anti-GBM disease / Goodpasture syndrome) ^[27] Senior notes: Ryan Ho Rheumatology.pdf (p83 — Systemic Sclerosis)

Tier 1: Bedside Investigations

These are the investigations you order immediately on every dyspnoeic patient. They are fast, cheap, and highly informative.

What it measures: Percentage of oxygenated haemoglobin using infrared/red light absorption through a finger probe
Normal: ≥ 95% on room air (target 88–92% in known COPD with CO₂ retention risk)
Why it matters: Gives you a real-time, non-invasive estimate of oxygenation

Key interpretive pitfalls:

Situation	Problem	Why
CO poisoning	SpO₂ falsely normal	Conventional pulse oximeter cannot distinguish COHb from O₂Hb — both absorb at similar wavelengths. Need co-oximetry via ABG ^[12]
Methaemoglobinaemia	SpO₂ plateaus ~85% regardless of true saturation	MetHb absorbs red and infrared equally → ratio approaches 1 → oximeter reads ~85%
Severe anaemia	SpO₂ may be normal despite inadequate O₂ delivery	SpO₂ reflects proportion of Hb that is oxygenated, not total O₂ content. Patient can be 100% saturated but still profoundly hypoxic if Hb is 4 g/dL
Poor peripheral perfusion	SpO₂ unreliable/unreadable	Vasoconstriction → inadequate pulsatile signal
Dark nail polish	May interfere	Absorbs light at oximeter wavelengths

SpO₂ vs PaO₂ — Know the Difference

SpO₂ measures the percentage of Hb carrying O₂. PaO₂ (from ABG) measures the partial pressure of dissolved O₂ in arterial blood. Because of the sigmoid shape of the O₂-Hb dissociation curve, SpO₂ remains > 90% until PaO₂ drops below ~60 mmHg — then it falls steeply. This means SpO₂ gives you a false sense of security until the patient is already significantly hypoxaemic. Always get an ABG if the clinical picture is concerning.

The single most informative investigation in acute dyspnoea. It tells you about oxygenation, ventilation, and acid-base status simultaneously.

Normal values (room air):

Parameter	Normal	Interpretation
pH	7.35–7.45	Acidosis < 7.35; Alkalosis > 7.45
PaO₂	80–100 mmHg	< 60 mmHg = respiratory failure ^[28]
PaCO₂	35–45 mmHg	> 50 mmHg = Type 2 RF ^[28]
HCO₃⁻	22–26 mmol/L	Metabolic component
Base excess	-2 to +2	Metabolic acid-base balance
Lactate	< 2 mmol/L	↑ in tissue hypoperfusion (shock, sepsis)

Key ABG patterns in dyspnoea:

Pattern	pH	PaO₂	PaCO₂	HCO₃⁻	Likely Diagnosis
Type 1 RF	N/↑	↓ < 60	N/↓	N	PE, pneumonia, asthma (early), ARDS, ILD
Type 2 RF	↓	↓ < 60	↑ > 50	↑ (if chronic)	COPD exacerbation, sedative OD, NMD, OHS
Respiratory alkalosis	↑	N/↑	↓	N	Hyperventilation (psychogenic, early PE, early asthma)
Metabolic acidosis	↓	N/↓	↓ (compensatory)	↓	DKA, lactic acidosis, uraemia, salicylate OD
Mixed	Variable	Variable	Variable	Variable	Severe sepsis, combined pathology

A-a gradient (alveolar-arterial oxygen gradient):

Calculated: A-a = PAO₂ - PaO₂, where PAO₂ = FiO₂(Patm - PH₂O) - PaCO₂/0.8
Normal: < 10–15 mmHg (increases ~3 mmHg per decade of age)
Why it matters: Helps distinguish where the gas exchange problem is:
- Normal A-a gradient + hypoxia → hypoventilation (Type 2 RF from neuromuscular or central cause) — the lung itself is fine, it's just not being ventilated enough
- ↑A-a gradient + hypoxia → parenchymal disease (V/Q mismatch, shunt, diffusion impairment) — the lung itself is abnormal

ABG findings in PE: Type 1 RF (↓PaO₂, N/↓PaCO₂) with ↑A-a gradient; metabolic acidosis if massive PE with obstructive shock ^[28]

Why ECG in dyspnoea? Because cardiac causes are common and many are life-threatening. The ECG is fast, free, and enormously informative.

Finding	Suggests	Pathophysiological Basis
ST elevation/depression	ACS / MI	Transmural (ST elevation) or subendocardial (ST depression) ischaemia → current of injury
New LBBB	Possible acute MI	Ischaemia → conduction system damage
S1Q3T3 pattern	PE (massive) ^[9]	Deep S in lead I, Q wave and inverted T in lead III — reflects acute RV strain rotating the heart clockwise
Right axis deviation, P pulmonale	RV strain (PE, pulmonary HTN) ^[28]	↑RV workload → right axis shift; ↑RA pressure → peaked P waves in lead II
New onset RBBB	PE ^[28]	Acute RV dilatation → stretching of RV conduction system
Inverted T in V1-V4	RV strain ^[28]	RV ischaemia from acute pressure overload
AF / atrial arrhythmias	PE, thyrotoxicosis, HF, MS	AF may be cause (precipitating HF) or consequence (atrial stretch from ↑filling pressures)
Low voltage QRS	Pericardial effusion / tamponade	Fluid around heart attenuates electrical signal
LVH criteria	AS, HTN, HCMP	↑LV mass → ↑voltage on ECG
Sinus tachycardia	Non-specific — present in PE, HF, sepsis, anaemia, anxiety	Sympathetic activation

S1Q3T3 — What Does It Really Mean?

The classic "S1Q3T3" pattern in PE reflects acute right ventricular strain ^[9]^[28]. The acutely dilated RV shifts the electrical axis rightward and posteriorly: deep S in lead I (leftward forces reduced), Q and inverted T in lead III (rightward and inferior forces). However, this pattern is present in < 20% of PE cases and is not specific — it can occur in any cause of acute RV strain. Its absence does NOT rule out PE. The most common ECG finding in PE is simply sinus tachycardia.

CXR is essential in virtually every dyspnoeic patient ^[2]^[28]^[29]. It provides information about the lungs, heart, pleura, mediastinum, and chest wall in a single image.

CXR Finding	Diagnosis Suggested	Why This Appearance
Cardiomegaly (CTR > 50% on PA film)	Heart failure	Dilated ventricles
Upper lobe venous diversion (cephalisation)	LV failure / ↑LA pressure ^[2]^[29]	↑Pulmonary venous pressure → redistribution of blood to upper lobes (normally lower lobes receive more blood due to gravity)
Bilateral perihilar hazy opacification ("bat wing")	Pulmonary oedema	Fluid transudation into alveoli, worse perihilarly
Kerley B lines	Interstitial oedema / lymphangitis	Thickened interlobular septa from fluid (oedema) or tumour (lymphangitis carcinomatosa)
Bilateral pleural effusion	HF, hypoalbuminaemia	Transudative fluid in pleural space
Hyperinflation: flattened diaphragm, elongated heart, ↑lung volume, hyperlucency	COPD / emphysema ^[29]	Air trapping → ↑TLC → pushes diaphragm down, heart appears narrow and elongated
Bullae	Emphysema ^[29]	Destruction of alveolar walls → large air spaces
Consolidation (air bronchograms)	Pneumonia	Alveoli filled with inflammatory exudate; air in bronchi remains visible against opacified lung
Unilateral white-out with mediastinal shift (away)	Massive pleural effusion	Fluid pushes mediastinum contralaterally
Unilateral white-out with mediastinal shift (towards)	Lung collapse / atelectasis	Loss of volume pulls mediastinum ipsilaterally
Absent lung markings + visible lung edge	Pneumothorax	Air in pleural space → lung falls away from chest wall
Peripheral wedge-shaped opacity (Hampton hump)	PE with pulmonary infarction ^[28]	Infarction of peripheral lung tissue → wedge of consolidated, necrotic lung
Focal oligaemia (Westermark sign)	PE ^[28]	Occluded pulmonary artery → ↓blood flow to affected segment → appears hyperlucent
Enlarged pulmonary artery	PE, pulmonary HTN ^[28]	↑pressure in pulmonary trunk
Reticular shadowing (bilateral, basal)	ILD / IPF ^[29]	Fibrosis of lung parenchyma
Widened mediastinum	Aortic dissection, mediastinal mass	Blood/tumour/lymphadenopathy expanding mediastinum
Normal CXR with hypoxia	PE, early pneumonia, asthma, anaemia	No parenchymal pathology visible but V/Q mismatch (PE), bronchospasm (asthma), or ↓Hb (anaemia)

Remember: CXR requires ~200 mL of fluid to be visible as a pleural effusion ^[29]. Small effusions may be missed. Ultrasound is more sensitive.

Tier 2: Blood Investigations

Parameter	Finding	Significance
Haemoglobin	↓ → anaemia	Anaemia is an important d/dx in chronic SOB ^[29] — always check Hb. Even mild anaemia exacerbates dyspnoea in patients with coexisting cardiac or respiratory disease
WCC	↑ → infection, stress response	Pneumonia, sepsis; also ↑ in stress (MI, PE)
Eosinophils	↑ → asthma, parasites, eosinophilic lung disease, allergic reaction	Atopic asthma; ↑eosinophils on CBC supports eosinophilic airway inflammation
Platelets	↑ → reactive thrombocytosis in IDA; ↓ → DIC (sepsis, massive PE)	Context-dependent
MCV	Micro/macro/normocytic → guides anaemia workup	E.g. microcytic → IDA or thalassaemia; macrocytic → B12/folate deficiency

Marker	What It Tells You	Key Cut-offs & Interpretation
Troponin (cTnT/cTnI)	Myocardial injury	Detection of ↑/↓ cardiac biomarker with ≥1 value above 99th URL = MI (when combined with clinical criteria) ^[30]. Also ↑ in PE (prognostic — indicates RV microinfarction), myocarditis, sepsis, renal failure
BNP / NT-proBNP	Ventricular wall stress	BNP > 100 pg/mL or NT-proBNP > 300 pg/mL suggests HF (age-adjusted cut-offs for NT-proBNP: > 450 if < 50y, > 900 if 50-75y, > 1800 if > 75y). Echocardiography if clinical findings suggestive of HF (to look for the cause, as it is diagnosed clinically) ^[2]^[29]. BNP has excellent NPV — a normal BNP effectively rules out HF
CK-MB	Myocardial necrosis (less specific than troponin)	Largely superseded by high-sensitivity troponin

BNP — The Dyspnoea Blood Test

BNP ("Brain" or "B-type" natriuretic peptide — originally discovered in brain tissue, but predominantly secreted by ventricular cardiomyocytes in response to wall stretch) is the single most useful blood test for discriminating cardiac from non-cardiac dyspnoea. A normal BNP/NT-proBNP virtually rules out heart failure as the cause of dyspnoea (NPV > 95%). Elevated BNP points you towards cardiac investigation (echocardiography). However, remember that BNP can be falsely low in obesity (adipocytes clear BNP) and flash pulmonary oedema (not enough time for BNP to rise).

Test	What to Look For	Relevance to Dyspnoea
RFT (U/Cr, electrolytes)	↑U/Cr → AKI (shock-induced) or CKD; electrolyte disturbance ^[3]	Uraemic acidosis → Kussmaul breathing; hyperkalaemia from renal failure can precipitate arrhythmia → HF
LFT	↑ALT/AST → shock liver; cholestatic pattern → RHF ^[3]	Hepatic congestion from RHF → ↑bilirubin, ↑ALP, ↑GGT
Coagulation profile	Baseline for anticoagulation treatment ^[28]	Essential before starting heparin for PE/DVT
Lactate	↑ → tissue hypoperfusion ^[3]	Lactic acidosis in shock of any cause → metabolic acidosis → compensatory hyperventilation
TFT	Hyper/hypothyroidism	Thyrotoxicosis → ↑O₂ demand + AF → HF; hypothyroidism → pericardial effusion, ↓respiratory drive
Blood glucose	Hyper/hypoglycaemia	DKA with Kussmaul breathing
CRP/Procalcitonin	Infection markers	Pneumonia, sepsis; procalcitonin more specific for bacterial infection

Tier 3: Targeted Confirmatory Investigations

These are ordered based on the clinical picture and results of Tier 1 and 2.

Echocardiography if clinical findings suggestive of HF (to look for the cause, as it is diagnosed clinically) ^[2]^[29].

Mode	What It Shows	When to Use
TTE (transthoracic)	LV/RV function (LVEF), wall motion abnormalities, valvular disease, pericardial effusion, chamber dimensions, estimated PAP, diastolic function	First-line cardiac imaging for HF, suspected valvular disease, tamponade; also useful as bedside in unstable PE (RV dilatation, septal bowing, McConnell sign)
TOE (transoesophageal)	Better visualisation of valves, LA appendage (thrombus in AF), aortic dissection	When TTE inadequate or specific pathology suspected

Key echocardiographic findings by diagnosis:

Diagnosis	Key Echo Findings
LV systolic dysfunction	↓LVEF ( < 40%), regional wall motion abnormalities (if ischaemic), dilated LV
Diastolic dysfunction (HFpEF)	Preserved LVEF ( ≥ 50%), abnormal relaxation pattern on Doppler (E/A ratio), ↑E/e' ratio ( > 14), ↑LA volume index
Valvular disease	Stenotic or regurgitant valve with quantification of severity
HCMP	Asymmetric septal hypertrophy, systolic anterior motion (SAM) of mitral valve, LVOT gradient
Tamponade	Pericardial effusion + RV diastolic collapse + RA systolic collapse + respiratory variation
Acute PE (massive)	RV dilatation, RV free wall hypokinesis with apical sparing (McConnell sign), septal bowing into LV, TR with ↑RVSP
Pulmonary HTN	↑estimated PAP ( > 35 mmHg), RV dilatation/hypertrophy, TR

12. Lung Function Tests (Pulmonary Function Tests / PFT)

The cornerstone investigation for chronic dyspnoea of suspected respiratory origin ^[2]^[29].

Parameter	What It Measures	Key Findings
FEV₁	Volume expired in 1st second of forced expiration	↓ in obstructive and restrictive disease
FVC	Total volume of forced expiration	↓ in restrictive disease; may be ↓ in severe obstruction (air trapping)
FEV₁/FVC ratio	Proportion of FVC expired in 1st second	< 70% → obstructive (COPD diagnostic criterion: post-bronchodilator FEV₁/FVC < 70%) ^[29]; ≥ 70% with ↓FVC → restrictive

Pattern	TLC	RV	FRC	Significance
Obstructive	↑	↑ (air trapping)	↑	COPD, emphysema ^[29]
Restrictive	↓	↓	↓	ILD, chest wall disease, NMD

DLCO: ↓ in ILD (a/w ↓lung volumes), emphysema (a/w ↑lung volumes), pulmonary vascular disease (a/w normal lung volumes) ^[2]^[29]

DLCO	Lung Volumes	Likely Diagnosis
↓	↓	ILD (fibrosis thickens alveolar membrane + ↓surface area)
↓	↑	Emphysema (destruction of alveolar-capillary units)
↓	Normal	Pulmonary vascular disease (↓capillary blood volume), early ILD
Normal/↑	Normal	Asthma (unless acute attack), extrapulmonary restriction

When: Suspected ILD, bronchiectasis, atypical infection, lung cancer staging, when CXR is non-diagnostic
Key patterns:

Pattern	Diagnosis	Description
GGO with peripheral reticulonodular changes → patchy basal reticular shadowing → honeycombing	IPF (UIP pattern) ^[29]	Progressive fibrosis, peripheral and basal predominance
GGO predominant	NSIP, HP, organising pneumonia	Less fibrosis, potentially more treatable
Centrilobular nodules + air trapping	Hypersensitivity pneumonitis	Inhaled antigen → granulomatous inflammation
Tram-track sign, signet ring sign	Bronchiectasis	Dilated, thick-walled bronchi

Test	When to Use	Key Interpretive Points
Exercise tolerance test (ETT)	Low-intermediate pre-test probability (15-65%) for CAD; normal baseline ECG; not on anti-ischaemic drugs ^[30]	+ve test = horizontal or downsloping ST depression ≥ 0.1 mV (1 mm) 80 ms after J point during exercise ^[30]; NOT useful if abnormal baseline ECG (LBBB, paced rhythm, WPW, AF, LVH, digoxin) or limited exercise tolerance ^[30]
Coronary CT angiography	Low-intermediate PTP (15-50%); adequate breath holding; HR ≤ 65 bpm; Agatston calcium score < 400; younger individuals; LVH ^[30]	Excellent NPV (99-100%); significant stenosis = ≥ 70% stenosis; NOT for severe obesity, CKD, prior CABG/stenting, asymptomatic screening ^[30]
Stress echocardiography / MRI / PET	When ETT is non-diagnostic or baseline ECG is abnormal	Provoked regional wall motion abnormalities or perfusion defects
Invasive coronary angiography	High-risk features on non-invasive testing, ACS	Gold standard for coronary anatomy; allows simultaneous PCI
Cardiac MRI	Myocarditis, cardiomyopathy characterisation, infiltrative disease	Late gadolinium enhancement patterns distinguish ischaemic vs non-ischaemic cardiomyopathy

Test	Indication	Key Findings
Diagnostic thoracocentesis	ALL effusions except bilateral effusion strongly suggestive of transudative process ^[29]	Light's criteria (exudative if ≥1 positive): pleural:serum protein > 0.5; pleural:serum LDH > 0.6; pleural LDH > 2/3 URL for serum. ↓Glucose + ↓pH ( < 7.30) in empyema, CTD, malignancy, TB. Cytology for malignancy (60% sens with 1 tap, 75% with 2). Microbiology: Gram stain, culture, TB workup ^[29]
Bronchoscopy ± BAL	Suspected endobronchial lesion, infection in immunocompromised, ILD characterisation	Direct visualisation, washings for cytology/microbiology, transbronchial biopsy
Polysomnography	OSA diagnosis	AHI ≥ 5/h + symptoms = OSA syndrome ^[32]
NCS/EMG	Neuromuscular causes of dyspnoea (GBS, MG)	GBS: demyelinating pattern (usually appears after 1 week) ^[33]; MG: decremental response on repetitive nerve stimulation
Anti-AChR / anti-MuSK antibodies	Suspected MG	Confirmatory of autoimmune MG
CO-oximetry (via ABG)	Suspected CO poisoning or methaemoglobinaemia	Directly measures COHb and MetHb levels ^[12]
Serology	Autoimmune/inflammatory causes	ANA, ANCA, anti-GBM (for pulmonary-renal syndromes), RF/anti-CCP

Specific Diagnostic Criteria for Key Conditions Causing Dyspnoea

Heart failure is diagnosed clinically and confirmed with investigations:

Category	LVEF	Key Features
HFrEF (HF with reduced EF)	< 40%	Systolic dysfunction; most drug trial evidence applies here
HFmrEF (HF with mildly reduced EF)	40–49%	Intermediate phenotype
HFpEF (HF with preserved EF)	≥ 50%	Diastolic dysfunction; requires evidence of structural/functional cardiac abnormality (↑E/e', ↑LA volume index, ↑BNP)

Diagnostic requirements: Symptoms/signs of HF + objective evidence of cardiac dysfunction (abnormal echo) + elevated natriuretic peptides (BNP or NT-proBNP)

Diagnostic approach depends on haemodynamic stability and pre-test probability ^[28]:

For haemodynamically unstable patients (sBP < 90 or drop ≥ 40 mmHg): definitive testing is NOT indicated ^[28]:

Obtain presumptive diagnosis by LL venous duplex (for DVT) or TTE (for RV strain or clot-in-transit)
Treat empirically: immediate parenteral anticoagulant + initiate thrombolysis

For stable patients: use Wells score to stratify pre-test probability ^[10]:

Wells Score Item	Points
Clinical symptoms of DVT	3.0
Other diagnosis less likely than PE	3.0
Immobilisation ≥ 3 days or surgery in previous 4 weeks	1.5
Previous DVT/PE	1.5
Tachycardia (HR > 100)	1.5
Hemoptysis	1.0
Malignancy	1.0

Interpretation (simplified/modified Wells): PE likely > 4.0; PE unlikely ≤ 4.0 ^[10]

Type	Definition	ABG
Type 1	↓PaO₂ < 60 mmHg + ↓/normal PaCO₂ ≤ 50 mmHg	↑A-a gradient; respiratory alkalosis or normal pH
Type 2	↓PaO₂ < 60 mmHg + ↑PaCO₂ > 50 mmHg	May be acute (↓pH, normal HCO₃⁻) or chronic (compensated pH, ↑HCO₃⁻)

Suspected Cause	Essential Investigations
Cardiac (HF, ACS)	ECG, troponin, BNP/NT-proBNP, CXR, echocardiography, ± ETT/CT coro
Asthma	Spirometry with bronchodilator reversibility, PEF diary, ± methacholine challenge, CXR to r/o alternatives
COPD	Post-bronchodilator spirometry, CXR, ± HRCT, ± α₁-antitrypsin (if young Caucasian), CBC, ABG
PE	Wells score → D-dimer (if low probability) → CTPA; ECG, ABG, LL duplex, ± V/Q scan (if pregnant/CKD)
Pneumonia	CXR, CBC, CRP, blood cultures, sputum culture, ABG if severe
Pneumothorax	CXR (erect PA), ± CT thorax if uncertain
Pleural effusion	CXR, USS, diagnostic thoracocentesis with Light's criteria, cytology, microbiology
ILD	HRCT, PFT (restrictive + ↓DLCO), serology, ± BAL, ± surgical lung biopsy
Anaemia	CBC, reticulocyte count, iron studies, B12/folate, ± haemolysis screen
Metabolic acidosis	ABG, glucose, U&E, lactate, anion gap, ± salicylate/toxicology levels
Neuromuscular	FVC (serial), NCS/EMG, anti-AChR/MuSK Ab, ± CSF
OSA	Polysomnography (AHI), Epworth Sleepiness Scale
Psychogenic	Diagnosis of exclusion; ABG (respiratory alkalosis), negative organic workup

High Yield Summary

Every dyspnoeic patient gets: SpO₂, ABG (if acute/severe), ECG, CXR — these four tests answer most questions
ABG: Type 1 RF (↓PaO₂, N/↓PaCO₂) = parenchymal problem; Type 2 RF (↓PaO₂, ↑PaCO₂) = pump failure. A-a gradient normal = hypoventilation; A-a gradient elevated = V/Q mismatch/shunt/diffusion
BNP/NT-proBNP: Best blood test to distinguish cardiac from non-cardiac dyspnoea. Normal BNP effectively rules out HF
D-dimer: High NPV in low-risk PE patients. Useless if high clinical probability — go straight to CTPA
Wells score for PE: ≤ 4 → D-dimer → if positive → CTPA. > 4 → CTPA directly. Unstable → bedside echo/duplex → empiric anticoag + thrombolysis
Spirometry: FEV₁/FVC < 70% post-bronchodilator = COPD. > 12% and 200 mL reversibility = asthma
DLCO: ↓ with ↓volumes = ILD; ↓ with ↑volumes = emphysema; ↓ with normal volumes = pulmonary vascular disease
CXR: Normal CXR with hypoxia → think PE, early pneumonia, asthma, anaemia
CTPA vs V/Q scan: CTPA is default; V/Q preferred in pregnancy (lower radiation, no contrast), renal impairment
Light's criteria: Exudative effusion if protein ratio > 0.5, LDH ratio > 0.6, or pleural LDH > 2/3 serum URL
Pulse oximetry is unreliable in CO poisoning, MetHb, severe anaemia, and poor perfusion — always correlate with ABG
IPF diagnosis: Clinical + HRCT (UIP pattern) + exclusion of alternatives ± multidisciplinary discussion ± biopsy

Active Recall - Diagnostic Criteria, Algorithm and Investigations for Dyspnoea

ABCDE Approach

This is your default starting point for any acutely dyspnoeic patient ^[3]^[34].

A — Airway

Emergent airway management ^[5]^[34]:

Visual inspection of airway + suction of debris
Airway manoeuvres: head tilt-chin lift or jaw thrust to open up airway
Ventilation: BVM with reservoir + 15 L/min high-flow O₂ ± airway adjuncts
ETT intubation with rapid-sequence induction (RSI) if fail any of above

Specific upper airway obstruction management ^[5]:

UA inflammatory swelling: nebulised adrenaline in O₂ (5 mL 1:1000), IV dexamethasone 8 mg
Post-op haematoma: consult surgeons → open surgical incision to allow evacuation
Blocked tracheostomy: remove inner tube, deflate cuff, suction → remove tracheostomy tube if failed
If failed intubation and cannot oxygenate → NEEDLE CRICOTHYROTOMY if all else fail ^[5]

Indications for endotracheal intubation ^[34]:

Acute respiratory failure
Inadequate oxygenation
Inadequate ventilation (e.g. status asthmaticus, severe COPD with fatigue)
Airway protection in patients with decreased mental status (GCS < 8)

Contraindications to ETT ^[34]:

Trauma to the upper airway
Total upper airway obstruction (severe laryngeal oedema)
Cervical spine injury (relative — use in-line stabilisation)

ETT vs. Tracheostomy

Feature	ETT	Tracheostomy
Advantages	Easier and quicker insertion; no surgical procedure; no stoma complications	Ease of suctioning; ease of replacement; patient comfort; reduced sedation needs; enhanced mobility, speech and swallowing; reduces work of breathing by decreasing dead space
Disadvantages	Injury to nose/mouth/vocal cords; difficult replacement; patient discomfort; need to be sedated	More invasive; stomal complications

^[34]

B — Breathing: Oxygen Therapy

Principles of oxygen therapy — this is crucial to understand from first principles:

Target SpO₂	Patient Group	Why This Target
94–98%	Most acutely ill patients	Ensures adequate tissue oxygenation
88–92%	COPD with known/suspected CO₂ retention ^[35]	Higher O₂ may suppress hypoxic ventilatory drive → ↑CO₂ retention → ↓consciousness. Also: Haldane effect (O₂ displaces CO₂ from Hb) and release of hypoxic pulmonary vasoconstriction (worsens V/Q matching)
93–95%	Acute asthma ^[36]	Reasonable target; avoid unnecessary hyperoxia

Modes of O₂ delivery (in order of ↑FiO₂):

Device	Flow Rate	Approximate FiO₂	When to Use
Nasal cannulae	1–6 L/min	24–44%	Mild hypoxia, chronic O₂ therapy
Simple face mask	6–10 L/min	40–60%	Moderate hypoxia
Venturi mask	Preset	24–60% (precise)	COPD — allows controlled O₂ delivery
Non-rebreather mask	10–15 L/min	60–90%	Severe hypoxia, CO poisoning
BVM with reservoir	15 L/min	~100%	Pre-oxygenation, peri-arrest
High-flow nasal cannula (HFNC)	Up to 60 L/min	21–100%	Acute hypoxic RF, post-extubation

C — Circulation

IV access (two large-bore cannulae)
Fluid resuscitation if hypovolaemic or distributive shock
Vasopressors if persistent hypotension despite fluids (septic shock, distributive)
Inotropes (e.g. IV dobutamine) if adequate filling pressure for cardiogenic shock ^[37]
Monitor: BP, HR, UO, lactate

D — Disability

GCS, pupils, blood glucose
Treat seizures, hypoglycaemia, opioid overdose (naloxone)

E — Exposure

Full exposure for examination; temperature; look for rashes (anaphylaxis), leg swelling (DVT)

Phase 2: Non-Invasive and Invasive Ventilatory Support

This deserves its own section because it cuts across multiple causes of dyspnoea.

NIV delivers positive pressure ventilation via a mask interface without intubation ^[35].

Mode	Mechanism	Primary Indications
CPAP	Continuous positive airway pressure applied throughout breathing cycle ^[35]	Acute pulmonary oedema (↑intrathoracic pressure → ↓preload → ↓pulmonary congestion) ^[37]; OSA
BiPAP	Higher inspiratory pressure (IPAP) and lower expiratory pressure (EPAP) ^[35]	COPD exacerbation with respiratory acidosis (pCO₂ ≥ 6 kPa, pH ≤ 7.35) ^[35]^[36]; severe dyspnoea with respiratory muscle fatigue; persistent hypoxaemia despite O₂

Why BiPAP works in COPD: The IPAP assists inspiration (↓work of breathing, ↑tidal volume, ↓CO₂), while the EPAP acts like intrinsic PEEP to splint open collapsed small airways during expiration (↓air trapping). This is analogous to the patient's own pursed-lip breathing, but much more effective.

Why CPAP works in pulmonary oedema: Continuous positive pressure → ↑intrathoracic pressure → ↓venous return (↓preload) → ↓pulmonary capillary hydrostatic pressure → ↓pulmonary oedema. Also recruits collapsed alveoli → ↑FRC → ↑oxygenation.

Typical pressure settings ^[35]:

CPAP/EPAP: 8–12 cmH₂O (for pulmonary oedema), 4–5 cmH₂O (for COPD)
IPAP: start at 8–15 cmH₂O and titrate up to 20 cmH₂O in COPD (aim TV ~7 mL/kg and RR ≤ 25/min)

Contraindications to NIV ^[35]:

Respiratory arrest and medical instability
Inability to protect airway and copious secretions
Uncooperative or agitated status and unfitting mask
Recent upper airway or GI surgery

Key precautions ^[35]:

Monitor ABG ≤ 1–2 h after start to determine success
Consider invasive mechanical ventilation if no objective signs of improvement after 1 h
Watch out for gastric distension

Indications ^[35]:

Respiratory failure not adequately treated by other means
Failure to protect the airway (GCS < 8)
Cardiac and/or respiratory arrest
Clinical instability (e.g. severe hypotension)

Laboratory criteria suggesting need ^[35]:

PaO₂ < 7.3 kPa despite O₂ supplement
PaCO₂ > 6.7 kPa with pH < 7.32
Vital capacity < 10 mL/kg; FEV₁ < 10 mL/kg

Modes (simplified) ^[35]:

Mode	Description	Use
Volume-limited (VC)	Guarantees tidal volume	Risk of barotrauma; used when consistent TV needed
Pressure-limited (PC)	↓Risk of barotrauma	Preferred in ARDS, stiff lungs
SIMV	Allows spontaneous breaths between mandatory breaths	Weaning mode
Pressure support (PS)	Patient-triggered, pressure-assisted	Active weaning, spontaneous breathing trial

Phase 3: Cause-Specific Management

Severity grading ^[5]^[36]:

Mild/Moderate	Severe	Life-threatening
Talks in phrases; prefers sitting; calm; ↑RR; no accessory muscles; HR 100-120; SpO₂ 90-95%; PEF > 50%	Talks in words; sits hunched forwards; agitated; RR > 30; accessory muscles; HR > 120; SpO₂ < 90%; PEF ≤ 50% ^[36]	Silent chest; hypotension; PEF < 33%; cyanosis; confusion ^[36]

Management ^[5]^[36]:

High flow O₂ to keep SpO₂ 94–98% (93–95% per GINA)
Repeated 5 mg salbutamol nebulised with O₂ — β₂-agonist → bronchial smooth muscle relaxation. Can give 4–10 puffs every 20 min for the first hour via MDI + spacer (non-inferior to nebuliser)
IV hydrocortisone 100 mg or PO prednisolone 40–50 mg ^[5] (oral is as effective as IV ^[36]) — corticosteroids reduce airway inflammation, ↓oedema, restore β₂-receptor sensitivity. Takes 4–6 hours to work, so must give EARLY
If unresponsive ^[5]:
- Slow IV MgSO₄ 2 g over 20 min — thought to ↓Ca²⁺ influx in airway smooth muscle → bronchodilation. Useful in severe attacks
- Add nebulised ipratropium 0.5 mg — anticholinergic → additive bronchodilation. SAMA with SABA = ↓hospitalisation and ↑PEF/FEV₁ improvement vs. SABA alone in moderate-severe attack ^[36]
Repeated reassessment every 15 min
ABG if SpO₂ < 92% or life-threatening ^[5]
Consider discharge if PEF > 75% 1 h after treatment ^[5]

Features warranting ICU care ^[36]:

Life-threatening features
Deterioration in PEF/FEV₁
Worsening or persistent hypoxia or hypercapnia
Respiratory failure requiring IPPV

Avoid ^[36]: antibiotics (unless strong evidence of infection), aminophylline/theophylline (narrow therapeutic range, poor efficacy), sedatives/cough suppressants, mucolytics

Management depends on primary vs. secondary and size/symptoms (BTS 2010/2023):

Type	Small/Minimal Symptoms	Large/Symptomatic	Tension PTX
Primary spontaneous	Observe 4–6 h + repeat CXR; if stable → discharge with review	Needle aspiration (2nd ICS MCL) → if fails, chest drain (4th-5th ICS mid-axillary line)	Immediate needle decompression (2nd ICS MCL) → chest drain
Secondary spontaneous	Admit + high-flow O₂ + observe; consider aspiration or drain	Chest drain (intercostal tube drainage)	Same as above

Definitive procedure and preventing recurrence ^[39]:

Risk of recurrence: 10–30% at 1–5 y (1st PSP), 50% at 3 y (SSP)
Indications for surgical opinion: 2nd ipsilateral PTX, 1st contralateral PTX, synchronous bilateral PTX, persistent air leak despite 5–7 days drainage, spontaneous haemothorax, specific professions (pilots, divers), pregnancy ^[39]
Surgical treatment: resection of visible bullae/blebs + obliteration of pleural space by pleurectomy or pleurodesis ^[39]
VATS: 5% recurrence but ↓hospital stay and ↓morbidity vs. open (1% recurrence) ^[39]
Stop smoking; avoid diving permanently unless bilateral pleurodesis ^[39]

Chronic HF management follows a disease-modifying + symptom-relief approach:

Disease-modifying pharmacotherapy (for HFrEF — the "four pillars"):

Drug Class	Mechanism	Why It Helps	Key Considerations
ACEi/ARB (or ARNI = sacubitril/valsartan)	↓RAAS activation → ↓afterload, ↓remodelling	↓Mortality, ↓hospitalisation	Monitor K⁺ and creatinine; contraindicated in bilateral RAS, angioedema (ACEi)
β-blockers (bisoprolol, carvedilol, metoprolol succinate)	↓HR → ↑diastolic filling time, ↓myocardial O₂ demand, ↓remodelling	↓Mortality, ↓SCD	Start low, go slow; contraindicated in acute decompensated HF, severe bradycardia
MRA (spironolactone, eplerenone)	↓Aldosterone → ↓Na⁺/H₂O retention, ↓fibrosis	↓Mortality	Risk of hyperkalaemia; monitor K⁺
SGLT2 inhibitors (dapagliflozin, empagliflozin)	Glycosuric natriuresis → ↓preload; also ↓inflammation, ↓fibrosis (mechanisms still being elucidated)	↓Mortality + ↓HF hospitalisation (even in non-diabetics)	Risk of genital mycotic infections, euglycaemic DKA

Symptom relief:

Loop diuretics (frusemide, bumetanide): ↓congestion; titrate to lowest dose that maintains euvolaemia
Digoxin: if symptomatic despite above + AF for rate control; ↓hospitalisation but NOT mortality

Follows a stepwise, individualised approach (GOLD 2024) ^[35]^[36]:

Non-pharmacological ^[36]:

Smoking cessation — the single most effective intervention to slow FEV₁ decline
Pulmonary rehabilitation: exercise training + education → ↑exercise capacity, ↓dyspnoea, ↓hospitalisation
Vaccination: influenza, pneumococcal, COVID-19, RSV, Zoster
Nutritional support for cachexia; psychotherapy and education ^[36]

Pharmacological — stepwise ^[36]:

Step	Dyspnoea-predominant	Exacerbation-predominant
Initial	LABA or LAMA monotherapy	LABA or LAMA → step to LABA/LAMA if eos < 0.3; or ICS/LABA if eos ≥ 0.3
Escalation	LABA/LAMA dual	LABA/LAMA/ICS (triple therapy) if eos ≥ 0.1
Further	Non-pharmacological + investigate alternative causes	Add roflumilast or azithromycin; stop ICS if adverse effects or lack of efficacy

Long-term O₂ therapy (LTOT) — demonstrated to ↓mortality ^[36]:

Indication: start when clinically stable for 3–4 weeks
Continuous ≥ 15 h/d when resting PaO₂ < 7.3 kPa (55 mmHg) or SaO₂ ≤ 88% × 2 over 3 weeks
Or PaO₂ < 8 kPa if cor pulmonale, pulmonary HTN, or polycythaemia ^[36]

Long-term NIV: if severe chronic hypercapnia + history of hospitalisation for acute respiratory failure ^[36]

Surgical options for advanced COPD ^[36]:

Lung volume reduction surgery (LVRS): resection of lung to ↓hyperinflation and improve mechanical efficiency of muscles — for upper-lobe emphysema
Bullectomy: removal of large non-functional bulla
Bronchoscopic interventions: endobronchial valves, thermal ablation, coils
Lung transplantation in very severe COPD

Follows the GINA 2023/2024 stepwise approach ^[36]:

Two treatment tracks:

Track 1 (Preferred): Uses ICS-formoterol as both controller and reliever (maintenance and reliever therapy, MART)

Reliever: as-needed low-dose ICS-formoterol
Advantage: reduces the risk of exacerbations compared with using a SABA reliever, and is a simpler regimen ^[36]

Track 2 (Alternative): Uses SABA as reliever with separate controller

Reliever: as-needed ICS-SABA or as-needed SABA (always with ICS taken whenever SABA is taken)

Step-up approach (simplified):

Step	Track 1	Track 2
1	As-needed low-dose ICS-formoterol	As-needed ICS-SABA or ICS whenever SABA taken
2	Low-dose ICS-formoterol maintenance + prn	Low-dose ICS daily or LTRA
3	Medium-dose ICS-formoterol maintenance + prn	Medium-dose ICS, or add LTRA or HDM SLIT
4	Medium/high-dose ICS-formoterol + add LAMA	Add LAMA or LTRA or HDM SLIT; switch to high-dose ICS
5	Refer for phenotyping ± biologics (anti-IgE, anti-IL5, anti-IL4R)	Add low-dose OCS but consider side effects

Condition	Key Management Points
Pneumonia	Antibiotics (empiric → targeted), O₂, fluid resuscitation, consider NIV/IPPV if RF
Anaemia	Treat underlying cause (iron replacement, B12/folate, EPO for CKD); transfuse if Hb dangerously low or symptomatic (typically < 7 g/dL, or < 8 g/dL in cardiac disease)
CO poisoning	Supplemental O₂ (speeds up CO dissociation; half-life 4–5 h room air → 50–60 min on 100% O₂ → 22–23 min with hyperbaric O₂) ^[12]; consider hyperbaric O₂ if severe (LOC, cardiac ischaemia, pregnancy)
Methaemoglobinaemia	Supplementary O₂ + IV 1% methylene blue ^[12] (acts as electron carrier → reduces Fe³⁺ back to Fe²⁺)
DKA	IV fluids (NS) → IV insulin infusion → K⁺ replacement → monitor glucose/K⁺/pH hourly; treat precipitant
OSA	Nasal CPAP, dental appliance ± surgery ^[40]; weight loss, positional therapy, avoid alcohol/sedatives
ILD/IPF	Antifibrotics (pirfenidone or nintedanib) — slow progression; immunosuppressive therapy NOT useful for IPF ^[41]; lung transplant for end-stage disease ^[35]
Neuromuscular (GBS)	Monitor respiratory function (FVC, ABG); mechanical ventilation if ↑CO₂, ↓O₂, FVC < 15 mL/kg, inefficient cough ^[42]; IV immunoglobulin 0.4 g/kg/d × 5 days OR plasmapheresis ^[42]
Pleural effusion	Treat underlying cause; diagnostic thoracocentesis for ALL effusions ^[29]; therapeutic drainage if symptomatic; pleurodesis for malignant effusion ^[43]
Psychogenic hyperventilation	Reassurance; breathing retraining (diaphragmatic breathing, slow breathing exercises); treat underlying anxiety/panic disorder (CBT, SSRIs) ^[44]

Depends on type of respiratory failure and underlying cause ^[35]:

Type	Treatment Approach
T1RF	Treat underlying cause (e.g. bronchodilators for asthma, thrombolysis for PE); O₂ therapy as palliative treatment to reverse hypoxaemia; CPAP then BiPAP then IPPV if persistent hypoxaemia despite O₂
T2RF	Treat underlying cause (e.g. stop sedatives, relieve airway obstruction); Controlled O₂ therapy (to avoid ↓hypoxic drive in background chronic T2RF); BiPAP then IPPV — some form of ventilatory support generally required to reverse ↑pCO₂

Chronic respiratory failure ^[35]:

Home non-invasive ventilation: early stages → overnight NIV sufficient to restore daytime pCO₂; late stages → extended to daytime NIV
Lung transplantation for end-stage lung disease refractory to maximal medical treatment ^[35]

Indications for lung transplantation ^[35]:

COPD (27%), CF (26%), IPF (17%), α₁-antitrypsin deficiency (6%), pulmonary HTN (5%)
High (> 50%) risk of death ≤ 2 y if not performed
High (> 80%) likelihood of surviving ≥ 90 d post-transplant
High (> 80%) likelihood of 5 y survival with adequate graft function

High Yield Summary

ABCDE first — always stabilise before investigating. Inability to speak = life-threatening
O₂ targets: 94–98% for most; 88–92% for COPD (avoid abolishing hypoxic drive)
ADHF: Sit up + O₂ + IV frusemide + IV nitrate ± morphine. CPAP if persistent hypoxia. Inotropes if cardiogenic shock
Acute asthma: O₂ + nebulised salbutamol + systemic steroids. Escalate to IV MgSO₄ + ipratropium. Avoid aminophylline and sedatives. Silent chest = ICU
AE-COPD: Controlled O₂ + SABA ± SAMA + prednisolone + Abx if purulent sputum. BiPAP if acidotic. Intubate if NIV fails
PE: Anticoagulation for all; thrombolysis for massive (haemodynamically unstable) PE
Tension PTX: Needle decompression → chest drain. Do NOT wait for CXR
NIV modes: CPAP for pulmonary oedema (↓preload); BiPAP for COPD (↓CO₂, ↓work of breathing)
Chronic HF: Four pillars — ACEi/ARNI + β-blocker + MRA + SGLT2i. Loop diuretics for symptom relief only
Chronic COPD: Smoking cessation most important. LABA/LAMA ± ICS. LTOT if PaO₂ < 55 mmHg. NIV if chronic hypercapnia
Chronic asthma (GINA 2024): ICS-formoterol as both controller and reliever is now the preferred track. Never use SABA alone without ICS
Intubation indications: RF despite other measures, GCS < 8, cardiac/respiratory arrest, clinical instability
Lung transplant: End-stage lung disease (COPD, CF, IPF, α₁-AT, pHTN) refractory to maximal therapy

Active Recall - Management of Shortness of Breath

Dyspnoea, regardless of cause, can lead to a common final pathway of deterioration if untreated:

Complication	Mechanism	Why It Matters
Respiratory failure (Type 1 or 2)	Any untreated cause of dyspnoea → progressive gas exchange failure	Hypoxaemia → end-organ damage (brain, heart, kidneys); hypercapnia → CO₂ narcosis → coma
Respiratory arrest	Diaphragmatic fatigue (paradoxical breathing) → complete ventilatory failure	Fatal unless immediately ventilated
Cardiac arrest	Profound hypoxaemia → myocardial ischaemia → arrhythmia → VF/asystole	Most common final cause of death in respiratory emergencies
Hypoxic brain injury	PaO₂ critically low → neuronal death (irreversible after ~4–6 min without O₂)	Permanent cognitive impairment, vegetative state
Multi-organ failure	Prolonged tissue hypoxia → cellular injury across all organs	High mortality once established

B. Complications by Specific Underlying Condition

Complication	Mechanism	Clinical Significance
Cardiogenic shock	Progressive ↓CO → ↓organ perfusion → lactic acidosis	↓systolic function → ↓coronary perfusion → ↓supply → ischaemia; ↓diastolic function → ↑pulmonary congestion → hypoxaemia → ischaemia — a downward spiral ^[45]
Arrhythmias (AF, VT, VF)	Atrial stretch → AF; ventricular remodelling/ischaemia → VT/VF	Leading cause of sudden cardiac death in HF
Pulmonary oedema	↑LV filling pressure → transudation into alveoli	Acute respiratory failure with pink frothy sputum
Renal failure (cardiorenal syndrome)	↓CO → ↓renal perfusion → pre-renal AKI; also ↑venous congestion → ↑renal venous pressure	Worsens fluid overload (can't diurese) → vicious cycle
Hepatic congestion ("cardiac cirrhosis")	↑RA pressure → ↑hepatic venous pressure → centrilobular necrosis	↑Bilirubin, ↑ALP; chronic: fibrosis
Thromboembolic events	Low CO → stasis in dilated chambers → intracardiac thrombus (esp. in AF) → stroke/systemic embolism; also ↑DVT risk from immobility	Stroke prevention with anticoagulation in AF
Cardiac cachexia	Chronic neurohormonal activation (↑TNF-α, ↑IL-6) → catabolic state + anorexia	Poor prognosis marker; involuntary weight loss > 6% over 6–12 months

Complications of MI indicate extensive myocardial damage → poor prognosis (↑likelihood of other complications) ^[45]:

Timing	Complication	Mechanism
Immediate	Arrhythmias (VF, VT, bradyarrhythmias)	Ischaemic myocardium is electrically unstable; acidotic tissue → K⁺ shifts → abnormal automaticity
Early (days)	Pump failure → cardiogenic shock ^[45]	Loss of contractile myocardium
Early	Acute mitral regurgitation	Papillary muscle rupture (usually posteromedial papillary muscle — supplied by single vessel, PDA)
Early (3–5 d)	Ventricular septal rupture	Necrosis of interventricular septum → L-to-R shunt → ↑pulmonary blood flow → acute HF
Early (3–7 d)	Free wall rupture	Necrosis of ventricular wall → haemopericardium → tamponade → sudden death
Early	Pericarditis (fibrinous)	Transmural MI → epicardial inflammation
Late (weeks)	Ventricular aneurysm	Scar tissue formation → paradoxical outward movement → ↓CO, source of thrombus
Late (weeks)	Dressler syndrome	Autoimmune pericarditis (anti-myocardial antibodies) → fever, pleuritic pain, pericardial effusion
Late	Post-infarct angina	Residual stenosis → up to 50% in thrombolysis patients ^[45]

Complication	Mechanism	Clinical Features
Acute RV failure / cardiogenic shock	Massive PE → acute ↑RV afterload → RV dilatation → ↓LV filling → ↓CO	Hypotension, ↑JVP, clear lungs — the primary cause of death in PE
Pulmonary infarction	Distal small-vessel PE → lung tissue necrosis (only occurs in ~10% because bronchial circulation provides collateral supply)	Pleuritic chest pain, haemoptysis, wedge-shaped opacity on CXR (Hampton hump)
Chronic thromboembolic pulmonary hypertension (CTEPH)	Incomplete resolution of thrombus → organised thrombus → chronic ↑PVR → progressive RV failure	Progressive exertional dyspnoea months-years after PE; diagnosis by V/Q scan + right heart catheterisation; treatment: pulmonary endarterectomy
Recurrent VTE	Underlying risk factors persist → new DVT/PE	10–30% recurrence rate at 5 years if anticoagulation stopped; higher if unprovoked
Post-thrombotic syndrome	Chronic venous insufficiency from DVT → valvular damage → venous hypertension ^[46]	Chronic leg swelling, pain, skin changes, ulceration
Death	RV failure, arrhythmia	1–3% case mortality overall; up to 30% if massive PE untreated

Complications of DVT specifically ^[46]:

Pulmonary embolism
Chronic venous insufficiency → leads to pulmonary hypertension
Chronic venous obstruction → leads to pulmonary hypertension

Complications of pneumonia ^[47]:

Complication	Mechanism	Management
Respiratory failure	Extensive alveolar consolidation → shunt → severe hypoxaemia	O₂, NIV, or IPPV
Lung abscess formation	Necrotising infection → cavitation (esp. Klebsiella, S. aureus, anaerobes, aspiration)	Prolonged antibiotics ± percutaneous/surgical drainage
Septicaemia with multi-organ failure	Bacteraemia → systemic inflammatory response → distributive shock → organ dysfunction	Sepsis bundle: fluids, broad-spectrum Abx, vasopressors, source control
Parapneumonic effusion ± empyema thoracis	Inflammatory exudate into pleural space → if infected → empyema	Thoracocentesis → if pus/low pH ( < 7.2)/positive culture → chest drain ± surgical decortication
Electrolyte abnormalities (hypoNa from SIADH)	Lung inflammation → ↑ADH secretion from posterior pituitary → water retention → dilutional hypoNa	Fluid restriction; treat underlying pneumonia
Cardiac complications: acute MI, arrhythmia (esp AF)	Systemic inflammation + hypoxia → myocardial stress → demand ischaemia; atrial inflammation → AF	Standard ACS/AF management

Causes of unresolving pneumonia ^[47]: host factors (COPD, aspiration, immunosuppression), resistant organisms (Pseudomonas, MRSA, Acinetobacter), unusual pathogens (TB, fungi, Nocardia), complicated pneumonia (empyema, abscess), non-infectious mimics (malignancy, organising pneumonia)

Complication	Mechanism	Clinical Features
Acute exacerbations	Viral/bacterial infection + air pollution → ↑airway inflammation → ↑airflow obstruction → acute-on-chronic respiratory failure	↑SOB, ↑cough, ↑sputum; if hospitalised, 5-year mortality ~50%
Cor pulmonale	Chronic hypoxia → hypoxic pulmonary vasoconstriction → ↑PVR → chronic ↑PAP → RV hypertrophy → RV failure	↑JVP, peripheral oedema, hepatomegaly, RV heave, loud P2, TR murmur
Polycythaemia	Chronic hypoxia → ↑EPO → ↑RBC production	↑Hct → hyperviscosity → ↑risk of thrombosis (stroke, DVT/PE)
Respiratory failure (Type 2)	Decompensated hypoventilation → ↑CO₂ + ↓O₂	CO₂ narcosis, flapping tremor, headache, confusion
Pneumothorax	Bullae rupture → air enters pleural space	Especially in emphysema; can be tension
Lung cancer	Shared risk factor (smoking) → 4× ↑risk	Weight loss, haemoptysis, new persistent cough
Depression and anxiety	Chronic breathlessness + functional limitation → psychological distress	↓QoL, ↓adherence, ↑exacerbations
Osteoporosis	Chronic steroid use + systemic inflammation + inactivity + smoking	Vertebral fractures → kyphosis → further ↓chest wall compliance

Complication	Mechanism	Clinical Features
Status asthmaticus (near-fatal asthma)	Severe bronchospasm + mucus plugging → respiratory failure	Silent chest, exhaustion, respiratory arrest
Pneumothorax / pneumomediastinum	Air trapping → alveolar rupture	Sudden pleuritic pain, subcutaneous emphysema
Irreversible airflow obstruction	Chronic airway remodelling (subepithelial fibrosis, smooth muscle hypertrophy) → fixed narrowing	Progressive decline in FEV₁ despite treatment; asthma-COPD overlap
Steroid side effects (chronic/repeated oral steroids)	Iatrogenic Cushing's, osteoporosis, DM, adrenal suppression, cataracts, immunosuppression	Minimise OCS use; emphasise ICS + biologics for severe asthma

Complication	Mechanism
Progressive respiratory failure	Inexorable fibrosis → ↓gas exchange area → ↓DLCO → exertional then resting hypoxaemia
Pulmonary hypertension	Destruction of pulmonary vascular bed + hypoxic vasoconstriction → ↑PVR → RV failure ^[48]
Acute exacerbation of IPF	Rapid, unexplained worsening (diffuse alveolar damage superimposed on UIP) → bilateral GGO on HRCT → high mortality ( > 50%)
Lung cancer	IPF is an independent risk factor (8–14% of IPF patients develop lung cancer)
Infections	Immunosuppressive therapy (if used for non-IPF ILD) → opportunistic infections ^[48]

Complications of obstructive sleep apnoea ^[49]:

Complication	Mechanism
Hypertension	Repetitive arousals → intermittent sympathetic surges → sustained ↑SNS activity → ↑BP; also ↑oxidative stress → endothelial dysfunction
Diabetes mellitus / metabolic syndrome	Intermittent hypoxia → insulin resistance; also shared risk factor (obesity)
Cardiovascular events (MI, stroke, AF)	Chronic intermittent hypoxia + sympathetic activation + endothelial dysfunction → accelerated atherosclerosis; intrathoracic pressure swings → atrial stretch → AF
Motor vehicle accidents	Excessive daytime sleepiness → ↓reaction time → ↑crash risk (2–7× ↑ risk)
Pulmonary hypertension	Chronic nocturnal hypoxia → HPV → ↑PVR → RV strain
Cognitive impairment and mood disturbance	Fragmented sleep → ↓memory, ↓attention; also ↑depression and irritability

Post-operative complications causing dyspnoea are extremely high-yield ^[50]^[51]:

Pulmonary complications ^[50]:

Atelectasis — the commonest cause of post-op fever in the first 24–48 hours. Mechanism: anaesthesia + pain + immobility → ↓deep breathing → small airway collapse → V/Q mismatch → hypoxia
Pneumonia — especially aspiration pneumonia (↓consciousness post-GA) and hospital-acquired pneumonia (immobility, mechanical ventilation)
Bronchospasm — pre-existing asthma/COPD exacerbated by intubation/anaesthetic agents
ARDS — systemic inflammation (sepsis, massive transfusion, aspiration) → diffuse alveolar damage
Acute exacerbation of COPD
Pulmonary embolism — immobility + surgery + hypercoagulability (Virchow's triad all triggered)
Respiratory failure

Cardiac complications ^[50]:

AF — most common post-operative arrhythmia, especially after thoracic/oesophageal surgery (atrial irritation from surgical manipulation + sympathetic surge + electrolyte disturbances)
Myocardial infarction — stress-induced demand ischaemia (Type 2 MI) in patients with underlying CAD

Other post-operative causes of dyspnoea ^[51]:

Post-operative haematoma (after thyroid surgery): usually in paratracheal region below strap muscles → venous obstruction → acute laryngeal oedema → risk of airway compromise; S/S: large, tense, firm immobile neck swelling + SOB; Mx: cut subcuticular stitches and stitches holding strap muscles (evacuate all blood) → call seniors for intubation ^[51]
Bilateral RLN injury (after thyroid surgery): dyspnoea + stridor upon extubation → require immediate re-tube ± tracheostomy ^[51]
Laryngospasm from hypocalcaemia (after total thyroidectomy → hypoPTH): severe hypoCa can lead to laryngospasm requiring emergency intubation/surgical airway ^[51]
Tracheomalacia (after removal of large goitre): floppy tracheal wall collapses on inspiration ^[51]
Chylothorax (after oesophageal surgery): thoracic duct damage → milky pleural effusion → ↓lung volume ^[50]

Post-Thyroidectomy Dyspnoea — DDx

When a patient develops acute dyspnoea after thyroidectomy, consider these causes in order of urgency ^[51]:

Haematoma → neck swelling + hypovolaemic shock + laryngeal oedema → open wound immediately
Bilateral RLN irritation/injury → stridor + airway obstruction → re-intubate ± tracheostomy
Laryngospasm from hypocalcaemia → check calcium → IV calcium gluconate → intubate if needed
Injury to trachea / pneumothorax → CXR → chest drain
Tracheomalacia → floppy trachea → positive pressure ventilation ± tracheostomy

This is a classic exam question. The first step for haematoma is open the wound at the bedside — do NOT wait to go to theatre.

C. Complications of Treatment Modalities

Complication	Mechanism	When to Worry
CO₂ narcosis in COPD	Excessive O₂ → ↓hypoxic drive → hypoventilation → ↑CO₂ → respiratory acidosis → ↓consciousness	Always use controlled O₂ (SpO₂ 88–92%) in known/suspected CO₂ retainers
Oxygen toxicity	Prolonged high FiO₂ ( > 60% for > 24–48 h) → free radical generation → oxidative damage to alveolar epithelium → ARDS-like picture	Minimise FiO₂ to lowest level maintaining target SpO₂
Absorption atelectasis	High FiO₂ → nitrogen washout from alveoli → ↓alveolar splinting → collapse of poorly ventilated alveoli	Especially in alveoli with low V/Q ratios
Retinopathy of prematurity	Excessive O₂ in neonates → abnormal retinal vessel proliferation	Strict O₂ monitoring in NICU

Complications of mechanical ventilation ^[35]:

Complication	Mechanism	Prevention
Ventilator-associated pneumonia (VAP)	Endotracheal tube bypasses upper airway defences → aspiration of oropharyngeal secretions → nosocomial pneumonia	Head-of-bed elevation 30–45°, oral hygiene, subglottic suction, minimise sedation, daily sedation holidays
Barotrauma (pneumothorax, pneumomediastinum, subcutaneous emphysema)	Volume-limited ventilation → ↑alveolar pressure → alveolar rupture ^[35]	Use pressure-limited ventilation; lung-protective strategy (TV 6 mL/kg IBW, plateau pressure < 30 cmH₂O)
Atelectasis	Inadequate PEEP → alveolar collapse; endobronchial intubation → single-lung ventilation	Appropriate PEEP; confirm ETT position (4–6 cm above carina)
Patient-ventilator asynchrony	↑SOB, ↑work of breathing, ↑duration of ventilation; causes: airway-related (ETT malposition, blocked tube), ventilator-related (circuit leak, inadequate humidification), inappropriate settings, underlying disease, complications (VAP, PTX), or anxiety/pain ^[35]	Identify and treat reversible causes; sedation if needed
VILI (ventilator-induced lung injury)	Volutrauma (overdistension), atelectrauma (cyclic opening/closing of alveoli), biotrauma (inflammatory cascade from mechanical stress)	Lung-protective ventilation: low TV, adequate PEEP
Haemodynamic compromise	Positive pressure → ↓venous return → ↓preload → ↓CO	Particularly in hypovolaemic patients; may need fluid bolus
ICU-acquired weakness	Prolonged immobility + corticosteroids + neuromuscular blocking agents → critical illness myopathy/neuropathy	Early mobilisation, minimise NMBAs, daily sedation holidays
Tracheal stenosis (late)	Prolonged ETT cuff pressure → tracheal mucosal ischaemia → fibrosis → stenosis	Monitor cuff pressure ( < 25 cmH₂O); consider tracheostomy if ventilation > 10–14 days

Complication	Mechanism	Management
Major bleeding	Excessive anticoagulation → ↓clotting	For warfarin: vitamin K ± PCC/FFP; for heparin: protamine; for DOACs: specific reversal agents (idarucizumab for dabigatran, andexanet alfa for factor Xa inhibitors)
Heparin-induced thrombocytopenia (HIT)	Anti-PF4/heparin antibodies → platelet activation → paradoxical thrombosis	Stop all heparin immediately; switch to non-heparin anticoagulant (argatroban, fondaparinux)
Warfarin skin necrosis	Protein C (short half-life) depleted before other factors → transient hypercoagulable state → microvascular thrombosis in skin	Bridge with heparin during warfarin initiation

Complication	Risk	Mitigation
Intracranial haemorrhage	~1–3%	Strict adherence to contraindications; lower dose if possible
Major extracranial bleeding	~5–10%	Careful patient selection; avoid in recent surgery, active bleeding
Reperfusion injury	Sudden restoration of flow → inflammatory cascade → transient worsening	Supportive care; usually self-limiting

Drug	Side Effects	Mechanism
Salbutamol (SABA)	Tremor, tachycardia, hypokalaemia, palpitations	β₂ stimulation in skeletal muscle (tremor) and heart (↑HR); β₂-mediated K⁺ shift into cells
Ipratropium (SAMA)	Dry mouth, urinary retention (rare), acute glaucoma (if nebulised into eyes)	Anticholinergic effects
Theophylline	Nausea, vomiting, tachycardia, seizures, arrhythmias	Narrow therapeutic index; phosphodiesterase inhibition

Relevant because many dyspnoea-causing conditions require long-term steroids (asthma, COPD, ILD):

System	Complication	Mechanism
Metabolic	Cushing syndrome, DM, weight gain	↑Gluconeogenesis, insulin resistance, ↑appetite
MSK	Osteoporosis, avascular necrosis, myopathy	↓Osteoblast activity, ↑osteoclast; ↓protein synthesis in muscle
Immune	Immunosuppression → infections (TB reactivation, fungal, PJP)	↓T-cell function, ↓inflammatory response
GI	Peptic ulcer (esp. with NSAIDs)	↓Prostaglandin → ↓mucosal protection
Adrenal	Adrenal suppression → adrenal crisis on abrupt withdrawal	Exogenous steroid → ↓ACTH → adrenal atrophy
Other	Cataracts, glaucoma, skin thinning, easy bruising	Multiple mechanisms

Complication	Mechanism	Prevention/Management
Malposition	Insertion too high/low/deep	Confirm position with CXR; use ultrasound guidance
Infection / empyema	Contamination through drain site	Aseptic technique; prophylactic antibiotics not routinely indicated
Intercostal vessel injury → haemothorax	Insertion above rib → damage to neurovascular bundle running below each rib	Always insert above the upper border of the rib below
Re-expansion pulmonary oedema	Rapid re-expansion with restoration of blood flow into compressed capillaries → capillary damage with leakage; RFs: lung collapse > 3 days, high-volume drainage, early suction use; S/S: cough, SOB, desaturation; Mx: supportive + clamp drain ^[39]
Subcutaneous emphysema	Air leak along drain tract into subcutaneous tissue	Usually self-limiting; ensure drain is functioning
Organ injury (liver, spleen, diaphragm)	Incorrect level of insertion	Safe triangle: bordered by anterior border of latissimus dorsi, lateral border of pectoralis major, line superior to the horizontal level of the nipple, and apex below the axilla

D. Complications of Specific Systemic Conditions Presenting with Dyspnoea

Complications of DKA treatment — these are as important as the disease itself:

Complication	Mechanism	Prevention
Hypokalaemia	Insulin drives K⁺ intracellularly; also ongoing renal K⁺ losses	Always check K⁺ before starting insulin; replace K⁺ when < 5.5 mmol/L; do NOT give insulin if K⁺ < 3.5
Hypoglycaemia	Insulin therapy without adequate glucose monitoring	Monitor glucose hourly; add dextrose when glucose < 14 mmol/L
Cerebral oedema	Rapid correction of hyperosmolality → osmotic shift of water into brain cells	More common in children; avoid too-rapid fluid correction and too-rapid glucose drop
ARDS	Unclear; possibly related to fluid overload or pulmonary inflammation	Careful fluid management
Aspiration pneumonia	↓Consciousness + vomiting → aspiration	NGT if altered consciousness; protect airway

Pancreatic ascites and pleural effusion ^[56]:

Due to disruption of pancreatic duct or ruptured pseudocyst with fistulation into peritoneal/pleural cavity
S/S: abdominal distension, dyspnoea, chest pain
Dx: ↑↑amylase concentration in pleural or ascitic fluid
Mx: octreotide (↓pancreatic secretion), endoscopic stents, surgical fistula correction if fail

High Yield Summary

Dyspnoea → Respiratory failure → Respiratory arrest → Cardiac arrest: this is the common final pathway of all severe dyspnoea if untreated
Heart failure complications: cardiogenic shock (downward spiral of ↓CO → ↓coronary perfusion → more ischaemia), arrhythmias, cardiorenal syndrome, thromboembolic events
MI mechanical complications: papillary muscle rupture (acute MR), VSD, free wall rupture (tamponade) — all present with acute haemodynamic collapse and new SOB
PE complications: acute RV failure (cause of death), pulmonary infarction, CTEPH (chronic complication), post-thrombotic syndrome (DVT complication)
Pneumonia complications: sepsis/MOF, empyema, lung abscess, SIADH with hypoNa, cardiac complications (AF, MI)
COPD complications: cor pulmonale, polycythaemia, pneumothorax (bullae rupture), lung cancer, respiratory failure
Post-thyroidectomy dyspnoea: haematoma → bilateral RLN injury → hypocalcaemic laryngospasm → tracheomalacia — classic exam question
Mechanical ventilation complications: VAP, barotrauma, VILI, haemodynamic compromise, tracheal stenosis, ICU-acquired weakness
O₂ therapy risks: CO₂ narcosis in COPD (too much O₂), oxygen toxicity (prolonged high FiO₂), absorption atelectasis
TACO vs TRALI: TACO = volume overload (↑CVP, pulmonary oedema, responds to diuretics); TRALI = immune-mediated capillary leak (normal CVP, diuretics not helpful)
DKA treatment complications: hypokalaemia (check K⁺ before insulin), hypoglycaemia, cerebral oedema (children)
Re-expansion pulmonary oedema: after rapid re-expansion of collapsed lung; Mx: clamp drain + supportive

Active Recall - Complications of Conditions Causing Shortness of Breath

High Yield Summary

Dyspnoea = unexpected awareness of breathing due to mismatch between ventilatory demand and capacity
Mechanism: sensation of ↑effort by respiratory muscles when ventilatory rate is insufficient to meet physiological drive; driven by chemoreceptors (hypoxia, hypercapnia, acidosis) and mechanoreceptors (J-receptors, stretch receptors)
Cardiac vs. Respiratory dyspnoea: Key discriminators are PND (cardiac), orthopnoea (cardiac > respiratory), associated symptoms (angina/palpitation vs. cough/sputum/wheeze), signs (↑JVP/oedema/basal creps vs. inflated chest/wheeze)
Acute causes: Upper airway obstruction, asthma, AECOPD, ADHF, pneumonia, PE, pneumothorax, ARDS, tamponade, metabolic acidosis, anaphylaxis
Chronic causes: COPD, chronic HF, ILD, chronic asthma, pulmonary HTN, anaemia, obesity/OHS, neuromuscular disease, deconditioning
Respiratory failure: Type 1 (hypoxaemic, normal/low CO₂) vs. Type 2 (hypoxaemic + hypercapnic). CO₂ is easier to eliminate than O₂, so T2RF means the ventilatory pump is truly failing
Inability to speak = life-threatening — immediate ABCDE approach
Paradoxical breathing = impending respiratory arrest — diaphragmatic fatigue
PE: patients die from RV failure (cardiogenic shock) rather than hypoxaemia
CO poisoning: particularly relevant in HK (charcoal burning suicide); cherry-pink skin, treat with high-flow O₂
Always ABCDE first in acute dyspnoea, then systematic history and examination to differentiate cardiac vs. respiratory vs. other causes

High Yield Summary

Organise differentials by system (Respiratory, Cardiac, Haematological, Metabolic, Neuromuscular/Psychogenic) and by acuity (Acute vs. Chronic)
Life-threatening "don't miss" diagnoses: Tension PTX, massive PE, acute MI, tamponade, anaphylaxis, near-fatal asthma, epiglottitis
Cardiac vs. Respiratory: PND + orthopnoea + oedema = cardiac; Wheeze + cough + sputum = respiratory
PE is the great mimic — always consider in acute dyspnoea with risk factors; patients die from RV failure, not hypoxaemia
Silent chest in asthma = pre-arrest sign — ominous loss of wheeze means negligible airflow
Kussmaul breathing = metabolic acidosis — DKA, uraemia, lactic acidosis, salicylate OD
CO poisoning: cherry-pink, SpO₂ falsely normal, treat with O₂; MetHb: chocolate blood, treat with methylene blue
Psychogenic hyperventilation — sighing at rest, perioral tingling, rarely disturbs sleep — but is a diagnosis of exclusion
Murtagh's framework: Probability diagnosis (MSK, psychogenic, angina) → Serious not to miss (MI, dissection, PE, PTX) → Pitfalls (GORD, biliary, MVP) → Masquerades (depression, anaemia, spinal) → Functional causes
Always ABCDE first in acute presentations

High Yield Summary

Every dyspnoeic patient gets: SpO₂, ABG (if acute/severe), ECG, CXR — these four tests answer most questions
ABG: Type 1 RF (↓PaO₂, N/↓PaCO₂) = parenchymal problem; Type 2 RF (↓PaO₂, ↑PaCO₂) = pump failure. A-a gradient normal = hypoventilation; A-a gradient elevated = V/Q mismatch/shunt/diffusion
BNP/NT-proBNP: Best blood test to distinguish cardiac from non-cardiac dyspnoea. Normal BNP effectively rules out HF
D-dimer: High NPV in low-risk PE patients. Useless if high clinical probability — go straight to CTPA
Wells score for PE: ≤ 4 → D-dimer → if positive → CTPA. > 4 → CTPA directly. Unstable → bedside echo/duplex → empiric anticoag + thrombolysis
Spirometry: FEV₁/FVC < 70% post-bronchodilator = COPD. > 12% and 200 mL reversibility = asthma
DLCO: ↓ with ↓volumes = ILD; ↓ with ↑volumes = emphysema; ↓ with normal volumes = pulmonary vascular disease
CXR: Normal CXR with hypoxia → think PE, early pneumonia, asthma, anaemia
CTPA vs V/Q scan: CTPA is default; V/Q preferred in pregnancy (lower radiation, no contrast), renal impairment
Light's criteria: Exudative effusion if protein ratio > 0.5, LDH ratio > 0.6, or pleural LDH > 2/3 serum URL
Pulse oximetry is unreliable in CO poisoning, MetHb, severe anaemia, and poor perfusion — always correlate with ABG
IPF diagnosis: Clinical + HRCT (UIP pattern) + exclusion of alternatives ± multidisciplinary discussion ± biopsy

High Yield Summary

ABCDE first — always stabilise before investigating. Inability to speak = life-threatening
O₂ targets: 94–98% for most; 88–92% for COPD (avoid abolishing hypoxic drive)
ADHF: Sit up + O₂ + IV frusemide + IV nitrate ± morphine. CPAP if persistent hypoxia. Inotropes if cardiogenic shock
Acute asthma: O₂ + nebulised salbutamol + systemic steroids. Escalate to IV MgSO₄ + ipratropium. Avoid aminophylline and sedatives. Silent chest = ICU
AE-COPD: Controlled O₂ + SABA ± SAMA + prednisolone + Abx if purulent sputum. BiPAP if acidotic. Intubate if NIV fails
PE: Anticoagulation for all; thrombolysis for massive (haemodynamically unstable) PE
Tension PTX: Needle decompression → chest drain. Do NOT wait for CXR
NIV modes: CPAP for pulmonary oedema (↓preload); BiPAP for COPD (↓CO₂, ↓work of breathing)
Chronic HF: Four pillars — ACEi/ARNI + β-blocker + MRA + SGLT2i. Loop diuretics for symptom relief only
Chronic COPD: Smoking cessation most important. LABA/LAMA ± ICS. LTOT if PaO₂ < 55 mmHg. NIV if chronic hypercapnia
Chronic asthma (GINA 2024): ICS-formoterol as both controller and reliever is now the preferred track. Never use SABA alone without ICS
Intubation indications: RF despite other measures, GCS < 8, cardiac/respiratory arrest, clinical instability
Lung transplant: End-stage lung disease (COPD, CF, IPF, α₁-AT, pHTN) refractory to maximal therapy

High Yield Summary

Dyspnoea → Respiratory failure → Respiratory arrest → Cardiac arrest: this is the common final pathway of all severe dyspnoea if untreated
Heart failure complications: cardiogenic shock (downward spiral of ↓CO → ↓coronary perfusion → more ischaemia), arrhythmias, cardiorenal syndrome, thromboembolic events
MI mechanical complications: papillary muscle rupture (acute MR), VSD, free wall rupture (tamponade) — all present with acute haemodynamic collapse and new SOB
PE complications: acute RV failure (cause of death), pulmonary infarction, CTEPH (chronic complication), post-thrombotic syndrome (DVT complication)
Pneumonia complications: sepsis/MOF, empyema, lung abscess, SIADH with hypoNa, cardiac complications (AF, MI)
COPD complications: cor pulmonale, polycythaemia, pneumothorax (bullae rupture), lung cancer, respiratory failure
Post-thyroidectomy dyspnoea: haematoma → bilateral RLN injury → hypocalcaemic laryngospasm → tracheomalacia — classic exam question
Mechanical ventilation complications: VAP, barotrauma, VILI, haemodynamic compromise, tracheal stenosis, ICU-acquired weakness
O₂ therapy risks: CO₂ narcosis in COPD (too much O₂), oxygen toxicity (prolonged high FiO₂), absorption atelectasis
TACO vs TRALI: TACO = volume overload (↑CVP, pulmonary oedema, responds to diuretics); TRALI = immune-mediated capillary leak (normal CVP, diuretics not helpful)
DKA treatment complications: hypokalaemia (check K⁺ before insulin), hypoglycaemia, cerebral oedema (children)
Re-expansion pulmonary oedema: after rapid re-expansion of collapsed lung; Mx: clamp drain + supportive

Shortness Of Breath

Definition

Neurophysiology of Dyspnoea

Dyspnoea in Cardiac Failure — The Frank-Starling Link

Epidemiology

Risk Factors

Anatomy and Physiology of Breathing

Airways

Lung Parenchyma

Chest Wall and Respiratory Muscles

Pulmonary Vasculature

Gas Exchange

Oxygen Transport

Etiology (Hong Kong Focus)

A. Acute Dyspnoea

Upper Airway Obstruction [8]

Lower Airway / Pulmonary Causes [8]

Cardiac Causes [8]

Neurological Causes [8]

Toxic/Metabolic Causes [8]

Other Acute Causes [8]

B. Chronic Dyspnoea

Cardiac Causes

Respiratory Causes

Other Causes

Classification

By Acuity

By System [1][2][3]

By Mechanism (Pathophysiological)

Respiratory Failure Classification [3][14]

Severity Grading — mMRC Dyspnoea Scale

NYHA Functional Classification (Heart Failure)

Clinical Features

Symptoms

Character and Onset

Relationship to Position

Associated Symptoms

Signs

General Inspection

Respiratory System Signs

Cardiovascular Signs

Other Systemic Signs

Pathophysiological Framework Summary

Specific Pathophysiology Deep-Dives

Pulmonary Embolism (PE) [6][7]

Respiratory Failure [3][14]

CO Poisoning and Methaemoglobinaemia [9]

Active Recall - Shortness of Breath (Definition, Epidemiology, Etiology, Pathophysiology, Classification, Clinical Features)

References

Organising Framework

A. Respiratory Causes

Airway Diseases

Parenchymal/Alveolar Diseases

Pleural Diseases

Pulmonary Vascular Disease

B. Cardiac Causes

C. Haematological / Oxygen-Carrying Capacity

D. Metabolic / Toxic / Endocrine

E. Neuromuscular / Chest Wall / Other

F. Psychogenic / Functional

Differential Diagnosis by DVT/PE Specifically

Clinical Reasoning Flowchart

Key Discriminating Features — Summary Table

"Don't Miss" Diagnoses — The Life-Threatening Differentials

Approach to the Differential — History-Driven Strategy

Goodpasture Syndrome — A Rare but Must-Know Differential

Systemic Sclerosis — Respiratory Differentials

Active Recall - Differential Diagnosis of Shortness of Breath

Diagnostic Approach to Shortness of Breath

Stepwise Diagnostic Algorithm

Tier 1: Bedside Investigations

1. Pulse Oximetry (SpO₂)

2. Arterial Blood Gas (ABG)

3. ECG (12-lead)

4. Chest X-ray (CXR)

Tier 2: Blood Investigations

5. Complete Blood Count (CBC)

6. Cardiac Biomarkers

7. D-dimer

8. Other Tier 2 Blood Tests