Dyspnea

Last updated: May 30, 2024

Summary

Dyspnea, or shortness of breath, is a subjective feeling of breathing discomfort. It is a commonly reported symptom in acute care and outpatient settings. Causes of dyspnea include pulmonary (e.g., pneumonia, asthma exacerbation), cardiac (e.g., acute coronary syndrome, congestive heart failure), toxic-metabolic (e.g., metabolic acidosis, medication use), upper airway (e.g., epiglottitis, foreign body aspiration), psychological, and neuromuscular pathologies. On initial presentation, it is important to immediately evaluate the patient for any urgent or life-threatening causes of dyspnea using patient history, physical examination, and diagnostic testing. Once immediately life-threatening causes have been ruled out, a more detailed patient history should be obtained and further testing performed to narrow the differential diagnosis.

See also “Respiratory failure and arrest.”

Initial management

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

Assume that all dyspnea is life-threatening until proven otherwise and perform the following steps concurrently, not sequentially.

Perform an ABCDE survey and place the patient in a position of comfort.
Manage respiratory failure if present, e.g., airway management; , oxygen therapy if SpO₂ < 95%, respiratory support ^[2].
Begin pulse oximetry and cardiac monitoring; establish IV access.
Initiate treatment for life-threatening reversible causes of dyspnea.
Identify and treat the underlying cause.
- Focused history and examination
- Basic diagnostics: initial laboratory studies , CXR, ECG, POCUS
- Advanced diagnostic testing based on initial findings

Prioritize rapid identification and treatment of critical causes of dyspnea over advanced testing to obtain a definitive diagnosis. ^[4]

When evaluating a patient with dyspnea, always consider infection control and the need for PPE and patient isolation.

Red flags in dyspnea

The presence of any of these red flags suggests that dyspnea is the result of a serious pathologic process.

Symptoms
- Dyspnea at rest
- Chest pain
- Diaphoresis
Signs
- Pulmonary: low SpO₂, cyanosis, stridor, signs of increased work of breathing
- Cardiac: hypotension, distant heart sounds, new murmur, pulsus paradoxus
- Neurological: decreased level of consciousness, agitation, focal neurological deficits
Laboratory findings
- Hypoxemia
- Respiratory acidosis

Anticipate rapid clinical deterioration in patients with red flag features.

Immediately life-threatening causes of dyspnea

The severity of symptoms reported by the patient may not correlate with disease severity. Remain vigilant for life-threatening causes of dyspnea. ^[2]

Diagnostics

The diagnostic evaluation of undifferentiated dyspnea aims to first rule out immediately life-threatening causes of dyspnea and then determine the etiology, guided by the pretest probability of the diagnoses under consideration.

Initial evaluation ^[2]^[5]^[6]

Applicable to most patients with undifferentiated dyspnea

Laboratory studies
- ABG
- Troponin
- CBC
- BMP
- D-dimer
- BNP or pro-BNP
- Influenza and COVID-19 testing
Imaging
- CXR
- POCUS ^[6]
Other: ECG

Additional evaluation

Guided by clinical assessment and pretest probability

Laboratory studies
- Respiratory viral panel
- Sputum and blood cultures
- Serum salicylate level
- Thyroid function tests
- Lumbar puncture
Imaging
- Echocardiogram ^[7]
- CTPA or V/Q scan ^[8]^[9]
- CT brain without IV contrast
- CT neck with IV contrast
Other: peak expiratory flow

Pulmonary causes

	Clinical features	Diagnostic findings	Acute management
Pneumonia ^[10]	Fever, chills Cough, dyspnea Hypoxemia Crackles, egophony	Labs: leukocytosis, ↑ ESR/CRP, ↑ procalcitonin Positive sputum culture CXR: consolidation, pleural effusion CT chest with IV contrast: hyperdense consolidation	See “Acute management checklist for pneumonia.”
COPD exacerbation (AECOPD) ^[11]^[12]	Dyspnea, cough, purulent sputum Tachypnea, hypoxemia Diffuse wheezing, decreased breath sounds Increased work of breathing Signs of imminent respiratory arrest: confusion, absent breath sounds, bradycardia	ABG: ↓ pH, ↑ PaCO₂, ↓ PaO₂ (respiratory acidosis) CXR: hyperinflated lungs; signs of pneumonia, pneumothorax, and/or pleural effusion may be present POCUS: A-lines ^[6]	See “Acute management checklist for AECOPD.”
Asthma exacerbation ^[13]	Dyspnea, cough Tachycardia Tachypnea, hypoxemia Diffuse wheezing, decreased or absent breath sounds Signs of increased work of breathing	ABG Moderate disease: ↑ pH, ↓ PaCO₂, ↓ or normal PaO₂ (respiratory alkalosis) Severe disease: ↓ pH, ↑ PaCO₂, ↓ PaO₂ (respiratory acidosis) ^[14] Peak expiratory flow: ↓ compared to predicted or personal best POCUS: A-lines ^[6]	See “Acute management checklist for asthma exacerbation.”
Tension pneumothorax ^[15]^[16]	Severe, sharp chest pain Dyspnea, hypoxemia History of trauma Hyperresonance, decreased breath sounds, tracheal deviation Tachycardia, hypotension	Clinical diagnosis CXR: absent lung markings, tracheal deviation, pneumomediastinum	See “Acute management checklist for tension pneumothorax.”
Spontaneous pneumothorax ^[15]^[17]^[18]	Sudden, sharp unilateral chest pain Acute dyspnea Hypoxemia Hyperresonance, decreased breath sounds on affected side Crepitus History of lung disease or trauma	CXR (in inspiration): increased lucency, displaced lung markings, subcutaneous emphysema POCUS: absent lung sliding, absent seashore sign	See “Acute management checklist for spontaneous pneumothorax.”
Pulmonary embolism ^[19]	Pleuritic chest pain Acute onset dyspnea, hypoxemia Cough, hemoptysis Unilateral leg swelling or history of DVT Hypotension, shock (if massive PE)	Wells criteria for pulmonary embolism Elevated D-dimer ↑ Troponin, BNP ECG: normal sinus rhythm (most common), sinus tachycardia, signs of right ventricular strain CTA chest: pulmonary artery filling defect V/Q scan: perfusion-ventilation mismatch TTE: right ventricle hypokinesis with normal apical movement	See “Acute management checklist for pulmonary embolism.”
Fat embolism ^[20]	Triad of hypoxia, neurological abnormalities, and petechiae Associated with orthopedic trauma, e.g., long bone fractures	Thrombocytopenia Fat droplets in urine or sputum CXR: often normal; may show patchy bilateral infiltrates CT chest: ground-glass opacities, pulmonary consolidation ^[21]	Supportive care in the ICU Management of ARDS
Acute chest syndrome ^[22]^[23]	Chest pain Fever Cough, shortness of breath, wheezing Signs of vaso-occlusive crisis Rib or sternal pain	Clinical diagnosis (see diagnostic criteria for acute chest syndrome) ↓ Hb, leukocytosis CXR: new pulmonary infiltrate	See “Acute management checklist for acute chest syndrome.”
ARDS ^[24]^[25]	Acute hypoxemic respiratory failure (within 1 week of inciting event ) Diffuse, bilateral crackles	ABG: ↓ PaO₂, ↑ A-a gradient, P/F ratio < 300 mm Hg CXR: bilateral patchy diffuse or homogeneous lung infiltrates TTE: normal systolic function	See “Acute management checklist for ARDS.”

Lobar consolidation A-lines on lung ultrasound Illustration of seashore sign on lung ultrasound

Cardiac causes

	Clinical features	Diagnostic findings	Acute management
Acute coronary syndrome ^[26]^[27]	Heavy, dull, pressure/squeezing sensation Substernal pain with radiation to left shoulder Nausea, vomiting Diaphoresis, anxiety Dizziness, lightheadedness, syncope Pain may improve with nitroglycerin.	ECG: nonspecific changes, ST-segment elevation/depression, T-wave inversions, Q waves Increased or normal troponin TTE: hypokinesis, regional wall motion abnormalities	See “Acute management checklist for STEMI” and “Acute management checklist for NSTEMI/UA.”
Cardiac tamponade ^[28]	Tachypnea, dyspnea Tachycardia Pulsus paradoxus Cardiogenic shock Beck triad	ECG: low voltage, electrical alternans CXR: enlarged cardiac silhouette TTE: circumferential fluid layer, collapsible chambers , high EF, dilated IVC Inspiration: Both ventricular and atrial septa move sharply to the left. Expiration: Both ventricular and atrial septa move sharply to the right.	See “Acute management checklist for cardiac tamponade.”
Heart failure exacerbation ^[29]^[30]^[31]^[32]	Chest pressure Cough, dyspnea Hypoxemia Crackles, JVD, peripheral edema Chronic exertional dyspnea and paroxysmal nocturnal dyspnea	Clinical diagnosis Labs: ↑ BNP, ↑ troponin, hyponatremia CXR: diffuse opacities, Kerley B lines TTE: global or focal wall abnormalities, systolic and/or diastolic dysfunction, decreased LVEF POCUS: multiple B-lines ^[6]	See “Acute management checklist for heart failure exacerbation.”
Hypertrophic cardiomyopathy ^[33]^[34]	Signs of heart failure Angina Presyncope or syncope Arrhythmias	ECG signs of LVH TTE: asymmetrically thickened LV wall, LV outflow obstruction	See “Treatment of hypertrophic cardiomyopathy.”
Atrial fibrillation with RVR ^[35]^[36]	Dyspnea Palpitations Dizziness Hypotension, syncope	ECG: irregularly irregular rhythm, absent P waves CXR: pulmonary edema, left atrial enlargement	See “Acute management checklist for atrial fibrillation with RVR.”
Acute mitral regurgitation ^[37]	Tachycardia, hypotension, cardiogenic shock Tachypnea, dyspnea Weakness, dizziness, altered mental state Faint systolic decrescendo murmur	ECG: tachycardia, nonspecific ST-wave and T-wave changes; in some cases, signs of ischemia CXR: pulmonary edema TTE: mitral regurgitation, normal left ventricular size , ejection fraction intact, signs of the underlying pathology (e.g., chordal rupture)	See “Acute management checklist for acute mitral regurgitation.”

Acute inferior ST-segment elevation myocardial infarction (STEMI) Acute anterior ST-elevation myocardial infarction (STEMI) Electrical alternans Illustration of B-lines on lung ultrasound

Upper airway causes

	Clinical features	Diagnostic findings	Acute management
Anaphylaxis ^[2]^[38]^[39]	Hives, angioedema Stridor, wheezing, dyspnea Hypotension Nausea, vomiting, diarrhea	Clinical diagnosis (see “Diagnostic criteria for anaphylaxis”)	See “Acute management checklist for anaphylaxis.”
Angioedema ^[40]^[41]	Swelling of the face, upper airway, body Urticaria, hypotension, and/or bronchospasm	Clinical diagnosis ↑ Serum tryptase (in histamine-mediated forms) ↓ C4 (during hereditary angioedema attacks)	See “Acute management checklist for angioedema.”
Foreign body aspiration ^[42]	Choking, coughing Respiratory distress, cyanosis, altered mental state Wheezing, stridor, absent breath sounds In chronic cases : cough, recurrent pulmonary infections	X-ray chest: radio-opacity in the trachea or bronchi, atelectasis CT chest : direct identification of the foreign body Rigid or flexible bronchoscopy: visualization of the foreign body	See “Acute management checklist for foreign body aspiration.”
Epiglottitis ^[43]^[44]	Odynophagia, pain over larynx on palpation Respiratory distress, hypoxia, toxic appearance Dysphagia, stridor, drooling, muffled voice Absence of hoarseness, cough	↑ WBC, ↑ CRP X-ray of lateral neck soft tissue: thumb sign (i.e., a swollen epiglottis), vallecula sign Endoscopy : edematous, inflamed epiglottis	See “Acute management checklist for epiglottitis.”
Deep neck infection ^[45]	Fever, fatigue Dysphagia, dysphonia, otalgia Unilateral erythema and neck swelling/lymphadenopathy Trismus, drooling, dyspnea, stridor Ludwig angina: bilateral neck swelling, lingual swelling, woody/brawny cellulitis	↑ WBC, ↑ CRP Ultrasound: abscess, lymphadenitis, jugular thrombophlebitis X-ray of the lateral neck: widening of retropharyngeal tissues CT neck with contrast: decreased definition of anatomic spaces, abscess, lymphadenitis, gas collections	See “Acute management checklist for deep neck infection.”

Toxic-metabolic and other causes

	Clinical features	Diagnostic findings	Acute management
Salicylate toxicity ^[46]^[47]	Tachypnea, nausea/vomiting, tinnitus Lethargy, dizziness, restlessness, diaphoresis Severe toxicity: coma, seizures, AKI, pulmonary edema	↑ BUN and creatinine, elevated anion gap ^[47] ABG Early/mild toxicity: respiratory alkalosis Moderate/severe toxicity: mixed primary respiratory alkalosis with primary high anion gap metabolic acidosis ↑ Serum salicylate levels (> 40 mg/dL)	See “Acute management checklist for salicylate toxicity.”
Organophosphate poisoning ^[2]^[48]	Cholinergic crisis Bronchospasm, bronchorrhea Bradycardia and hypotension Weakness, paralysis Diarrhea, vomiting, abdominal pain	↓ Plasma cholinesterase activity level	See “Organophosphates.”
DKA ^[49]^[50]	Polyuria, polydipsia Nausea and vomiting Signs of volume depletion Altered mental status, coma	Hyperglycemia, high anion gap metabolic acidosis, ketonuria/ketonemia	See “Acute management checklist for hyperglycemic crises.”
Carbon monoxide poisoning ^[51]^[52]	Headache, dizziness, confusion, loss of consciousness Nausea, vomiting Shortness of breath, tachypnea Chest pain, tachycardia, hypotension “Cherry red” skin Hypoxia	Clinical diagnosis: history of exposure, typical symptoms, and ↑ COHb CXR: usually normal ABG: ↓ PaO₂, ↑ Serum COHb (nonsmokers > 3–4%, smokers > 10%)	See “Acute management checklist for carbon monoxide toxicity.”
Anemia ^[53]^[54]	Postural hypotension, dizziness, tachycardia Altered mental status Cool and/or clammy skin Pallor, signs of bleeding (e.g., melena) Tachypnea	Normal or ↓ Hb	See “Acute management checklist for anemia.”

Anything that can cause metabolic acidosis (e.g., DKA, lactic acidosis, salicylate toxicity) can also cause acute dyspnea.

Overview of causes of dyspnea by speed of onset

Causes of dyspnea by speed of onset ^[1]^[2]^[55]^[56]^[57]
System	Sudden onset	Acute onset	Chronic onset
Upper airway	Anaphylaxis Angioedema Foreign body aspiration	Epiglottitis Croup Epstein-Barr virus infection Deep neck infection	Head and neck malignancy
Pulmonary	Pulmonary embolism Pneumothorax Pulmonary contusion Hemothorax Fat emboli	Pneumonia Bronchitis COPD exacerbation Asthma exacerbation Acute respiratory distress syndrome Pleural effusion Pleuritis Diffuse alveolar hemorrhage Pneumomediastinum	COPD Restrictive lung disease Lung cancer Pulmonary hypertension
Cardiac	Acute coronary syndrome Papillary muscle rupture Arrhythmias Cardiac tamponade	Congestive heart failure Myocarditis Pericarditis	Coronary artery disease Valvular dysfunction Cardiomyopathy Deconditioning
Gastrointestinal	Gastric aspiration	Acute abdominal infection Intestinal ischemia Abdominal compartment syndrome	Ascites Large hiatal hernia Abdominal obesity Hepatopulmonary syndrome
Musculoskeletal	Rib fractures Flail chest	Diaphragmatic paralysis Pain ^[58]	Severe kyphosis Muscular dystrophy
Neurological	Spinal cord injury Stroke	Myasthenic crisis Guillain-Barré syndrome Multiple sclerosis	Amyotrophic lateral sclerosis
Toxic/metabolic	Salicylate poisoning Carbon monoxide poisoning Organophosphate poisoning	Metabolic acidosis Diabetic ketoacidosis	Thyrotoxicosis
Psychogenic	Panic attack		Anxiety Somatization
Hematologic	Acute chest syndrome		Anemia
Obstetric	Amniotic fluid embolism	N/A	Pregnancy
Renal	Hemodialysis ^[59]	Acute renal failure Electrolyte abnormalities	Chronic renal disease

Cardiopulmonary disease may be mistaken for panic attacks, as symptoms and pathogenesis overlap. Consider organic causes before attributing dyspnea to anxiety. ^[2]^[60]

Differential diagnoses of dyspnea

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