Fact 1: While most presentations of chest pain have non-cardiac origins, prompt evaluation is crucial to identify potentially life-threatening cardiac conditions like Acute Coronary Syndrome (ACS).

Related Key Facts:

• Initial assessment must rapidly differentiate between cardiac and non-cardiac causes, prioritizing conditions requiring immediate intervention.
• Non-cardiac causes are diverse, encompassing pulmonary (e.g., PE, pneumonia, pleurisy), gastrointestinal (e.g., GERD, PUD, esophageal spasm, Boerhaave's), musculoskeletal (e.g., costochondritis, radiculopathy), and other (e.g., anxiety, herpes zoster) etiologies.
• Key historical features suggesting cardiac ischemia include substernal pressure/squeezing, radiation to arm/jaw, exertional nature, duration >20 minutes (for ACS), and association with diaphoresis or nausea.
• Atypical presentations of cardiac ischemia (e.g., dyspnea, fatigue, epigastric pain) are more common in women, diabetic patients, and postoperative patients.
• Vital signs, physical examination (including cardiac, pulmonary, abdominal, and musculoskeletal exams), and an early ECG are fundamental first steps in the evaluation.

Fact 2: Acute Coronary Syndrome (ACS) encompasses a spectrum from unstable angina (UA) to non-ST-elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI), primarily differentiated by ECG findings and cardiac biomarkers.

Related Key Facts:

• ACS results from myocardial ischemia, often progressing to necrosis (infarction), typically triggered by acute atherosclerotic plaque rupture, erosion, or fissuring leading to thrombus formation.
• STEMI is characterized by significant ST-segment elevation on ECG and requires immediate reperfusion therapy (PCI or fibrinolytics).
• NSTEMI presents without ST elevation (may have ST depression or T-wave inversion) but shows elevated cardiac biomarkers (e.g., troponin), indicating myocardial necrosis.
• Unstable Angina (UA) involves ischemic symptoms similar to NSTEMI, often with transient ECG changes (ST depression/T-wave inversion) or normal ECG, but without elevation of cardiac biomarkers.
• The distinction between UA and NSTEMI relies solely on biomarker levels (troponin), while STEMI is identified by characteristic ECG changes; management strategies differ significantly, especially acutely for STEMI.

Fact 3: STEMI diagnosis requires specific ECG criteria involving new ST-segment elevation at the J-point in at least two contiguous leads, with varying thresholds depending on the leads and patient demographics.

Related Key Facts:

• Standard criteria: ≥1 mm (0.1 mV) ST elevation in two contiguous leads, except leads V2-V3.
• Criteria in V2-V3: ≥2 mm in men ≥40 years, ≥2.5 mm in men <40 years, or ≥1.5 mm in women.
• STEMI equivalents requiring urgent reperfusion include new or presumed new Left Bundle Branch Block (LBBB) with concerning clinical presentation, and posterior (inferobasal) MI.
• Posterior MI may show ST depression in V1-V3; obtaining posterior leads (V7-V9) can reveal ST elevation (≥0.5 mm threshold, or ≥1 mm in men <40 years).
• Early STEMI may manifest as hyperacute T waves (tall, broad-based, symmetrical) preceding overt ST elevation.

Fact 4: ECG findings suggestive of UA or NSTEMI typically include new horizontal or downsloping ST-segment depression (≥0.5 mm) or T-wave inversion (≥1 mm) in two contiguous leads.

Related Key Facts:

• Contiguous leads group anatomically: Anterior (V1-V4), Inferior (II, III, aVF), Lateral (I, aVL, V5-V6).
• While ST depression and T-wave inversions are characteristic, the ECG can be normal or non-specific in UA/NSTEMI.
• Dynamic ECG changes (changes occurring over time or with pain) increase the likelihood of ACS.
• Conditions like LVH, LBBB, paced rhythms, pericarditis, and electrolyte abnormalities (e.g., hyperkalemia) can mimic or mask ischemic ECG changes, complicating interpretation.
• In patients with LBBB, concordant ST elevation (≥1 mm in leads with a positive QRS) strongly suggests acute MI.

Fact 5: While atherosclerotic plaque rupture is the most frequent cause of ACS, other etiologies include coronary artery vasospasm, spontaneous coronary artery dissection (SCAD), coronary embolism, and stent thrombosis.

Related Key Facts:

• Coronary artery vasospasm (Prinzmetal's angina) causes transient, often nocturnal or early morning, chest pain potentially with ST elevation; triggers include smoking, cocaine, and amphetamines. Myocardial infarction can occur, especially with underlying CAD.
• SCAD is an important cause of ACS, particularly in younger women, often occurring in the peripartum period or associated with fibromuscular dysplasia or connective tissue disease.
• Coronary embolism should be considered in patients with arrhythmias (especially atrial fibrillation), valvular heart disease, or intracardiac thrombus.
• Stent thrombosis is a critical complication post-PCI; early thrombosis (<30 days) is more typical for bare-metal stents, while late/very late thrombosis can occur years after drug-eluting stent placement, often related to antiplatelet therapy cessation.
• Risk factors for underlying CAD (the substrate for plaque rupture) include age, male sex, smoking, hypertension, hyperlipidemia, diabetes, inactivity, and family history of premature CAD (MI/sudden death <55 yrs male, <65 yrs female first-degree relative).

Fact 6: Stable angina pectoris involves transient myocardial ischemia due to a fixed coronary stenosis, causing predictable chest discomfort triggered by increased myocardial oxygen demand (e.g., exertion) and relieved by rest or nitrates.

Related Key Facts:

• Unlike ACS, stable angina involves a stable atherosclerotic plaque that limits coronary blood flow reserve but does not cause acute thrombosis or necrosis at rest.
• Symptoms are typically brief (usually <10-15 minutes) and reproducible at a similar level of exertion or stress.
• Hospitalized patients can experience stable angina symptoms due to "supply/demand mismatch" from conditions like tachycardia, anemia, hypoxemia, or sepsis increasing demand or reducing supply.
• Diagnosis often involves stress testing (exercise or pharmacologic) combined with ECG or imaging (echocardiography or nuclear perfusion) to demonstrate inducible ischemia.
• Management focuses on risk factor modification, antiplatelet therapy (aspirin), statins, beta-blockers, nitrates, and potentially calcium channel blockers or ranolazine, with revascularization (PCI or CABG) for refractory symptoms or high-risk anatomy.

Fact 7: Severe aortic stenosis (AS) can cause exertional chest pain (angina), syncope, and heart failure symptoms, often accompanied by a late-peaking crescendo-decrescendo systolic murmur and signs of left ventricular hypertrophy.

Related Key Facts:

• The murmur is typically best heard at the right upper sternal border with radiation to the carotids; severity correlates with later peaking of the murmur, diminished/absent A2 sound, pulsus parvus et tardus (weak and delayed carotid upstroke), and narrow pulse pressure.
• Angina in AS occurs due to increased myocardial oxygen demand from LV hypertrophy combined with potentially limited coronary flow reserve and reduced diastolic filling time, even without obstructive CAD.
• ECG often shows evidence of Left Ventricular Hypertrophy (LVH) (e.g., voltage criteria like R in aVL ≥ 11 mm) and potentially left axis deviation or strain pattern (ST depression/T-wave inversion in lateral leads).
• An S4 gallop (heard just before S1, low-pitched, best heard at apex with bell) is common due to forceful atrial contraction into a non-compliant, hypertrophied left ventricle.
• Once symptoms (angina, syncope, heart failure) develop in severe AS, prognosis is poor without valve replacement; mean survival is approximately 5 years with angina, 3 years with syncope, and 2 years with heart failure symptoms. Definitive treatment is aortic valve replacement (surgical or transcatheter).

Fact 8: Acute pericarditis classically presents with sharp, pleuritic chest pain that is often relieved by sitting up and leaning forward and worsened by lying down or inspiration.

Related Key Facts:

• The most common causes are idiopathic or viral (e.g., Coxsackie B, echovirus, influenza). Other causes include post-MI (Dressler syndrome), uremia, malignancy, autoimmune disease, radiation, and certain medications.
• A pericardial friction rub (a high-pitched, scratching, or grating sound with up to three components per cardiac cycle) is pathognomonic but may be transient or absent.
• ECG typically shows diffuse, concave-up ST-segment elevation across multiple precordial and limb leads (not fitting a specific coronary territory) and PR-segment depression (PR elevation in aVR is often seen). These changes evolve over days to weeks.
• Cardiac biomarkers (troponin) may be mildly elevated if there is associated epicardial inflammation (myopericarditis), but significant elevation suggests alternative diagnoses like ACS.
• Treatment primarily involves NSAIDs (e.g., ibuprofen, indomethacin) and colchicine, which has been shown to reduce recurrence rates. Corticosteroids are reserved for refractory cases or specific indications (e.g., autoimmune etiology).

Fact 9: Acute aortic dissection presents with severe, sudden-onset "tearing" or "ripping" chest pain, often radiating to the back, and may be associated with significant blood pressure differentials between arms or pulse deficits.

Related Key Facts:

• Major risk factors include chronic hypertension (most common), connective tissue diseases (e.g., Marfan syndrome, Ehlers-Danlos syndrome), bicuspid aortic valve, prior aortic aneurysm, aortic instrumentation/surgery, and vasculitis.
• Physical exam findings may include hypertension (more common in distal, Type B dissections) or hypotension/shock (suggesting complications like tamponade or rupture, often with proximal, Type A dissections), new aortic regurgitation murmur, and neurological deficits (e.g., stroke, paraplegia).
• Initial imaging often includes chest X-ray, which may show a widened mediastinum, abnormal aortic contour, or pleural effusion, but a normal CXR does not rule out dissection.
• Definitive diagnosis requires urgent imaging with CT angiography (CTA) of the chest/abdomen/pelvis, transesophageal echocardiography (TEE), or MR angiography (MRA).
• Management differs drastically based on location (Stanford classification): Type A (involving ascending aorta) requires emergent surgical repair, while uncomplicated Type B (descending aorta only) is typically managed medically initially with strict blood pressure and heart rate control (target SBP 100-120 mmHg, HR <60 bpm, often using IV beta-blockers like labetalol or esmolol +/- sodium nitroprusside).

Fact 10: Pulmonary embolism (PE) is a critical consideration in patients with pleuritic chest pain, dyspnea, and tachypnea, particularly if risk factors for venous thromboembolism (VTE) are present.

Related Key Facts:

• Risk factors for VTE include recent surgery or trauma, prolonged immobility, active malignancy, estrogen use (OCPs, HRT), pregnancy/postpartum state, inherited thrombophilias, obesity, and prior VTE.
• Clinical presentation is highly variable; besides chest pain and dyspnea, symptoms/signs can include cough, hemoptysis, syncope, tachycardia, hypoxemia, and signs of right heart strain (e.g., elevated JVP, RV heave, loud P2).
• ECG is often abnormal but non-specific; findings may include sinus tachycardia (most common), new atrial fibrillation, right axis deviation, new incomplete or complete Right Bundle Branch Block (RBBB), anteroseptal T-wave inversions (V1-V4), or the classic S1Q3T3 pattern (deep S in lead I, Q wave in III, inverted T in III), suggestive of right ventricular strain. A normal ECG does not exclude PE.
• Diagnostic workup typically involves assessing pre-test probability (e.g., Wells score), D-dimer testing (useful to rule out PE in low-probability patients), and definitive imaging such as CT pulmonary angiography (CTPA) or ventilation-perfusion (V/Q) scanning.
• Treatment involves anticoagulation (e.g., heparin, LMWH, DOACs) and, in cases of massive PE with hemodynamic instability, thrombolysis or embolectomy.

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Source

Frameworks for Internal Medicine

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