**Textbook:** Harrison’s Principles of Internal Medicine (21st Edition)  
**Chapter Number & Name:** Chapter 14 – Chest Discomfort  
**Topics Covered:**  
- Epidemiology & Common Causes of Acute Chest Discomfort  
- Myocardial Ischemia (Stable Angina, ACS)  
- Other Cardiopulmonary Causes (Aortic Emergencies, PE, Pericarditis, Pneumothorax)  
- Non-Cardiopulmonary Causes (GI, MSK, Psychological)  
- Diagnostic Approach & Initial Triage  
- Laboratory & Imaging (ECG, Chest X-ray, Cardiac Biomarkers, Stress Testing, CT Angio)  
**Page Numbers:** 1016–1035 (Approx.)  

Chest Discomfort

INTRODUCTION

• Chest discomfort is one of the most common ED presentations (6–7 million visits/year in the U.S.).

• Minority (~10–20%) have acute coronary syndrome (ACS), but missed MI is dangerous (doubled 30-day mortality).

• Other life-threatening causes: Aortic dissection, Pulmonary embolism (PE), Pneumothorax, Pericarditis with tamponade.

🔵 Clinical Pearl: The goal is to quickly identify life-threatening causes while avoiding unnecessary testing in low-risk patients.

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EPIDEMIOLOGY & NATURAL HISTORY

• Chest pain accounts for up to 10% of ED visits.

• <15% of patients end with a final diagnosis of ACS.

• GI causes (e.g., reflux, esophageal spasm) are most common non-cardiac etiologies.

• The 1-year mortality rate in patients with presumed non–cardiopulmonary chest pain is <2%.

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CAUSES OF CHEST DISCOMFORT

1. Myocardial Ischemia/Injury

• Pathophysiology: Mismatch of myocardial oxygen supply & demand → ischemia → potential infarction.

• Most common: Atherosclerotic coronary artery disease → stable angina vs. acute coronary thrombosis → ACS.

  • Unstable angina (UA): No biomarker rise, no ST-elevation.

  • Non-ST-elevation MI (NSTEMI): Elevated biomarkers, no ST-elevation.

  • ST-elevation MI (STEMI): Complete occlusion → transmural ischemia + ST-elevation.

• Clinical features (Angina):

  • Squeezing, pressure-like retrosternal pain ± radiation (arms, neck, jaw).

  • Often triggered by exertion/stress; relieved by rest/nitroglycerin.

  • Unstable patterns: lower threshold, at rest, or more severe/longer.

  • MI: Usually >30 min, often with diaphoresis, anxiety, possible dyspnea, nausea.

🟡 High-Yield: Radiation to both arms strongly suggests ischemic origin.

2. Other Cardiopulmonary Causes

a) Pericarditis/Myocarditis

• Pericarditis: Often sharp, pleuritic chest pain improved by sitting up, leaning forward.

  • May have pericardial friction rub.

  • Diffuse ST-elevation on ECG (concave pattern).

• Myocarditis: Can mimic ACS or present with heart failure.

  • Elevated cardiac biomarkers (troponin), but can be from nonischemic injury.

b) Aortic Emergencies (Acute Aortic Syndrome)

• Aortic Dissection: Sudden severe “tearing/ripping” chest or back pain.

  • Look for unequal pulses, possible aortic regurg murmur, hypotension if rupture or tamponade.

  • Risk factors: Hypertension, Marfan syndrome, bicuspid aortic valve.

• Intramural Hematoma / Penetrating Ulcer: Similar presentation; can evolve into dissection or rupture.

c) Pulmonary Embolism (PE)

• Classically sudden onset pleuritic pain, dyspnea, tachypnea, tachycardia, hypoxia.

• Large PE → syncope, shock, possible “heaviness” that can mimic MI.

• Risk factors: Recent surgery, immobilization, hypercoagulable states.

d) Pneumothorax

• Primary spontaneous in tall, thin, young males (or underlying lung disease).

• Sudden pleuritic pain, dyspnea; absent breath sounds on affected side.

• Tension pneumothorax: Hypotension, JVD, tracheal deviation → emergency needle decompression.

3. Noncardiopulmonary Causes

a) Gastrointestinal

• Esophageal reflux/spasm: Burning, retrosternal, can mimic angina. May respond to nitroglycerin.

• Peptic ulcer: Epigastric burning, can radiate to chest. Often 60–90 min post-meal, improves with antacids.

• Gallbladder disease: RUQ or epigastric, may radiate to the back.

b) Musculoskeletal

• Costochondritis (Tietze’s): Reproducible with palpation over costochondral junctions.

• Cervical disk disease: Radiates to arms/shoulders; may worsen with neck movement.

c) Emotional / Psychiatric

• Panic disorder: Tightness, hyperventilation, anxiety, variable location & duration.

• Somatic symptom disorders: Often recurrent, nonspecific chest discomfort.

🔴 Exam Alert: Always exclude dangerous cardiopulmonary etiologies before attributing chest pain to anxiety or musculoskeletal origin.

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APPROACH TO THE PATIENT

1. Assess stability & rule out “can’t-miss” diagnoses:

   • STEMI or unstable ischemia

   • Aortic dissection

   • Pulmonary embolism

   • Tension pneumothorax

   • Pericarditis/tamponade

   • Esophageal rupture (rare but severe)

2. History & Physical

   • Quality, location (radiation), duration/pattern, provoking/relieving factors, associated sx (dyspnea, diaphoresis, syncope), risk factors (CAD, HTN, coagulopathy).

   • Inspect vital signs: Tachycardia, hypotension, tachypnea, fever → can guide.

   • Chest exam: Murmurs (e.g. aortic regurg → dissection), friction rub, absent breath sounds, JVP changes, local reproducible tenderness.

3. ECG

   • Obtain within 10 min of presentation if suspect ACS.

   • Repeat serially (q30–60 min) if suspicion persists.

   • ST elevations → STEMI vs. pericarditis (diffuse).

   • ST depressions/T inversions → non-ST elevation ischemia, or other conditions.

4. Cardiac Biomarkers (Troponin)

   • High-sensitivity troponin → earlier detection of myocardial injury.

   • Serial sampling: 0 & 1–3 h (HS troponin) or 0 & 3–6 h (conventional).

   • Rise/fall pattern + clinical context → type 1 MI (atherothrombosis) vs. type 2 MI (O2 mismatch) vs. nonischemic injury (myocarditis).

5. Chest X-Ray

   • Useful to evaluate for pneumothorax, pneumonia, widened mediastinum (dissection), or heart failure signs.

6. Advanced Testing

   • CT Pulmonary Angiography: Suspected PE, or triple rule-out (PE, aortic dissection, coronary disease) if stable.

   • Coronary CT Angiography: High negative predictive value for ACS.

   • Stress Testing (exercise ECG, nuclear perfusion, stress echo): For intermediate risk after negative troponins/ECG.

   • Echocardiography: Evaluate for wall motion abnormalities, valvular lesions, tamponade.

   • MRI: Detailed structural evaluation (myocarditis, infiltrative disease) or aortic pathology.

🔵 Clinical Pearl: In low-risk patients with no abnormal ECG changes or troponin elevation, the yield of routine stress imaging is low. An accelerated diagnostic pathway can be used to safely discharge many patients.

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CRITICAL PATHWAYS

• Chest Pain Units and standardized protocols help:

  1. Rapid triage of high-risk conditions.

  2. Quick “rule out” of ACS (e.g., with serial HS-troponins + ECG ± imaging).

  3. Avoid unnecessary admissions in very low-risk patients.

🔵 Clinical Pearl: Decision tools like the HEART Score or EDACS integrate History, ECG, Age, Risk factors, Troponin to risk-stratify patients quickly.

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OUTPATIENT EVALUATION

• In primary care, chest pain is common.

• If suspicion of acute ACS → immediate ED referral (troponin + ECG).

• Otherwise, detailed history & exam, plus baseline ECG, guide further testing (e.g., stress testing, GI evaluation).

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MERMAID DIAGRAM: APPROACH TO ACUTE CHEST PAIN

flowchart LR
    A[Acute Chest Discomfort] --> B{Stable vs. Unstable?}
    B -- Unstable Vitals or Suspected Life-Threat? --> C[Immediate Workup: ECG<10min, Troponin, Chest X-ray, +/- Emergent Imaging]
    B -- Stable --> D[Obtain ECG + Troponin, Focused H&P]
    D --> E{High Suspicion ACS?}
    E -- Yes --> F[Serial Troponins, +/- Stress/CT Angio, Possible Admission]
    E -- No --> G[Consider Non-Cardiac Etiologies: GI, MSK, Psych, Outpatient Workup]

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HIGH-YIELD DIFFERENTIAL TABLE

Condition	Key Features	Diagnostic Clues
Myocardial Ischemia	Pressure, heaviness; exertional or stress-induced; can radiate to arm/jaw	ECG changes (ST/T), ↑ Troponin
Aortic Dissection	Sudden severe tearing pain, can migrate; difference in BP between arms	Widened mediastinum on CXR, CT/MRI diagnostic
Pulmonary Embolism	Sudden onset pleuritic chest pain, dyspnea, tachycardia, hypoxia	D-dimer, CT Pulm Angio, risk factors for VTE
Pericarditis	Sharp, positional (worse supine), friction rub, diffuse ST elevation	ECG (diffuse ST-elevation), rub on auscultation
Pneumothorax	Sudden pleuritic pain, absent breath sounds, hyperresonance	CXR: visible visceral pleural line
Esophageal Reflux/Spasm	Retrosternal burning/squeezing, may mimic angina, relief w/ acid suppression	pH study, endoscopy, trial of PPI
Costochondritis	Reproducible tenderness on palpation of costosternal junctions	Localized chest wall tenderness
Anxiety/Panic	May have chest tightness, hyperventilation, normal investigations; often recurrent	Diagnosis of exclusion; normal cardiac tests

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MANAGEMENT PEARLS

1. Rapid STEMI Recognition: Immediate reperfusion therapy (PCI or fibrinolysis).

2. Suspected Aortic Dissection: Control BP/HR, emergent surgical consult.

3. PE: Anticoagulation ± thrombolysis if massive.

4. Pneumothorax: Needle decompression if tension, otherwise chest tube if large or symptomatic.

5. Pericarditis: NSAIDs/Colchicine; watch for tamponade.

6. Non-ischemic GI issues: acid suppression, antispasmodics, cholecystitis management.

7. Musculoskeletal: NSAIDs, physical therapy.

8. Anxiety: Reassure after thorough evaluation, consider psychotherapy or anxiolytics.

🔴 Exam Alert: Always re-evaluate patients with persistent, worsening, or recurrent symptoms—misdiagnosis can be fatal.

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REFERENCES (APA Style, Annotated)

• Amsterdam, E. A., et al. (2010). Testing of low-risk patients presenting to the emergency department with chest pain: A scientific statement from the American Heart Association. Circulation, 122(17), 1756–1776.

  — Outlines guidelines for evaluating low-risk chest pain, emphasizing appropriate testing strategies.

• Chapman, A. R., et al. (2017). Association of high-sensitivity cardiac troponin I concentration with cardiac outcomes in patients with suspected acute coronary syndrome. JAMA, 318(19), 1913–1924.

  — Landmark study detailing the prognostic power of high-sensitivity troponin in suspected ACS.

• Fanaroff, A. C., et al. (2015). Does this patient with chest pain have acute coronary syndrome? JAMA, 314(18), 1955–1965.

  — Reviews key clinical features to distinguish ACS from non-ACS chest pain.

• Mahler, S. A., et al. (2018). Safely identifying emergency department patients with acute chest pain for early discharge: HEART pathway accelerated diagnostic protocol. Circulation, 138(22), 2456–2468.

  — Demonstrates how structured protocols (e.g., HEART Score) can reduce admissions and miss rates.

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Final Check:

• Chest discomfort can arise from multiple systems; triage protocols and a structured approach with ECG + troponin + targeted imaging ensure life-threatening causes aren’t missed.

• Rapid, systematic evaluation saves lives and avoids overuse of resources.

[▶️ Video Placeholder: “Bedside Ultrasound for Cardiac Tamponade Evaluation”]

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If you need further clarifications or a deeper dive into specific diagnostic algorithms, let me know!