Undifferentiated Chest Pain & Dyspnea in the ED
Rule out the six killers at the bedside before anyone calls it reflux
The first ten minutes
Parallel start. Every patient with chest pain gets a 12-lead ECG read within 10 minutes of arrival, plus cardiac monitoring, IV access, pulse oximetry, and blood pressure in both arms. Give oxygen only if SpO₂ is below 90%. Suspected ACS gets 162–325 mg of chewed aspirin unless dissection is suspected. A STEMI activates the catheterization laboratory, with a door-to-balloon goal of 90 minutes or less.
Nondiagnostic first ECG. If symptoms persist, repeat the ECG every 15–30 minutes. ST depression in V1–V3 prompts posterior leads (V7–V9) to seek a posterior MI, and an inferior STEMI prompts right-sided leads for right ventricular infarction.
The six killers. Acute coronary syndrome, aortic dissection, pulmonary embolism, tension pneumothorax, cardiac tamponade, and esophageal rupture must be considered in every patient. Each has a bedside signature.
| Killer | Bedside clue | Key test | First action |
|---|---|---|---|
| ACS | Pressure-like pain, diaphoresis, ECG changes | ECG, serial high-sensitivity troponin | Aspirin; PCI for STEMI |
| Aortic dissection | Tearing pain to the back, arm BP differential, pulse deficit | CT angiography (TEE if unstable) | Rate then BP control; no antithrombotics |
| Pulmonary embolism | Pleuritic pain, tachycardia, hypoxemia, leg swelling | Wells/PERC → D-dimer or CT pulmonary angiography | Anticoagulation; thrombolysis if in shock |
| Tension pneumothorax | Absent breath sounds, hypotension, JVD, tracheal shift | Clinical diagnosis | Needle decompression, then chest tube |
| Tamponade | Beck triad, pulsus paradoxus | Bedside echo | Pericardiocentesis (if from type A dissection: emergency surgery, at most controlled drainage as a bridge) |
| Esophageal rupture | Pain after forceful vomiting, subcutaneous emphysema, Hamman crunch | Water-soluble contrast esophagram or CT | NPO, antibiotics, surgery |
Acute coronary syndrome
Presentation. Pressure-like pain radiating to the arm or jaw, exertional onset, diaphoresis, or vomiting raises the likelihood of ACS. Women, older adults, and diabetics often present with dyspnea, fatigue, nausea, or epigastric discomfort alone. Sharp, positional, or reproducible pain lowers but does not eliminate the probability. STEMI goes to emergent PCI; ST depression or dynamic T-wave changes with a rising troponin mean NSTE-ACS, which needs treatment and admission.
High-sensitivity troponin. Draw it on arrival and repeat at 1–3 hours; MI is ruled in or out by the absolute value and the change (delta). A single very low value can rule out MI when symptoms began at least 3 hours earlier. Troponin marks myocardial injury, not only MI: it also rises in PE (right ventricular strain), myocarditis, sepsis, heart failure, and chronic kidney disease.
| Component | 0 points | 1 point | 2 points |
|---|---|---|---|
| History | Slightly suspicious | Moderately suspicious | Highly suspicious |
| ECG | Normal | Nonspecific repolarization changes | Significant ST deviation |
| Age | <45 | 45–64 | ≥65 |
| Risk factors | None | 1–2 | ≥3 or known atherosclerotic disease |
| Troponin | ≤ normal limit | 1–3× normal limit | >3× normal limit |
Aortic dissection
Recognition. Abrupt, maximal-at-onset tearing pain radiating to the back, usually with hypertension; other risks are Marfan and other connective-tissue diseases, bicuspid aortic valve, cocaine, and pregnancy. Look for a systolic difference above 20 mmHg between arms, a pulse deficit, a new aortic regurgitation murmur, a focal neurologic deficit, and a widened mediastinum. The aortic dissection detection risk score counts high-risk conditions, pain features, and exam findings: a score of 2 or more goes straight to imaging, while 0–1 with a negative D-dimer makes dissection unlikely.
Dissection can extend into the right coronary artery and mimic an inferior STEMI. Check both arm pressures before giving heparin or a thrombolytic; antithrombotics can extend the tear or cause fatal bleeding.
Management. A stable patient gets CT angiography of the chest; an unstable patient or one with renal failure gets bedside transesophageal echo. Lower heart rate first with IV esmolol or labetalol (target below 60), then add a vasodilator such as nitroprusside for a systolic pressure of 100–120 mmHg; starting the vasodilator first causes reflex tachycardia. Type A (ascending) dissection needs emergency surgery; type B is usually treated medically.
Pulmonary embolism
Pretest probability. Estimate with the Wells score or gestalt. If PE is unlikely (Wells ≤4) and gestalt is low, apply PERC; when all eight criteria are met, no testing is needed:
- Age <50, heart rate <100, SpO₂ ≥95%
- No hemoptysis, no estrogen use, no prior VTE
- No unilateral leg swelling, no recent surgery or trauma
D-dimer versus CT. A low-probability patient who fails PERC, or one with Wells ≤4 whose gestalt is not low enough for PERC, gets a D-dimer, age-adjusted after 50 (age × 10 μg/L); a negative result excludes PE. A positive D-dimer, or PE likely (Wells above 4), leads directly to CT pulmonary angiography, because a negative D-dimer cannot safely exclude PE when probability is high.
Special situations. When contrast is contraindicated (severe allergy, renal failure) or in pregnancy with a normal chest radiograph, use a V/Q scan, or start with leg compression ultrasound if DVT symptoms are present, since a clot there justifies treatment. A hypotensive patient too unstable for CT gets bedside echocardiography: a dilated, hypokinetic right ventricle supports massive PE and systemic thrombolysis.
Tension pneumothorax, tamponade, and esophageal rupture
Tension pneumothorax. Respiratory distress, hypotension, absent breath sounds, hyperresonance, JVD, and late tracheal deviation away from the affected side make a clinical diagnosis, often after trauma, central line placement, or positive-pressure ventilation. Decompress with a needle before any imaging, at the 4th–5th intercostal space just anterior to the midaxillary line or the 2nd intercostal space in the midclavicular line, then place a chest tube in the 4th–5th space within the "triangle of safety."
Cardiac tamponade. Beck triad (hypotension, JVD, muffled heart sounds) with pulsus paradoxus (an inspiratory fall in systolic pressure above 10 mmHg, not to be confused with Kussmaul sign, an inspiratory rise in JVP), tachycardia, and ECG low voltage or electrical alternans. Bedside echo shows effusion with right atrial or ventricular diastolic collapse and a plethoric IVC. IV fluids bridge to pericardiocentesis or surgical drainage (tamponade from type A aortic dissection needs emergency surgery; full pericardiocentesis can worsen bleeding, so at most a small controlled drainage as a bridge); diuretics, nitrates, and positive-pressure ventilation reduce preload and can precipitate arrest.
Boerhaave syndrome. Forceful vomiting, often after an alcohol binge, ruptures the full thickness of the distal esophagus, usually the left posterolateral wall. Expect severe retrosternal pain, subcutaneous emphysema, Hamman crunch (a mediastinal crackle with each heartbeat), a left pleural effusion, and pneumomediastinum on the radiograph. Confirm with CT with oral contrast or a water-soluble contrast esophagram; barium can cause mediastinitis, and endoscopy may extend the tear. Treat with NPO status, broad-spectrum antibiotics, and emergent surgical repair.
Point-of-care ultrasound. Focused ultrasound speeds diagnosis in the hypotensive or dyspneic patient: pericardial effusion with chamber collapse (tamponade), a dilated right ventricle with septal flattening (acute PE), diffuse B-lines (pulmonary edema), and absent lung sliding (pneumothorax). Absent sliding alone is nonspecific (mainstem intubation, pleural adhesions, apnea), whereas a lung point, where sliding resumes, confirms pneumothorax.
Dyspnea, cocaine, and disposition
Undifferentiated dyspnea. Add a chest radiograph, BNP, and blood gas to the ECG. BNP below 100 pg/mL makes acute heart failure unlikely; obesity lowers BNP and renal failure raises it. Diffuse B-lines favor pulmonary edema over COPD or asthma, which show normal A-lines, and hypoxemia with a clear chest radiograph should raise suspicion for PE.
Cocaine-associated chest pain. Cocaine causes coronary vasospasm, raises myocardial oxygen demand, and promotes thrombosis, producing MI and dissection. Give benzodiazepines first to calm the sympathetic surge, plus aspirin and nitroglycerin; add a calcium channel blocker or phentolamine for persistent hypertension, and treat STEMI with PCI.
Avoid acute β-blockade after cocaine: unopposed α-adrenergic vasoconstriction can worsen coronary spasm and hypertension.
Disposition. Musculoskeletal pain, GERD, and anxiety are diagnoses of exclusion. Reproducible chest wall tenderness, relief with a GI cocktail, and relief with nitroglycerin do not rule out ACS; nitroglycerin also relaxes esophageal smooth muscle, so esophageal spasm responds too. Low-risk patients (HEART 0–3, nondiagnostic ECG, negative serial troponins) are discharged with outpatient follow-up and any further testing, rather than admitted.