USMLE Diagnosis Calculator

Persistent Truncus Arteriosus
Persistent Truncus Arteriosus

Failure of truncus arteriosus to divide into pulmonary artery and aorta.

  • 🟪 Overview
    Rare congenital heart defect often associated with DiGeorge syndrome.
  • 🧠 Pathophysiology
    Single great vessel causes mixed oxygenated/deoxygenated blood to circulate systemically.
  • 🩻 Clinical Presentation
    Early cyanosis, loud single S2, heart failure signs like tachypnea or poor feeding in infants.
  • 🩺 Diagnosis
    Echocardiogram confirms a single outflow tract with associated VSD.
  • 💊 Management
    Surgical correction early in life; may need diuretics or inotropes pre-op.
  • 📊 Epidemiology
    Estimated incidence: ~1 in 10,000 live births in the U.S.
🏷️ Tags
cyanosis,heart failure,murmur,truncus arteriosus,newborn,congenital
D-Transposition of the Great Vessels
D-Transposition of the Great Vessels

Aorta and pulmonary artery are switched, causing parallel circulation.

  • 🟪 Overview
    Most common cyanotic lesion in neonates; requires mixing lesion to survive.
  • 🧠 Pathophysiology
    Failure of aorticopulmonary septum to spiral → separate systemic and pulmonary circuits.
  • 🩻 Clinical Presentation
    Severe cyanosis at birth, no murmur, often in large, well-developed babies.
  • 🩺 Diagnosis
    Echo shows transposed vessels; CXR may show "egg on a string" heart.
  • 💊 Management
    Prostaglandin E1 to keep ductus open; balloon atrial septostomy; arterial switch surgery.
  • 📊 Epidemiology
    Occurs in ~1 in 3,500 to 5,000 live births; more common in males.
🏷️ Tags
Tricuspid Atresia
Tricuspid Atresia

Absence of tricuspid valve and hypoplastic right ventricle.

  • 🟪 Overview
    Always requires both ASD and VSD to maintain circulation.
  • 🧠 Pathophysiology
    Complete lack of tricuspid valve causes no connection between RA and RV; systemic venous return must cross ASD and VSD.
  • 🩻 Clinical Presentation
    Cyanosis in newborn, often with a murmur due to VSD, failure to thrive.
  • 🩺 Diagnosis
    Echocardiography confirms absence of tricuspid valve and presence of ASD/VSD.
  • 💊 Management
    PGE1 to maintain ductus arteriosus; staged surgical repair (e.g., Fontan procedure).
  • 📊 Epidemiology
    Accounts for ~1–3% of congenital heart defects; more common in males.
🏷️ Tags
Tetralogy of Fallot
Tetralogy of Fallot

Most common cyanotic congenital heart disease beyond infancy, due to 4 structural abnormalities.

  • 🟪 Overview
    Consists of VSD, pulmonary stenosis, right ventricular hypertrophy (RVH), and overriding aorta.
  • 🧠 Pathophysiology
    Pulmonary stenosis increases RV pressure, causing right-to-left shunt across VSD.
  • 🩻 Clinical Presentation
    Cyanosis, tet spells (sudden cyanosis and dyspnea relieved by squatting), boot-shaped heart on CXR.
  • 🩺 Diagnosis
    Echocardiogram confirms all 4 defects; CXR shows classic silhouette.
  • 💊 Management
    Initial oxygen and knee-chest positioning for tet spells; definitive surgical repair in infancy.
  • 📊 Epidemiology
    Occurs in ~3.5 per 10,000 live births; associated with DiGeorge syndrome and Down syndrome.
🏷️ Tags
TAPVR
Total Anomalous Pulmonary Venous Return (TAPVR)

Pulmonary veins drain into right heart circulation instead of the left atrium.

  • 🟪 Overview
    Requires ASD or PDA for systemic circulation to receive oxygenated blood.
  • 🧠 Pathophysiology
    Oxygenated pulmonary venous blood returns to right atrium → right heart overload and left heart hypoplasia.
  • 🩻 Clinical Presentation
    Cyanosis, respiratory distress, heart failure signs, and "snowman sign" on CXR in supracardiac type.
  • 🩺 Diagnosis
    Echocardiography to visualize pulmonary vein drainage; CXR and cardiac MRI may assist.
  • 💊 Management
    Immediate stabilization with oxygen and ventilation; surgical correction is definitive.
  • 📊 Epidemiology
    Accounts for ~1–2% of congenital heart defects; higher risk in males and infants of diabetic mothers.
🏷️ Tags
Ebstein Anomaly
Ebstein Anomaly

Apical displacement of the tricuspid valve leaflets into the right ventricle.

  • 🟪 Overview
    Congenital malformation linked to maternal lithium exposure in early pregnancy.
  • 🧠 Pathophysiology
    Displaced tricuspid valve causes "atrialization" of part of the right ventricle and leads to tricuspid regurgitation.
  • 🩻 Clinical Presentation
    Cyanosis, right heart failure, widely split S2, tricuspid regurgitation murmur.
  • 🩺 Diagnosis
    Echocardiography shows apical displacement of tricuspid valve leaflets.
  • 💊 Management
    Medical therapy for heart failure, arrhythmia management, and surgical repair for severe cases.
  • 📊 Epidemiology
    Represents less than 1% of congenital heart defects; linked to maternal lithium or benzodiazepine use.
🏷️ Tags
Ventricular Septal Defect
Ventricular Septal Defect (VSD)

Abnormal opening in the interventricular septum allowing blood flow between ventricles.

  • 🟪 Overview
    Most common congenital heart defect; often closes spontaneously in childhood.
  • 🧠 Pathophysiology
    Left-to-right shunt increases pulmonary blood flow and volume load on the left heart.
  • 🩻 Clinical Presentation
    Harsh holosystolic murmur at the lower left sternal border, failure to thrive, dyspnea, frequent respiratory infections.
  • 🩺 Diagnosis
    Echocardiogram visualizes septal defect and estimates shunt size and direction.
  • 💊 Management
    Small VSDs may close spontaneously; large ones may need surgical closure or medical management for heart failure.
  • 📊 Epidemiology
    Occurs in ~2–6 per 1,000 live births; most common congenital heart lesion in infants.
🏷️ Tags
Atrial Septal Defect
Atrial Septal Defect (ASD)

A persistent opening between the atria that allows left-to-right shunting.

  • 🟪 Overview
    Commonly due to ostium secundum defect; often asymptomatic until adulthood.
  • 🧠 Pathophysiology
    Left-to-right shunt causes right atrial and ventricular dilation, increasing pulmonary blood flow.
  • 🩻 Clinical Presentation
    Wide fixed splitting of S2, systolic murmur at left upper sternal border, fatigue, recurrent respiratory infections.
  • 🩺 Diagnosis
    Echocardiography with bubble study confirms shunt; TEE better for adults.
  • 💊 Management
    Small ASDs may close spontaneously; large defects closed percutaneously or surgically.
  • 📊 Epidemiology
    Occurs in ~1 per 1,500 live births; second most common congenital heart defect after VSD.
🏷️ Tags
Patent Ductus Arteriosus
Patent Ductus Arteriosus (PDA)

Persistence of a fetal connection between the aorta and pulmonary artery.

  • 🟪 Overview
    Common in premature infants and those with congenital rubella infection.
  • 🧠 Pathophysiology
    Left-to-right shunt increases pulmonary flow, causing pulmonary hypertension and heart failure.
  • 🩻 Clinical Presentation
    Continuous "machine-like" murmur at left infraclavicular area, bounding pulses, widened pulse pressure.
  • 🩺 Diagnosis
    Echocardiogram confirms left-to-right shunting and ductal patency.
  • 💊 Management
    Indomethacin or ibuprofen to close the ductus; surgery if medical therapy fails.
  • 📊 Epidemiology
    Seen in ~1 per 2,000 term births; significantly higher in preterm infants.
🏷️ Tags
Persistent Pulmonary Hypertension of the Newborn
Persistent Pulmonary Hypertension of the Newborn (PPHN)

Failure of normal circulatory transition after birth, with persistently high pulmonary pressures.

  • 🟪 Overview
    Occurs when pulmonary vascular resistance remains abnormally elevated after birth.
  • 🧠 Pathophysiology
    Sustained high PVR leads to right-to-left shunting through ductus arteriosus and foramen ovale, causing hypoxemia.
  • 🩻 Clinical Presentation
    Severe cyanosis shortly after birth, tachypnea, respiratory distress, low oxygen saturation despite oxygen therapy.
  • 🩺 Diagnosis
    Pre- and post-ductal oxygen saturation difference; echocardiography shows right-to-left shunting.
  • 💊 Management
    Supportive care, mechanical ventilation, inhaled nitric oxide, ECMO for refractory cases.
  • 📊 Epidemiology
    Affects ~2 per 1,000 live births; more common in term/post-term neonates with birth stress or meconium aspiration.
🏷️ Tags
Hypertension
Hypertension

Chronic elevation of systemic arterial pressure, often asymptomatic but with long-term vascular damage.

  • 🟪 Overview
    Defined as systolic BP ≥130 mmHg or diastolic BP ≥80 mmHg (ACC/AHA guidelines); classified as primary (essential) or secondary.
  • 🧠 Pathophysiology
    Multifactorial: genetic predisposition, increased sympathetic tone, RAAS activation, renal sodium retention, and vascular remodeling.
  • 🩺 Diagnosis
    Requires ≥2 elevated readings on ≥2 separate occasions. Ambulatory or home BP monitoring may improve accuracy.
  • 💊 Management
    Lifestyle changes (diet, exercise, sodium restriction); meds include thiazides, ACE inhibitors/ARBs, calcium channel blockers, beta-blockers.
  • 🌍 Epidemiology
    Affects ~45% of U.S. adults. Leading modifiable risk factor for cardiovascular disease and stroke globally.
Xanthomas
Xanthomas

Lipid-rich, yellowish skin deposits associated with hyperlipidemia and systemic disorders.

  • 🟪 Overview
    Xanthomas are subcutaneous lipid accumulations due to abnormal lipid metabolism, often indicating elevated LDL, triglycerides, or systemic diseases.
  • 🧠 Pathophysiology
    Macrophages engulf excess lipids and form foam cells, which deposit in skin and tendons, forming yellowish plaques or nodules.
  • 🩺 Diagnosis
    Clinical diagnosis based on appearance; lipid panel, family history, and screening for metabolic syndromes guide workup.
  • 💊 Management
    Treat underlying lipid disorder; statins, fibrates, niacin; lesions may regress with lipid control or require removal if symptomatic.
  • 🌍 Epidemiology
    Relatively uncommon; often seen in familial hypercholesterolemia and rare lipid metabolism disorders.
Tendinous Xanthoma
Tendinous Xanthoma

Firm nodules on tendons, especially Achilles or extensor tendons, seen in familial hypercholesterolemia.

  • 🟪 Overview
    A type of xanthoma characterized by lipid deposits in tendons, most commonly associated with familial hypercholesterolemia.
  • 🧠 Pathophysiology
    LDL particles accumulate in the connective tissue of tendons, where they are taken up by macrophages and form foam cells.
  • 🩺 Diagnosis
    Palpable, firm nodules in typical locations; lipid panel typically shows markedly elevated LDL. Often diagnostic in clinical context.
  • 💊 Management
    Aggressive lipid-lowering therapy (statins, ezetimibe, PCSK9 inhibitors); may require surgery if painful or disabling.
  • 🌍 Epidemiology
    Seen in ~30–50% of individuals with familial hypercholesterolemia. Rare in the general population.
Corneal Arcus
Corneal Arcus

Lipid deposits in the corneal periphery, often seen with hyperlipidemia or aging.

  • 🟪 Overview
    Corneal arcus appears as a white-gray ring at the edge of the cornea, typically associated with elevated lipids or age-related changes.
  • 🧠 Pathophysiology
    Lipid infiltration into the peripheral corneal stroma leads to light-scattering deposits without impairing vision.
  • 🩺 Diagnosis
    Diagnosed by slit-lamp exam; lipid panel often reveals hypercholesterolemia if seen in patients less than 50 years old.
  • 💊 Management
    Treat underlying dyslipidemia if present. No treatment is needed if age-related and asymptomatic.
  • 🌍 Epidemiology
    Common in elderly; if present before age 50, it suggests familial hypercholesterolemia or secondary dyslipidemia.
Atherosclerosis
Atherosclerosis

Chronic inflammatory disease of the arterial wall, causing plaque buildup and vascular narrowing.

  • 🟪 Overview
    A progressive condition where lipids and inflammatory cells form plaques within arteries, leading to ischemic complications like MI and stroke.
  • 🧠 Pathophysiology
    Endothelial injury triggers LDL infiltration, oxidation, macrophage foam cell formation, and smooth muscle proliferation forming fibrous plaques.
  • 🩺 Diagnosis
    Doppler US, CT angiography, coronary calcium scoring, and lipid profiles used to assess vascular involvement and risk.
  • 💊 Management
    Lifestyle changes, statins, antihypertensives, antiplatelet agents, and glucose control. Severe cases may require stenting or bypass.
  • 🌍 Epidemiology
    Leading cause of death globally. Risk increases with age, smoking, hypertension, diabetes, and high LDL.
Cholesterol Emboli Syndrome
Cholesterol Emboli Syndrome

Microemboli of cholesterol crystals cause multi-organ ischemia after vascular manipulation.

  • 🟪 Overview
    Cholesterol emboli syndrome (CES) is an iatrogenic complication of vascular procedures, often presenting with AKI, livedo reticularis, and eosinophilia.
  • 🧠 Pathophysiology
    Atherosclerotic plaques rupture and release cholesterol crystals that embolize to small arteries, causing ischemia and inflammation.
  • 🩺 Diagnosis
    Clinical diagnosis; biopsy (skin/kidney) shows biconvex cholesterol clefts. Often triggered by angiography or anticoagulation.
  • 💊 Management
    Supportive care; discontinue anticoagulation if safe. Statins may stabilize plaques. Prognosis depends on organ involvement.
  • 🌍 Epidemiology
    Rare, often underdiagnosed. Incidence ~1–4% in patients undergoing cardiac catheterization.
Arteriolosclerosis
Arteriolosclerosis

Thickening of small arteries/arterioles due to chronic hypertension or diabetes.

  • 🟪 Overview
    Arteriolosclerosis refers to the hardening and narrowing of arterioles, often secondary to chronic conditions like hypertension or diabetes.
  • 🧠 Pathophysiology
    Two types: hyaline (protein leakage, thickened walls in diabetes/HTN) and hyperplastic ("onion-skin" smooth muscle proliferation in severe HTN).
  • 🩺 Diagnosis
    Histopathology reveals hyaline deposits or concentric smooth muscle layers. Often inferred based on clinical background.
  • 💊 Management
    Manage underlying cause: blood pressure control, glucose control, statins, lifestyle changes.
  • 🌍 Epidemiology
    Extremely common in patients with long-standing hypertension and/or diabetes, especially in the elderly.
Aortic Aneurysm
Aortic Aneurysm

Abnormal dilation of the aorta due to wall weakening, often from atherosclerosis or genetic disorders.

  • 🟪 Overview
    Aneurysms can occur in thoracic or abdominal aorta, commonly due to atherosclerosis (abdominal) or connective tissue disorders (thoracic).
  • 🧠 Pathophysiology
    Degradation of elastin and smooth muscle in the aortic media leads to wall thinning and dilation; smoking is a major risk factor.
  • 🩺 Diagnosis
    Ultrasound (screening), CT angiography (pre-op or rupture). Defined as ≥3 cm dilation for abdominal aorta.
  • 💊 Management
    Monitor size regularly; surgical repair if ≥5.5 cm or rapid growth. Risk reduction: smoking cessation, BP control.
  • 🌍 Epidemiology
    Prevalence ~4–8% in men >65. Major cause of sudden death in older adults; more common in smokers.
Traumatic Aortic Rupture
Traumatic Aortic Rupture

Tearing of the aortic wall due to high-speed trauma, most commonly at the aortic isthmus.

  • 🟪 Overview
    Life-threatening injury caused by deceleration trauma (e.g., motor vehicle accidents). Often fatal at the scene.
  • 🧠 Pathophysiology
    Sudden deceleration shears the aortic isthmus (just distal to left subclavian artery), leading to rupture of the intima and media.
  • 🩺 Diagnosis
    CT angiography is the gold standard. Chest X-ray may show widened mediastinum. High suspicion in trauma settings.
  • 💊 Management
    Urgent surgical or endovascular repair. Blood pressure and heart rate control are critical to reduce further stress.
  • 🌍 Epidemiology
    Accounts for up to 20% of deaths in high-speed trauma. Most survivors need rapid diagnosis and intervention.
Aortic Dissection
Aortic Dissection

Tear in the aortic intima allows blood to track between layers, forming a false lumen.

  • 🟪 Overview
    Aortic dissection is a medical emergency that classically presents with sudden, tearing chest or back pain. Associated with hypertension and connective tissue disorders.
  • 🧠 Pathophysiology
    A tear in the tunica intima allows blood to enter the media layer, creating a false lumen; can compress true lumen and lead to ischemia of major organs.
  • 🩺 Diagnosis
    CT angiography is the diagnostic test of choice. Look for mediastinal widening on chest X-ray. May have asymmetrical pulses.
  • 💊 Management
    Type A (ascending) requires surgery; Type B (descending) treated medically with beta blockers and BP control unless complications arise.
  • 🌍 Epidemiology
    Incidence ~3 per 100,000/year. Risk factors include hypertension, Marfan syndrome, and cocaine use.
Subclavian Steal Syndrome
Subclavian Steal Syndrome

Blood is diverted from the brain to the arm due to subclavian artery stenosis proximal to the vertebral artery.

  • 🟪 Overview
    Occurs when proximal subclavian artery stenosis causes retrograde flow in the ipsilateral vertebral artery, “stealing” blood from cerebral circulation during arm exertion.
  • 🧠 Pathophysiology
    Stenosis of the proximal subclavian artery drops pressure distal to the lesion, reversing flow in the vertebral artery during exercise or arm use.
  • 🩺 Diagnosis
    Duplex ultrasound shows reversed vertebral artery flow. Confirm with CT or MR angiography.
  • 💊 Management
    Manage atherosclerosis risk factors; stenting or bypass for severe symptomatic cases.
  • 🌍 Epidemiology
    Uncommon; more frequent in older adults with widespread atherosclerosis. Often asymptomatic.
Angina
Angina

Chest discomfort due to transient myocardial ischemia without infarction.

  • 🟪 Overview
    Angina is categorized as stable (predictable with exertion), unstable (worsening or new), or Prinzmetal/variant (vasospasm).
  • 🧠 Pathophysiology
    Coronary artery narrowing from atherosclerosis impairs oxygen delivery to myocardium, particularly during stress or exertion.
  • 🩺 Diagnosis
    ECG, stress testing, and imaging (e.g., nuclear perfusion scan, coronary angiography) used to confirm ischemia and guide treatment.
  • 💊 Management
    Lifestyle changes, beta blockers, nitrates, calcium channel blockers. Consider PCI or CABG in high-risk patients.
  • 🌍 Epidemiology
    Affects millions globally. Stable angina is a common early symptom of coronary artery disease.
Coronary Steal Syndrome
Coronary Steal Syndrome

Vasodilation diverts blood from ischemic myocardial regions due to collateral-dependent perfusion.

  • 🟪 Overview
    Occurs when vasodilators (e.g., dipyridamole) cause dilation of healthy coronary vessels, reducing perfusion to areas dependent on collateral flow.
  • 🧠 Pathophysiology
    Vasodilators preferentially dilate non-ischemic vessels, "stealing" flow from post-stenotic areas that rely on autoregulated collaterals.
  • 🩺 Diagnosis
    Observed during pharmacologic stress testing with agents like dipyridamole or adenosine; reversible perfusion defects seen on imaging.
  • 💊 Management
    Avoid vasodilators in patients with known ischemia. Revascularization may be needed for symptomatic or high-risk patients.
  • 🌍 Epidemiology
    Primarily encountered as a phenomenon during stress testing in those with obstructive coronary artery disease.
Sudden Cardiac Death
Sudden Cardiac Death

Unexpected death due to cardiac causes, typically from ventricular arrhythmia within 1 hour of symptom onset.

  • 🟪 Overview
    SCD most often results from ischemic heart disease triggering a fatal arrhythmia, especially ventricular fibrillation or tachycardia.
  • 🧠 Pathophysiology
    Myocardial ischemia alters electrical stability, creating reentry circuits and increased excitability leading to lethal rhythms.
  • 🩺 Diagnosis
    Clinical event; autopsy may show coronary artery disease, hypertrophic cardiomyopathy, or channelopathies like long QT.
  • 💊 Management
    Immediate CPR and defibrillation. ICD placement for survivors or high-risk patients (e.g., EF less than 35%).
  • 🌍 Epidemiology
    Accounts for ~50% of all cardiac deaths. Most common in older men with known or silent CAD.
Chronic Ischemic Heart Disease
Chronic Ischemic Heart Disease

Progressive myocardial dysfunction from longstanding coronary insufficiency.

  • 🟪 Overview
    A consequence of repeated ischemic insults or post-MI remodeling that leads to heart failure and arrhythmias over time.
  • 🧠 Pathophysiology
    Chronic hypoperfusion impairs myocardial contractility, causing ventricular remodeling, fibrosis, and systolic dysfunction.
  • 🩺 Diagnosis
    Echocardiography, nuclear imaging, or cardiac MRI shows prior infarcts, wall motion abnormalities, or reduced EF.
  • 💊 Management
    Standard CHF treatment: ACE inhibitors, beta blockers, diuretics, aldosterone antagonists. Revascularization if viable myocardium present.
  • 🌍 Epidemiology
    Common in post-MI patients and those with long-standing coronary artery disease.
Myocardial Infarction
Myocardial Infarction (MI)

Necrosis of myocardial tissue due to prolonged ischemia, usually from plaque rupture and thrombosis.

  • 🟪 Overview
    MI is classified as STEMI or NSTEMI depending on ECG findings. Both are types of acute coronary syndrome due to coronary occlusion.
  • 🧠 Pathophysiology
    Atherosclerotic plaque rupture → thrombosis → occlusion of coronary artery → myocardial ischemia and necrosis.
  • 🩺 Diagnosis
    Elevated troponins, ST elevation (STEMI), or ST depression/T-wave inversion (NSTEMI) on ECG. Imaging may show wall motion abnormalities.
  • 💊 Management
    Aspirin, P2Y12 inhibitor, anticoagulation, beta-blockers, nitrates. STEMI requires urgent PCI or thrombolysis.
  • 🌍 Epidemiology
    Leading cause of death globally. Risk increases with age, smoking, hypertension, diabetes, and dyslipidemia.
Atrial Fibrillation
Atrial Fibrillation (AFib)

Irregularly irregular rhythm due to chaotic atrial electrical activity, leading to loss of atrial contraction.

  • 🟪 Overview
    AFib is the most common sustained arrhythmia, increasing risk for stroke, heart failure, and thromboembolism.
  • 🧠 Pathophysiology
    Ectopic foci (often near pulmonary veins) trigger fibrillatory waves, causing disorganized atrial activity and variable ventricular response.
  • 🩺 Diagnosis
    ECG shows no P waves, irregularly irregular R-R intervals. Evaluate for underlying causes with labs and echocardiogram.
  • 💊 Management
    Rate control (beta-blockers, CCBs), anticoagulation (CHA₂DS₂-VASc score), rhythm control (antiarrhythmics, cardioversion) when needed.
  • 🌍 Epidemiology
    Prevalence ~2–3% in general population; increases significantly with age.
Multifocal Atrial Tachycardia
Multifocal Atrial Tachycardia (MAT)

An irregular atrial rhythm with ≥3 distinct P wave morphologies, often seen in pulmonary disease.

  • 🟪 Overview
    MAT is a supraventricular tachycardia frequently associated with COPD, hypoxia, and electrolyte abnormalities.
  • 🧠 Pathophysiology
    Multiple ectopic atrial pacemakers fire in a disorganized pattern due to increased atrial automaticity from hypoxia or stretch.
  • 🩺 Diagnosis
    ECG shows ≥3 different P wave morphologies, irregular rhythm, and HR >100 bpm. Often in patients with lung disease.
  • 💊 Management
    Treat underlying cause (e.g., hypoxia). Beta-blockers or CCBs may be used for rate control if needed.
  • 🌍 Epidemiology
    Primarily affects elderly patients with chronic lung disease or electrolyte imbalances.
Atrial Flutter
Atrial Flutter

Rapid, regular atrial contractions with characteristic sawtooth flutter waves on ECG.

  • 🟪 Overview
    Atrial flutter is a macro-reentrant atrial arrhythmia usually involving a circuit around the tricuspid annulus.
  • 🧠 Pathophysiology
    A single reentrant loop causes atria to contract rapidly (~300 bpm) with some AV node filtering to the ventricles.
  • 🩺 Diagnosis
    ECG shows sawtooth flutter waves best seen in leads II, III, and aVF. Regular ventricular rate unless variable block.
  • 💊 Management
    Rate control, anticoagulation, cardioversion, or catheter ablation targeting the cavotricuspid isthmus.
  • 🌍 Epidemiology
    Less common than AFib but frequently coexists. Seen in structural heart disease and post-MI.
PSVT
Paroxysmal Supraventricular Tachycardia (PSVT)

Sudden onset and offset of rapid regular heartbeat originating above the ventricles.

  • 🟪 Overview
    PSVT includes AV nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT), both of which use reentry circuits.
  • 🧠 Pathophysiology
    Reentry circuit between fast and slow AV node pathways or between AV node and accessory pathway causes rapid regular rhythm.
  • 🩺 Diagnosis
    ECG shows narrow QRS complex tachycardia, regular rhythm. P waves often buried in T waves or retrograde.
  • 💊 Management
    Vagal maneuvers, adenosine (first-line), beta-blockers or CCBs. Refractory cases may benefit from ablation.
  • 🌍 Epidemiology
    More common in younger individuals. May present with palpitations, dizziness, or syncope.
Wolff-Parkinson-White Syndrome
Wolff-Parkinson-White (WPW)

Pre-excitation syndrome due to accessory pathway between atria and ventricles (Bundle of Kent).

  • 🟪 Overview
    WPW allows early ventricular depolarization through the accessory pathway, which can facilitate reentrant tachyarrhythmias.
  • 🧠 Pathophysiology
    Bundle of Kent bypasses the AV node, creating a direct electrical connection between atria and ventricles, enabling AVRT.
  • 🩺 Diagnosis
    ECG shows delta wave, short PR interval, wide QRS. May be found incidentally or during SVT episode.
  • 💊 Management
    Avoid AV node blockers (e.g., adenosine, beta-blockers) in AF with WPW. Use procainamide or ablation of accessory pathway.
  • 🌍 Epidemiology
    Prevalence ~0.1–0.3% of population. Symptoms often begin in adolescence or early adulthood.
Ventricular Tachycardia
Ventricular Tachycardia

A wide complex tachycardia originating in the ventricles, often life-threatening if sustained.

  • 🟪 Overview
    VT is a potentially lethal rhythm commonly seen after myocardial infarction or with structural heart disease.
  • 🧠 Pathophysiology
    Reentrant circuits or abnormal automaticity in the ventricles trigger rapid, ineffective contractions with wide QRS.
  • 🩺 Diagnosis
    ECG shows regular wide QRS complexes, usually >120 bpm. May have AV dissociation or capture/fusion beats.
  • 💊 Management
    Stable: antiarrhythmics (amiodarone, lidocaine). Unstable: immediate synchronized cardioversion. ICD for recurrent VT.
  • 🌍 Epidemiology
    Common in patients with ischemic heart disease and cardiomyopathy. Major cause of sudden cardiac death.
Torsades de Pointes
Torsades de Pointes

A polymorphic VT with twisting QRS complexes, associated with prolonged QT interval.

  • 🟪 Overview
    Torsades is a specific type of polymorphic VT that can degenerate into VF and often presents with syncope or sudden death.
  • 🧠 Pathophysiology
    Triggered by early afterdepolarizations due to prolonged repolarization (long QT). Drugs and electrolyte imbalances are common causes.
  • 🩺 Diagnosis
    ECG shows sinusoidal or “twisting” morphology with varying QRS amplitude and axis around the baseline.
  • 💊 Management
    IV magnesium sulfate, discontinue QT-prolonging drugs. Correct electrolytes. Defibrillation if pulseless.
  • 🌍 Epidemiology
    Rare but potentially fatal. Associated with congenital long QT, antiarrhythmics, antipsychotics, and hypokalemia/hypomagnesemia.
Ventricular Fibrillation
Ventricular Fibrillation

Disorganized, chaotic ventricular rhythm resulting in no cardiac output and death without intervention.

  • 🟪 Overview
    VF is the terminal arrhythmia in many cases of cardiac arrest. Characterized by erratic electrical activity with no effective heartbeat.
  • 🧠 Pathophysiology
    Multiple ectopic foci or reentry pathways cause chaotic depolarization of the ventricles, halting coordinated contraction.
  • 🩺 Diagnosis
    ECG shows irregular, fibrillatory baseline with no identifiable QRS complexes or P waves. Pulse is absent.
  • 💊 Management
    Immediate defibrillation (unsynchronized shock), CPR, epinephrine. Long-term: ICD placement in survivors.
  • 🌍 Epidemiology
    VF is responsible for most sudden cardiac deaths. Common in MI and structural heart disease.
Brugada Syndrome
Brugada Syndrome

Genetic disorder causing ST elevations and risk of ventricular arrhythmias and sudden death.

  • 🟪 Overview
    Brugada syndrome is an inherited channelopathy most often seen in Asian males, presenting with sudden cardiac death or syncope.
  • 🧠 Pathophysiology
    SCN5A mutation leads to decreased sodium current, predisposing to ventricular arrhythmias and conduction abnormalities.
  • 🩺 Diagnosis
    ECG shows pseudo–right bundle branch block with ST elevations in V1–V3. Provocative testing with sodium channel blockers may unmask.
  • 💊 Management
    Implantable cardioverter-defibrillator (ICD) is first-line. Avoid drugs that prolong QT or reduce Na⁺ current.
  • 🌍 Epidemiology
    Most common in Southeast Asian men; rare overall. Often presents in 3rd or 4th decade of life.
Congenital Long QT Syndrome
Congenital Long QT Syndrome

Inherited ion channel disorder prolonging cardiac repolarization, increasing risk of torsades and sudden death.

  • 🟪 Overview
    Congenital LQTS is caused by mutations in potassium or sodium channels, leading to prolonged QT on ECG and syncope or SCD.
  • 🧠 Pathophysiology
    Defective ion channels prolong the action potential, increasing risk of early afterdepolarizations and torsades de pointes.
  • 🩺 Diagnosis
    QTc >460 ms in females or >440 ms in males on ECG. Genetic testing may confirm subtype (e.g., Jervell, Romano-Ward).
  • 💊 Management
    Beta-blockers (esp. propranolol), ICD if high risk. Avoid QT-prolonging drugs and strenuous exertion.
  • 🌍 Epidemiology
    Prevalence estimated ~1 in 2,000. Leading cause of sudden death in the young.
Sick Sinus Syndrome
Sick Sinus Syndrome

SA node dysfunction causing bradycardia, sinus arrest, or alternating brady-tachy episodes.

  • 🟪 Overview
    Sick sinus syndrome is a collection of arrhythmias caused by failure of the sinus node to generate or propagate impulses.
  • 🧠 Pathophysiology
    Fibrosis, ischemia, or degeneration of the SA node impairs pacemaking ability, causing pauses or rhythm instability.
  • 🩺 Diagnosis
    ECG or Holter may show sinus pauses, arrest, or alternating brady-tachycardia. Symptoms include dizziness or syncope.
  • 💊 Management
    Permanent pacemaker for symptomatic bradycardia. Treat underlying causes and avoid bradycardia-inducing drugs.
  • 🌍 Epidemiology
    Most common in elderly patients. Major indication for pacemaker implantation in the U.S.
First Degree AV Block
First Degree AV Block

Prolonged PR interval (>200 ms) due to delayed conduction through the AV node.

  • 🟪 Overview
    Often asymptomatic and found incidentally. Rarely requires treatment.
  • 🧠 Pathophysiology
    Conduction is slowed but not blocked through the AV node, prolonging the PR interval uniformly.
  • 🩺 Diagnosis
    ECG shows PR interval >200 ms. No dropped beats.
  • 💊 Management
    Usually no treatment needed. Monitor and manage underlying causes (e.g., electrolyte imbalance, drug effect).
  • 🌍 Epidemiology
    Common in older adults and athletes. May be drug-induced (e.g., beta-blockers, CCBs).
Mobitz I
Second Degree AV Block (Mobitz I - Wenckebach)

Progressively lengthening PR intervals until a beat is dropped.

  • 🟪 Overview
    Benign AV block typically seen in athletes or with high vagal tone. Usually asymptomatic.
  • 🧠 Pathophysiology
    Impaired conduction through the AV node results in increasing PR intervals until a P wave fails to conduct.
  • 🩺 Diagnosis
    ECG shows progressive PR prolongation followed by a dropped QRS complex.
  • 💊 Management
    Usually no treatment. Monitor and correct reversible causes. Rarely requires pacemaker.
  • 🌍 Epidemiology
    Common in young, healthy individuals and during sleep.
Mobitz II
Second Degree AV Block (Mobitz II)

Intermittent dropped QRS complexes without PR prolongation.

  • 🟪 Overview
    More dangerous than Mobitz I due to unpredictable dropped beats. Can progress to complete heart block.
  • 🧠 Pathophysiology
    Conduction failure occurs below the AV node (e.g., His-Purkinje system) without progressive delay.
  • 🩺 Diagnosis
    ECG shows constant PR intervals with sudden dropped QRS complexes (e.g., 2:1 or 3:1 block).
  • 💊 Management
    Requires pacemaker due to risk of progression. Discontinue AV node-blocking agents.
  • 🌍 Epidemiology
    Less common than Mobitz I but more likely to be symptomatic or require intervention.
Third Degree AV Block
Third Degree AV Block

Complete dissociation between atrial and ventricular activity due to failure of AV conduction.

  • 🟪 Overview
    Medical emergency. The atria and ventricles beat independently with a slow escape rhythm.
  • 🧠 Pathophysiology
    Total conduction block below the AV node prevents impulses from reaching ventricles. Escape rhythm takes over.
  • 🩺 Diagnosis
    ECG shows P waves and QRS complexes that occur independently. Atrial rate > ventricular rate.
  • 💊 Management
    Requires permanent pacemaker. Temporary pacing if unstable. Stop AV nodal blockers.
  • 🌍 Epidemiology
    Often seen in older adults or due to ischemic heart disease, Lyme carditis, or congenital causes.
Bundle Branch Block
Bundle Branch Block

Delay or block in electrical conduction through right or left bundle branches.

  • 🟪 Overview
    Can be benign or associated with structural heart disease. Right BBB may be normal; left BBB usually pathologic.
  • 🧠 Pathophysiology
    Damage or delay in His-Purkinje system impairs conduction to ventricles, causing QRS widening and abnormal morphology.
  • 🩺 Diagnosis
    ECG shows wide QRS (>120 ms) with specific features for RBBB (rsR' in V1) or LBBB (broad notched R in I, aVL, V5-V6).
  • 💊 Management
    Treat underlying disease. LBBB may mask MI; consider advanced imaging if suspected.
  • 🌍 Epidemiology
    RBBB more common in general population. LBBB associated with aging and hypertension or ischemic heart disease.
Premature Atrial Contraction
Premature Atrial Contraction (PAC)

Early depolarization originating from ectopic atrial focus, often benign.

  • 🟪 Overview
    Common in healthy individuals or with stimulants like caffeine. Usually asymptomatic.
  • 🧠 Pathophysiology
    Atrial cells outside the SA node spontaneously depolarize, producing a premature P wave.
  • 🩺 Diagnosis
    ECG shows early P wave with abnormal morphology, followed by normal QRS. May be followed by a compensatory pause.
  • 💊 Management
    No treatment needed unless symptomatic. Avoid triggers. Beta-blockers for frequent symptomatic PACs.
  • 🌍 Epidemiology
    Very common. Seen in all age groups, especially with stress, caffeine, or alcohol.
Premature Ventricular Contraction
Premature Ventricular Contraction (PVC)

Early ventricular beat due to ectopic focus in the ventricles, leading to wide QRS.

  • 🟪 Overview
    PVCs are common and often benign. May cause palpitations or be asymptomatic.
  • 🧠 Pathophysiology
    Ectopic focus in ventricles fires before the next sinus beat, leading to abnormal ventricular contraction.
  • 🩺 Diagnosis
    ECG shows wide, bizarre QRS not preceded by a P wave, often with compensatory pause.
  • 💊 Management
    No treatment if asymptomatic. Beta-blockers or ablation if frequent or causing cardiomyopathy.
  • 🌍 Epidemiology
    Prevalence increases with age. Often seen in healthy hearts and in structural heart disease.
Cardiac Arrhythmia
Cardiac Arrhythmia

Abnormal heart rhythm due to irregular electrical conduction.

  • 🟪 Overview
    Umbrella term for rhythm disturbances including bradycardia, tachycardia, fibrillation, and more.
  • 🧠 Pathophysiology
    Caused by abnormalities in impulse generation (automaticity), conduction (reentry), or both.
  • 🩺 Diagnosis
    ECG monitoring, Holter monitor, event recorder, or implantable loop recorder.
  • 💊 Management
    Depends on type; includes antiarrhythmics, ablation, pacemakers, or defibrillators.
  • 🌍 Epidemiology
    Very common, especially in elderly populations or those with structural heart disease.
Peri-Infarction Pericarditis
Peri-Infarction Pericarditis

Inflammation of pericardium days after myocardial infarction.

  • 🟪 Overview
    Occurs 1–3 days post-MI due to transmural inflammation. Different from Dressler syndrome (which is autoimmune).
  • 🧠 Pathophysiology
    Inflammatory response to myocardial necrosis spreads to adjacent pericardium.
  • 🩺 Diagnosis
    Pleuritic chest pain, friction rub, ECG may show diffuse ST elevation (less common post-MI).
  • 💊 Management
    High-dose aspirin is preferred (NSAIDs avoided post-MI due to healing interference).
Papillary Muscle Rupture
Papillary Muscle Rupture

Acute mitral regurgitation following myocardial infarction.

  • 🟪 Overview
    Typically occurs 2–7 days after inferior MI, especially with RCA occlusion.
  • 🧠 Pathophysiology
    Infarction weakens the papillary muscle, causing rupture and inability to hold mitral valve closed.
  • 🩺 Diagnosis
    Sudden-onset pulmonary edema, new holosystolic murmur at apex. Confirm with echocardiogram.
  • 💊 Management
    Emergency surgical repair. Stabilize with vasodilators, diuretics, and inotropes.
Interventricular Septal Rupture
Interventricular Septal Rupture

Life-threatening post-MI complication causing VSD and cardiogenic shock.

  • 🟪 Overview
    Occurs 3–5 days post-MI, more common with anterior infarcts (LAD occlusion).
  • 🧠 Pathophysiology
    Necrotic septum ruptures, creating left-to-right shunt and decreased cardiac output.
  • 🩺 Diagnosis
    Harsh holosystolic murmur with thrill, signs of shock. Confirm with echo + Doppler.
  • 💊 Management
    Urgent surgical closure. Stabilize with vasopressors, intra-aortic balloon pump.
Ventricular Pseudoaneurysm
Ventricular Pseudo-aneurysm

Contained rupture of the ventricular free wall post-MI.

  • 🟪 Overview
    A false aneurysm formed when myocardial rupture is sealed by pericardium or scar tissue.
  • 🧠 Pathophysiology
    Incomplete rupture of the ventricular wall allows blood to pool in pericardial space, bounded externally.
  • 🩺 Diagnosis
    Echocardiogram or cardiac MRI shows narrow-necked outpouching. May present with chest pain or hypotension.
  • 💊 Management
    Surgical repair is often required due to risk of rupture.
Free Wall Rupture
Ventricular Free Wall Rupture

Catastrophic rupture of the ventricular wall post-MI, often fatal.

  • 🟪 Overview
    Usually occurs within 1–7 days of MI, especially with first-time anterior MIs.
  • 🧠 Pathophysiology
    Transmural infarction weakens the wall, leading to rupture and pericardial tamponade.
  • 🩺 Diagnosis
    Sudden hypotension, electromechanical dissociation. Echo shows hemopericardium. Often diagnosed postmortem.
  • 💊 Management
    Emergency surgical repair if identified. Prevent with reperfusion therapy.
True Ventricular Aneurysm
True Ventricular Aneurysm

Outpouching of scarred ventricular wall post-MI, with low risk of rupture.

  • 🟪 Overview
    Develops weeks after MI. True aneurysms are lined by myocardium and pericardium.
  • 🧠 Pathophysiology
    Fibrotic remodeling leads to a thinned, dyskinetic myocardial segment.
  • 🩺 Diagnosis
    ECG shows persistent ST elevation. Echo or MRI confirms outpouching with wide neck.
  • 💊 Management
    Medical therapy unless refractory heart failure or thrombus → consider surgical repair.
Post-Cardiac Injury Syndrome
Post-Cardiac Injury Syndrome

Autoimmune pericarditis following myocardial infarction or surgery.

  • 🟪 Overview
    Also called Dressler syndrome. Occurs weeks after injury to the heart.
  • 🧠 Pathophysiology
    Immune response to myocardial antigens causes pericardial inflammation.
  • 🩺 Diagnosis
    Pleuritic chest pain, pericardial friction rub, fever, leukocytosis. Confirm with ECG and echo.
  • 💊 Management
    NSAIDs and colchicine. Avoid steroids if possible. Monitor for effusion.
Dilated Cardiomyopathy
Dilated Cardiomyopathy

Most common type of cardiomyopathy with ventricular dilation and systolic dysfunction.

  • 🟪 Overview
    Causes include genetic mutations, alcohol, doxorubicin, viral myocarditis, and peripartum cardiomyopathy.
  • 🧠 Pathophysiology
    Dilated ventricles have impaired contractility, leading to systolic heart failure and reduced ejection fraction.
  • 🩺 Diagnosis
    Echocardiogram shows enlarged ventricles with reduced EF. MRI, biopsy, or labs for underlying cause.
  • 💊 Management
    Guideline-directed HF therapy (ACEi, beta-blockers, diuretics), ICD if severe EF, transplant in refractory cases.
Hypertrophic Cardiomyopathy
Hypertrophic Cardiomyopathy

Genetic condition characterized by asymmetric septal hypertrophy and diastolic dysfunction.

  • 🟪 Overview
    Autosomal dominant mutation in sarcomere proteins (e.g., beta-myosin heavy chain).
  • 🧠 Pathophysiology
    Myocardial hypertrophy leads to decreased compliance, outflow obstruction, and increased risk of arrhythmias.
  • 🩺 Diagnosis
    Echocardiogram shows asymmetric septal thickening. EKG may show LVH or deep Q waves. Confirm with MRI/genetics.
  • 💊 Management
    Beta-blockers, non-dihydropyridine CCBs. Avoid preload/afterload reducers. ICD if high risk of SCD.
Restrictive Cardiomyopathy
Restrictive Cardiomyopathy

Stiff ventricles impair diastolic filling with preserved systolic function.

  • 🟪 Overview
    Associated with infiltrative diseases: amyloidosis, sarcoidosis, hemochromatosis, and radiation fibrosis.
  • 🧠 Pathophysiology
    Decreased compliance prevents ventricular relaxation and filling during diastole → right-sided HF symptoms.
  • 🩺 Diagnosis
    Echo shows normal EF with biatrial enlargement. Cardiac MRI or biopsy confirms etiology.
  • 💊 Management
    Treat underlying cause. Diuretics for symptom relief. Consider transplant in advanced cases.
Heart Failure
Heart Failure

Syndrome of reduced cardiac output leading to symptoms of congestion and/or hypoperfusion.

  • 🟪 Overview
    Includes HFrEF and HFpEF. Etiologies include ischemia, HTN, valvular disease, and cardiomyopathy.
  • 🧠 Pathophysiology
    Inadequate forward flow (low output) and/or increased filling pressures (congestion).
  • 🩺 Diagnosis
    Echo for EF. BNP/NT-proBNP, CXR, ECG. Use Framingham criteria for clinical Dx.
  • 💊 Management
    Lifestyle changes + GDMT (ACEi/ARB/ARNI, beta-blockers, diuretics, SGLT2i). ICD, CRT if indicated.
Shock
Shock

Critical condition of inadequate tissue perfusion leading to cellular dysfunction.

  • 🟪 Overview
    Types include hypovolemic, cardiogenic, distributive (septic, anaphylactic), and obstructive.
  • 🧠 Pathophysiology
    Failure to deliver sufficient oxygen to tissues due to low flow, vasodilation, or pump failure.
  • 🩺 Diagnosis
    Hypotension, tachycardia, cold/clammy skin, lactate elevation. Confirm with labs and hemodynamic monitoring.
  • 💊 Management
    Depends on type. Volume resuscitation, vasopressors, antibiotics, inotropes, or relieving obstruction.
Cardiac Tamponade
Cardiac Tamponade

Life-threatening accumulation of fluid in the pericardial sac compressing the heart.

  • 🟪 Overview
    Caused by trauma, malignancy, uremia, pericarditis, or rupture. Rapid onset worsens outcome.
  • 🧠 Pathophysiology
    Pressure prevents ventricular filling → decreased stroke volume → shock.
  • 🩺 Diagnosis
    Beck triad: hypotension, JVD, muffled heart sounds. Confirm with echo. Pulsus paradoxus >10 mmHg.
  • 💊 Management
    Emergency pericardiocentesis or surgical drainage.
Syncope
Syncope

Transient loss of consciousness due to global cerebral hypoperfusion.

  • 🟪 Overview
    Classified as vasovagal, orthostatic, cardiac, or neurologic. Most cases are benign.
  • 🧠 Pathophysiology
    Mismatch in autonomic tone or structural heart issues reduce blood to brain transiently.
  • 🩺 Diagnosis
    History and physical. ECG, tilt table, echo, or Holter monitoring as needed.
  • 💊 Management
    Treat underlying cause. Educate on triggers. Pacemaker if bradycardia-related.
Infective Endocarditis
Infective Endocarditis

Infection of the endocardial surface, typically affecting heart valves.

  • 🟪 Overview
    Risk factors: prosthetic valves, IV drug use, dental procedures, structural heart disease.
  • 🧠 Pathophysiology
    Bacteremia seeds valve → vegetations → inflammation, emboli, valve destruction.
  • 🩺 Diagnosis
    Duke criteria: blood cultures, echo (vegetation), clinical signs (Janeway, Osler, Roth spots).
  • 💊 Management
    IV antibiotics 4–6 weeks. Valve surgery if severe dysfunction or abscess. Prophylaxis in high-risk patients.
Nonbacterial Thrombotic Endocarditis
Nonbacterial Thrombotic Endocarditis

Sterile vegetations on valves, often associated with hypercoagulable states.

  • 🟪 Overview
    Seen in malignancy (esp. mucinous adenocarcinomas), lupus (Libman-Sacks), and antiphospholipid syndrome.
  • 🧠 Pathophysiology
    Endothelial injury or hypercoagulable states promote sterile fibrin/platelet deposition on valves.
  • 🩺 Diagnosis
    Echocardiogram shows vegetations. Negative blood cultures. Associated thromboembolic events.
  • 💊 Management
    Treat underlying cause and anticoagulate to reduce embolic risk.
Rheumatic Fever
Rheumatic Fever

Autoimmune inflammatory disease following group A strep pharyngitis.

  • 🟪 Overview
    Common in developing countries. Can cause chronic rheumatic heart disease, especially mitral stenosis.
  • 🧠 Pathophysiology
    Molecular mimicry → cross-reactivity of antibodies against M protein with cardiac tissue.
  • 🩺 Diagnosis
    Jones criteria: migratory polyarthritis, carditis, nodules, erythema marginatum, chorea.
  • 💊 Management
    Penicillin for strep, anti-inflammatories, long-term prophylaxis to prevent recurrence.
Syphilitic Heart Disease
Syphilitic Heart Disease

Late manifestation of tertiary syphilis affecting the aorta and valves.

  • 🟪 Overview
    Rare in developed countries. May lead to aortic aneurysm, aortic regurgitation, or coronary ostial narrowing.
  • 🧠 Pathophysiology
    Obliterative endarteritis of vasa vasorum weakens aortic wall leading to dilation.
  • 🩺 Diagnosis
    Serologic tests for syphilis. Imaging (CXR, CT) for aortic dilation or aneurysm.
  • 💊 Management
    IV penicillin G for tertiary syphilis. Surgical intervention if severe aortic damage.
Acute Pericarditis
Acute Pericarditis

Inflammation of the pericardium causing pleuritic chest pain and friction rub.

  • 🟪 Overview
    Common causes: viral (coxsackie), uremia, autoimmune, post-MI, neoplasm.
  • 🧠 Pathophysiology
    Pericardial inflammation leads to pain and possible effusion. Can be fibrinous or serous.
  • 🩺 Diagnosis
    ECG: diffuse ST elevation, PR depression. Friction rub on auscultation. Echo to assess effusion.
  • 💊 Management
    NSAIDs + colchicine. Avoid steroids unless refractory. Treat underlying cause.
Constrictive Pericarditis
Constrictive Pericarditis

Fibrosis and calcification of pericardium impair diastolic filling.

  • 🟪 Overview
    Can be idiopathic or follow TB, viral pericarditis, or cardiac surgery/radiation.
  • 🧠 Pathophysiology
    Thickened pericardium restricts ventricular compliance → equalization of diastolic pressures.
  • 🩺 Diagnosis
    Signs: Kussmaul sign, pericardial knock. Echo or CT/MRI shows pericardial thickening.
  • 💊 Management
    Diuretics for symptom relief. Pericardiectomy in refractory cases.
Myocarditis
Myocarditis

Inflammation of myocardium often leading to dilated cardiomyopathy.

  • 🟪 Overview
    Common causes: Coxsackievirus B, adenovirus, COVID, autoimmune, drugs (doxorubicin, cocaine).
  • 🧠 Pathophysiology
    Inflammatory infiltrate damages myocytes → decreased contractility, arrhythmia, HF.
  • 🩺 Diagnosis
    Cardiac MRI is most sensitive. Confirm with biopsy if needed. Troponins often elevated.
  • 💊 Management
    Supportive care ± heart failure treatment. Avoid strenuous activity. Treat underlying cause.
Acute Coronary Syndrome
Acute Coronary Syndrome (ACS)

Spectrum of myocardial ischemia: unstable angina, NSTEMI, STEMI.

  • 🟪 Overview
    Most often due to atherosclerotic plaque rupture and thrombosis.
  • 🧠 Pathophysiology
    Plaque rupture → platelet aggregation → thrombus → reduced perfusion to myocardium.
  • 🩺 Diagnosis
    ECG (ST elevation, T wave inversion), elevated troponins, clinical presentation (chest pain).
  • 💊 Management
    MONA-BASH (morphine, oxygen, nitro, aspirin, beta-blocker, ACEi, statin, heparin) + PCI.
Hereditary Hemorrhagic Telangiectasia
Hereditary Hemorrhagic Telangiectasia

Autosomal dominant disorder causing AV malformations and bleeding.

  • 🟪 Overview
    Also known as Osler-Weber-Rendu syndrome. Affects skin, mucosa, GI tract, lungs, liver.
  • 🧠 Pathophysiology
    Mutations in ENG, ACVRL1 disrupt TGF-beta signaling → fragile vessels prone to rupture.
  • 🩺 Diagnosis
    Clinical: epistaxis, telangiectasias, visceral AVMs, family history. Genetic testing confirms.
  • 💊 Management
    Supportive: iron, transfusions, laser ablation, embolization. Monitor AVMs in vital organs.
Myxoma
Myxoma

Most common primary cardiac tumor, usually in left atrium.

  • 🟪 Overview
    Benign tumor composed of gelatinous material. Often pedunculated and mobile.
  • 🧠 Pathophysiology
    Can obstruct mitral valve inflow → syncope or embolize → stroke.
  • 🩺 Diagnosis
    Echocardiography is diagnostic. May hear early diastolic "tumor plop."
  • 💊 Management
    Surgical resection is curative. Monitor for recurrence.
Rhabdomyoma
Rhabdomyoma

Most common cardiac tumor in children, often associated with tuberous sclerosis.

  • 🟪 Overview
    Benign hamartoma of striated muscle. Usually regresses spontaneously.
  • 🧠 Pathophysiology
    Located in ventricles; may cause obstruction or arrhythmia.
  • 🩺 Diagnosis
    Prenatal or postnatal echo/MRI. Clinical features of tuberous sclerosis may prompt screening.
  • 💊 Management
    Observation unless symptomatic. Rarely requires surgery.