Detect Cardiac Arrhythmia ECG Quiz

Rhythm analysis follows a systematic approach to prevent missed findings. Evaluating P waves confirms atrial activity, QRS width identifies ventricular involvement, rhythm regularity assesses conduction stability, P–QRS relationship confirms AV conduction, and heart rate determines clinical severity.

Lead II aligns closely with the heart’s electrical axis, producing upright P waves and clear QRS complexes. This makes it ideal for identifying rhythm patterns and conduction abnormalities.

Supraventricular rhythms originate above the ventricles, allowing atrial depolarization and visible P waves. Ventricular rhythms bypass atrial activation, eliminating P waves.

AV nodal rhythms suppress SA node activity, resulting in absent or hidden P waves. Ventricular depolarization follows normal pathways, keeping QRS complexes narrow.

Ventricular rhythms originate outside the normal conduction system, causing slow cell-to-cell conduction and wide QRS complexes with absent P waves.

Sinus arrhythmia maintains a normal PR interval but varies with respiration, causing slight rhythm irregularity while remaining physiologically normal.

Supraventricular arrhythmias arise from the atria or AV node, distinguishing them from ventricular-origin rhythms.

Atrial fibrillation lacks organized atrial depolarization, producing a chaotic baseline and unpredictable ventricular response, described as irregularly irregular.

Rate control in AFib with RVR prevents hemodynamic compromise. IV diltiazem or beta blockers slow AV nodal conduction effectively.

AFib with RVR often causes palpitations, dyspnea, chest discomfort, and fatigue due to rapid ventricular rates and poor cardiac output.

Cardioversion and radiofrequency ablation restore organized atrial conduction without relying on medications.

Cardioversion after prolonged AFib risks dislodging atrial thrombi, leading to stroke or systemic embolism.

Atrial flutter involves a single reentrant atrial circuit, producing rapid but regular atrial depolarizations.

Flutter waves create a saw-tooth ECG appearance, especially visible in inferior leads.

Leads II, III, and aVF visualize the inferior heart wall supplied by the right coronary artery.

Rate-control medications slow AV conduction, stabilizing ventricular response in atrial flutter.

DC cardioversion rapidly restores sinus rhythm in unstable atrial flutter patients.

PSVT originates above the ventricles, producing narrow complexes and very rapid rates.

Vagal maneuvers increase parasympathetic tone, while adenosine transiently blocks AV conduction.

Wide QRS complexes indicate ventricular origin or aberrant conduction.

PSVT conduction uses normal ventricular pathways, resulting in narrow QRS complexes.

Adenosine terminates AV nodal reentry, making it first-line for PSVT.

Unstable tachyarrhythmias require immediate electrical cardioversion to restore perfusion.

Antiarrhythmics suppress ventricular automaticity and stabilize myocardial conduction.

Ventricular fibrillation causes no effective cardiac output and requires immediate defibrillation.

Escape rhythms activate when primary pacemakers fail, resulting in very slow heart rates.

AIVR originates in ventricular tissue but at slower, transient rates.

PVCs arise prematurely from ventricles, producing wide, early QRS complexes.