ECG QUIZZES PART II CHALK TALKS | Graded to Pass | Rhythm Interpretation & Cardiology Exam Prep | Pass Guaranteed - A+ Graded

Pass your ECG Quizzes Part II (Chalk Talks) on the first attempt with this comprehensive guide featuring graded questions and detailed rhythm interpretations! This A+ Graded resource for the Advanced ECG / EKG Chalk Talks Quizzes Part II contains verified questions with complete solutions covering essential electrocardiography concepts for medical, nursing, and paramedic students. Featuring comprehensive coverage of cardiac anatomy and conduction system (SA node, AV node, Bundle of His, Purkinje fibers), sinus rhythms (normal sinus rhythm (NSR) (rate 60-100, P before every QRS, P wave morphology normal, PR interval 0.12-0.20, QRS 0.12), sinus bradycardia (60, regular, normal P waves), sinus tachycardia (100, 150 typically, regular, normal P waves, can exceed 150 with fever, exercise, hypovolemia, hyperthyroidism, but if 150 suspect SVT), sinus arrhythmia (irregular rhythm that varies with respiration, P-P interval varies by 0.12 seconds, P wave morphology normal, rate often 50-100, benign especially in young healthy patients)), atrial rhythms (premature atrial complexes (PACs) (early P wave with different morphology, often hidden in T wave, P wave may be flattened or peaked or biphasic (left atrial or right atrial origin), PR interval may be normal or slightly prolonged, QRS usually narrow unless aberrant conduction (right or left bundle branch block pattern (RBBB or LBBB)), atrial bigeminy (every other beat is PAC), compensatory pause incomplete (PAC resets SA node, pause less than two full cycles), PACs described as unifocal (identical P wave morphology) or multifocal (varying P wave morphology and PR interval), treatment often none unless symptomatic causing palpitations, consider beta-blockers (metoprolol, propranolol) for symptom control, worsen with stimulants (caffeine, nicotine, alcohol)), atrial tachycardia (atrial rate 100-250, P waves morphology differs from sinus P, may have isoelectric baseline between P waves (distinguishes from atrial flutter which has sawtooth baseline and rate usually 250-350), PR interval variable, QRS narrow (unless aberrancy), paroxysmal atrial tachycardia (PAT) often due to triggered activity or automatic focus, may be refractory to vagal maneuvers, treat with AV nodal blocking agents (adenosine (6 mg rapid IV push, may repeat 12 mg) will transiently block AV node causing pause, stopping the tachycardia if it is dependent on AV node (AVRT, AVNRT), but pure atrial tachycardia may continue despite AV block, then better treated with beta-blockers, calcium channel blockers (verapamil, diltiazem)), multifocal atrial tachycardia (MAT) (atrial rate 100, P waves with at least three different morphologies in same lead, variable PR intervals, irregularly irregular (but note: MAT has P waves before each QRS, atrial fibrillation has no P waves), usually associated with COPD, pulmonary disease, theophylline toxicity, treat underlying pulmonary condition, rate control with verapamil, diltiazem, magnesium, avoid beta-blockers in COPD), atrial flutter (sawtooth flutter waves (F waves) at rate 250-350 typically 300 bpm, AV node conducts in variable ratio (2:1 most common, 3:1, 4:1), ventricular rate often 150 with 2:1 block, 100 with 3:1 block), carotid sinus massage or adenosine may increase AV block to unmask flutter waves, not treat sustained flutter but may help diagnosis. Treatment for atrial flutter similar to atrial fibrillation (rate control with beta-blockers, nondihydropyridine CCBs (verapamil, diltiazem), rhythm control with dofetilide, ibutilide, or synchronized cardioversion (50-100 J biphasic for atrial flutter, lower than for atrial fibrillation)), anticoagulation per CHA₂DS₂-VASc score (congestive heart failure, hypertension, age ≥75 (2 points), diabetes, prior stroke/TIA (2 points), vascular disease, age 65-74, female sex)), atrial fibrillation (AFib) (no P waves, irregularly irregular baseline, fibrillatory (f) waves coarse or fine, atrial rate 350-600, ventricular rate variable (rapid ventricular response 100, if slow AFib 60 consider conduction system disease or drugs), classification: paroxysmal (7 days self-terminating), persistent (7 days requires cardioversion), long-standing persistent (12 months), permanent (patient and provider accept AFib no further rhythm control), rate control vs rhythm control strategy, anticoagulation (apixaban (Eliquis), rivaroxaban (Xarelto), dabigatran (Pradaxa), edoxaban (Savaysa), warfarin (Coumadin)), tell‑tale irregularly irregular rhythm and absent P waves, QRS narrow unless aberrancy or pre-existing conduction delay), junctional rhythms (junctional escape rhythm (rate 40-60, inverted P wave before or after QRS or absent, PR interval 0.12 if P before QRS, QRS narrow), accelerated junctional rhythm (rate 60-100), junctional tachycardia (rate 100), premature junctional complexes (PJCs) (early narrow QRS with absent or inverted P wave)), ventricular rhythms (premature ventricular complexes (PVCs) (wide QRS 0.12, no preceding P wave, fully compensatory pause despite earlier belief may not always be full in some contexts, T wave opposite polarity to QRS, unifocal (identical morphology), multifocal (different morphologies), couplets (2 PVCs in a row), triplet (3 PVCs in a row), bigeminy (PVC every other beat), trigeminy (PVC every third beat), quadrigeminy (PVC every fourth beat), R‑on‑T phenomenon (PVC falling on T wave (vulnerable period) can provoke ventricular tachycardia or fibrillation), treatment: reassurance if asymptomatic and no structural heart disease, beta-blockers for symptomatic, antiarrhythmics for high burden (10-15% of beats) or polymorphic PVCs), ventricular tachycardia (VT) (wide QRS 0.12, rate 100 typically 150-250, monomorphic VT (same QRS morphology, usually due to re-entry, may be sustained (30 seconds) or non-sustained (runs of 3+ PVCs terminating spontaneously 30 seconds), atrioventricular dissociation (P waves not related to QRS), capture beats and fusion beats diagnostic of VT, differentiate from SVT with aberrancy using Brugada criteria, Vereckei algorithm (aVR lead: initial R wave 0.04 seconds? Or in lead II: notching? Many criteria), treatment: monomorphic VT hemodynamically unstable (syncope, angina, dyspnea, SBP 90) → synchronized cardioversion (100 J biphasic, escalate 150-200 J), stable VT → IV amiodarone (150 mg over 10 min, then 1 mg/min infusion for 6 hours), lidocaine, procainamide, polymorphic VT (torsades de pointes) (twisting of peaks around baseline, usually in setting of long QT, congenital long QT syndrome (LQTS type 1,2,3), acquired LQT (medications (many), hypokalemia, hypomagnesemia, hypocalcemia), treat with IV magnesium sulfate (2 g over 1-2 minutes, may repeat 2g), isoproterenol (overdrive pacing), shared decision to treat QT prolonging medication), ventricular fibrillation (VF) (chaotic irregular waveform, no identifiable QRS, rate unmeasurable, immediate defibrillation (unsynchronized, 200 J biphasic following CPR (push hard, push fast 100-120/min, depth 2-2.4 inches, allow full chest recoil, minimize interruptions, after every 2 minutes of CPR rhythm check, alternating with epinephrine 1 mg IV q3-5 minutes and amiodarone 300 mg IV for refractory VF/pulseless VT after first shock and epinephrine), also consider lidocaine 100 mg IV)), idioventricular rhythm (wide QRS, rate 20-40, no P waves, usually seen in complete heart block or post cardiac arrest), accelerated idioventricular rhythm (rate 50-110, commonly after reperfusion in myocardial infarction, usually benign and not treated unless hemodynamic compromise), asystole (flatline, no electrical activity, treat with high-quality CPR, epinephrine 1 mg IV q3-5 minutes, check for loose leads, reversible causes (hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia, tension pneumothorax, tamponade (cardiac), toxins, thrombosis (coronary or pulmonary)), PEA (pulseless electrical activity, organized rhythm but no palpable pulse, treat same as asystole, identify and treat reversible causes (4H and 4T etc.)), heart blocks (first‑degree AV block (PR interval 0.20 seconds, all P waves conducted, QRS normal, rate regular, usually benign, no treatment unless symptomatic or progresses to higher grade)), second‑degree AV block Mobitz I (Wenckebach) (progressive prolongation of PR interval until a QRS is dropped, RR interval shortens, Wenckebach periodicity, usually at AV node level, narrow QRS, often benign, treat only if symptomatic (atropine 0.5 mg IV, pacing rarely needed)), second‑degree AV block Mobitz II (constant PR interval with non-conducted P waves, typically infra-Hisian, QRS often wide, high risk of progressing to third‑degree AV block, requires pacemaker), 2:1 AV block (cannot classify as Mobitz I or II easily, often infra-Hisian if wide QRS, requires pacemaker, vagal maneuvers increase block), third‑degree AV block (complete heart block) (no relation between P waves and QRS, atrial rate 60-100, ventricular rate 30-60 if junctional escape, 20-40 if ventricular escape, QRS narrow if junctional (in congenital block or acquired in setting of inferior MI), QRS wide if ventricular (often in anterior MI), treatment urgent pacing, transcutaneous or transvenous, atropine not effective for Mobitz II or third-degree AV block, consider isoproterenol if needed temporarily), package and fascicular blocks (right bundle branch block (RBBB) (QRS ≥0.12, rsR' (rabbit ears) in V1, wide slurred S wave in V6 left precordial leads, secondary ST‑T changes opposite terminal QRS direction, causes: pulmonary embolism, right heart strain, congenital, but also idiopathic; can be rate‑dependent (bradycardia‑dependent, tachycardia‑dependent) when conduction block occurs at certain heart rates); left bundle branch block (LBBB) (QRS ≥0.12, monophasic notched or slurred R wave in V5-V6 (wide tall), broad S wave in V1, no septal q waves in lateral leads (because septum depolarizes left to right), ST‑T discordant (opposite direction to wide QRS), LBBB associated with ischemic heart disease, dilated cardiomyopathy makes it more difficult to interpret ST segments for ischemia (Sgarbossa criteria)), left anterior fascicular block (LAFB) (left axis deviation (usually -45° to -90°), qR pattern in lead aVL, R peak time 45 ms in aVL, QRS duration 0.12, no other cause of LAD), left posterior fascicular block (LPFB) (right axis deviation (+90° but +180°, provided no other cause of RAD (right ventricular hypertrophy, lateral MI, COPD, pulmonary embolism)), rS in leads I and aVL, qR in leads III and aVF, QRS duration 0.12, exceedingly rare because left posterior fascicle has dual blood supply from LAD and PDA), ischemia and infarction patterns (hyperacute T waves (tall, symmetric, peaked, more than 5mm in limb leads or 10mm in precordial leads? no, but at least 50% increase in amplitude or new, asymmetrical, diagnostic of very early transmural ischemia before ST elevation), ST elevation (≥1 mm in limb leads (except aVR, V2-V3 ≥2 mm in men ≥40 years in V2-V3, ≥2.5 in V2-V3 for men 40, ≥1.5 for women), leads corresponding to myocardial injury, suspect STEMI (ST elevation myocardial infarction) and activate cath lab, reciprocal ST depression in opposite leads); Q waves (pathologic if 0.04 seconds and depth 25% of R wave, indicates transmural infarction); ST depression (horizontal or downsloping ≥0.5 mm in two contiguous leads suggests subendocardial ischemia (unstable angina, NSTEMI, or reciprocal changes of posterior MI), also seen in LVH with strain (downsloping ST and T inversion in leads V5-V6 but asymmetric inversion), digoxin effect (scooping ST segment with short QT, also ST depression in lateral leads with downsloping, but distinguished from ischemia by absence of reciprocal changes and presence of other digoxin signs (arrhythmias from increased automaticity (PVCs, atrial tachycardia with block), shortened PR, prolonged QT, visual colors, nausea)), wellens syndrome (biphasic T waves in V2-V3 or deeply inverted symmetric T waves in V2-V4, high grade proximal LAD stenosis, not associated with enzyme elevation (troponin may be elevated but not), do not exercise stress, these patients need angiography), de winters sign (upwardly convex ST depression in precordial leads V1-V6 with hyperacute peaked T waves, no ST elevation, anterior LAD occlusion), electrolyte disturbances (hyperkalemia (peaked T waves (tall tented symmetric T waves with narrow base), prolongs PR interval, QRS widening, sine wave (sinoventricular rhythm) before VF, treat with calcium gluconate (10% solution 10 ml IV over 2-3 minutes), insulin + glucose, albuterol, kayexalate, furosemide, dialysis); hypokalemia (U waves after T waves (most prominent in V2-V4), flattened T waves, ST depression, increased amplitude and duration of P wave, treat potassium chloride IV 10-20 mEq/hour depending on cardiac monitoring (max 20 mEq/hour peripheral, 40 mEq/hour central), also PO supplements (K-Dur, Klor-Con, potassium chloride liquid)); hypercalcemia (short QT interval, Osborn waves? no, Osborn waves in hypothermia, hypercalcemia short QT, JT segment shortening, prolonged PR and QRS may occur in severe cases); hypocalcemia (prolonged QT interval, ST segment lengthening (prominent), no U wave (helps distinguish from hypokalemia)), drug effects (digoxin (scooped ST segment, prolonged PR, short QT, arrhythmias (PAT with block, accelerated junctional rhythm, PVCs, bidirectional ventricular tachycardia))); quinidine and Class 1A antiarrhythmics causing QT prolongation (torsades), amiodarone causing QT prolongation and pulmonary toxicity, thyroid dysfunction); chalk talk focus for part II includes clinical case quizzes where you are given a short patient presentation (vital signs, symptoms, ECG rhythm strip) and must identify rhythm, discuss rate, regularity, P waves, PR interval, QRS width, management decisions (defibrillation vs cardioversion, medication administration (adenosine, amiodarone, beta-blockers), atropine for symptomatic bradycardia, pacing), potential pitfalls: differentiating SVT with aberrancy vs VT (Brugada signs (V lead: no RS complex positive, presence of any RS complex 100ms in any precordial lead?), in a study 80% accuracy, but more reliable having prior ECG, stabilization, tachycardia above 150 with unstable, direct cardioversion; if stable, use adenosine to slow AV node and reveal underlying atrial flutter or sinus rhythm, note that adenosine terminates AV nodal reentrant tachycardia (AVNRT) and atrioventricular reentrant tachycardia (AVRT) with accessory pathway (WPW syndrome), but not atrial tachycardia or flutter. Also learn about verapamil-sensitive (or adenosine-sensitive) idiopathic left ventricular tachycardia (fascicular ventricular tachycardia) that originates in left posterior fascicle with RBBB morphology and left axis deviation, slower 160 bpm, responsive to verapamil but not adenosine. Distinguishing characteristics: RBBB pattern with left axis deviation, left ventricular origin near fascicles, verapamil 5-10 mg IV over 2-3 minutes may terminate. The ECG patterns also include accelerated idioventricular rhythm, idioventricular escape rhythms, demand pacemaker rhythms (ventricular paced, atrial paced, AV paced) with pacer spikes, failure to capture (spike no QRS), failure to sense (spike delivered on intrinsic QRS), oversensing (pacing inhibited due to sensing of T wave or muscle artifact). Chalk talks part II often includes pacemaker ECGs: identify atrial paced with spike before P wave, ventricular paced with spike before wide QRS), fusion beats (intrinsic and paced QRS overlap), pseudofusion (spike appears on top of intrinsic QRS but does not depolarize myocardium because it fell in refractory period). In addition, ECG artifact: muscle tremor (pseudofibrillation) vs VF (artifact has consistent baseline not chaotic?), movement artifact, lead reversal (e.g., arm leads swapped, precordial leads placed incorrectly (V1-V2 upside down or V3-V6 misplaced). Sinus rhythm with limb lead reversal (right arm to left arm) produces P wave negative in lead I and all leads reversed, can diagnose. Also dextrocardia (right‑sided placement of precordial leads V1-V6 as mirror images showing low voltage in V1, tall R wave in V6, but if we place leads on right side corrected then true mirror. Dextrocardia with situs inversus presents with right axis deviation, P wave inversion in lead I, but the QRS may be upright but negative in I? Not needed). This guide provides complete solutions for each quiz question, with step‑by‑step analysis, identifying rhythms, recognition of abnormalities, appropriate nursing and clinician response (call rapid response team or activate code blue for VF/pulseless VT, prepare for defibrillation), and pharmacology dosages based on ACLS guidelines (American Heart Association). With detailed rationales, multiple practice quizzes, rhythm strips, and our Pass Guarantee, this is the definitive tool for nursing students, medical residents, paramedics, ECG technicians, and healthcare providers preparing for advanced ECG examinations, certification, or board exams. Download now and become a confident ECG interpreter!