Emergency Medicine Rotation (EOR) Exam Topic List — ALL TOPICS (New 2026 Topic List)

What is an atrial arrhythmia?

A supraventricular dysrhythmia originating in atrial tissue above the AV node, including atrial fibrillation, atrial flutter, multifocal atrial tachycardia, and paroxysmal SVT.

What is the immediate ED management of atrial fibrillation with hemodynamic instability?

Immediate synchronized cardioversion at 120–200 J biphasic; do not delay the shock for rate control, and start anticoagulation as early as possible.

What are first-line rate-control agents for stable atrial fibrillation with RVR in the ED?

IV diltiazem or IV metoprolol; use amiodarone or digoxin instead when the patient is hypotensive or has decompensated heart failure.

What ECG pattern suggests atrial fibrillation with WPW, and which drugs are contraindicated?

Irregularly irregular WIDE-complex tachycardia with varying QRS morphology; avoid all AV nodal blockers (adenosine, beta-blockers, calcium channel blockers, digoxin) and IV amiodarone; give procainamide or cardiovert.

What ECG finding defines atrial flutter and what is the classic ventricular rate?

Sawtooth flutter waves best seen in II, III, aVF with an atrial rate near 300 and a ventricular rate near 150 from 2:1 conduction.

What is multifocal atrial tachycardia and what condition is it most associated with?

Irregular tachycardia with at least 3 distinct P-wave morphologies and varying PR intervals, classically in COPD exacerbation — treat the underlying pulmonary disease, not the rhythm.

What is the 48-hour rule for cardioversion of atrial fibrillation?

Stable AF of less than 48 hours duration may be cardioverted in the ED; if 48 hours or longer or unknown, anticoagulate 3 weeks or obtain TEE first because of atrial thrombus and stroke risk, then anticoagulate at least 4 weeks after cardioversion.

What is the ED treatment sequence for stable narrow-complex SVT?

Vagal maneuvers (modified Valsalva is most effective), then adenosine 6 mg rapid IV push followed by 12 mg, then diltiazem or beta-blocker if refractory.

What is a heart block?

A conduction disorder in which impulse transmission from the atria to the ventricles is delayed or interrupted at the AV node or His-Purkinje system.

What defines first-degree AV block and how is it managed in the ED?

PR interval greater than 200 ms with every P wave conducted; benign, requires no ED treatment, review AV nodal blocking medications.

What defines Mobitz type I (Wenckebach) second-degree AV block?

Progressive PR prolongation until a P wave fails to conduct and a QRS is dropped; usually AV nodal, benign, and managed with observation.

What defines Mobitz type II second-degree AV block and why is it an ED emergency?

Constant PR interval with sudden non-conducted P waves; the lesion is infranodal and can progress abruptly to complete heart block or asystole, so it requires pacing.

What are the ECG and exam findings of third-degree (complete) heart block?

Complete AV dissociation with the atrial rate faster than and independent of the ventricular escape rate, plus cannon A waves and variable S1 intensity on exam.

What is the ACLS management of symptomatic bradycardia from high-grade heart block?

Atropine 1 mg IV every 3–5 minutes to a maximum of 3 mg, then transcutaneous pacing and/or dopamine or epinephrine infusion; atropine is often ineffective in Mobitz II and third-degree block.

Which MI territory causes which type of AV block, and why does it matter?

Inferior MI causes AV nodal block that is usually transient and atropine-responsive; anterior MI causes infranodal block that carries a poor prognosis and typically requires pacing.

What is a junctional arrhythmia?

A rhythm arising from pacemaker tissue in the AV junction when the sinus node fails or when junctional automaticity becomes abnormally enhanced.

What are the characteristic ECG findings of a junctional rhythm?

Narrow QRS with absent, inverted (in II, III, aVF), or retrograde P waves that may precede, be buried within, or follow the QRS complex.

What are the rate ranges for junctional escape, accelerated junctional, and junctional tachycardia?

Junctional escape 40–60 bpm, accelerated junctional rhythm 60–100 bpm, and junctional tachycardia greater than 100 bpm.

What toxic ingestion classically produces accelerated junctional rhythm or paroxysmal atrial tachycardia with block?

Digoxin toxicity — treat significant toxicity or hyperkalemia with digoxin immune Fab.

Why does a junctional escape rhythm appear, and what should the ED evaluation target?

It is a backup rhythm from sinus node failure or high-grade AV block, so evaluate for ischemia, hyperkalemia, hypothyroidism, increased vagal tone, and AV nodal blocking drugs.

How is symptomatic junctional bradycardia managed in the ED?

Atropine and transcutaneous pacing for symptoms or instability, with simultaneous correction of the underlying cause; asymptomatic junctional rhythm needs no rhythm-specific treatment.

What is a premature beat?

An early ectopic depolarization arising from the atria (PAC), AV junction (PJC), or ventricles (PVC) that interrupts the underlying sinus rhythm.

What ECG features distinguish a PAC?

An early, abnormally shaped P wave followed by a normal narrow QRS, typically with an incomplete (non-compensatory) pause; aberrantly conducted PACs may appear wide.

What ECG features distinguish a PVC?

A wide (greater than 120 ms), bizarre QRS with no preceding P wave, discordant T wave, and a full compensatory pause.

What is the R-on-T phenomenon and why is it dangerous?

A PVC landing on the T wave during the vulnerable repolarization period, which can trigger ventricular tachycardia, ventricular fibrillation, or torsades.

What do bigeminy, trigeminy, and couplets describe?

Bigeminy is every other beat a PVC, trigeminy is every third beat, a couplet is two consecutive PVCs, and three or more consecutive PVCs constitutes non-sustained VT.

Which PVC features warrant ED concern rather than reassurance?

Multifocal morphology, couplets or runs, PVCs in the setting of syncope, ischemic chest pain, structural heart disease, or a prolonged QT.

What is the ED workup and treatment for isolated premature beats?

Check potassium and magnesium, review stimulants and drugs, obtain an ECG; asymptomatic premature beats need no antiarrhythmic therapy.

What is a ventricular arrhythmia?

A wide-complex dysrhythmia originating below the bundle of His, including ventricular tachycardia, torsades de pointes, and ventricular fibrillation.

What is the immediate management of pulseless VT or ventricular fibrillation?

Immediate unsynchronized defibrillation with high-quality CPR, epinephrine 1 mg IV every 3–5 minutes, and amiodarone 300 mg IV (or lidocaine) after the third shock.

How is stable monomorphic ventricular tachycardia with a pulse treated?

Amiodarone 150 mg IV over 10 minutes or procainamide 20–50 mg/min; procainamide has the best evidence for termination of stable VT.

How is unstable ventricular tachycardia with a pulse treated?

Synchronized cardioversion starting at 100 J, with sedation if time permits.

What is torsades de pointes and what is the first-line treatment?

Polymorphic VT with a twisting QRS axis on a prolonged QT; treat with magnesium sulfate 2 g IV (even if Mg is normal), correct potassium, stop offending drugs; overdrive pacing or isoproterenol for recurrent pause-dependent (acquired) torsades; defibrillate if unstable

What is the safest ED assumption for any wide-complex tachycardia of uncertain origin?

Treat it as ventricular tachycardia — never give a calcium channel blocker, which can precipitate hemodynamic collapse if the rhythm is truly VT.

What is Brugada syndrome and why does it matter in the ED?

A sodium channelopathy with coved ST elevation and RBBB pattern in V1–V3, often unmasked by fever, that causes syncope and sudden cardiac death and requires ICD referral.

What is dilated cardiomyopathy?

Ventricular chamber dilation with impaired systolic contraction and reduced ejection fraction not explained by abnormal loading conditions or coronary disease alone.

What are the major causes of dilated cardiomyopathy?

Ischemic disease is most common overall; nonischemic causes include alcohol, viral myocarditis (coxsackie B), peripartum state, doxorubicin, cocaine, thiamine deficiency, and Chagas disease.

What exam findings suggest dilated cardiomyopathy?

S3 gallop, laterally and inferiorly displaced PMI, functional mitral or tricuspid regurgitation murmurs, elevated JVP, and bibasilar rales.

What are the echocardiographic findings of dilated cardiomyopathy?

Four-chamber dilation with global hypokinesis and an ejection fraction typically below 40 percent.

What is peripartum cardiomyopathy and when does it occur?

New systolic heart failure occurring from the last month of pregnancy through 5 months postpartum without another identifiable cause.

What complications of dilated cardiomyopathy should the ED anticipate?

Mural thrombus with systemic embolization, ventricular arrhythmias and sudden death, and acute decompensation requiring diuresis and afterload reduction.

What is hypertrophic cardiomyopathy?

An autosomal dominant sarcomere disorder producing asymmetric left ventricular hypertrophy that can cause dynamic outflow tract obstruction and sudden cardiac death.

What murmur is heard in hypertrophic cardiomyopathy and how do maneuvers change it?

A harsh crescendo-decrescendo systolic murmur at the left lower sternal border that increases with Valsalva and standing (decreased preload) and decreases with squatting and passive leg raise.

What ECG findings suggest hypertrophic cardiomyopathy?

Left ventricular hypertrophy with deep, narrow dagger-like Q waves in the inferior and lateral leads and diffuse T-wave inversions.

Why is exertional syncope in a young athlete a red-flag ED presentation?

Hypertrophic cardiomyopathy is the leading cause of sudden cardiac death in young athletes, and exertional syncope is its highest-risk warning symptom, requiring echocardiography and cardiology evaluation before discharge.

Which medications worsen hypertrophic cardiomyopathy and which help?

Avoid nitrates, diuretics, and other preload reducers plus inotropes like digoxin; treat with beta-blockers, and give IV fluids and phenylephrine for acute hypotension.

What echocardiographic findings confirm hypertrophic cardiomyopathy?

Asymmetric septal hypertrophy with septal thickness of 15 mm or greater and systolic anterior motion of the mitral valve producing dynamic outflow obstruction.

What is restrictive cardiomyopathy?

A disorder of impaired diastolic filling caused by stiff, non-compliant ventricles with normal or near-normal ejection fraction and non-dilated chambers.

What are the major causes of restrictive cardiomyopathy?

Amyloidosis (most common in the US), sarcoidosis, hemochromatosis, radiation, scleroderma, and endomyocardial fibrosis.

What ECG-echo mismatch is classic for cardiac amyloidosis?

Low voltage on ECG despite increased wall thickness on echocardiography, often with a granular sparkling myocardial texture.

What is Kussmaul sign and what does it indicate?

A paradoxical rise in JVP with inspiration, seen in restrictive cardiomyopathy and constrictive pericarditis rather than in tamponade.

Why is distinguishing restrictive cardiomyopathy from constrictive pericarditis important?

Constrictive pericarditis is surgically curable with pericardiectomy, so cardiac MRI, CT, or catheterization is needed to make the distinction.

What is the ED pitfall in managing restrictive cardiomyopathy?

These patients are preload dependent and rate sensitive — aggressive diuresis or loss of atrial kick from new atrial fibrillation can cause abrupt hemodynamic collapse.

What is acute coronary syndrome?

A spectrum of myocardial ischemia from coronary plaque rupture and thrombosis that includes unstable angina, NSTEMI, and STEMI.

What ECG criteria define a STEMI?

New ST elevation at the J point in two contiguous leads of at least 1 mm, or at least 2 mm in men and 1.5 mm in women in leads V2–V3.

What are the major STEMI equivalents that require emergent catheterization?

Posterior MI, de Winter T waves, Wellens syndrome, ST elevation in aVR with diffuse ST depression, and LBBB or a paced rhythm that meets the Sgarbossa criteria. A new LBBB by itself is no longer an automatic STEMI equivalent.

What are the reperfusion time goals in STEMI?

Door-to-balloon within 90 minutes at a PCI-capable center, or fibrinolysis within 30 minutes if PCI cannot be performed within 120 minutes.

Why must you obtain right-sided leads in an inferior STEMI?

Up to 40 percent have RV infarction, which is preload dependent — these patients need IV fluids and will become profoundly hypotensive with nitroglycerin or morphine.

What is the core ED pharmacologic therapy for ACS?

Aspirin 325 mg chewed, nitroglycerin for ongoing pain if not contraindicated, anticoagulation with heparin, high-intensity statin, and a P2Y12 inhibitor per cardiology.

How does the HEART score guide ED disposition in chest pain?

History, ECG, Age, Risk factors, and Troponin generate a score where 0–3 is low risk and generally dischargeable, 4–6 is moderate risk warranting observation, and 7–10 is high risk requiring admission.

What distinguishes unstable angina from NSTEMI?

Both have ischemic symptoms without ST elevation, but NSTEMI has elevated troponin while unstable angina has a normal troponin.

What is vasospastic (Prinzmetal) angina?

Transient myocardial ischemia caused by focal coronary artery spasm rather than fixed obstructive plaque.

What is the classic presentation of vasospastic angina?

Recurrent chest pain at rest, typically at night or in the early morning, in a younger smoker, with transient ST elevation that resolves spontaneously or with nitroglycerin.

What substance use is strongly associated with coronary vasospasm?

Cocaine and amphetamines, along with tobacco smoking.

How is vasospastic angina definitively diagnosed?

Coronary angiography demonstrating non-obstructive vessels with provocative testing using ergonovine or acetylcholine to induce reversible spasm.

What is the treatment of vasospastic angina and which drug class must be avoided?

Calcium channel blockers are first-line with nitrates as adjuncts; avoid beta-blockers, which allow unopposed alpha stimulation and worsen spasm.

Why is cocaine-associated chest pain treated with benzodiazepines first?

Benzodiazepines reduce sympathetic drive, blood pressure, and coronary spasm; nitroglycerin and phentolamine are added and non-selective beta-blockers avoided.

What is heart failure?

A clinical syndrome in which structural or functional cardiac impairment prevents the ventricle from filling or ejecting adequately to meet metabolic demand.

How are HFrEF and HFpEF defined by ejection fraction?

HFrEF is an ejection fraction of 40 percent or less from systolic dysfunction; HFpEF is an ejection fraction of 50 percent or greater from diastolic dysfunction.

How is BNP used in the ED evaluation of dyspnea?

BNP below 100 pg/mL or NT-proBNP below 300 pg/mL makes acute heart failure very unlikely; values are falsely low in obesity and falsely elevated in renal failure, sepsis, and atrial fibrillation.

What chest radiograph findings support acute decompensated heart failure?

Cardiomegaly, cephalization of pulmonary vessels, Kerley B lines, perihilar bat-wing edema, and bilateral pleural effusions.

What is the ED management of acute decompensated heart failure with pulmonary edema?

Sit the patient upright, apply non-invasive positive pressure ventilation, give IV nitroglycerin for afterload and preload reduction, and give an IV loop diuretic if volume overloaded.

What is SCAPE and how does its management differ?

Sympathetic Crashing Acute Pulmonary Edema is hypertensive flash pulmonary edema from fluid redistribution rather than volume overload — treat with high-dose nitroglycerin and BiPAP, since diuretics are secondary and these patients are often euvolemic.

Which heart failure interventions should be avoided in the ED?

Aggressive fluid boluses, initiation or uptitration of beta-blockers during acute decompensation, and NSAIDs.

What is a hypertensive emergency?

Severe blood pressure elevation, generally 180/120 mmHg or higher, accompanied by acute end-organ damage.

What end-organ injuries define a hypertensive emergency?

Hypertensive encephalopathy, intracranial hemorrhage or ischemic stroke, acute pulmonary edema, ACS, aortic dissection, acute kidney injury, retinal hemorrhage or papilledema, and eclampsia.

What is the blood pressure reduction target in most hypertensive emergencies?

Lower mean arterial pressure by no more than 10–25 percent in the first hour, then toward 160/100 mmHg over the next 2–6 hours, because rapid drops cause watershed ischemia.

Which IV agents are preferred for hypertensive emergency?

Nicardipine or clevidipine infusions and labetalol or esmolol; nitroprusside is reserved for short-term use because of cyanide and thiocyanate toxicity.

What is the specific BP target and agent for aortic dissection?

Heart rate below 60 and systolic pressure 100–120 mmHg using IV esmolol or labetalol FIRST, adding nicardipine only after beta-blockade to prevent reflex tachycardia and propagation.

What are the blood pressure thresholds for treatment in acute ischemic stroke?

Treat above 185/110 mmHg if the patient is a thrombolytic candidate, otherwise permit up to 220/120 mmHg to preserve penumbral perfusion.

How is hypertensive emergency from cocaine or pheochromocytoma managed?

Benzodiazepines plus phentolamine or nicardipine; avoid unopposed beta-blockade, which produces unopposed alpha vasoconstriction.

What is severe asymptomatic hypertension (hypertensive urgency)?

Blood pressure of 180/120 mmHg or higher with no evidence of acute end-organ damage.

What is the appropriate ED workup for asymptomatic severe hypertension?

A focused history and exam for end-organ symptoms; routine labs, ECG, and imaging are not required in a truly asymptomatic patient with reliable follow-up.

Why is rapid blood pressure lowering harmful in hypertensive urgency?

Chronic hypertension shifts cerebral autoregulation, so acute lowering risks watershed stroke, myocardial ischemia, and acute kidney injury.

What is the correct ED treatment of hypertensive urgency?

Restart or adjust oral antihypertensives, avoid IV agents and as-needed clonidine or nifedipine, and arrange outpatient recheck within 24–72 hours.

What is the appropriate disposition for asymptomatic severe hypertension?

Discharge with primary care follow-up; admission and ED observation do not improve outcomes.

What is the most common reason for markedly elevated blood pressure in the ED?

Medication nonadherence or untreated chronic hypertension, often compounded by pain, anxiety, or the ED environment itself.

What is orthostatic hypotension?

A fall in systolic blood pressure of at least 20 mmHg or diastolic pressure of at least 10 mmHg within 3 minutes of moving from supine to standing.

How should orthostatic vital signs be measured correctly?

Measure supine after 5 minutes of rest, then repeat at 1 and 3 minutes after standing, recording heart rate along with blood pressure.

What are the major categories of orthostatic hypotension?

Volume depletion (hemorrhage, dehydration), medication effect, and autonomic failure from diabetes, Parkinson disease, or amyloidosis.

What dangerous conditions must the ED consider in a patient with new orthostasis?

Occult GI bleeding, ruptured ectopic pregnancy or AAA, sepsis, adrenal insufficiency, and dehydration from any cause.

Which medication classes most commonly cause orthostatic hypotension?

Alpha-blockers, diuretics, nitrates, tricyclic antidepressants, antipsychotics, and antihypertensives generally.

How is orthostatic hypotension managed?

IV or oral volume repletion, elimination of offending medications, slow position changes and compression stockings, with midodrine or fludrocortisone for chronic autonomic cases.

What is vasovagal syncope?

Transient loss of consciousness from a reflex surge in vagal tone causing bradycardia and vasodilation with cerebral hypoperfusion, followed by rapid spontaneous recovery.

What prodrome is characteristic of vasovagal syncope?

Nausea, diaphoresis, warmth, tunnel vision, and lightheadedness after a trigger such as pain, prolonged standing, emotional stress, or blood draw.

What features suggest cardiac rather than vasovagal syncope?

Syncope during exertion or while supine, absent prodrome, preceding palpitations or chest pain, family history of sudden death, or an abnormal ECG.

Why is an ECG mandatory in every ED syncope evaluation?

It screens for the dangerous causes that history alone can miss — ischemia, heart block, prolonged QT, WPW, Brugada, and hypertrophic cardiomyopathy.

What tools help risk-stratify ED syncope for discharge?

The Canadian Syncope Risk Score and San Francisco Syncope Rule; low-risk young patients with a classic vasovagal prodrome and a normal ECG can be safely discharged.

What is the treatment for recurrent vasovagal syncope?

Reassurance and education, trigger avoidance, adequate hydration and salt intake, and physical counterpressure maneuvers at symptom onset.

What is cardiogenic shock?

Tissue hypoperfusion caused by primary cardiac pump failure despite adequate intravascular volume.