Common Causes of Acute and Acute-on-Chronic Breathlessness
The majority of acute and acute-on-chronic dyspnea cases originate from cardiac and pulmonary pathology, with acute exacerbations often triggered by respiratory infections, cardiac decompensation, pulmonary embolism, or exacerbations of concomitant chronic diseases rather than isolated worsening of the primary respiratory condition. 1
Acute Dyspnea: Primary Causes
Pulmonary Causes
- Acute airway obstruction: Asthma exacerbations cause bronchospasm with characteristic "chest tightness," laryngospasm obstructs the upper airway, and foreign body aspiration creates mechanical obstruction 1
- Pneumonia: Impairs gas exchange through alveolar consolidation, stimulating pulmonary receptors and chemoreceptors 1
- Pulmonary embolism: Stimulates vascular receptors, increases dead space ventilation, and causes acute hypoxemia 1, 2
- Pneumothorax: Causes sudden lung collapse with mechanical receptor stimulation 1
- Acute pulmonary edema: Results from cardiac decompensation with interstitial fluid accumulation activating pulmonary receptors 1, 2
Cardiac Causes
- Acute heart failure/decompensation: Produces pulmonary congestion characterized by "air hunger" and "inability to get a deep breath" due to increased respiratory drive and limited tidal volume 1, 2, 3
- Acute coronary syndrome: Causes ischemia-induced ventricular dysfunction 1
- Arrhythmias: Atrial fibrillation, inappropriate tachycardia, or bradycardia reduce cardiac output and oxygen delivery 1
- Pericardial tamponade: Restricts cardiac filling 1
Metabolic and Hematologic Causes
- Metabolic acidosis: From renal failure or diabetic ketoacidosis, directly stimulates chemoreceptors increasing ventilatory drive 1, 2
- Severe anemia: Reduces oxygen-carrying capacity, triggering compensatory hyperventilation despite normal lung function; transfusion indicated when hemoglobin <4 g/dL or <6 g/dL with heart failure signs 1, 2, 4
Other Acute Causes
- Anxiety/panic attacks: Produce sensations of effort, suffocation, and rapid breathing through central mechanisms 1, 2
- Environmental hypoxia: Altitude or contained spaces with fire stimulate peripheral chemoreceptors 1
Acute-on-Chronic Dyspnea: Exacerbation Triggers
COPD Exacerbations
- Respiratory infections: Viral and bacterial infections are the primary triggers, causing acute inflammation superimposed on chronic airway inflammation 1, 5, 6
- Air pollution exposure: Triggers acute inflammatory response 6
- Dynamic hyperinflation: Worsens with exertion or supine positioning, producing "air hunger" and "inability to breathe deeply" 1, 2
Critical Insight: Extrapulmonary Mechanisms
In patients with COPD and multimorbidity, acute respiratory symptoms may be caused by exacerbations of concomitant chronic diseases rather than primary airway/lung involvement—making the term "COPD exacerbation" potentially misleading. 1, 6
Specific extrapulmonary triggers include:
- Acute heart decompensation: Systemic inflammation from infections triggers cardiac dysfunction in patients with underlying heart disease 1, 6
- Pulmonary embolism: Occurs with increased frequency in COPD patients 1, 6
- Atrial fibrillation: New-onset or rapid ventricular response 1
- Hypertensive crisis: Acute blood pressure elevation 1
Heart Failure Exacerbations
- Volume overload: From dietary indiscretion, medication non-adherence, or renal dysfunction 3
- Ischemic events: Acute coronary syndromes precipitate decompensation 1
- Arrhythmias: Particularly atrial fibrillation with rapid ventricular response 1
Interstitial Lung Disease Progression
- Acute exacerbations: Idiopathic worsening with increased receptor stimulation 1, 2
- Superimposed infections: Pneumonia on fibrotic lung 1
Diagnostic Approach Algorithm
Initial Clinical Assessment
Look specifically for:
- Respiratory signs: Use of accessory muscles, paradoxical thoracoabdominal motion (suggests diaphragm dysfunction), decreased breath sounds, wheezing, pleural friction rub 2
- Cardiac signs: Jugular venous distension, S3 gallop, peripheral edema, pulmonary crackles 2, 3
- Other findings: Clubbing, fever, tachycardia 2
First-Line Investigations
- Chest radiograph: Identifies pulmonary edema, pneumonia, pleural effusion, pneumothorax, cardiomegaly 1, 2, 3
- Electrocardiogram: Detects ischemia, arrhythmias, chamber enlargement 1, 2, 3
- Pulse oximetry: Quantifies hypoxemia 2
- Complete blood count: Identifies anemia, leukocytosis 2
- Basic metabolic panel: Detects acidosis, renal dysfunction 2
- B-natriuretic peptide (BNP): Has diagnostic utility for heart failure in appropriate clinical settings 2
Advanced Testing When Diagnosis Remains Elusive
- Echocardiography: Assesses cardiac function, particularly heart failure with preserved ejection fraction and valvular disease 1, 2
- Chest CT: Excludes pulmonary embolism, identifies interstitial disease 1
- Spirometry: With supine and upright measurements; >20% FVC drop when supine suggests diaphragm paralysis 3
- Cardiopulmonary exercise testing (CPET): Definitive noninvasive tool to differentiate cardiac, pulmonary, vascular, and deconditioning causes 2
Critical Clinical Caveats
Common Pitfalls
- Never dismiss symptoms because spirometry is normal: Dyspnea predicts mortality more strongly than FEV₁ in many conditions 2
- Recognize multimorbidity: In COPD patients, 26% of deaths are cardiovascular, 21% cancer, and only 35% directly attributable to COPD 1
- Consider cardiac causes in "respiratory" patients: Ischemic heart disease is particularly common in COPD, contributing to worsening health status and increased dyspnea 1
- Assess for anemia: Frequently coexists with cardiac dysfunction and aggravates dyspnea severity disproportionately 4
- Linguistic and cultural differences: Patients describe breathlessness differently; focus on quality descriptors like "chest tightness" (bronchospasm) versus "air hunger" (restrictive mechanics/hyperinflation) 1, 2