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

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

  
  
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  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 that occurs outside of the normal conduction system, whereas those with normal QRS durations originate from a focus either superior to or within the AV node that then travel through standard conduction pathways.

Cardiac dysrhythmias vary by etiology, severity, and treatment. Atrial fibrillation (AF), for example, is common and has multiple causes (Table 16-1). Although occasionally symptomatic and/or requiring emergent intervention, many patients are typically unaware when they are in AF. Asymptomatic bradycardia is also a very common rhythm, especially in young, athletic patients. It can be a normal finding in some people or result from medication use at therapeutic levels. Other bradydysrhythmias, such as third-degree heart block, always elicit emergent concern. Tachydysrhythmias vary in a similar manner, from an isolated asymptomatic atrial tachycardia to an emergently life-threatening ventricular fibrillation, the initial dysrhythmia for the majority of patients in cardiac arrest.

There are several important questions that need to be answered when attempting to identify a pathologic rhythm. First, determine the hemodynamic stability of the patient. Look for any signs of hypoperfusion, including systemic hypotension, cardiac chest pain, pronounced diaphoresis, altered mental status (AMS), or congestive heart failure. Second, quantify the rate of the dysrhythmia and classify as normal, slow, or fast. Third, identify the morphology of the rhythm (eg, narrow vs wide complex QRS). Next, determine whether the observed dysrhythmia is irregular or regular in cadence. Finally, assess for any evidence of an AV conduction block. AV blocks are divided into first, second, and third degrees based on the PR interval and the cardiac rhythm.

Narrow rhythms:

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  Fast: Atrial fibrillation, atrial flutter, SVT

  
  
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  Slow: Sinus bradycardia, junctional escape rhythm

Wide rhythms:

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  Fast: Ventricular tachycardia (VT), AF, or flutter with aberrant conduction

  
  
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  Slow: Hyperkalemia, third-degree (complete) heart block

History

Unstable patients may be too altered to offer any meaningful history. Employ any available friends, family, and emergency medical service personal for possible critical details. Unstable patients require immediate intervention, and time should not be wasted on an excessively detailed history. In stable patients, ask about any previous episodes, current medications, illicit drug use, and the timing of symptom onset. Inquire about a history of any underlying structural anomalies (eg, Wolf-Parkinson-White syndrome [WPW]), as this will help guide therapy (Figure 16-1).

Finally, ascertain about past medical history. Although sinus bradycardia is a common finding in healthy adults, older patients with underlying coronary artery disease (CAD) and slow heart rates often have a pathologic source for their bradydysrhythmia (eg, inferior wall ischemia, electrolyte abnormalities, or pharmacologic side effects). Similarly, although sinus tachycardia often accompanies conditions with increased sympathetic tone (eg, exercise, fever, cocaine use), older patients with a history of CAD, valvulopathy, or underlying pulmonary disease often have a pathologic source for their tachydysrhythmia.

Physical Examination

Evaluate the patient’s hemodynamic stability. Always note the triage vital signs and repeat frequently. Carefully palpate peripheral pulses to determine whether they correspond with the dysrhythmia displayed on the cardiac monitor. Assess for signs of end-organ hypoperfusion, including detailed cardiovascular (weak peripheral pulses), pulmonary (rales), and neurologic (AMS) examinations.