Cardiology

A

• Acute Aortic Dissection — Anti‑Impulse Therapy, Imaging, and Repair Pathways

  Tearing chest/back pain with pulse/BP differential warrants immediate anti‑impulse therapy and CTA. Type A → emergent surgery; Type B complicated → TEVAR/branch-first strategies; all receive strict BP/HR control, analgesia, and intensive monitoring.
• Acute Aortic Dissection — HR/BP Control, Imaging, and Surgical vs Medical Management

  Tearing chest/back pain with pulse deficits or mediastinal widening suggests dissection. Rapidly control HR (<60) and SBP (100–120) with beta-blockade and vasodilators; obtain CTA chest/abdomen/pelvis. Type A requires emergent surgery; Type B usually medical unless complications warrant TEVAR.
• Acute Coronary Syndrome — NSTEMI/Unstable Angina

  Non-ST-elevation acute coronary syndrome includes NSTEMI, defined by acute myocardial injury with evidence of ischemia, and unstable angina, in which ischemia occurs without biomarker-defined infarction. Modern high-sensitivity troponin assays have made true unstable angina less common. Evaluation requires serial ECGs, serial high-sensitivity troponin interpreted with symptom timing, and active assessment for alternative life-threatening causes of chest pain. Treatment combines anti-ischemic care, antithrom
• Acute Decompensated Heart Failure — Diuresis Strategy and Afterload Reduction

  Identify perfusion/congestion profile (wet/dry; warm/cold). Use IV loop diuretics (1–2× home dose), consider vasodilators in hypertensive pulmonary edema, and escalate to inotropes/ultrafiltration for diuretic resistance and hypoperfusion.
• Acute Decompensated Heart Failure — Diuretics, Vasodilators, and Noninvasive Ventilation

  Volume overload or flash pulmonary edema requires loop diuretics, vasodilators when blood pressure allows, and noninvasive ventilation to improve oxygenation. Identify precipitating factors (ischemia, arrhythmia, nonadherence) and tailor therapy by hemodynamic profile (warm/wet vs cold/wet).
• Acute Decompensated Heart Failure — ED Management

  Acute decompensated heart failure is a syndrome of congestion, elevated filling pressures, and sometimes impaired perfusion. In the emergency setting, identify respiratory failure and shock, determine whether the patient is wet or dry and warm or cold, give IV loop diuretics for significant fluid overload, use noninvasive ventilation and vasodilators when appropriate, and treat the precipitating cause while preserving or re-establishing guideline-directed therapy.
• Acute Decompensated Heart Failure — Pulmonary Edema

  Rapid dyspnea relief with noninvasive ventilation and nitrates when hypertensive; add diuretics and treat triggers such as ischemia or arrhythmia.
• Acute Decompensated Heart Failure with Pulmonary Edema — Nitrates, Diuretics, and NIV

  Acute dyspnea with rales and frothy sputum indicates pulmonary edema. Provide high-flow oxygen and early noninvasive ventilation, give IV nitrates to reduce preload/afterload (especially in hypertensive ADHF), and administer loop diuretics; investigate triggers (ischemia, arrhythmia, dietary/medication nonadherence).
• Acute Inferior ST-Elevation Myocardial Infarction (STEMI) — Diagnosis & Management

  Inferior STEMI presents with ST elevation in leads II, III, and aVF, often due to right coronary artery occlusion. Prompt reperfusion with PCI or fibrinolytics is essential. Assess for right ventricular infarction, avoid nitrates if present, and provide guideline-directed antithrombotic therapy.
• Acute Pericarditis — Diagnosis and Treatment

  Acute pericarditis is an inflammatory syndrome causing characteristic pleuritic chest pain, pericardial friction rub, diffuse ECG changes, and sometimes pericardial effusion. Exclude acute coronary syndrome, pulmonary embolism, aortic disease, and tamponade; treat uncomplicated inflammatory disease with aspirin or an NSAID plus colchicine and restrict exercise until inflammation resolves.
• Adult Congenital Heart Disease — Primary Care Essentials

  Adults with congenital heart disease require lifelong care based on their original anatomy, operations or catheter interventions, and residual physiology. Treat residual hemodynamic lesions and arrhythmias according to ACHD-specific guidance.
• Aortic Dissection — Diagnosis & Initial Treatment

  Acute aortic dissection is a form of acute aortic syndrome caused by an intimal tear with blood entering the aortic media. Mortality rises rapidly when proximal dissection is untreated. Diagnosis requires a high index of suspicion in patients with abrupt severe chest, back, or abdominal pain, pulse or blood-pressure differences, neurologic deficits, new aortic regurgitation, shock, or high-risk aortic disease. CT angiography is the usual definitive test in stable patients, while transesophageal echocardiogr
• Aortic Intramural Hematoma vs Penetrating Atherosclerotic Ulcer — Imaging and Management

  Acute chest/back pain with imaging showing intramural hematoma (IMH) or penetrating atherosclerotic ulcer (PAU)—entities within acute aortic syndrome.
• Atrial Fibrillation — Anticoagulation and Rhythm Control

  Atrial fibrillation management has four parallel goals: assess hemodynamic stability, control ventricular rate when needed, reduce thromboembolic risk, and decide whether rhythm control improves symptoms or long-term outcomes. Unstable AF causing shock, ongoing ischemia, pulmonary edema, or severe hypotension requires synchronized cardioversion.
• Atrial Fibrillation — Rate vs Rhythm

  Atrial fibrillation management is built on hemodynamic assessment, stroke prevention, symptom control, and treatment of modifiable risk factors. Unstable AF requires synchronized cardioversion. Stable patients may undergo rate or rhythm control, but long-term anticoagulation is based on thromboembolic risk rather than whether sinus rhythm is restored.
• Atrial Fibrillation with RVR — ED Rate vs Rhythm

  Atrial fibrillation with rapid ventricular response is managed according to hemodynamic stability, the cause of the tachycardia, ventricular function, symptom burden, and thromboembolic risk. Unstable AF causing hypotension, ischemia, shock, or acute pulmonary edema requires immediate synchronized electrical cardioversion. Stable patients usually receive rate control with a beta blocker or nondihydropyridine calcium-channel blocker when ventricular function permits, while rhythm control is selected when sym
• Atrial Fibrillation with RVR — Rate vs Rhythm Control and Anticoagulation

  Rapid AF can cause hypotension, ischemia, or heart failure. Stabilize ABCs; if unstable, perform synchronized cardioversion. If stable, choose rate control (β‑blocker or nondihydropyridine CCB; amiodarone if LV dysfunction/hypotension) versus rhythm control based on duration and comorbidities, and address anticoagulation using CHA₂DS₂‑VASc and bleeding risk.

B

• Brugada Syndrome — Fever Management, Drug Avoidance, and ICD Criteria

  Inherited sodium‑channelopathy with coved ST elevation (type 1) in V1–V3 and risk of polymorphic VT/VF. Avoid fever and offending drugs; treat electrical storms with isoproterenol and consider quinidine. ICD is indicated for survivors of VT/VF and often for syncope with spontaneous type‑1 ECG plus inducible arrhythmias; counsel family screening.

C

• Cardiac Amyloidosis — Clues, Workup, and Treatment

  Cardiac amyloidosis should be considered when increased ventricular wall thickness or HFpEF is accompanied by discordant low ECG voltage, restrictive physiology, unexplained neuropathy, bilateral carpal tunnel syndrome, lumbar spinal stenosis, biceps tendon rupture, proteinuria, or intolerance of conventional HF medications. Refer suspected AL amyloidosis urgently to hematology because plasma-cell-directed therapy is time-sensitive.
• Cardiac Tamponade — Recognition, Pericardiocentesis, and Reversal of Precipitants

  Beck’s triad and pulsus paradoxus with effusion on ultrasound suggests tamponade. Provide IV fluids as a bridge, avoid positive-pressure ventilation if possible, and perform urgent pericardiocentesis with echo guidance; reverse anticoagulation and treat underlying cause.
• Catecholaminergic Polymorphic Ventricular Tachycardia — Exertional Syncope & Sudden Death Prevention

  CPVT is an inherited arrhythmia syndrome in which adrenergic stimulation triggers bidirectional or polymorphic ventricular tachycardia despite a structurally normal heart and often normal resting ECG. Diagnosis relies on exercise-provoked arrhythmia and genetic evaluation, while treatment centers on nonselective beta-blockade, flecainide when needed, activity modification, and selective use of sympathetic denervation or ICD therapy.

D

• Deep Vein Thrombosis — ED Diagnosis and Initial Therapy

  Use Wells score and D dimer to guide ultrasound; start anticoagulation when DVT is confirmed or highly suspected without major contraindications.
• Digoxin Toxicity — Digoxin Immune Fab

  Life-threatening digoxin toxicity can cause nausea, confusion, hyperkalemia, bradyarrhythmias, atrioventricular block, ventricular dysrhythmias, and shock. Treat clinically significant cardiotoxicity with digoxin-specific immune Fab, correct contributing electrolyte disturbances, and do not rely on dialysis because digoxin is poorly removed extracorporeally.

H

• Heart Failure with Reduced EF — Guideline-Directed Therapy

  Heart failure with reduced ejection fraction is generally defined by LVEF 40% or lower and is treated with four foundational medication classes: an ARNI or other renin-angiotensin system inhibitor, an evidence-based beta blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor. These therapies should be initiated early and titrated as tolerated, with diuretics used for congestion rather than mortality reduction.
• HFrEF — Guideline‑Directed Medical Therapy Up‑Titration

  Heart failure with reduced ejection fraction is treated with four foundational disease-modifying medication classes: an angiotensin receptor-neprilysin inhibitor (or ACE inhibitor/ARB when ARNI is not feasible), an evidence-based beta blocker, a mineralocorticoid receptor antagonist, and an SGLT2 inhibitor. For a stable patient, introduce low doses of the four pillars over days to weeks and aim for maximally tolerated evidence-based doses over roughly three months, with earlier follow-up.
• Hypertensive Emergency — IV Management

  Hypertensive emergency is severe blood pressure elevation accompanied by acute target-organ injury. Confirm the pressure, identify the injured organ system, and use a titratable IV agent matched to the syndrome. For most emergencies, reduce pressure in a controlled fashion rather than normalizing it immediately, while recognizing exceptions such as acute aortic syndromes, pregnancy-related severe hypertension, and stroke-specific pathways.
• Hypertensive Emergency — IV Therapy in the ED

  Acutely elevated blood pressure with target organ damage requires controlled reduction using IV agents tailored to the condition.
• Hypertensive Emergency — Organ Protection, IV Drips, and Targeted Reductions

  Acute severe hypertension with target-organ damage (e.g., encephalopathy, pulmonary edema, ACS, AKI) requires rapid but controlled BP lowering with IV agents; general goal is ≤25% MAP reduction in the first hour, then to 160/100–110 mmHg over the next 2–6 hours, except in special conditions.

K

• Kounis Syndrome — Allergic Acute Coronary Syndrome

  Chest pain and ST‑changes during anaphylaxis or hypersensitivity reaction suggests Kounis syndrome (allergic ACS).

L

• Lipoprotein(a) — When to Measure & Treat

  Lipoprotein(a), or Lp(a), is a genetically determined apoB-containing lipoprotein that contributes to atherosclerotic cardiovascular disease and calcific aortic valve disease. There is not yet a broadly approved Lp(a)-specific drug with proven cardiovascular-outcome benefit as of 2026, so current management focuses on aggressive control of modifiable risk, especially LDL cholesterol.

M

• MINOCA — Workup & Secondary Prevention

  MINOCA—myocardial infarction with nonobstructive coronary arteries—is a working diagnosis, not a final mechanism. Treat the identified mechanism rather than giving every MINOCA patient identical lifelong therapy.
• Myocarditis — Diagnosis & Return‑to‑Activity

  Myocarditis is inflammatory injury of heart muscle that can range from mild chest pain with troponin elevation to fulminant cardiogenic shock, malignant arrhythmia, or advanced heart failure. Treat heart-failure physiology and arrhythmias according to standard principles while avoiding unnecessary exercise and cardiotoxic exposures.

N

• NSTEMI — Early Invasive Strategy, DAPT, Anticoagulation, and Secondary Prevention

  Chest pain with troponin rise and non-ST elevation ECG changes. Start aspirin, P2Y12 inhibitor, and anticoagulation; apply high-intensity statins and anti-ischemic therapy. Use risk scores (TIMI/GRACE) to guide timing of angiography and revascularization.
• NSTEMI Unstable Angina — Early Risk-Guided Care

  Non-ST-elevation acute coronary syndrome includes NSTEMI, defined by acute myocardial injury from ischemia without persistent diagnostic ST elevation, and unstable angina, in which ischemic symptoms occur without biomarker-defined infarction. Management combines rapid ECG and serial high-sensitivity troponin testing, aspirin and additional antithrombotic therapy, anti-ischemic treatment, risk stratification, and an invasive strategy for high-risk patients. Dynamic instability, recurrent ischemia, heart fail

P

• Pericardial Tamponade — Emergency Management

  Cardiac tamponade is obstructive shock caused by pericardial pressure that limits cardiac filling. Diagnosis is clinical and hemodynamic, supported by echocardiography. Hypotension, tachycardia, elevated venous pressure, pulsus paradoxus, and dyspnea can occur, but classic findings may be incomplete. Hemodynamically significant tamponade requires urgent drainage, usually image-guided pericardiocentesis or surgical drainage depending on cause. Temporizing fluids or vasoactive support must not delay definitiv
• Pericardial Tamponade — Rapid Diagnosis and Pericardiocentesis

  Beck triad is uncommon; rely on echocardiography showing chamber collapse and IVC plethora. Resuscitate, avoid positive-pressure ventilation if possible, and perform pericardiocentesis (ultrasound-guided) for hemodynamic compromise.
• Pericarditis & Pericardial Tamponade — Recognition & Management

  Acute pericarditis is inflammation of the pericardium, usually diagnosed from a compatible syndrome that includes pleuritic positional chest pain, a pericardial friction rub, characteristic ECG changes, or a new or worsening pericardial effusion. Most uncomplicated idiopathic or presumed viral cases respond to anti-inflammatory therapy plus colchicine. Pericardial tamponade is a separate hemodynamic emergency in which pressure from pericardial fluid impairs cardiac filling. Tamponade is diagnosed from clini
• Peripartum Cardiomyopathy — Management & Prognosis

  Peripartum cardiomyopathy is new systolic heart failure arising toward the end of pregnancy or in the months after delivery, usually with LVEF below 45%, when no other cause explains the dysfunction. During pregnancy, treat congestion with judicious diuretics and use pregnancy-compatible afterload reduction such as hydralazine/nitrates when needed; selected beta blockers are used carefully.
• Post‑MI Secondary Prevention — Medications & Cardiac Rehab

  Secondary prevention after myocardial infarction starts before discharge and continues indefinitely. Dual antiplatelet therapy duration is individualized by ACS/PCI features and bleeding risk; aspirin is usually continued long-term in patients with atherosclerotic coronary disease unless another strategy is chosen.
• Pulmonary Embolism — ED Risk Stratification and Anticoagulation

  Use pretest probability and D dimer to guide imaging; stratify risk for disposition; anticoagulate when diagnosis is likely or confirmed unless contraindicated.

S

• Spontaneous Coronary Artery Dissection — ED Diagnosis and Conservative Management

  Younger women with ACS symptoms, often without classic risk factors; angiography shows coronary dissection not due to atherosclerosis.
• ST-Elevation MI — ED to Reperfusion

  ST-elevation myocardial infarction is usually caused by acute coronary artery occlusion and requires immediate reperfusion unless a clear contraindication or alternative diagnosis exists. The operational goal is to identify STEMI rapidly, activate the reperfusion system, provide evidence-based antithrombotic therapy, and minimize total ischemic time. Primary PCI is preferred when it can be delivered promptly by an experienced system. When timely PCI is not achievable and symptom onset is within the fibrinol
• ST‑Elevation Myocardial Infarction — Reperfusion Times, Antithrombotics, and Post‑PCI Care

  Activate the cath lab for PCI‑capable patients with goal first‑medical‑contact‑to‑device ≤90 min (≤120 min for transfers). If PCI unavailable in time, give fibrinolysis within 30 min of arrival if no contraindications and plan pharmaco‑invasive strategy. Load antiplatelets and anticoagulate; control pain and blood pressure; initiate secondary prevention.
• STEMI — Reperfusion First

  ST-elevation myocardial infarction is an acute coronary occlusion syndrome in which rapid reperfusion is the central treatment goal. Activate the PCI pathway immediately when diagnostic ECG findings and clinical context support STEMI. Primary PCI is preferred when it can be performed promptly by an experienced team; fibrinolysis is an alternative for eligible patients with early presentation when timely PCI cannot be achieved and bleeding risk is acceptable. Give aspirin, appropriate P2Y12 inhibition and an
• Supraventricular Tachycardia — Acute Termination

  Regular narrow-complex supraventricular tachycardia is usually caused by AV nodal reentrant tachycardia or AV reentrant tachycardia. First determine whether the tachycardia is causing hypotension, shock, ischemic chest discomfort, acute heart failure, or altered mental status. Unstable patients require synchronized cardioversion. Stable regular narrow-complex SVT is treated with a vagal maneuver followed by rapid IV adenosine, 6 mg then 12 mg if needed, while recurrent episodes may require beta blocker or c
• Supraventricular Tachycardia — Vagal, Adenosine, Cardioversion

  Stable narrow complex tachycardia responds to vagal maneuvers and adenosine; unstable rhythms need synchronized cardioversion.

T

• Takotsubo Cardiomyopathy — Diagnosis & Management

  Takotsubo syndrome is a transient stress cardiomyopathy that mimics acute coronary syndrome with chest pain, dyspnea, ECG abnormalities, troponin elevation, and characteristic ventricular wall-motion patterns extending beyond a single coronary territory. Treatment is supportive and phenotype-specific.
• Torsades de Pointes — Magnesium and Overdrive Pacing

  Torsades de pointes is a polymorphic ventricular tachycardia associated with a prolonged QT interval and commonly triggered by medications, hypokalemia, hypomagnesemia, bradycardia, or congenital long-QT syndrome. Unstable or pulseless torsades requires immediate unsynchronized shock; magnesium, electrolyte correction, removal of QT-prolonging causes, and rate acceleration are used to prevent recurrence.
• Torsades de Pointes — Magnesium, Electrolyte Repletion, and Overdrive Pacing

  Polymorphic VT with prolonged QT requires IV magnesium sulfate regardless of serum level, aggressive potassium repletion, and cessation of QT-prolonging drugs. Unstable patients need immediate defibrillation; recurrent cases benefit from overdrive pacing or isoproterenol if pause-dependent.
• Torsades de Pointes — Magnesium, Overdrive Pacing, and QT Hygiene

  Polymorphic VT with prolonged QT; correct precipitants (electrolytes, QT-prolonging meds), give magnesium, increase heart rate via overdrive pacing or isoproterenol if bradycardic, and treat hemodynamic instability per ACLS.

V

• Ventricular Tachycardia — ED Management

  Ventricular tachycardia is a wide-complex tachyarrhythmia that can cause hypotension, ischemia, heart failure, or cardiac arrest. Treat unstable VT with immediate synchronized cardioversion when a pulse is present, defibrillate pulseless VT, and manage stable monomorphic VT with expert-supported antiarrhythmic therapy while correcting ischemia, electrolytes, drug toxicity, and other triggers.