Skip to Main Content

We have a new app!

Take the Access library with you wherever you go—easy access to books, videos, images, podcasts, personalized features, and more.

Download the Access App here: iOS and Android

Key Points

  • Quickly address airway, breathing, and circulation (the ABCs), provide supplemental O2, secure intravenous access, and initiate continuous cardiac monitoring.

  • Rapidly distinguish between stable versus unstable presentations, as unstable patients require immediate intervention.

  • Order a 12-lead electrocardiogram on stable patients and address potential etiologies, including acute coronary syndrome, electrolyte abnormalities, toxic ingestions, and medication side effects.


The recognition of dysrhythmia is an essential skill for all emergency physicians, as patients presenting with dysrhythmias are relatively common and have the potential for rapid hemodynamic deterioration. Clinically, dysrhythmias are classified as stable or unstable based on the presence or absence of adequate end-organ perfusion (ie, systemic hypotension, cardiac ischemia, pulmonary edema, or mental status changes). Dysrhythmias are further divided by their rate into either bradydysrhythmias (heart rate [HR] <60) or tachydysrhythmias (HR >100). An additional subset of dysrhythmia, atrioventricular blocks, can present with any HR and represent a malfunction in electrical conduction between the sinoatrial (SA) node, atrioventricular (AV) node, and bilateral ventricles.

A thorough understanding of the origins of normal cardiac rhythm and electrical conduction is essential to properly comprehend cardiac dysrhythmia. Normal cardiac conduction originates in the SA node and conducts through the atria to the AV node. In the majority of patients, the AV node is the only site where electrical signals can transmit between the atria and ventricles and therefore functions as the ultimate “gatekeeper” to the ventricles. Impulses then travel sequentially from the AV node to the bundle of His, the right and left bundle branches, the Purkinje fibers, and ultimately the ventricular myocardium.

The normal electrocardiogram (ECG) waveform contains a P wave, QRS complex, and T wave. The P wave represents atrial depolarization. It is immediately followed by the PR interval, which normally lasts between 120 and 200 msec in duration. The QRS complex represents ventricular depolarization and is normally <100 msec in duration. Delays in intraventricular conduction result in a widened (>100 msec) QRS complex. The ST segment represents the plateau of ventricular depolarization and is normally isoelectric in appearance. Finally, the T wave represents ventricular repolarization. Of note, the segment extending from the end of a T wave to the beginning of the next P wave, known as the TP segment, should be used as the isoelectric baseline when performing any type of ECG analysis.

Bradydysrhythmias occur either because of depressed sinus node activity or inhibited electrical signal conduction. These are common in patients with structural heart damage, excessive vagal tone, taking certain cardioactive medications, or with specific electrolyte abnormalities (eg, hyperkalemia). Tachydysrhythmias occur because of enhanced automaticity from either the SA node or an ectopic focus and can originate from both atrial and ventricular sources. Supraventricular tachycardia (SVT) occurs when re-entry loops are present in the AV node or accessory conduction pathways.

Rhythms with a wide QRS complex represent ventricular depolarization ...

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.