Medical School · Year 3 · Internal Medicine · includes a quiz and discussion video

Seminar 01: Approach to Chest Pain

Year 3: Internal Medicine Clerkship

Learning Objectives

By the end of this seminar, students will be able to:

1. Develop a systematic approach to evaluating chest pain
2. Differentiate cardiac from non-cardiac causes of chest pain
3. Identify clinical features that suggest acute coronary syndrome
4. Describe the evaluation and initial management of chest pain
5. Recognize life-threatening causes requiring immediate intervention
6. Apply risk stratification tools in chest pain assessment

I. Overview of Chest Pain

Chest pain represents one of the most common chief complaints encountered in emergency departments, accounting for approximately five to eight percent of all visits. Among patients presenting with chest pain, acute coronary syndrome is identified in fifteen to twenty-five percent of cases, making rapid and accurate assessment essential for patient outcomes. The majority of chest pain presentations ultimately have non-cardiac etiologies, yet the consequences of missing a cardiac cause can be catastrophic. Studies have demonstrated that two to five percent of myocardial infarctions are missed in the emergency department, underscoring the need for systematic evaluation protocols.

The anatomical structures within the thorax that can generate pain include the heart, great vessels, esophagus, lungs, pleura, and musculoskeletal components of the chest wall. Cardiac pain typically manifests as pressure or heaviness with radiation to the arms or jaw and often occurs with exertion. Esophageal pain frequently presents as burning discomfort that worsens with swallowing or changes in position. Pulmonary and pleural pain characteristically has a pleuritic quality, worsening with respiratory movements. Musculoskeletal pain tends to be localized, reproducible with palpation, and positional in nature.

Life-threatening causes of chest pain that require immediate recognition include acute coronary syndrome presenting with pressure, radiation, diaphoresis, and dyspnea, as well as aortic dissection characterized by tearing pain radiating to the back with blood pressure differentials between arms. Pulmonary embolism presents with pleuritic chest pain, dyspnea, and identifiable risk factors for venous thromboembolism. Tension pneumothorax causes acute dyspnea with absent breath sounds on the affected side, while esophageal rupture typically follows forceful vomiting and presents with subcutaneous emphysema. Cardiac tamponade manifests with Beck's triad of hypotension, jugular venous distension, and muffled heart sounds along with pulsus paradoxus.

The initial assessment of any patient with chest pain must proceed with urgency and follow established priorities. Vital signs including blood pressure in both arms and oxygen saturation should be obtained immediately. An electrocardiogram must be performed within ten minutes of presentation to identify ST-elevation myocardial infarction or other acute changes. History taking should focus on pain quality, location, radiation, and timing. A focused cardiopulmonary physical examination completes the initial evaluation and guides subsequent workup.

<image>Panel A: Emergency department triage algorithm showing immediate ECG, vital sign assessment, and risk stratification pathways. Panel B: Anatomical cross-section of the thorax demonstrating cardiac, esophageal, pulmonary, and musculoskeletal pain generators with characteristic radiation patterns. Panel C: Clinical photographs depicting Beck's triad findings in cardiac tamponade including jugular venous distension. Panel D: Comparison of ECG findings in the six life-threatening causes of chest pain including STEMI, PE strain pattern, and pericarditis.</image>

II. History Taking

The PQRST approach provides a systematic framework for characterizing chest pain through careful questioning. Provocation and palliation assess what activities or interventions worsen or improve the pain, with exertional onset suggesting cardiac ischemia and relief with antacids pointing toward gastrointestinal causes. Quality of pain is described in the patient's own words, with pressure, squeezing, or heaviness suggesting cardiac origin, while sharp or tearing qualities raise concern for dissection or pleuritic causes. Radiation patterns are highly informative, as classic cardiac pain radiates to the left arm, jaw, or shoulder, while dissection pain typically radiates to the back. Severity is assessed on a standardized scale to track response to treatment, and timing encompasses onset, duration, and pattern of symptoms.

Cardiac history features require specific attention during the interview process. Exertional chest pain that occurs predictably with physical activity and resolves with rest represents classic stable angina pectoris. Rest pain or pain occurring with minimal exertion suggests unstable angina or myocardial infarction and demands urgent evaluation. Associated symptoms including diaphoresis, nausea, and dyspnea increase the likelihood of acute coronary syndrome. Cardiovascular risk factors such as hypertension, diabetes mellitus, smoking history, hyperlipidemia, and family history of premature coronary disease must be systematically assessed. Prior cardiac history including previous myocardial infarction, percutaneous coronary intervention, or coronary artery bypass grafting provides essential context.

Non-cardiac features of chest pain help identify alternative diagnoses requiring different management approaches. Pleuritic pain that worsens with breathing suggests pulmonary embolism, pericarditis, or pleuritis from various causes. Positional pain that improves with sitting forward is characteristic of pericarditis, while musculoskeletal pain often worsens with certain movements or positions. Pain associated with swallowing suggests esophageal pathology including esophagitis or esophageal spasm. Reproducible pain with chest wall palpation supports a musculoskeletal diagnosis, though this finding does not exclude concurrent cardiac disease. Post-prandial symptoms raise suspicion for gastrointestinal causes including gastroesophageal reflux disease or biliary disease.

Red flags in the history mandate immediate attention and aggressive evaluation. Severe tearing pain radiating to the back raises strong concern for aortic dissection, particularly in patients with hypertension, connective tissue disorders, or known aortic pathology. Sudden severe dyspnea suggests pulmonary embolism or tension pneumothorax requiring immediate imaging or intervention. Chest pain following forceful vomiting indicates possible esophageal rupture, a surgical emergency. Syncope associated with chest pain may indicate massive pulmonary embolism, arrhythmia, or aortic dissection. New heart failure symptoms accompanying chest pain suggest significant myocardial injury or mechanical complications of infarction.

<image>Panel A: Flow diagram illustrating PQRST questioning technique with branching pathways based on responses. Panel B: Body diagram showing pain radiation patterns for different etiologies including cardiac, aortic, and esophageal sources. Panel C: Clinical decision tree for distinguishing red flag symptoms requiring emergent workup. Panel D: Comparison table of typical versus atypical chest pain presentations across different patient populations.</image>

III. Physical Examination

Vital sign assessment provides immediate prognostic information and guides the urgency of subsequent evaluation. Hypotension indicates shock states that may result from massive pulmonary embolism, cardiac tamponade, or cardiogenic shock from extensive myocardial infarction. Hypertension commonly accompanies acute coronary syndrome and aortic dissection, where severe elevation requires aggressive management. Tachycardia may reflect pain, anxiety, pulmonary embolism, or hemodynamic compromise from any cause. Hypoxia suggests pulmonary pathology including pneumothorax, pulmonary edema, or pulmonary embolism. Blood pressure differential greater than twenty millimeters of mercury between arms strongly suggests aortic dissection and mandates immediate imaging evaluation.

The cardiovascular examination yields critical diagnostic information in chest pain evaluation. An S3 gallop indicates left ventricular dysfunction that may result from acute myocardial infarction with significant myocardial damage or decompensated heart failure. An S4 gallop suggests decreased ventricular compliance from ischemia or chronic hypertension. New murmurs during acute chest pain raise concern for mechanical complications of myocardial infarction including papillary muscle rupture causing acute mitral regurgitation or ventricular septal defect. A pericardial friction rub is pathognomonic for pericarditis and has a scratchy, positional quality best heard with the diaphragm. Jugular venous distension indicates elevated right heart pressures seen in right heart failure, tamponade, and massive pulmonary embolism.

Pulmonary examination findings help differentiate among various chest pain etiologies. Crackles or rales suggest pulmonary edema from cardiogenic causes including acute heart failure or may indicate pneumonia causing pleuritic chest pain. Absent or diminished breath sounds on one side indicate pneumothorax, with tension pneumothorax being a clinical diagnosis requiring immediate needle decompression. A pleural friction rub indicates pleuritis, which may accompany pulmonary embolism, pneumonia, or connective tissue disease. Wheezing may indicate bronchospasm from asthma or chronic obstructive pulmonary disease, but can also occur with pulmonary edema as cardiac asthma.

Additional physical findings provide important diagnostic clues in chest pain assessment. Chest wall tenderness with palpation supports musculoskeletal etiology, though this finding does not exclude acute coronary syndrome and should not provide false reassurance. Unilateral leg swelling suggests deep vein thrombosis as a source for pulmonary embolism. Subcutaneous emphysema, palpable as crepitus in the neck or chest wall, indicates esophageal rupture or pneumomediastinum requiring urgent evaluation. Marfanoid habitus with tall stature, long extremities, and joint hypermobility identifies patients at increased risk for aortic dissection. Skin findings may suggest systemic diseases associated with specific chest pain etiologies.

<image>Panel A: Physical examination technique demonstrating jugular venous pressure assessment with patient positioning at 45 degrees. Panel B: Auscultation landmarks for cardiac examination with audio waveform representations of S3, S4, murmurs, and friction rub. Panel C: Comparison of normal versus abnormal pulmonary examination findings with corresponding chest radiograph correlates. Panel D: Clinical photographs demonstrating chest wall palpation technique and assessment of peripheral pulses.</image>

IV. Acute Coronary Syndrome

Acute coronary syndrome encompasses a spectrum of clinical presentations resulting from atherosclerotic plaque rupture or erosion with subsequent thrombus formation. ST-elevation myocardial infarction represents complete coronary artery occlusion requiring emergent reperfusion therapy within established time windows. Non-ST-elevation myocardial infarction involves partial coronary occlusion with evidence of myocardial injury demonstrated by elevated cardiac biomarkers despite absence of ST elevation on electrocardiogram. Unstable angina represents the mildest form of acute coronary syndrome with clinical symptoms but no detectable troponin elevation, indicating ischemia without myocardial necrosis. All three conditions represent a continuous spectrum of acute plaque pathology with thrombosis.

The typical presentation of acute coronary syndrome involves substernal or left-sided chest pressure, squeezing, or heaviness that patients may describe using a clenched fist over the sternum known as Levine's sign. Radiation to the left arm, jaw, shoulder, or back occurs in the majority of patients and increases diagnostic specificity. Associated symptoms including diaphoresis, nausea, vomiting, and dyspnea reflect autonomic activation and cardiac dysfunction. Duration greater than twenty minutes suggests myocardial infarction rather than stable angina, as the latter typically resolves with rest or nitroglycerin within minutes. The intensity of symptoms does not reliably predict the extent of myocardial injury or prognosis.

Atypical presentations of acute coronary syndrome occur frequently in specific populations and require heightened clinical awareness. Women with myocardial infarction more commonly present with fatigue, dyspnea, and nausea rather than classic substernal chest pressure, leading to diagnostic delays and worse outcomes. Elderly patients may present with confusion, weakness, or falls rather than chest pain, with dyspnea being the most common symptom in patients over age eighty-five. Diabetic patients frequently experience silent ischemia due to autonomic neuropathy, presenting with dyspnea or heart failure rather than chest discomfort. Atypical pain locations including epigastric, back, or right arm distribution occur in up to thirty percent of myocardial infarctions.

Electrocardiographic findings provide essential diagnostic and prognostic information in acute coronary syndrome. ST-segment elevation in two or more contiguous leads indicates transmural ischemia requiring emergent reperfusion through percutaneous coronary intervention or thrombolytic therapy. ST-segment depression suggests subendocardial ischemia and defines high-risk non-ST-elevation acute coronary syndrome requiring urgent intervention. T-wave inversions indicate myocardial ischemia and, when deep and symmetric, suggest critical coronary stenosis. New left bundle branch block in the setting of chest pain should be considered a STEMI equivalent requiring emergent evaluation. Q waves indicate established myocardial necrosis and prior infarction, helping distinguish acute from chronic coronary disease.

<image>Panel A: Pathophysiology illustration showing atherosclerotic plaque rupture, thrombus formation, and resulting coronary occlusion patterns for STEMI versus NSTEMI. Panel B: Serial ECG strips demonstrating evolution of ST-elevation myocardial infarction with hyperacute T waves, ST elevation, Q wave development, and T wave inversion. Panel C: Anatomical diagram correlating ECG lead groups with coronary artery territories and wall segments. Panel D: Clinical presentation comparison showing typical versus atypical symptoms across demographic groups.</image>

V. Non-ACS Cardiac Causes

Pericarditis presents as sharp, pleuritic chest pain that characteristically improves when the patient sits forward and worsens when supine. The pain may radiate to the trapezius ridge, a finding relatively specific for pericardial inflammation. Electrocardiographic findings include diffuse ST-segment elevation with upward concavity and PR-segment depression, distinguishing pericarditis from the regional ST changes of acute coronary syndrome. A pericardial friction rub on auscultation has a scratchy, leathery quality and may be intermittent, requiring repeated examination in different positions. Common etiologies include viral infection, post-myocardial infarction inflammation known as Dressler syndrome, uremic pericarditis in renal failure, and autoimmune diseases. Treatment depends on etiology but typically includes anti-inflammatory therapy with NSAIDs or colchicine.

Myocarditis represents inflammatory disease of the myocardium that frequently follows viral infection, particularly with coxsackievirus, adenovirus, or parvovirus B19. Patients present with chest pain that may mimic acute coronary syndrome, often accompanied by symptoms of heart failure including dyspnea and edema, or arrhythmias including ventricular tachycardia. Troponin elevation occurs due to myocyte injury and may be substantial, complicating differentiation from acute coronary syndrome. The diagnosis is established clinically with supportive imaging, particularly cardiac magnetic resonance imaging showing myocardial edema and late gadolinium enhancement in non-coronary distributions. Treatment is supportive with standard heart failure therapy; immunosuppression is reserved for specific histologic subtypes identified on endomyocardial biopsy.

Aortic dissection presents with sudden-onset severe chest pain described as tearing or ripping that radiates to the back and may migrate as the dissection propagates. Blood pressure differential between arms greater than twenty millimeters of mercury and pulse deficits in extremities suggest branch vessel involvement. Type A dissection involves the ascending aorta and represents a surgical emergency with mortality increasing approximately one to two percent per hour without intervention. Type B dissection involves only the descending aorta distal to the left subclavian artery and is typically managed medically with blood pressure control unless complications develop. Computed tomographic angiography of the chest has become the primary diagnostic modality, with transesophageal echocardiography serving as an alternative in unstable patients.

Aortic stenosis produces anginal chest pain through demand-supply mismatch as the fixed valvular obstruction limits cardiac output augmentation during exertion while simultaneously increasing myocardial oxygen demand from pressure overload. The classic triad of aortic stenosis includes angina, exertional syncope, and heart failure, with onset of symptoms marking a critical transition in the disease course requiring valve replacement. Physical examination reveals a systolic crescendo-decrescendo murmur best heard at the right upper sternal border radiating to the carotids, with diminished and delayed carotid upstroke known as pulsus parvus et tardus. Echocardiography confirms the diagnosis and quantifies stenosis severity through valve area calculation and transvalvular gradient measurement. Surgical or transcatheter aortic valve replacement is indicated for symptomatic severe aortic stenosis.

<image>Panel A: ECG comparison of pericarditis showing diffuse ST elevation and PR depression versus STEMI with regional ST elevation and reciprocal changes. Panel B: Cardiac MRI images demonstrating myocarditis with patchy mid-wall and epicardial enhancement distinct from subendocardial infarction pattern. Panel C: CT angiography cross-sections showing Type A versus Type B aortic dissection with intimal flap and true and false lumens labeled. Panel D: Echocardiographic images of severe aortic stenosis with continuous wave Doppler demonstrating high transvalvular gradient.</image>

VI. Pulmonary Causes

Pulmonary embolism presents with acute dyspnea and pleuritic chest pain, though the clinical presentation varies widely based on the size and location of the embolic burden. Risk factors following Virchow's triad include stasis from immobility or prolonged travel, endothelial injury from surgery or trauma, and hypercoagulability from malignancy, estrogen use, or inherited thrombophilias. The diagnosis requires a structured approach using pretest probability assessment with the Wells score for pulmonary embolism, followed by D-dimer testing in low-probability patients and computed tomographic pulmonary angiography in those with elevated probability or positive D-dimer. Ventilation-perfusion scanning remains an alternative when CT angiography is contraindicated due to contrast allergy or renal dysfunction. Treatment involves anticoagulation with direct oral anticoagulants preferred for most patients, with thrombolysis reserved for massive pulmonary embolism with hemodynamic instability.

Pneumothorax causes sudden onset pleuritic chest pain accompanied by dyspnea, with severity depending on the size of the pneumothorax and underlying pulmonary reserve. Physical examination reveals decreased breath sounds and hyperresonance to percussion on the affected side, findings that may be subtle in small pneumothoraces. Risk factors include tall thin body habitus, smoking, underlying lung disease particularly chronic obstructive pulmonary disease, and recent trauma or procedures. Tension pneumothorax develops when air accumulates under pressure, causing mediastinal shift with tracheal deviation away from the affected side, jugular venous distension, and hemodynamic collapse. Tension pneumothorax is a clinical diagnosis requiring immediate needle decompression at the second intercostal space in the midclavicular line, followed by chest tube placement.

Pneumonia causes pleuritic chest pain through inflammation of the visceral and parietal pleura adjacent to the infected lung parenchyma. Associated symptoms include productive cough with purulent sputum, fever, chills, and dyspnea, though elderly patients may present atypically with confusion or falls. Physical examination reveals inspiratory crackles over the affected area, with consolidation producing bronchial breath sounds, egophony, and dullness to percussion. Chest radiography confirms the diagnosis by demonstrating pulmonary infiltrates, though early pneumonia may not be radiographically apparent. Treatment involves empiric antibiotic therapy directed at likely pathogens based on community versus healthcare-associated acquisition and patient risk factors.

Pleuritis or pleurisy refers to inflammation of the pleural membranes causing sharp chest pain that worsens with breathing and coughing. The pain results from friction between inflamed visceral and parietal pleura during respiratory movements. Etiologies include viral infection as the most common cause, pneumonia extending to the pleural surface, pulmonary embolism with infarction, autoimmune diseases particularly systemic lupus erythematosus, and malignancy. Physical examination may reveal a pleural friction rub, a grating sound heard during both inspiration and expiration, though this finding is often transient as pleural fluid accumulation separates the inflamed surfaces. Treatment addresses the underlying cause while providing symptomatic relief with NSAIDs for analgesia.

<image>Panel A: CT pulmonary angiography demonstrating saddle pulmonary embolism at the bifurcation of the main pulmonary artery with extension into both main pulmonary arteries. Panel B: Chest radiograph series comparing simple pneumothorax with visible pleural line to tension pneumothorax with mediastinal shift. Panel C: Chest radiograph and CT images of right lower lobe pneumonia with air bronchograms and adjacent pleural effusion. Panel D: Anatomical illustration of pleural inflammation with friction rub mechanism and audio waveform representation.</image>

VII. Gastrointestinal Causes

Gastroesophageal reflux disease and esophageal spasm represent common causes of chest pain that can closely mimic cardiac ischemia. The pain quality may be burning or pressure-like, occurring post-prandially or nocturnally when supine. Both nitroglycerin and antacids may provide relief, as nitroglycerin relaxes esophageal smooth muscle in addition to coronary vasodilation, making treatment response unreliable for differentiating cardiac from esophageal pain. Diagnostic evaluation includes a trial of proton pump inhibitor therapy, which supports the diagnosis if symptoms resolve. Endoscopy may reveal erosive esophagitis or Barrett's esophagus in chronic cases. Esophageal manometry diagnoses motility disorders including diffuse esophageal spasm and achalasia that present with chest pain and dysphagia.

Esophageal rupture, also known as Boerhaave syndrome, is a life-threatening cause of chest pain typically occurring after forceful vomiting against a closed glottis. Mackler's triad consists of vomiting, chest pain, and subcutaneous emphysema, though the complete triad is present in fewer than half of cases. Chest radiography may demonstrate pleural effusion, pneumomediastinum, or pneumothorax, though early imaging may appear normal. The diagnosis is confirmed with esophagography using water-soluble contrast or computed tomography with oral contrast demonstrating extravasation. Mortality is extremely high without prompt recognition and treatment, which includes broad-spectrum antibiotics, nothing by mouth, and surgical consultation for operative repair or drainage. Delayed diagnosis beyond twenty-four hours dramatically worsens outcomes.

Peptic ulcer disease causes epigastric pain that may radiate to the chest, particularly with posterior duodenal ulcers that can irritate the diaphragm. The pain typically relates to meals, with duodenal ulcer pain classically improving with eating and worsening hours later, while gastric ulcer pain may worsen with food intake. Risk factors include nonsteroidal anti-inflammatory drug use and Helicobacter pylori infection, both of which should be addressed in management. Complications including perforation cause sudden severe pain with peritonitis, while bleeding ulcers present with hematemesis, melena, or hemodynamic instability. Upper endoscopy establishes the diagnosis and allows for therapeutic intervention including hemostasis for bleeding and biopsy for gastric ulcers to exclude malignancy.

Biliary disease including cholelithiasis and cholecystitis causes right upper quadrant pain that may radiate to the chest, back, or right shoulder through diaphragmatic irritation. Pain is often post-prandial, particularly following fatty meals that stimulate gallbladder contraction. Associated symptoms include nausea and vomiting, with fever suggesting acute cholecystitis or cholangitis. Murphy's sign, inspiratory arrest during palpation of the right upper quadrant, suggests acute cholecystitis. Diagnosis is established with right upper quadrant ultrasound demonstrating gallstones, gallbladder wall thickening, and pericholecystic fluid in cholecystitis. Treatment involves cholecystectomy, with urgent intervention required for complicated cases including gangrene, perforation, or cholangitis.

<image>Panel A: Endoscopic images comparing normal esophageal mucosa with erosive esophagitis and Barrett's esophagus demonstrating intestinal metaplasia. Panel B: Chest radiograph and CT scan of Boerhaave syndrome showing pneumomediastinum, pleural effusion, and esophageal perforation site. Panel C: Upper endoscopy images of gastric and duodenal ulcers with comparison of clean-based versus high-risk bleeding stigmata. Panel D: Right upper quadrant ultrasound demonstrating cholelithiasis, gallbladder wall thickening, and positive sonographic Murphy sign.</image>

VIII. Musculoskeletal Causes

Costochondritis represents inflammation at the costochondral or costosternal junctions, presenting as parasternal chest pain that is reproducible with palpation. The pain may be sharp or aching and worsens with movement, deep breathing, or coughing. No visible swelling occurs, distinguishing costochondritis from Tietze syndrome, which produces localized swelling at the affected junction. Costochondritis affects multiple levels in the majority of cases, most commonly the second through fifth costal cartilages. The diagnosis is clinical, based on reproducible tenderness at the costochondral junctions without evidence of alternative pathology. Treatment consists of nonsteroidal anti-inflammatory drugs, application of local heat, and activity modification, with symptoms typically resolving over weeks to months.

Chest wall strain results from overuse, trauma, or excessive coughing, affecting the intercostal muscles or other chest wall musculature. Patients can often identify a precipitating event such as heavy lifting, new exercise routine, or prolonged coughing spell. Physical examination reveals localized tenderness over the affected muscle group, with pain reproduction on specific movements or resisted muscle testing. The pain characteristically worsens with activity and improves with rest, the opposite pattern from inflammatory causes. Treatment includes rest, ice, analgesics, and gradual return to activity. Severe or refractory cases may benefit from muscle relaxants or physical therapy, though most cases resolve spontaneously within several weeks.

Herpes zoster produces dermatomal pain that may precede the characteristic vesicular rash by days, causing diagnostic confusion with cardiac or other visceral causes of chest pain. The pain has a burning or electric quality and follows a thoracic dermatomal distribution, not crossing the midline. Cutaneous hyperesthesia and allodynia in the affected dermatome provide clues to the diagnosis even before rash appearance. When the rash emerges, grouped vesicles on an erythematous base in a dermatomal pattern confirm the diagnosis. Treatment with antiviral therapy including acyclovir, valacyclovir, or famciclovir is most effective when initiated within seventy-two hours of rash onset and reduces the risk of postherpetic neuralgia. Pain management often requires multimodal therapy including anticonvulsants, tricyclic antidepressants, and topical lidocaine.

Rib fracture causes point tenderness at the fracture site with pain worsening on deep inspiration, coughing, or direct compression of the chest wall. History typically reveals trauma, though fractures may occur spontaneously in patients with osteoporosis or with severe coughing in those with bone disease or chronic steroid use. Chest radiography may demonstrate the fracture, though non-displaced fractures are frequently radiographically occult and CT scan has higher sensitivity. The primary concern with rib fractures involves associated injuries including pneumothorax, hemothorax, or pulmonary contusion, particularly with multiple fractures or significant mechanism. Treatment is supportive with adequate analgesia to maintain pulmonary toilet and prevent atelectasis and pneumonia. Intercostal nerve blocks or epidural analgesia may be necessary for severe cases.

<image>Panel A: Anatomical illustration of chest wall showing costochondral junctions and intercostal musculature with palpation landmarks for examination. Panel B: Clinical photograph of thoracic herpes zoster demonstrating dermatomal vesicular rash with underlying anatomical nerve distribution diagram. Panel C: Chest radiograph and CT images showing rib fractures with associated pneumothorax and pulmonary contusion. Panel D: Physical examination maneuvers for assessing musculoskeletal chest pain including palpation technique and provocative movements.</image>

IX. Diagnostic Workup

Initial diagnostic tests should be obtained promptly in all patients presenting with chest pain to identify life-threatening conditions. The electrocardiogram remains the essential first test, capable of diagnosing ST-elevation myocardial infarction requiring emergent reperfusion, and should be obtained within ten minutes of presentation. Troponin measurement detects myocardial injury with high sensitivity, though the optimal timing depends on symptom duration and assay sensitivity. High-sensitivity troponin assays allow for earlier rule-out protocols, with serial measurements at zero and three hours in low-risk patients. Chest radiography evaluates for pneumonia, pneumothorax, widened mediastinum suggesting aortic pathology, and cardiomegaly with pulmonary edema suggesting heart failure. Basic metabolic panel and complete blood count provide baseline assessment and identify contributing factors.

Advanced imaging studies are selected based on clinical suspicion and initial test results. Computed tomographic angiography of the chest serves as the primary modality for evaluating suspected pulmonary embolism and aortic dissection, providing rapid definitive diagnosis. Echocardiography assesses left ventricular function, wall motion abnormalities suggesting coronary disease, valvular pathology, pericardial effusion, and right ventricular strain from pulmonary embolism. Stress testing with exercise or pharmacologic provocation combined with imaging through nuclear perfusion or echocardiography identifies inducible ischemia in stable patients without clear acute coronary syndrome. Coronary angiography provides definitive coronary anatomy assessment and allows for percutaneous intervention when significant disease is identified.

Risk stratification tools guide disposition and intensity of evaluation in chest pain patients. The HEART score incorporates history features, electrocardiogram findings, age, risk factors, and troponin to stratify patients into low, intermediate, and high-risk categories for major adverse cardiac events. Low HEART scores of zero to three identify patients potentially safe for outpatient evaluation with thirty-day event rates under two percent. The TIMI score applies to patients with known or suspected acute coronary syndrome and predicts risk of death, myocardial infarction, or urgent revascularization. For suspected pulmonary embolism, the Wells score establishes pretest probability to guide D-dimer testing or immediate imaging, while the PERC rule identifies patients in whom pulmonary embolism can be excluded without further testing. The YEARS algorithm combines clinical assessment with D-dimer to efficiently evaluate suspected pulmonary embolism.

The HEART score deserves detailed understanding given its widespread application in chest pain evaluation. History receives zero points for clearly non-cardiac features, one point for moderately suspicious features, and two points for highly suspicious features. ECG interpretation assigns zero points for normal, one point for nonspecific changes, and two points for significant ST deviation. Age scoring gives zero points for those under forty-five, one point for forty-five to sixty-four, and two points for sixty-five and older. Risk factors including hypertension, hyperlipidemia, diabetes, smoking history, family history, and obesity contribute zero points if none or one is present, one point for two factors, and two points for three or more factors or known atherosclerotic disease. Troponin receives zero points if normal, one point if one to three times the upper limit, and two points if greater than three times the upper limit. Scores of zero to three indicate low risk, four to six indicate moderate risk, and seven to ten indicate high risk.

<image>Panel A: ECG interpretation guide showing STEMI criteria by coronary territory, ischemic ST depression patterns, and comparison with early repolarization and pericarditis. Panel B: CT imaging protocols for chest pain showing PE protocol, aortic dissection protocol, and triple rule-out technique with radiation considerations. Panel C: HEART score worksheet with component scoring criteria and risk category interpretation with corresponding management recommendations. Panel D: Diagnostic algorithm flowchart integrating clinical assessment, laboratory testing, and imaging for undifferentiated chest pain.</image>

X. Initial Management

General management principles apply to all patients presenting with significant chest pain regardless of presumed etiology. Intravenous access should be established promptly to allow medication administration and potential resuscitation. Continuous cardiac monitoring detects arrhythmias that may complicate acute coronary syndrome or result from other causes of chest pain. Supplemental oxygen is administered to maintain oxygen saturation above ninety-four percent, though routine oxygen in non-hypoxic patients may not provide benefit and is no longer recommended. Adequate analgesia provides patient comfort and reduces sympathetic activation that increases myocardial oxygen demand. Close monitoring with frequent reassessment ensures timely recognition of clinical deterioration.

Acute coronary syndrome management follows established protocols aimed at restoring coronary perfusion and preventing further thrombosis. Aspirin at a dose of three hundred twenty-five milligrams should be chewed for rapid absorption in all patients with suspected acute coronary syndrome without contraindication. Anticoagulation with heparin, either unfractionated or low-molecular-weight, prevents thrombus propagation. P2Y12 inhibitors including clopidogrel, ticagrelor, or prasugrel provide additional platelet inhibition and improve outcomes, with timing depending on invasive strategy. Nitroglycerin provides symptomatic relief through coronary vasodilation and reduction in preload, though it should be avoided in right ventricular infarction and recent phosphodiesterase inhibitor use. Morphine may be administered for refractory pain but should be used judiciously given potential hemodynamic effects. ST-elevation myocardial infarction requires emergent cardiac catheterization laboratory activation for primary percutaneous coronary intervention within ninety minutes of first medical contact.

Pulmonary embolism management depends on hemodynamic stability and risk stratification. Stable patients with low-risk pulmonary embolism receive anticoagulation with direct oral anticoagulants preferred for most patients due to efficacy and convenience. Submassive pulmonary embolism with right ventricular dysfunction or elevated cardiac biomarkers requires close monitoring and consideration of thrombolytic therapy if deterioration occurs. Massive pulmonary embolism with hemodynamic instability warrants systemic thrombolysis with alteplase, surgical embolectomy, or catheter-directed intervention depending on institutional capabilities and patient factors. Anticoagulation should not be delayed for confirmatory imaging in high-probability cases with hemodynamic compromise. Patients with contraindications to anticoagulation require inferior vena cava filter placement to prevent recurrent embolism.

Other chest pain emergencies require specific interventions tailored to the underlying pathology. Aortic dissection management prioritizes blood pressure control with intravenous beta-blockers as first-line therapy, targeting systolic blood pressure below one hundred twenty millimeters of mercury and heart rate below sixty beats per minute. Type A dissection requires emergency surgery, while uncomplicated Type B dissection is managed medically. Tension pneumothorax requires immediate needle decompression at the second intercostal space followed by chest tube placement, a clinical decision that should not await radiographic confirmation in unstable patients. Cardiac tamponade is treated with pericardiocentesis, which may be performed emergently at the bedside in hemodynamically unstable patients. Esophageal rupture mandates nothing by mouth, broad-spectrum antibiotics, and surgical consultation for operative management.

<image>Panel A: Acute coronary syndrome treatment protocol flowchart showing medication timing, dosing, and decision points for invasive versus conservative management. Panel B: Pulmonary embolism management algorithm stratified by hemodynamic status and risk category with treatment options at each decision node. Panel C: Emergency procedure diagrams for needle decompression of tension pneumothorax and pericardiocentesis with anatomical landmarks. Panel D: Blood pressure control targets and medication options for aortic dissection management with continuous monitoring parameters.</image>

Summary

• Chest pain requires systematic approach to identify life-threatening causes including acute coronary syndrome, aortic dissection, pulmonary embolism, tension pneumothorax, cardiac tamponade, and esophageal rupture
• PQRST history with focus on quality, radiation, and associated symptoms guides differential diagnosis
• Electrocardiogram must be obtained within ten minutes of presentation; troponin detects myocardial injury
• Typical acute coronary syndrome presents with pressure, radiation to arm or jaw, and diaphoresis; atypical presentations common in women, elderly, and diabetics
• Risk stratification with HEART score guides disposition and further evaluation
• ST-elevation myocardial infarction requires emergent reperfusion through primary percutaneous coronary intervention or thrombolysis
• Pulmonary embolism workup guided by Wells score and D-dimer with CT pulmonary angiography for confirmation
• Aortic dissection presents with tearing pain radiating to back and blood pressure differential between arms
• Musculoskeletal chest pain is a diagnosis of exclusion; reproducible tenderness does not rule out cardiac disease
• Initial management includes aspirin for acute coronary syndrome, anticoagulation for pulmonary embolism, and blood pressure control for aortic dissection

Key Terms

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