Urgent considerations

See Differentials for more details

Acute chest pain warrants rapid clinical assessment, as underlying disease can be life-threatening.[13] Continuous monitoring of pulse, blood pressure, and oxygen saturation is standard care. Use a C-A-B (circulation, airway, breathing) approach to systematically assess and treat the patient. Treat life-threatening problems before moving onto the next part of the assessment.[14][15][16]​​​​​

Recommendations regarding supplemental oxygen and target ranges may vary depending on each guideline and/or disorder. One systematic review and meta-analysis found that the liberal use of oxygen was associated with increased mortality in acutely ill patients when compared with a conservative oxygen strategy.[17][18]

Supplemental oxygen has not been proven to be helpful and may be harmful in patients with acute coronary syndrome (ACS) who have normal oxygen saturations.​[19][20]​ Guidelines recommend that oxygen should not be routinely administered in normoxic patients with suspected or confirmed ACS.[20]​​[21]​​[22]

European guidelines do not recommend oxygen routinely if the oxygen saturation is ≥90% for patients with presumed ACS.[23] British Thoracic Society guidelines recommend a target oxygen saturation of 94% to 98% for most acutely ill patients, or 88% to 92% (or a patient-specific target range) for those at risk of hypercapnic respiratory failure.[24]

Opiates (e.g., morphine) may be necessary to relieve severe pain.

Immediate investigations include a 12-lead ECG, chest x-ray, cardiac biomarkers, complete blood count, and renal profile.[20][23][25]​​​​​ The patient may need to be transferred to an intensive care setting. Once the patient is stable, further tests such as computed tomography, echocardiography or angiography should be requested to confirm the diagnosis. 

Acute coronary syndrome

ACS refers to acute myocardial ischemia caused by atherosclerotic coronary disease and includes ST-elevation myocardial infarction (STEMI), non-STEMI, and unstable angina.[26] These terms are used as a framework for guiding management.

Patients with STEMI need to be urgently assessed, as they may have life-threatening arrhythmias, cardiogenic shock, or pulmonary edema. STEMI typically presents with a severe central chest pressure radiating to the jaw or upper extremities. There can be associated nausea and vomiting. The treatment is anticoagulation and acute reperfusion therapy with angioplasty (if available within 2 hours) or thrombolytics (if no contraindications and angioplasty not available).[20][22]​​[23]​​​[26]​​[27][28]

Spontaneous coronary artery dissection (SCAD)

An unusual, but important cause of ACS. SCAD is defined as a separation of the layers of an epicardial coronary artery wall by intramural hemorrhage, with or without an intimal tear, and usually presents with chest pain that often radiates to the arms, shoulders or back.[29]​ It is not associated with trauma, iatrogenic injury, or atherosclerosis. Approximately 90% of patients with SCAD are women ages 47 to 53 years.[29]​ SCAD causes approximately 15% to 20% of myocardial infarctions during pregnancy and the peripartum period.[29][30][31]

Patients with SCAD most often present with STEMI or NSTEMI, with only a minority presenting with ventricular dysrhythmias.[29][32]​​ Diagnosis of SCAD is made by coronary angiography. SCAD is generally managed medically. Due to the pathophysiology, patients with SCAD treated with percutaneous coronary intervention (PCI) may have worse outcomes.[32]​ Thrombolytic use is not recommended and anticoagulation should generally be discontinued once SCAD is diagnosed. Patients with SCAD should receive dual antiplatelet therapy acutely and for a year afterwards.[29][33]​ Beta-blockers appear to be the most useful in both treatment and prevention of recurrence of SCAD.[29][34][35]

Aortic dissection

Aortic dissection typically presents with sudden, severe pain described as a tearing sensation radiating to the mid-back. A chest x-ray may show a widened mediastinum. Computed tomography chest scan with intravenous contrast or transesophageal echocardiogram confirms the diagnosis.

Patients should immediately receive intravenous beta-blockade for heart rate and blood pressure control.[36]​ Additional titratable vasodilators may be required.[36]

Definitive management depends on the type of aortic dissection and includes urgent surgical replacement or ongoing medical therapy. Uncomplicated dissections involving the ascending aorta (Stanford A) are generally managed surgically and necessitate urgent surgical consultation. Uncomplicated dissections involving solely the descending aorta (Stanford B) are generally managed medically. Complicated Stanford B dissections may be managed endovascularly.[13][37]

Tension pneumothorax

Tension pneumothorax occurs when there is a disruption of the tissues of the lung or pleura causing a one-way valve that lets air enter, but not exit, the pleural space. In severe cases, the tension pneumothorax causes mediastinal shift with compression of the great vessels, reducing blood flow to the heart, leading to shock. Tension pneumothorax may begin as acute, sharp, pleuritic pain. Needle decompression followed by tube thoracostomy should be done immediately to prevent acute decompensation.

Needle decompression of tension pneumothorax: animated demonstration
Needle decompression of tension pneumothorax: animated demonstration

How to decompress a tension pneumothorax. Demonstrates insertion of a large-bore intravenous catheter into the fourth intercostal space in an adult.

Pulmonary embolism

Pulmonary embolism (PE) typically presents with pleuritic chest pain, dyspnea, and tachycardia. Hemoptysis occurs less commonly. Patients who have a high-risk (hemodynamically unstable) PE will have features of hypotension, shock, or tachycardia, and can be hypoxemic at rest. Computed tomographic pulmonary angiography and ventilation/perfusion (V/Q) scan are key diagnostic modalities.[41]​​

Patients with suspected PE can be classified into distinct categories of clinical (pretest) probability that correspond to confirmed PE prevalence using the original Wells Criteria (modified), simplified Wells Criteria (modified), original Geneva Score (revised), or the simplified Geneva Score (revised).[42][43][44] Each of these clinical decision tools assigns a value (a single point, or points) to a series of historic and physical exam features, the sum of which determines whether PE is likely or unlikely.

Cardiac tamponade

Cardiac tamponade may occur suddenly as a result of trauma, aortic dissection, or gradual accumulation of fluid in the pericardial space. Early recognition and appropriate drainage of pericardial fluid is vital. The condition can present with muffled heart sounds, distended neck veins, and pulsus paradoxus. Diagnosis is made by point-of-care ultrasonography or transthoracic echocardiography. Patients presenting in shock from tamponade require emergency pericardiocentesis.[45]

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