Arrhythmia take 1

PAS  |  CAM II  |  Spring 2026

Arrhythmias Part 1

50-Question High-Yield Clinical Application Practice Exam

Select the single best answer for each clinical scenario.

Answer Key with Clinical Explanations on Page 2

Section 1: Cardiac Conduction System & ECG Basics (Questions 1–6)

1.  A medical student is reviewing the cardiac conduction system. She asks about the primary pacemaker of the heart and its normal intrinsic rate.

Which structure serves as the dominant pacemaker and what is its intrinsic rate?

A.  AV node — intrinsic rate 40-60 bpm; greatest degree of automaticity

B.  Bundle of His — intrinsic rate 60-100 bpm; generates the QRS complex

C.  SINOATRIAL (SA) NODE — dominant pacemaker with greatest automaticity; intrinsic rate 60-100 bpm; its depolarization wave proceeds outward to both atria, producing the P wave on ECG

D.  Purkinje fibers — intrinsic rate 20-40 bpm; serve as backup pacemaker only

2.  A teaching attending explains why there is a brief pause between the P wave and QRS complex on the ECG.

What does this pause represent and what ion is responsible for conduction through this structure?

A.  Ventricular repolarization — potassium ions leaving myocytes cause the electrical pause

B.  CONDUCTION DELAY AT THE AV NODE — the AV node is the SOLE PATHWAY to conduct impulses from atria to ventricles; depolarization SLOWS here to allow ventricular filling; conduction is carried by SLOWER CALCIUM (Ca2+) ions (not sodium); this delay is represented as the PR INTERVAL on ECG; AV node intrinsic rate = 40-60 bpm

C.  Bundle branch block — the right and left bundle branches each delay conduction sequentially

D.  The pause represents junctional escape rhythm taking over the pacemaker function

3.  A 45-year-old presents with a syncopal episode. On his ECG, the QT interval is prolonged. The attending explains which wave corresponds to ventricular repolarization.

Which ECG waveform represents ventricular REPOLARIZATION and what ion is primarily responsible?

A.  P wave — atrial depolarization using sodium ions exiting the cell

B.  QRS complex — ventricular depolarization as sodium floods into cells

C.  T WAVE — represents rapid phase of ventricular REPOLARIZATION; accomplished by POTASSIUM (K+) leaving the myocytes; the ST segment represents the plateau phase of repolarization; ventricular contraction persists from the QRS until the end of the T wave (encompassed in the QT interval)

D.  U wave — represents repolarization of the SA node

4.  An emergency medicine resident reviews the autonomic nervous system effects on the heart before treating a bradycardic patient.

Stimulation of the SYMPATHETIC nervous system produces which cardiac effects?

A.  Decrease in SA node rate, decrease in conduction velocity, decrease in contractility, decrease in irritability of foci — all inhibitory effects

B.  INCREASES in SA node pacing rate, INCREASES in conduction rate, INCREASES in force of contraction, and INCREASES in irritability of foci; mediated by norepinephrine binding to cardiac Beta-1 adrenergic receptors — all excitatory effects

C.  Decreases SA node rate but increases contractility — a mixed effect mediated by acetylcholine

D.  Only increases SA node rate with no effect on contractility or conduction

5.  A student is asked about the cardiac action potential phases during a pharmacology lecture on antiarrhythmics.

During Phase 0 of the cardiac action potential, what net action occurs and what ion is responsible?

A.  Plateau phase — calcium and sodium influx balances potassium efflux (slow channels)

B.  Initial repolarization — transient potassium efflux creates a brief downward deflection

C.  RAPID DEPOLARIZATION — fast SODIUM (Na+) influx through fast channels causes rapid depolarization; this phase is the target of Class I antiarrhythmic drugs (sodium channel blockers); Phase 1 = initial repolarization (transient K efflux); Phase 2 = plateau (Ca/Na influx vs K efflux); Phase 3 = repolarization (K efflux); Phase 4 = slow depolarization (slow Na influx)

D.  Slow depolarization — slow sodium influx during diastole (phase 4)

6.  A PA student is asked to identify a mnemonic for causes of bradycardia before seeing a patient with heart rate of 38 bpm.

Using the mnemonic HE DIES, which of the following is NOT included as a cause of bradycardia?

A.  Hypothyroidism — metabolic cause of bradycardia

B.  Elevated intracranial pressure — Cushing's reflex includes bradycardia

C.  Sick sinus syndrome — dysfunction of SA node automaticity

D.  HYPERKALEMIA is a cause of bradycardia (E = Electrolytes in HE DIES); HYPERNATREMIA is NOT listed — the mnemonic includes: Hypothyroidism, Elevated ICP, Drugs, Ischemia, Electrolytes, Sick sinus syndrome

Section 2: Antiarrhythmic Medications (Questions 7–14)

7.  A 58-year-old with new-onset atrial fibrillation and reduced ejection fraction (EF 30%) needs rate control. The attending notes the patient has borderline blood pressure at 90/60 mmHg.

Which agent is preferred for rate control in a patient with atrial fibrillation AND heart failure with reduced EF (HFrEF)?

A.  Diltiazem — non-dihydropyridine CCB is first-line for all AFib rate control

B.  Metoprolol — always first-line regardless of EF; diltiazem second-line

C.  DIGOXIN (or amiodarone if anticoagulated or ≤48 hours) — diltiazem and beta-blockers are to be AVOIDED in HFrEF due to negative inotropy (reduced EF) and hypotension; digoxin directly suppresses AV node conduction and provides positive inotropic effect without worsening systolic dysfunction; amiodarone is an option if anticoagulated

D.  Adenosine — first-line for AFib rate control in HFrEF patients

8.  A pharmacy student asks about the mechanism of adenosine and its clinical use during a PSVT case.

What is the mechanism of adenosine, what is its most important adverse effect, and what route/technique must be used?

A.  Adenosine blocks beta-1 receptors to slow the SA node; most common side effect is hypotension; given slowly over 2 minutes

B.  Adenosine blocks Ca2+ channels in the AV node; most common side effect is nausea; given as a slow IV push

C.  ADENOSINE slows AV node conduction and interrupts RE-ENTRY pathways to restore NSR; ADVERSE EFFECT = CHEST PAIN (highly uncomfortable — warn the patient); EXTREMELY SHORT half-life (<10 seconds); must be given IV RAPID BOLUS in the MOST PROXIMAL peripheral line followed by a RAPID saline flush to ensure rapid delivery to the heart; USE = PSVT (paroxysmal supraventricular tachycardia)

D.  Adenosine directly cardioverts all supraventricular arrhythmias including AFib; side effect is complete heart block

9.  A 72-year-old with chronic AFib is admitted with nausea, anorexia, and visual disturbances (yellow-green halos around lights). His rhythm shows bidirectional ventricular tachycardia on ECG.

What is the most likely diagnosis and what is the class of medication responsible?

A.  Amiodarone toxicity — pulmonary fibrosis and thyroid dysfunction are the classic toxicity presentations

B.  Class I antiarrhythmic (lidocaine) toxicity — CNS toxicity causes visual changes and nausea

C.  DIGOXIN TOXICITY — symptoms include nausea, anorexia, visual changes (yellow-green halos/chromatopsia), and BIDIRECTIONAL VENTRICULAR TACHYCARDIA on ECG; digoxin is a cardiac glycoside derived from the foxglove plant; toxicity is monitored with serum plasma digoxin levels; hypokalemia increases toxicity risk

D.  Quinidine toxicity — causes prolonged QT and torsades de pointes, not visual changes

10.  A patient with AFib and HFrEF is prescribed amiodarone. The intern asks why amiodarone is uniquely useful compared to other antiarrhythmics.

What is amiodarone's mechanism of action and why does its extensive pharmacology make it broadly effective?

A.  Amiodarone is a pure Class III (potassium channel blocker) with no other mechanisms; this makes it highly selective

B.  AMIODARONE blocks MULTIPLE CHANNELS: K+ channels (Class III — primary), Na+ channels (Class I), Ca2+ channels (Class IV), and ALSO blocks alpha and beta receptors; this multi-channel blockade decreases conduction and automaticity across multiple pathways; it has a half-life of 27-107 DAYS (longest of any antiarrhythmic); preferred in AFib with HF; better at MAINTAINING NSR than converting to NSR

C.  Amiodarone only blocks beta receptors; its long half-life means it accumulates dangerously

D.  Amiodarone is a Class II drug (pure beta-blocker) with an unusually long half-life

11.  A resident presents a case of SVT to the attending. The patient is stable. After failed vagal maneuvers, the team proceeds with pharmacologic management. The attending explains the difference between Class II and Class IV antiarrhythmics.

What is the mechanism difference between Class II (beta-blockers) and Class IV (non-dihydropyridine CCBs) antiarrhythmics?

A.  Class II blocks Ca2+ channels; Class IV blocks Na+ channels — they work on opposite ion channels

B.  Both block the same ion channel (potassium) but at different phases of the action potential

C.  CLASS II (Beta-blockers — metoprolol, atenolol): block BETA-1 receptors → ↓ SA node automaticity, ↓ cardiac conduction; CLASS IV (Non-DHP CCBs — diltiazem, verapamil): block Ca2+ entrance in myocardial cells → ↓ AV conduction, ↓ SA node automaticity, ↓ contractility; BOTH are used for Afib rate control and SVT; Class II also used for ventricular arrhythmias

D.  Class II blocks K+ channels to prolong repolarization; Class IV blocks Na+ channels to slow conduction

12.  A pharmacology student asks about Class Ia sodium channel blockers and their use in cardiac arrhythmias.

Which drugs are Class Ia sodium channel blockers, and in what clinical context are Class I antiarrhythmics generally reserved?

A.  Amiodarone, sotalol, and dofetilide — Class Ia drugs reserved for routine SVT management

B.  Lidocaine, mexiletine — Class Ia; reserved for all bradycardic arrhythmias

C.  PROCAINAMIDE, QUINIDINE, and DISOPYRAMIDE — Class Ia sodium channel blockers; Class Ib = lidocaine and mexiletine; Class Ic = flecainide and propafenone; Class I drugs as a group are RESERVED FOR LIFE-THREATENING VENTRICULAR ARRHYTHMIAS due to their proarrhythmic risk

D.  Diltiazem, verapamil — Class Ia; used for rate control in all tachyarrhythmias

13.  A student must explain why procainamide is a reasonable option in stable AFib with duration ≤48 hours, but ibutilide requires extended monitoring.

What is the primary concern with ibutilide used for AFib cardioversion, and which patient population should avoid it?

A.  Ibutilide causes negative inotropy and should be avoided in all patients with HFrEF

B.  IBUTILIDE has the HIGHEST CARDIOVERSION SUCCESS RATE for AFib but requires 24 HOURS of MONITORING afterwards due to the RISK OF TORSADES DE POINTES (polymorphic VT from prolonged QT); AVOID in patients with HYPOKALEMIA or PROLONGED QT at baseline; other options for pharmacologic cardioversion include procainamide and amiodarone

C.  Ibutilide causes AV block and complete heart block after cardioversion

D.  Ibutilide must be avoided in AFib >12 months because it only works in recent-onset AFib

14.  An attending explains synchronized versus unsynchronized cardioversion to a resident preparing to treat an unstable tachycardia.

What is the key difference between synchronized cardioversion and unsynchronized defibrillation, and when is each used?

A.  Synchronized = high energy, unsynchronized = low energy; both can be used interchangeably for any tachyarrhythmia

B.  SYNCHRONIZED = LOW ENERGY SHOCK delivered at the PEAK OF THE QRS COMPLEX (to avoid delivering shock during the vulnerable T wave period which could trigger VF); used for UNSTABLE TACHYCARDIAS with a pulse (unstable AFib, flutter, atrial tachycardia, SVT, unstable VT with pulse); UNSYNCHRONIZED (defibrillation) = HIGH ENERGY, not synced to QRS, delivered immediately upon pressing button; used for NO COORDINATED ELECTRICAL ACTIVITY (pulseless VT/VF — patient is essentially dead)

C.  Synchronized = no coordination needed; unsynchronized = timed to QRS peak; same energy levels

D.  Only unsynchronized cardioversion is appropriate for all cardiac arrhythmias; synchronized is only for asystole

Section 3: AV Blocks & Bradyarrhythmias (Questions 15–22)

15.  A 68-year-old on diltiazem is found to have a PR interval of 0.26 seconds on his ECG. There is one P wave before each QRS. He is asymptomatic.

What is the diagnosis and appropriate management?

A.  Second-degree Mobitz Type I — progressive PR prolongation before a dropped beat

B.  Third-degree heart block — P waves dissociated from QRS complexes

C.  FIRST-DEGREE AV BLOCK — FIXED PROLONGED PR INTERVAL (>0.20 sec = greater than one large box); one P wave before every QRS; BENIGN, ASYMPTOMATIC, REQUIRES NO TREATMENT; pathologic causes include increased vagal tone, drugs (CCBs, beta-blockers, digoxin), inferior MI, myocarditis, and hyperkalemia

D.  Second-degree Mobitz Type II — fixed PR with dropped QRS complexes

16.  A 55-year-old presents with dizziness. His ECG shows the following pattern: PR interval progressively lengthens over 4 beats, then a QRS is dropped, and the pattern repeats. P-P interval is constant.

What is this conduction disorder, where is the block located, and how is it managed in an asymptomatic patient?

A.  Third-degree AV block — P waves unrelated to QRS complexes; requires permanent pacemaker

B.  Second-degree Mobitz Type II — fixed PR interval with dropped QRS; requires admission and pacing

C.  SECOND-DEGREE MOBITZ TYPE I (Wenckebach) — reversible conduction block WITHIN (or just below) the AV node; PROGRESSIVE PR LENGTHENING until a QRS is DROPPED, then pattern REPEATS; constant P-P interval; QRS clustered in groups; ASYMPTOMATIC = no treatment required; symptomatic = atropine (then pacing if fails); most benign of the second-degree blocks

D.  Sinus arrhythmia — variable P-P intervals with respiratory cycle; benign

17.  A 72-year-old with a recent anterior MI presents with a new bradycardia. His ECG shows a CONSTANT PR interval, but there are dropped QRS complexes. The pattern appears to be 3:2 (3 P waves, 2 QRS complexes) and the QRS is wide.

What is the diagnosis and why does this require urgent management?

A.  Second-degree Mobitz Type I — progressive PR lengthening before dropped beat; relatively benign

B.  SECOND-DEGREE MOBITZ TYPE II — block at the level of the BUNDLE OF HIS; CONSTANT PR interval (P waves 'march through') with DROPPED QRS complexes; FIXED conduction ratio (3:2, 4:3, 2:1); QRS usually WIDE (below bundle); associated with ANTEROSEPTAL MI; can PROGRESS TO COMPLETE HEART BLOCK without warning; REQUIRES ADMISSION; atropine OFTEN NOT EFFECTIVE (block too low); transcutaneous/transvenous pacing needed

C.  Sinus bradycardia — no dropped P waves; slow but regular rhythm

D.  Third-degree block — P waves dissociated from QRS; not a fixed ratio

18.  A 78-year-old presents in complete cardiovascular collapse with a ventricular rate of 30 bpm. His ECG shows regular P waves at 75 bpm and wide QRS complexes at 30 bpm with no relationship between P waves and QRS complexes.

What is the diagnosis and why are the QRS complexes WIDE?

A.  Atrial fibrillation with complete heart block — irregular P waves and wide escape rhythm

B.  THIRD-DEGREE (COMPLETE) AV BLOCK — NO conduction between atria and ventricles (COMPLETE AV DISSOCIATION); regular P-P intervals UNRELATED to regular R-R intervals; WIDE QRS (ventricular escape rhythm) when block is BELOW the His bundle (<40 bpm — ventricles are pacing themselves); NARROW QRS (junctional escape) if block is above the His bundle (40-60 bpm); HIGH RISK of ventricular standstill and sudden cardiac death

C.  Atrial flutter with 4:1 block — sawtooth pattern at 300 bpm with regular ventricular response

D.  Sinus arrest with junctional escape — P waves absent, narrow QRS escape rhythm

19.  A patient with third-degree heart block is being treated. The team discusses why atropine may not be effective.

Why is atropine often INEFFECTIVE in second-degree Mobitz Type II and third-degree heart block?

A.  Atropine is always effective for all types of bradycardia regardless of block location

B.  ATROPINE works by blocking ACETYLCHOLINE at the AV NODE (antimuscarinic mechanism); if the block is BELOW the AV node (Bundle of His or infra-nodal), atropine cannot reverse the conduction problem because the block is distal to where atropine acts; Mobitz II block = Bundle of His level; third-degree block = can be above or below; atropine works well only for blocks AT or ABOVE the AV node (first-degree, Mobitz I, sinus bradycardia)

C.  Atropine works by blocking beta receptors, so it only helps when sympathetic tone is low

D.  Atropine is contraindicated in all AV blocks due to risk of accelerating ventricular rate dangerously

20.  A student asks about permanent pacemaker indications in patients with AV block.

Which AV block pattern in an ASYMPTOMATIC patient still requires consideration for a permanent pacemaker?

A.  First-degree AV block — all patients with PR >0.20 sec need permanent pacemaker

B.  SECOND-DEGREE MOBITZ TYPE II and THIRD-DEGREE (COMPLETE) HEART BLOCK — these high-grade blocks can cause sudden cardiac death even when asymptomatic; HIGH-GRADE ASYMPTOMATIC BLOCK = PACEMAKER indication; Mobitz I in asymptomatic patients generally does NOT require pacing

C.  Sinus bradycardia — all asymptomatic patients with HR <50 need permanent pacemaker

D.  Second-degree Mobitz I — always requires permanent pacemaker even when asymptomatic

21.  A 42-year-old hiker presents with progressive dyspnea, palpitations, and a new first-degree AV block. She recently returned from a camping trip in New England.

What is the cardiac significance of this finding in the context of her history?

A.  First-degree AV block after camping always represents occult coronary artery disease requiring urgent catheterization

B.  LYME CARDITIS — LYME DISEASE (Borrelia burgdorferi) is a known cause of cardiac involvement including first-degree AV block that may DEGENERATE INTO COMPLETE HEART BLOCK; camping in New England (tick-endemic area) with new AV block should prompt consideration of Lyme disease; early treatment with antibiotics can reverse the cardiac conduction abnormalities

C.  Sinus node dysfunction — SA node failure is the most common cardiac manifestation of Lyme disease

D.  This is an incidental finding — AV block after camping requires no cardiac workup

22.  A 28-year-old with no cardiac history presents with sudden onset palpitations for 2 hours. ECG shows a narrow, fast, regular rhythm at HR 195 bpm with no clearly visible P waves before each QRS.

What is the most likely diagnosis and what is the most common mechanism?

A.  Sinus tachycardia — rate of 195 is within the expected range and P waves may be hidden

B.  Atrial fibrillation — fast irregular narrow complex rhythm without visible P waves

C.  PAROXYSMAL SVT (PSVT) — rapid narrow QRS complex tachycardia originating from atria or AV node; ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA (AVNRT) is the MOST COMMON mechanism (re-entry at the AV node); ECG: narrow QRS, HR 160-220 bpm, RATE DOES NOT VARY (differentiates from sinus tach), absent or retrograde P waves; mechanism = RE-ENTRY (revolving pathway)

D.  Ventricular tachycardia — wide QRS complex tachycardia in young patients

Section 4: Sinus Tachycardia, PSVT & SVT (Questions 23–29)

23.  A 32-year-old with PSVT is stable with HR 170 and BP 132/84. Vagal maneuvers are attempted first. The modified Valsalva technique is performed.

What is the correct technique for the MODIFIED VALSALVA maneuver?

A.  Have the patient strain for 30 seconds while standing, then sit down and hold breath

B.  MODIFIED VALSALVA: Patient in SEMI-RECUMBENT position → blows into a 10 mL SYRINGE for 15 SECONDS (when the plunger moves, adequate force is achieved) → immediately placed SUPINE with PASSIVE LEG RAISE for 45 SECONDS; this combination is more effective than the classic Valsalva maneuver alone by increasing venous return

C.  Carotid massage for 30 seconds bilaterally while patient breathes normally

D.  Carotid massage only — never Valsalva for SVT in adults

24.  A 10-year-old boy with no cardiac history presents with palpitations and HR 177 bpm. He is stable. After vagal maneuvers fail, the decision is made to use adenosine.

What are the two doses of adenosine used sequentially for PSVT, and what must you tell the patient before administration?

A.  3 mg slow IV push, then 6 mg if no conversion; no patient preparation needed

B.  ADENOSINE 6 mg rapid IV bolus first → if no conversion after monitoring → ADENOSINE 12 mg rapid IV bolus; must WARN the patient about HIGHLY UNCOMFORTABLE CHEST PAIN before administration; give in the most proximal peripheral line with rapid saline flush; half-life <10 seconds

C.  Adenosine 12 mg always first; 6 mg is the second dose; given as slow infusion over 2 minutes

D.  Adenosine is contraindicated in pediatric patients; use synchronized cardioversion instead

25.  A 46-year-old woman presents with palpitations for 3 hours, HR 165, BP 80/45, and oxygen saturation 94%. ECG shows narrow complex regular tachycardia. She is diaphoretic and altered.

What is the correct management for this hemodynamically UNSTABLE tachycardia?

A.  Adenosine 6 mg IV bolus — even in unstable tachycardia, attempt pharmacologic cardioversion first

B.  Diltiazem IV — rate control is the priority before considering electrical therapy

C.  EMERGENT SYNCHRONIZED CARDIOVERSION — this patient is UNSTABLE (altered mental status, hypotension, signs of shock); synchronized cardioversion is the first-line treatment for UNSTABLE tachycardias; adenosine and vagal maneuvers are only for STABLE patients with SVT; signs of instability = altered mental status, hypotension, signs of shock, ischemic chest pain, acute heart failure

D.  IV amiodarone infusion over 10 minutes — preferred for all unstable narrow complex tachycardias

26.  A student asks how to differentiate sinus tachycardia from PSVT on ECG.

Which ECG feature BEST differentiates sinus tachycardia from PSVT?

A.  QRS width — PSVT has wide QRS while sinus tachycardia has narrow QRS

B.  RATE VARIABILITY — Sinus tachycardia has a rate that VARIES with activity/stimuli; PSVT has a FIXED RATE that does NOT VARY; sinus tach has a visible P wave before every QRS and rate typically not >150 bpm; PSVT rate is 160-220 bpm with absent or retrograde P waves; sinus tach responds to treating the underlying cause (pain, fever, dehydration)

C.  PR interval — sinus tachycardia has short PR; PSVT has long PR interval

D.  All narrow complex fast rhythms are indistinguishable on ECG without electrophysiology study

27.  An electrophysiologist tells a PA student that ablation is the DEFINITIVE treatment for certain SVT patients.

For which patients with SVT/PSVT is catheter ablation considered the definitive treatment?

A.  All patients with any episode of PSVT should proceed directly to ablation

B.  PATIENTS WHO HAVE FAILED MANAGEMENT WITH MEDICATIONS — ablation is the definitive treatment for those who fail pharmacologic therapy (adenosine, beta-blockers, CCBs); ablation destroys the re-entry pathway (e.g., the slow pathway in AVNRT) to prevent recurrence; ablation can be considered as first-line for patients who prefer a procedural cure over lifelong medication

C.  Only patients with Wolff-Parkinson-White syndrome are candidates for ablation

D.  Ablation is never appropriate for AVNRT and should only be considered for AVRT

28.  A 65-year-old presents with irregular palpitations. His ECG shows absent P waves and irregularly irregular RR intervals with a ventricular rate of 138 bpm. He has no prior cardiac history.

What is the diagnosis and what are the three GOALS of treatment?

A.  Atrial flutter — regular P waves at 300 bpm with fixed 2:1 block; treat with cardioversion only

B.  ATRIAL FIBRILLATION — most common arrhythmia; DISORGANIZED electrical activity from MULTIPLE ATRIAL FOCI; ECG = ABSENT DISCRETE P WAVES + IRREGULARLY IRREGULAR RR INTERVALS; THREE TREATMENT GOALS: (1) PREVENT STROKE (cardioembolic), heart failure, and VF/death; (2) CONTROL SYMPTOMS; (3) treatment options = anticoagulation + rate control + rhythm control ± electrical cardioversion

C.  Multifocal atrial tachycardia — multiple P wave morphologies at rate >100 bpm

D.  Wandering atrial pacemaker — multiple P wave morphologies at normal rate; benign

29.  A 70-year-old woman with newly diagnosed AFib has a history of hypertension, CHF, diabetes, and a prior TIA. She is asking about her stroke risk.

Using the CHA2DS2-VASc score, calculate her score and determine if anticoagulation is indicated.

A.  Score of 3 — only anticoagulate if score is ≥5 in females

B.  CHA2DS2-VASc score: C=CHF(1) + H=HTN(1) + A=Age(0, not >75) + D=DM(1) + S=Stroke/TIA(2) + V=Vascular disease(0) + A=Age 65-74(1) + Sc=FEMALE SEX(1) = SCORE OF 7 → SCORE ≥3 in FEMALES = YES, ANTICOAGULATE; the lecture table: female ≥3 = OAC (oral anticoagulant); preferred anticoagulants = DOACs (dabigatran, apixaban, rivaroxaban, edoxaban) or warfarin

C.  Score of 5 — only consider anticoagulation (Grade C recommendation at this score)

D.  Anticoagulation is not recommended because she already had a TIA and bleeding risk is too high

Section 5: Atrial Fibrillation & Atrial Flutter (Questions 30–42)

30.  A 58-year-old male with AFib has a CHA2DS2-VASc score of 1 (hypertension only). His physician discusses anticoagulation.

Based on CHA2DS2-VASc scoring for MALES, what is the recommendation at a score of 1?

A.  Score of 1 in males = definitely start anticoagulation (Grade A recommendation)

B.  SCORE OF 1 IN MALES = CONSIDER anticoagulation (individualize based on patient bleeding risk and preferences); Score 0 in males = No anticoagulation; Score ≥2 in males = YES to anticoagulation; the CHA2DS2-VASc specifically gives different thresholds for males and females due to female sex being an added risk factor

C.  Score of 1 in males = No anticoagulation (same threshold as females)

D.  CHA2DS2-VASc is not used for males; only the CHADS2 score applies

31.  A 54-year-old presents with AFib. The duration of AFib is unknown — he noticed it this morning but cannot confirm the onset. He is stable.

What must be done BEFORE performing pharmacologic or electrical cardioversion when AFib duration is UNKNOWN or >48 hours?

A.  Immediately cardiovert — the risk of stroke from cardioversion is negligible in the first 48 hours

B.  TRANSESOPHAGEAL ECHOCARDIOGRAM (TEE) to RULE OUT THROMBUS in the left atrial appendage before cardioversion; OR anticoagulate for 3 WEEKS (21 DAYS) before cardioversion; if patient is already anticoagulated, consult cardiology regarding cardioversion risks; cardioverting without ruling out thrombus can dislodge a clot → embolic stroke

C.  Perform transthoracic echo only — TEE is not necessary for routine AFib cardioversion

D.  Start rate control immediately and never attempt cardioversion if duration is unknown

32.  A 66-year-old with AFib, hypertension, and CKD stage 3 needs anticoagulation. His physician is choosing between warfarin and DOACs.

Which of the following is a DOAC (direct oral anticoagulant) and what is its mechanism?

A.  Warfarin (Coumadin) — vitamin K antagonist with INR goal 2-3; a DOAC by definition

B.  APIXABAN (ELIQUIS) — a FACTOR XA INHIBITOR; other Factor Xa inhibitors = rivaroxaban (Xarelto) and edoxaban (Savaysa); DABIGATRAN (Pradaxa) = DIRECT THROMBIN INHIBITOR; these are all DOACs; WARFARIN = vitamin K antagonist (NOT a DOAC); DOACs are preferred over warfarin for most non-valvular AFib patients (predictable pharmacokinetics, fewer drug interactions, no routine INR monitoring)

C.  Dabigatran is a Factor Xa inhibitor and apixaban is a direct thrombin inhibitor

D.  Enoxaparin (Lovenox) — a DOAC used for long-term AFib anticoagulation

33.  A patient with chronic AFib asks why she needs long-term anticoagulation even when she has no symptoms.

Why does asymptomatic atrial fibrillation still carry a significant stroke risk?

A.  Asymptomatic AFib does not carry stroke risk — only symptomatic AFib requires anticoagulation

B.  IN AFIB, the atria fibrillate and do not contract effectively; this causes blood to STAGNATE in the LEFT ATRIAL APPENDAGE → thrombus formation; when NSR is restored (spontaneously or with cardioversion) the thrombus can embolize → CARDIOEMBOLIC STROKE; this risk exists regardless of symptoms; AFib causes disorganized electrical activity from multiple atrial foci, abnormal rhythm AND tachycardia (both ↑ stroke risk)

C.  Stroke risk in AFib is only present during episodes of symptomatic palpitations

D.  DOACs eliminate all stroke risk in AFib patients regardless of CHA2DS2-VASc score

34.  A patient with stable atrial flutter for less than 48 hours presents to the ED. The attendant explains the relationship between AFib and atrial flutter treatment.

How does atrial flutter differ from AFib on ECG, and how does the treatment differ?

A.  Atrial flutter and AFib are identical conditions with the same ECG findings and treatment

B.  ATRIAL FLUTTER: RAPID REGULAR atrial activity with SAWTOOTH P waves (single morphology); atrial rate ~300 bpm; FIXED or VARIABLE ventricular rates (2:1, 3:1, 4:1 conduction); causes similar to AFib (hyperthyroidism, PE, valvular disease, cardiomyopathy); TREATMENT IS SAME AS AFib but if cardioverting electrically, use LOWER VOLTAGE; may be idiopathic

C.  Atrial flutter has completely irregular RR intervals like AFib; only ECG morphology differs

D.  Atrial flutter is always faster than AFib and requires double the cardioversion energy

35.  A 63-year-old male with AFib has been in AFib for 6 days. His physician wants to perform cardioversion.

What is the correct anticoagulation strategy for this patient before cardioversion?

A.  No anticoagulation needed since the AFib has been present less than 1 week

B.  ANTICOAGULATE FOR 3 WEEKS (21 DAYS) before cardioversion OR perform TEE first to rule out left atrial thrombus; AFib >48 hours or unknown duration = HIGH RISK for LA thrombus; this patient has been in AFib for 6 DAYS (>48 hours) → MUST anticoagulate 3 weeks or get TEE before cardioverting; after cardioversion, continue anticoagulation for AT LEAST 4 WEEKS (post-cardioversion anticoagulation period)

C.  Cardiovert immediately and start anticoagulation after successful cardioversion

D.  Only heparin is acceptable — DOACs are not appropriate for pericardioversion anticoagulation

36.  A patient with AFib and known HYPERTENSION and HEART FAILURE is in the ED with HR 145 and BP 105/68. Rate control is needed.

What is the MOST APPROPRIATE rate control agent in this clinical scenario?

A.  IV diltiazem — first-line CCB for all AFib rate control regardless of hemodynamics

B.  IV metoprolol — beta-blockers are always preferred in patients with hypertension

C.  DIGOXIN or AMIODARONE — this patient has HYPOTENSION (BP 105/68) and HEART FAILURE; AVOID diltiazem (negative inotrope — worsens HF, contraindicated in hypotension) and beta-blockers (negative inotrope — worsens HF, contraindicated in hypotension); digoxin (directly suppresses AV node + positive inotropic) or amiodarone (if anticoagulated or ≤48 hours) are the preferred agents for rate control in HFrEF or soft BP

D.  Adenosine — used for PSVT, not appropriate for AFib rate control

37.  AFib lasting less than 48 hours is being managed in the ED. The provider considers pharmacologic cardioversion options.

For pharmacologic cardioversion of STABLE AFib ≤48 hours, which option has the HIGHEST SUCCESS RATE but requires extended post-administration monitoring?

A.  Amiodarone — highest success rate for AFib cardioversion and requires no extended monitoring

B.  Procainamide — first-line pharmacologic cardioversion agent with no monitoring needed

C.  IBUTILIDE — highest success rate for pharmacologic AFib cardioversion; however, requires 24 HOURS of monitoring after administration due to RISK OF TORSADES DE POINTES; not commonly used in the ED; AVOID if hypokalemia or prolonged QT at baseline; other pharmacologic cardioversion options = procainamide and amiodarone

D.  Adenosine — appropriate for all AFib cardioversion with highest success rate

38.  A student creates a summary card of AFib classification. She is asked about the key duration thresholds.

Which of the following CORRECTLY describes the classification of atrial fibrillation by duration?

A.  Paroxysmal = <24 hours; Persistent = 1-7 days; Long-standing = >7 days; Permanent = >12 months

B.  Paroxysmal = <2 days; Persistent = 2-7 days; Long-standing = 8-12 months; Permanent = >12 months

C.  PAROXYSMAL = <7 DAYS (self-terminating, usually <48 hrs); PERSISTENT = >7 DAYS or prior cardioversion (not self-terminating); LONG-STANDING PERSISTENT = >12 MONTHS; PERMANENT = continues despite cardioversion or has given up on maintaining NSR; POSTOPERATIVE = self-limiting, 3-5 DAYS post-surgery

D.  Paroxysmal = <48 hours; Persistent = 48 hours to 7 days; Long-standing = 7 days to 6 months; Permanent = >6 months

39.  A 42-year-old healthy triathlete presents with palpitations for 2 hours. ECG shows irregular narrow complex tachycardia with no visible P waves, ventricular rate 140 bpm, and normal BP of 140/70. He has a history of HTN only and takes no medications.

What is the diagnosis, stability assessment, and the FIRST critical management step?

A.  PSVT — stable; give adenosine 6 mg IV bolus immediately

B.  Atrial flutter — unstable; synchronized cardioversion immediately at 100J

C.  ATRIAL FIBRILLATION (new onset ≤48 hours — onset 2 hours ago) — STABLE (normal BP, alert); first step = ASSESS DURATION (≤48 hours → lower thrombus risk; cardioversion is an option); consider anticoagulation dose before cardioversion; calculate CHA2DS2-VASc score (1 point for HTN) → score 1 for male = CONSIDER anticoagulation; rate control vs rhythm control decision based on clinical course

D.  Sinus tachycardia — treat the underlying cause; no specific rhythm management needed

40.  A 32-year-old female presents with sudden palpitations. Vital signs: HR 170, BP 132/84, O2 sat 98%. ECG shows narrow complex regular tachycardia, rate non-varying at 170 bpm. Vagal maneuvers fail to convert the rhythm.

According to the lecture case study (Miss Morgan), what is the CORRECT sequence of management for this stable SVT patient after failed vagal maneuvers?

A.  Synchronized cardioversion immediately after failed vagal maneuvers — pharmacologic therapy is not tried first in stable patients

B.  IV diltiazem first, then verapamil if fails, then adenosine as last resort

C.  ADENOSINE 6 mg RAPID IV BOLUS → if no conversion, ADENOSINE 12 mg RAPID IV BOLUS → if still no conversion and patient remains STABLE → synchronized cardioversion or other rate control agents; WARN the patient about chest pain before giving adenosine; establish IV first; the lecture specifically describes this exact case ('the longest 4 seconds of your life')

D.  Oral metoprolol plus bed rest — IV medications only for unstable patients

41.  A 55-year-old presents with palpitations. ECG reveals a QRS that is wide and the P waves are completely dissociated from the QRS complexes. Ventricular rate is 32 bpm, atrial rate 78 bpm. The patient is diaphoretic and has BP 72/45.

What is the diagnosis and what is the CORRECT treatment for this hemodynamically unstable patient?

A.  Atrial flutter with 4:1 block — use synchronized cardioversion at 100J

B.  Third-degree AV block (stable) — atropine 1 mg IV with monitoring; transcutaneous pacing if fails

C.  THIRD-DEGREE (COMPLETE) AV BLOCK with hemodynamic instability — complete AV dissociation (P waves unrelated to QRS, wide escape rhythm <40 bpm indicates infranodal block); TREATMENT: TRANSCUTANEOUS PACING IMMEDIATELY; atropine often INEFFECTIVE (infranodal block); also give sympathomimetics (epinephrine, dopamine) as bridge; arrange TRANSVENOUS PACING ASAP

D.  Give adenosine 6 mg IV to diagnose the block type before treating

42.  A pharmacology question: A patient is started on amiodarone. The pharmacist counsels on its unique properties.

Which statement about amiodarone is MOST ACCURATE regarding its pharmacokinetics and comparative effectiveness?

A.  Amiodarone has a half-life of 2-4 hours, requiring dosing every 6 hours for maintenance

B.  AMIODARONE has a half-life of 27-107 DAYS (extremely long); it is BETTER AT MAINTAINING NSR than CONVERTING to NSR; it blocks multiple ion channels (K+, Na+, Ca2+) and also blocks alpha and beta receptors; it is the PREFERRED antiarrhythmic in AFib WITH HEART FAILURE (other agents may worsen HF); 'pill in the pocket' strategy for AFib uses flecainide or propafenone instead

C.  Amiodarone has the shortest half-life of all antiarrhythmics and requires continuous IV infusion

D.  Amiodarone is better at converting AFib to NSR than maintaining NSR; it has a 6-hour half-life

Section 6: Integrated Clinical Scenarios (Questions 43–50)

43.  A PA student is given the following case: a patient with palpitations has a regular narrow complex tachycardia at a rate of 155 bpm. There are no visible P waves before the QRS. After the QRS you see a small deflection. The patient is stable.

Which rhythm is most consistent with this finding and what is the characteristic of AVNRT vs. AVRT?

A.  Sinus tachycardia — normal P waves are before each QRS at this rate

B.  PSVT — AVNRT (most common): Re-entry WITHIN the AV node; retrograde P waves often buried in or immediately after the QRS (RP' interval very short); AVRT uses an ACCESSORY PATHWAY outside the AV node (e.g., WPW); in AVRT retrograde P wave may be slightly further from QRS; BOTH present as narrow complex regular SVT at 160-220 bpm; mechanism is RE-ENTRY in both cases; AVNRT is more common

C.  Atrial flutter with 2:1 block — sawtooth P waves at 300 bpm with regular ventricular rate ~150

D.  Ventricular tachycardia — wide complex, regular, fast; P waves unrelated to QRS

44.  An attending asks a student to identify the clinical stability criteria they must always assess before treating any arrhythmia.

According to the lecture, what are the SIGNS OF CLINICAL INSTABILITY that mandate emergent treatment regardless of arrhythmia type?

A.  Palpitations, fatigue, and lightheadedness — these symptoms always indicate instability

B.  ALTERED MENTAL STATUS, HYPOTENSION, SIGNS OF SHOCK, ISCHEMIC CHEST DISCOMFORT, and ACUTE HEART FAILURE — these are the SIGNS OF INSTABILITY; the lecture emphasizes 'from now on, anytime you read a clinical vignette or have a patient scenario you must ask yourself: STABLE OR UNSTABLE'; symptoms like palpitations and dizziness alone do NOT equal instability

C.  Any heart rate above 150 bpm automatically makes the patient unstable

D.  Only patients with systolic BP <80 mmHg are considered clinically unstable

45.  A 74-year-old woman with a history of hypertension presents for a routine check-up. She is asymptomatic. HR is 42 bpm, BP 110/70, O2 sat 98%, and she is alert and in no distress. ECG shows sinus bradycardia.

Based on the lecture case example, how should this patient be assessed and managed?

A.  This patient is unstable — HR 42 requires immediate atropine and pacemaker consultation

B.  She is STABLE — BP 110/70, asymptomatic, alert, O2 sat 98%; asymptomatic sinus bradycardia in an otherwise stable patient requires EVALUATION FOR UNDERLYING CAUSE (HE DIES: hypothyroidism, elevated ICP, drugs, ischemia, electrolytes, sick sinus syndrome) but NO IMMEDIATE INTERVENTION; 'symptoms do NOT equal instability' — the HR alone does not mandate emergent treatment; symptomatic bradycardia would require atropine → pacing

C.  Immediately start transcutaneous pacing — any HR <50 in an elderly patient is an emergency

D.  Give IV atropine 1 mg immediately and arrange for permanent pacemaker

ANSWER KEY

Arrhythmias Part 1  —  Clinical Application Exam