Cardiac-Related Presentations in the Emergency Department

Cardiac complaints are among the most common and high-risk reasons for ED visits. A systematic approach—reason for visit, symptoms, vital signs, screening, diagnostics, pathophysiology, and disposition—ensures rapid recognition and appropriate triage of life-threatening conditions.1–8

1. Reasons for Visit

• Chest pain (ischemia, aortic dissection, pericarditis, musculoskeletal pain)1–2
• Shortness of breath (heart failure, arrhythmia, pulmonary embolism)3,5
• Palpitations (arrhythmias, stimulant use, anxiety)4
• Syncope or near-syncope (arrhythmia, structural heart disease, vasovagal)4
• Fatigue/weakness (low-output heart failure, anemia)3
• Peripheral edema/weight gain (volume overload from HF or valvular disease)3,7

2. Symptoms

3. Vital Signs

• Blood Pressure (BP): Hypertension in ACS/dissection; hypotension in shock or tamponade.1–3,6,8
• Heart Rate (HR): Tachycardia in sympathetic drive, HF, PE; bradycardia in AV block/inferior MI.2–4,6
• Respiratory Rate (RR): Tachypnea in PE or pulmonary edema.3,5
• Oxygen Saturation (SpO₂): Hypoxemia in HF, PE, ACS with pulmonary edema.2–3,5
• Temperature: Fever in myocarditis, endocarditis, or PE.5–7

4. Screening Tests

• ECG (within 10 minutes for chest pain)1–2
• Troponin, CK-MB1–2
• BNP/NT-proBNP for suspected HF3
• CBC, CMP, glucose
• Chest X-ray (cardiomegaly, pulmonary edema, dissection signs)3,8
• POCUS (LV function, pericardial effusion, IVC)3,6

5. Diagnostic Pathways with Vital Signs

6. Pathophysiology, Etiology, and Disposition

Acute Coronary Syndrome (ACS)1–2

Etiology: Atherosclerotic plaque rupture, coronary thrombosis, vasospasm.

Risks: Hypertension, diabetes, dyslipidemia, smoking, family history.

Age Spectrum: Rare in pediatrics; common after 40, especially >55 (men) and >65 (women).

Pathophysiology: Plaque rupture exposes subendothelial collagen, initiating platelet aggregation and thrombus formation. Coronary occlusion reduces oxygen delivery to the myocardium, producing ischemia that progresses to necrosis if not reversed. Ischemia triggers sympathetic activation (↑BP, ↑HR); as infarction enlarges and contractility falls, cardiogenic shock develops with hypotension, pulmonary edema, and hypoxemia.

Disposition: Telemetry for stable NSTEMI/angina; ICU for STEMI, shock, or malignant arrhythmias.

Heart Failure (HF)3

Etiology: Ischemic cardiomyopathy, long-standing HTN, valvular disease, myocarditis, chemotherapy toxicity.

Risks: CKD, diabetes, obesity, alcohol, aging.

Age Spectrum: Rare in youth (except myocarditis); highly prevalent in older adults.

Pathophysiology: Ventricular systolic/diastolic dysfunction lowers stroke volume and cardiac output. RAAS and sympathetic activation attempt to maintain perfusion but raise afterload and drive sodium/water retention, elevating filling pressures and causing pulmonary congestion/systemic edema. Early hypertension and tachycardia give way to hypotension, tachypnea, and hypoxemia as alveolar flooding progresses.

Disposition: Telemetry after stabilization with diuresis and oxygen; ICU for shock, severe pulmonary edema (BiPAP/intubation), or inotrope/mechanical support.

Arrhythmias (SVT, AFib, VT, Bradyarrhythmias)4

Etiology: CAD, structural remodeling, electrolyte/thyroid imbalance, drug toxicity, congenital conduction disease.

Risks: Hypertension, obstructive sleep apnea, stimulant use, older age, family history of sudden death.

Age Spectrum: SVT in young adults; AFib increases >65; bradyarrhythmias/VT more in elderly.

Pathophysiology: Re-entry circuits, ectopic foci, or conduction block disrupt synchronous contraction. Tachyarrhythmias shorten diastolic filling (↓preload, ↓CO) and may precipitate hypotension; ventricular arrhythmias can cause immediate collapse. Bradyarrhythmias lower heart rate and stroke volume, reducing cerebral perfusion (syncope) and oxygen delivery; SpO₂ varies with perfusion adequacy.

Disposition: Telemetry for controlled AFib/SVT; ICU for unstable VT/VF, high-grade AV block, or refractory AFib with RVR.

Pulmonary Embolism (PE)5

Etiology: Venous thromboembolism, hypercoagulable states, malignancy, pregnancy, immobility.

Risks: Surgery, trauma, OCP/HRT use, thrombophilia, cancer.

Age Spectrum: Rare in children; young adults with thrombophilia; common in older adults with comorbidities.

Pathophysiology: Pulmonary arterial obstruction acutely increases pulmonary vascular resistance, straining and dilating the RV. RV failure reduces LV preload and systemic CO. Ventilation–perfusion mismatch impairs oxygenation, causing hypoxemia and tachypnea; massive PE produces obstructive shock with hypotension and tachycardia.

Disposition: Telemetry for stable PE with mild O₂ needs; ICU for massive/submassive PE with shock, severe hypoxemia, RV failure, or need for thrombolysis/thrombectomy.

Pericarditis / Cardiac Tamponade6

Etiology: Viral infection, autoimmune disease, malignancy, renal failure, post-MI.

Risks: Cancer, uremia, connective tissue disease, trauma.

Age Spectrum: Viral pericarditis in younger adults; tamponade more common in older adults with malignancy/renal disease.

Pathophysiology: Pericardial inflammation leads to effusion; as volume rises, pericardial pressure exceeds diastolic ventricular pressures, restricting filling. Stroke volume and CO fall, causing hypotension, tachycardia, JVD, pulsus paradoxus, and systemic hypoperfusion; SpO₂ declines from inadequate oxygen delivery.

Disposition: Telemetry for uncomplicated pericarditis; ICU for tamponade with hemodynamic compromise (urgent drainage).

Valvular Disease (AS, AR, MR, MS)7

Etiology: Rheumatic fever, congenital lesions, calcific degeneration, infective endocarditis.

Risks: Rheumatic history, bicuspid aortic valve, older age, radiation, prior endocarditis.

Age Spectrum: Congenital in youth; rheumatic in middle age; calcific in elderly.

Pathophysiology: Stenosis imposes pressure overload (ventricular hypertrophy); regurgitation imposes volume overload (dilation). Progressive remodeling culminates in HF. Vital signs mirror lesion physiology: aortic stenosis narrows pulse pressure; aortic regurgitation widens pulse pressure; mitral disease predisposes to AFib and pulmonary edema with hypoxemia.

Disposition: Telemetry for stable chronic lesions; ICU for acute severe regurgitation/stenosis with pulmonary edema or shock (urgent intervention).

Aortic Dissection8

Etiology: Hypertension, Marfan/Ehlers-Danlos, bicuspid valve, trauma, cocaine, prior surgery.

Risks: Chronic HTN, connective tissue disorders, pregnancy, stimulant use, pre-existing aneurysm.

Age Spectrum: Younger with CTD; older with HTN/atherosclerosis.

Pathophysiology: An intimal tear permits blood to track into the media, creating a false lumen that can obstruct branch vessels (malperfusion) or rupture (tamponade). Early sympathetic surge produces severe hypertension and tachycardia; rupture precipitates hypotension, shock, and hypoxemia.

Disposition: Telemetry for stable Type B (medical management); ICU for Type A or unstable Type B (surgical/endovascular repair).

7. Quick Reference Table: ICU vs Telemetry Admission

References (AMA style)