Family Medicine EOR (Cardiovascular): New for 2026 Topic List (Smarty PANCE)

What is an Atrial Arrhythmia?

An abnormal heart rhythm originating from the atria, including atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and supraventricular tachycardia

What ECG findings define atrial fibrillation?

Irregularly irregular rhythm with no discernible P waves, fibrillatory baseline, and variable R-R intervals

What is the most common sustained arrhythmia and its biggest complication?

Atrial fibrillation; stroke from left atrial appendage thromboembolism

What ECG findings define atrial flutter?

"Sawtooth" flutter waves (best seen in II, III, aVF) with atrial rate ~300 bpm and typically 2:1 AV conduction (ventricular rate ~150)

What is the CHA2DS2-VASc score used for?

Stroke risk stratification in non-valvular AFib (CHF, HTN, Age ≥75 [2pts], DM, Stroke/TIA [2pts], Vascular disease, Age 65-74, Sex female); score ≥2 in men or ≥3 in women → anticoagulation

What is the immediate management of unstable atrial fibrillation/flutter?

Synchronized cardioversion (hypotension, altered mental status, chest pain, or pulmonary edema)

What is multifocal atrial tachycardia (MAT) and its classic association?

≥3 distinct P wave morphologies with irregular rhythm and rate >100 bpm; strongly associated with COPD exacerbations

What is the first-line treatment for stable SVT (AVNRT/AVRT)?

Vagal maneuvers (Valsalva, carotid massage) first, then adenosine 6 mg rapid IV push (12 mg if needed)

What is Heart Block?

A conduction disorder characterized by impaired electrical transmission through the AV node or His-Purkinje system, ranging from delayed conduction (1st degree) to complete dissociation (3rd degree)

What ECG findings define 1st degree AV block?

PR interval >200 ms (>5 small boxes) with every P wave conducted to a QRS

What ECG findings define Mobitz Type I (Wenckebach)?

Progressive PR prolongation until a dropped QRS, then cycle repeats; usually benign and at AV node level

What ECG findings define Mobitz Type II and why is it dangerous?

Fixed PR intervals with intermittent dropped QRS complexes; high risk of progression to complete heart block — requires permanent pacemaker

What ECG findings define 3rd degree (complete) heart block?

Complete AV dissociation — P waves and QRS complexes occur independently; atrial rate faster than ventricular escape rate

What is the acute treatment for symptomatic bradycardia from heart block?

Atropine 1 mg IV (repeat q3-5 min, max 3 mg); if ineffective → transcutaneous pacing, dopamine, or epinephrine infusion

Why is new LBBB with chest pain a critical finding?

Considered a STEMI equivalent; warrants immediate reperfusion therapy (use Sgarbossa criteria to confirm acute MI)

What is a Junctional Arrhythmia?

An arrhythmia originating from the AV junction (AV node or bundle of His) that takes over as the dominant pacemaker, typically when the SA node fails or slows

What are the ECG findings of a junctional rhythm?

Narrow QRS complexes with absent, inverted (in II, III, aVF), or retrograde P waves; rate 40-60 bpm (junctional escape), 60-100 (accelerated), or >100 (junctional tachycardia)

What is the most common cause of junctional rhythm?

Digoxin toxicity; also seen with inferior MI, increased vagal tone, beta-blockers, and post-cardiac surgery

What is the treatment of a symptomatic junctional escape rhythm?

Treat underlying cause (stop offending drug, treat ischemia); atropine for symptomatic bradycardia; pacemaker if persistent

Digoxin toxicity: discontinue digoxin, treat hyperkalemia, digoxin immune Fab (Digibind) if life-threatening

How do you distinguish accelerated junctional rhythm from sinus rhythm?

Accelerated junctional: rate 60-100 with absent/inverted P waves or P waves after QRS; sinus rhythm has upright P waves preceding each QRS in lead II

What is a Premature Beat?

An early cardiac depolarization originating from an ectopic focus, classified as PAC (atrial), PJC (junctional), or PVC (ventricular)

What ECG findings characterize a PAC (premature atrial complex)?

Early P wave (often abnormal morphology) followed by a narrow QRS, with a non-compensatory pause

What ECG findings characterize a PVC (premature ventricular complex)?

Early, wide (>120 ms), bizarre QRS without a preceding P wave, followed by a fully compensatory pause

What PVC patterns are concerning and may warrant evaluation?

Frequent PVCs (>10/hour), multifocal PVCs, R-on-T phenomenon, couplets/triplets, and PVCs in setting of acute ischemia

What is the treatment for asymptomatic PVCs in a structurally normal heart?

Reassurance; avoid caffeine, alcohol, stimulants; no antiarrhythmic therapy needed

When are beta-blockers indicated for premature beats?

Symptomatic PACs/PVCs, frequent PVCs causing cardiomyopathy, or PVCs in the setting of structural heart disease/ischemia

What is a Ventricular Arrhythmia?

An abnormal rhythm originating below the bundle of His, including VTach, VFib, and torsades de pointes — all potentially life-threatening

What ECG findings define monomorphic ventricular tachycardia?

≥3 consecutive wide-complex QRS beats (>120 ms) at rate >100 bpm with uniform morphology; AV dissociation may be present

What is the treatment of stable monomorphic VTach?

Amiodarone 150 mg IV (or procainamide); synchronized cardioversion if becomes unstable

What is the treatment of pulseless VTach or VFib?

Immediate unsynchronized defibrillation (200 J biphasic), CPR, epinephrine 1 mg IV every 3-5 min, amiodarone 300 mg IV bolus

What cause torsades de pointes?

hypomagnesemia, hypokalemia, QT-prolonging drugs (macrolides, fluoroquinolones, antipsychotics, methadone)

What is the treatment for torsades de pointes?

IV magnesium sulfate 2 g (first-line); correct electrolytes, discontinue offending drugs, overdrive pacing or isoproterenol if recurrent

What is Brugada syndrome?

Genetic sodium channelopathy causing RBBB-like pattern with coved ST elevation in V1-V3; high risk of sudden cardiac death — treat with ICD (implantable Cardioverter-Defibrillator)

What is Dilated Cardiomyopathy?

A myocardial disorder characterized by ventricular dilation and systolic dysfunction (reduced ejection fraction) in the absence of abnormal loading conditions or coronary disease

What are the major causes of dilated cardiomyopathy (mnemonic: ABCCCD)?

Alcohol, Beriberi (thiamine deficiency), Coxsackie B virus, Cocaine, Chagas disease, Doxorubicin (and other chemo)

What is the classic physical exam finding in dilated cardiomyopathy?

S3 gallop with laterally displaced PMI; signs of biventricular failure (JVD, rales, peripheral edema)

What echocardiographic findings define dilated cardiomyopathy?

LV ejection fraction

What is peripartum cardiomyopathy and its timing?

Dilated cardiomyopathy occurring in the last month of pregnancy or within 5 months postpartum, in women without prior heart disease

What is the treatment of dilated cardiomyopathy?

(HFrEF guideline-directed medical therapy):

• heart needs BASS to beat better:

  • Beta-blocker (carvedilol, metoprolol succinate, bisoprolol)

  • ACE inhibitor/ARB or ARNi — sacubitril/valsartan

  • Spironolactone (MRA)

  • SGLT2 inhibitor (dapagliflozin, empagliflozin) — the "four pillars"

• Diuretics for congestion (loop diuretics)

• ICD if EF ≤35% after ≥3 months of optimal therapy + NYHA II–III (mild-mod activity limitations)

• *MRA = Mineralocorticoid receptor antagonists

What is Hypertrophic Cardiomyopathy?

An autosomal dominant disorder of sarcomere proteins causing asymmetric LV hypertrophy (especially interventricular septum) leading to dynamic LVOT obstruction

What is the classic triad of HCM symptoms? What is heard on phys exam?

Exertional dyspnea, chest pain, and syncope (especially with exertion)
PE: S4 gallop

PE

Hypertrophic obstructive cardiomyopathy (HOCM)

What characterizes the HCM murmur?

Harsh systolic crescendo-decrescendo murmur at LLSB; INCREASES with Valsalva and standing (decreased preload); DECREASES with squatting and passive leg raise

What medications are contraindicated in obstructive HCM?

Nitrates, diuretics (decrease preload), digoxin and other inotropes (increase contractility) — all worsen LVOT obstruction

What is the treatment of symptomatic HCM?

Beta-blockers first-line (metoprolol, atenolol); verapamil/disopyramide if intolerant; septal myectomy or alcohol septal ablation for refractory cases; ICD for high-risk SCD

What is Restrictive Cardiomyopathy?

A cardiomyopathy characterized by impaired ventricular filling due to rigid, non-compliant ventricular walls, with preserved systolic function and non-dilated ventricles

What are the major causes of restrictive cardiomyopathy?

Amyloidosis (most common), sarcoidosis, hemochromatosis, scleroderma, endomyocardial fibrosis, radiation, Loffler endocarditis

How does restrictive cardiomyopathy dx?

Kussmaul sign and rapid early diastolic filling

• Echocardiogram: thickened walls, diastolic dysfunction, biatrial enlargement, preserved EF

What ECG and biopsy findings suggest cardiac amyloidosis?

ECG: low voltage with pseudoinfarct pattern (Q waves V1-V3); Biopsy: apple-green birefringence with Congo red staining under polarized light

What is the treatment of restrictive cardiomyopathy?

Treat underlying cause; phlebotomy for hemochromatosis, steroids for sarcoidosis, tafamidis for ATTR amyloidosis

• Diuretics cautiously for congestion

• transplant for end-stage disease

• Avoid digoxin in amyloidosis

What is Acyanotic Congenital Heart Disease?

Congenital cardiac defects with left-to-right shunting that do not initially cause cyanosis, including VSD, ASD, PDA, and coarctation of the aorta

What is the most common congenital heart defect?

Ventricular septal defect (VSD) — harsh holosystolic murmur at LLSB, smaller defects produce louder murmurs

What murmur characterizes an atrial septal defect (ASD)?

Fixed, wide split S2 with systolic ejection murmur at left upper sternal border (from increased pulmonary flow)

What is the classic presentation of patent ductus arteriosus (PDA)?

Continuous "machinery" murmur at left infraclavicular area; wide pulse pressure; bounding peripheral pulses

What is the closure treatment for symptomatic PDA in neonates?

Indomethacin or ibuprofen (inhibits prostaglandins, promoting ductal closure); in cyanotic lesions PDA is kept OPEN with prostaglandin E1

What is the classic presentation of coarctation of the aorta?

Hypertension in upper extremities with hypotension/diminished pulses in lower extremities; "3 sign" on CXR; rib notching from collateral vessels; associated with Turner syndrome and bicuspid aortic valve

What is Eisenmenger syndrome?

Reversal of a left-to-right shunt to right-to-left due to pulmonary hypertension from chronic shunting; results in late cyanosis — surgical correction is contraindicated once it develops

What is Cyanotic Congenital Heart Disease?

Congenital heart defects causing right-to-left shunting and deoxygenated blood entering systemic circulation, producing central cyanosis — the "5 Ts"

What are the 5 Ts of cyanotic congenital heart disease?

Tetralogy of Fallot, Transposition of great arteries, Truncus arteriosus, Tricuspid atresia, Total anomalous pulmonary venous return

What are the 4 components of Tetralogy of Fallot (mnemonic: PROVe)?

Pulmonary stenosis, RVH (right ventricular hypertrophy), Overriding aorta, VSD

What is a "tet spell" and how is it managed?

Hypercyanotic episode with worsening cyanosis during crying/feeding; treated with knee-to-chest position (increases SVR), oxygen, morphine, beta-blockers, and IV fluids

What is the classic CXR finding in Tetralogy of Fallot?

"Boot-shaped" heart (coeur en sabot) from RVH with concavity of pulmonary artery

What is the classic CXR finding in transposition of the great arteries?

"Egg on a string" appearance — narrow mediastinum with cardiomegaly; presents with severe cyanosis at birth — requires PGE1 to maintain PDA

What is Acute Coronary Syndrome?

A spectrum of conditions caused by acute myocardial ischemia, encompassing unstable angina, NSTEMI, and STEMI — all due to plaque rupture and thrombus formation

What are the ECG criteria for STEMI?

ST elevation ≥1 mm in ≥2 contiguous leads (≥2 mm in V2-V3 for men, ≥1.5 mm for women); new LBBB with symptoms; posterior STEMI shows ST depression V1-V3

What ECG leads correspond to which coronary artery in STEMI?

Anterior (V1-V4) = LAD; Inferior (II, III, aVF) = RCA (80%) or LCx; Lateral (I, aVL, V5-V6) = LCx; Posterior (V7-V9) = RCA/LCx

What is the door-to-balloon time goal for STEMI?

What is the initial management of ACS (mnemonic: MONA-BASH)?

Morphine (if refractory pain), Oxygen (if SpO2

How do you differentiate unstable angina from NSTEMI?

Both have ischemic symptoms and possible ECG changes (ST depression, T-wave inversion); NSTEMI has elevated troponin, unstable angina does not

What is Wellens syndrome and why is it critical?

Biphasic or deeply inverted T waves in V2-V3 during pain-free interval indicating critical proximal LAD stenosis — high risk for massive anterior MI; needs urgent catheterization, NOT stress test

What are absolute contraindications to fibrinolytic therapy?

Any prior intracranial hemorrhage, known structural cerebrovascular lesion, ischemic stroke within 3 months, suspected aortic dissection, active bleeding, significant closed head trauma within 3 months

What is Stable Angina?

Predictable chest discomfort due to fixed coronary artery stenosis, provoked by exertion or stress and relieved by rest or nitroglycerin within minutes

What is the diagnostic test of choice for stable angina?

Exercise stress test (preferred if patient can exercise and baseline ECG is normal); stress echo or nuclear imaging if baseline ECG abnormal; coronary angiography for high-risk findings

What are the characteristic features of stable angina pain?

Substernal pressure/squeezing lasting

What is the medical management of stable angina?

Antiplatelet (aspirin), high-intensity statin, beta-blocker (first-line for symptoms), nitrates as needed, ACE inhibitor if HTN/DM/CKD; calcium channel blocker if beta-blocker contraindicated

When is revascularization indicated in stable angina?

Failure of medical therapy, high-risk findings on stress testing, left main disease, 3-vessel disease (especially with DM or low EF), or proximal LAD disease

What is Vasospastic (Prinzmetal) Angina?

Coronary artery spasm causing transient ischemia, typically occurring at rest (especially early morning), in patients often without significant coronary atherosclerosis

What demographic is classically affected by Prinzmetal angina?

Younger patients (30s-50s), often female, often smokers, frequently with other vasospastic disorders (migraines, Raynaud phenomenon)

What is the diagnostic gold standard for vasospastic angina?

Coronary angiography with provocative testing using ergonovine, acetylcholine, or hyperventilation to induce reversible spasm

What ECG finding occurs during a Prinzmetal angina episode?

Transient ST elevation that resolves spontaneously or with nitrates (mimics STEMI); typically NO troponin elevation between attacks

What is the treatment of vasospastic angina?

Calcium channel blockers (diltiazem, amlodipine) first-line; long-acting nitrates added if needed; smoking cessation; AVOID non-selective beta-blockers (unopposed alpha may worsen spasm) and triptans/cocaine

What is Heart Failure?

A clinical syndrome of impaired ventricular filling or ejection of blood, manifesting as dyspnea, fatigue, and fluid retention, classified as HFrEF (EF ≤40%) or HFpEF (EF ≥50%)

What are the Framingham major criteria for heart failure?

Paroxysmal nocturnal dyspnea, JVD, rales, cardiomegaly, acute pulmonary edema, S3 gallop, hepatojugular reflux, weight loss >4.5 kg with treatment

What is the BNP cutoff that helps rule out acute heart failure?

BNP

What CXR findings suggest heart failure?

Cardiomegaly, cephalization of pulmonary vessels, Kerley B lines, perihilar "bat-wing" pattern, pleural effusions (often right-sided)

What 4 medication classes reduce mortality in HFrEF ("Four Pillars")?

ARNI (or ACEI/ARB), beta-blocker (carvedilol, metoprolol succinate, bisoprolol), MRA (spironolactone/eplerenone), SGLT2 inhibitor (dapagliflozin/empagliflozin)

What is the first-line treatment for acute decompensated heart failure?

IV loop diuretic (furosemide); supplemental O2, nitrates for preload reduction, BiPAP for severe respiratory distress; inotropes (dobutamine) if cardiogenic shock

What medications worsen heart failure outcomes and should be avoided?

NSAIDs (sodium retention, worsen renal function), thiazolidinediones (fluid retention), non-dihydropyridine CCBs in HFrEF, class I antiarrhythmics

What is Primary Hypertension?

Persistently elevated blood pressure (≥130/80 mmHg per ACC/AHA) without an identifiable secondary cause, accounting for ~90-95% of all hypertension cases

What are the ACC/AHA blood pressure categories?

Normal:

What lifestyle modifications lower blood pressure?

DASH diet, sodium restriction (

What are the first-line antihypertensive medications?

Thiazide diuretics, ACE inhibitors, ARBs, or calcium channel blockers; in Black patients without CKD, thiazides or CCBs preferred initially

What initial workup is recommended for newly diagnosed hypertension?

BMP (K, Cr, glucose), lipid panel, TSH, UA, urine albumin-to-creatinine ratio, ECG; consider echo if LVH suspected

What end-organ damage results from chronic hypertension?

LVH/heart failure, CAD, stroke, CKD, retinopathy, peripheral artery disease, aortic dissection/aneurysm

What is Secondary Hypertension?

Hypertension with an identifiable underlying cause (renal, endocrine, vascular, drug-induced), accounting for 5-10% of cases; often suggested by resistant HTN, onset

What is the most common cause of secondary hypertension?

Renal parenchymal disease (CKD); renovascular disease (fibromuscular dysplasia in young women, atherosclerosis in older adults) is the most common potentially curable cause

What endocrine causes of secondary HTN should be considered?

Primary hyperaldosteronism (most common endocrine cause), pheochromocytoma, Cushing syndrome, hyperthyroidism, hyperparathyroidism, acromegaly

What is the classic triad of pheochromocytoma?

Episodic headache, palpitations, and diaphoresis with paroxysmal hypertension; diagnose with plasma free metanephrines or 24-hour urine metanephrines

What is the work-up for renovascular hypertension?

Renal duplex ultrasound (screening), MRA or CTA (confirmatory); fibromuscular dysplasia shows "string of beads" on angiography

What suggests primary hyperaldosteronism?

Hypertension with hypokalemia (often unprovoked), metabolic alkalosis; screen with aldosterone-to-renin ratio (ARR) — elevated ratio confirms