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Chapter 79


The term dysrhythmia denotes any abnormality in cardiac rhythm. In this chapter, we review dysrhythmias outside the context of cardiac arrest specific toxidromes. We then review the physiology of normal and abnormal cardiac impulse formation and conduction. Finally, we discuss the diagnostic tools for evaluating the patient with a known or suspected dysrhythmia, including the history, physical examination, and surface electrocardiogram (ECG). For each rhythm disturbance, we identify the treatment options for prehospital and emergency department (ED) management.

Cardiac Cellular Electrophysiology

The function of individual cells in the conductive and contractile tissues of the heart depends on an intact resting membrane potential. Na+, K+, and Ca2+ ions create the membrane potential and regulate conduction and contractility. The membrane potential is the result of a differential concentration of Na+ and K+ on either side of the cell membrane, measuring approximately −90 mV in normal resting, nonpacemaker cells. This electrical gradient exists mainly because of the Na+-K+ exchange pump and the natural concentration-dependent flow of K+ out of the cell. Adenosine triphosphate (ATP) fuels Na+ transport out to the extracellular fluid, with Mg2+ used as a cofactor (Fig. 79-1). This process creates an osmotic gradient, allowing Ca2+ to be passively exchanged for Na2+ and promoting conduction as well as myofibril contraction. The resting membrane potential is generated from the flow of K+ down a concentration gradient toward the extracellular fluid. The cell membrane is far more permeable to potassium than sodium ions, resulting in a net loss of intracellular positive charge.

In normal nonpacemaker cells, the application of an electrical stimulus causes the membrane potential to become less negative, termed depolarization. When the membrane potential reaches −70 mV, specialized Na2+ channels open, causing a rapid influx of positive charge into the cell. This “fast” channel activity further decreases the membrane potential and is augmented at 30 to 40 mV by a second “slow” channel that allows Ca2+ influx. When these channels close, resting potential is restored by the sodium-potassium pump, an event known as repolarization (Fig. 79-2).

In nonpacemaker cells, additional depolarization from a second electrical stimulus is not possible when the membrane potential is more positive than −60 mV. This period is termed the effective refractory period (Fig. 79-3). At a membrane potential of −60 to −70 mV, a strong impulse can cause a response that is likely to be propagated, although abnormally; this response represents the relative refractory period. At a membrane potential of −70 mV or less, virtually all fast channels are ready for activity if properly stimulated (see Fig. 79-3).

Pacemaker cells differ from non–impulse-generating cells in two ways: their resting membrane potential is less negative, and they can spontaneously depolarize via slow Na+ influx . Pacemaker cells exist normally within the sinoatrial (SA) and atrioventricular (AV) nodes and can also be found on the atrial surfaces of the AV valves and within the His-Purkinje system. Nonpacemaker cells may undergo spontaneous depolarization under pathologic conditions, especially during ischemia.

Afterdepolarizations are fluctuations in membrane potential that occur as the resting potential is restored. These fluctuations may precipitate another depolarization, either just before full resting potential is reached (early afterdepolarizations) or after full resting potential is reached (delayed afterdepolarizations). Early afterdepolarizations are associated with high resting membrane potentials and are more likely with slower heart rates. Delayed afterdepolarizations can arise from ischemia, catecholamine excess, or electrolyte disturbances (especially K+, Mg2+, and Ca2+) and are enhanced by faster heart rates.

Anatomy and Conduction

The SA node is an area of specialized impulse-generating tissue located at the junction of the right atrium and the superior vena cava. Its blood supply is from the right coronary artery (RCA) in 55% of patients and the left circumflex artery (LCA) in 45%. The normal SA node produces spontaneous depolarizations at a faster rate than other pacemakers and functions as the dominant pacemaker. The SA node maintains a rate of 60 to 90 beats/min in most adults. Hypothermia and vagal stimulation slow the sinus rate, whereas hyperthermia and sympathetic stimulation increase the rate. In the setting of low or absent parasympathetic tone—for example, with certain drugs or after heart transplantation—the resting sinus rate tends to be faster.

In the absence of normal SA node activity, other myocardial tissues may assume the role of pacemaker. The AV node has an intrinsic impulse-generating rate of 45 to 60 beats/min. Infranodal pacemakers, found within the His bundle, the Purkinje system, and the bundle branches, maintain intrinsic rates ranging from 30 to 45 beats/min. Other atrial and ventricular tissues may assume pacemaker-like activity under conditions of ischemia or metabolic derangement. Rates of ectopic pacemaker activity vary widely depending on the underlying pathology.

Figure 79-4 correlates the surface ECG tracings with tissue electrical events. Impulses generated from within the SA node itself, imperceptible on the surface ECG, are propagated through the atrial tissue to the AV node. Atrial depolarization is characterized by the P wave on the surface ECG.

The AV node is an area of specialized tissue between the atria and the ventricles of the heart, located in the posterior-inferior region of the interatrial septum. Its blood supply is from a branch of the RCA in 90% of patients (right dominant) and from the LCA in the remaining 10% (left dominant). Transmission of impulses within the AV node is slower than in parts of the conducting system (Table 79-1) because of a dependence on slow-channel ion influx for membrane depolarization. In some patients, pathologic “accessory pathways” connect atrial and ventricular tissues. These accessory pathways do not share the normal conduction delay of the AV node and may allow for rapid ventricular rates. Preexcitation refers to the early depolarization of ventricular myocardium when accessory paths are used instead of the normal conduction system.

On the surface ECG, the PR interval (normally 0.10 to 0.20 second) represents the time it takes for conduction of a sinus impulse through the atria and AV node and into the ventricles. Impulses originating in lower atrial tissues are associated with a shortened PR interval, as are impulses conducted to the ventricles via accessory pathways outside the AV node. PR prolongation is usually a result of nodal or supranodal conduction system disease.

After passing through the AV node, impulses propagate down the His bundle to the three main bundle branch fascicles: the right bundle branch (RBB), the left anterior-superior bundle (LASB), and the left posterior-inferior bundle (LPIB). The RBB and LASB are typically supplied by the left anterior descending (LAD) artery, whereas the LPIB may be supplied by either the RCA or the LCA. After conduction down the three main bundle branches, impulses are delivered to the Purkinje fibers, which propagate impulses to myocardial tissues in a swift and orderly fashion, allowing for coordinated ventricular contraction. If an impulse arrives prematurely, it may be conducted aberrantly (if bundles are relatively refractory), or it may be blocked (if the bundles are completely refractory).

On the surface ECG, the QRS complex represents ventricular depolarization, and the normal QRS interval is 0.09 seconds or less, with a duration of 0.12 seconds or greater being clearly abnormal. The T wave corresponds to ventricular repolarization and varies in duration depending, among other things, on the length of the cardiac cycle. The total time of ventricular depolarization and repolarization is represented by the QT interval. Shorter cycle lengths (i.e., shorter R-R intervals) result in a shorter repolarization time. Conversely, longer cardiac cycles are associated with longer repolarization times.

Mechanisms of Dysrhythmia Formation

There are three electrophysiologic mechanisms: enhanced automaticity, triggered activity, and reentry. Enhanced automaticity includes spontaneous depolarization of nonpacemaker cells or a lower threshold for depolarization in normal pacemaker cells (Fig. 79-5). Both types of enhanced automaticity can occur in the setting of ischemia, electrolyte disturbances, or drugs. Examples of enhanced automaticity include idioventricular rhythms in the setting of acute myocardial infarction, and atrial tachycardias or junctional tachycardias (JTs) seen with digitalis toxicity.

Triggered activity occurs as the result of early or delayed afterdepolarizations. The classic dysrhythmia associated with early afterdepolarization is torsades de pointes. Triggered dysrhythmias caused by delayed afterdepolarizations are frequently found in the setting of intracellular Ca2+ overload as occurs with digitalis toxicity or with reperfusion therapy for acute myocardial infarction. Many ectopic atrial, junctional, and ventricular rhythms fall into this category and are amenable to treatment with medications that slow the heart rate or interfere with calcium entry into the cell.

Reentry dysrhythmias occur as a consequence of abnormal conduction (Fig. 79-6). For a reentry mechanism, two alternate pathways for conduction must be present and one path must have a longer refractory period. The unequal responsiveness of the limbs creates a functional unidirectional block such that when the impulse exits one limb, it may then reenter the other in retrograde fashion. The cycle is then repeated, creating a self-sustaining or “circus movement” tachycardia that can appear orderly or disorderly (i.e., fibrillatory).


Figure 79-6 Mechanism of reentry.

Reentry mechanisms are responsible for most narrow-complex tachycardias and many ventricular tachycardias (VTs). Treatment is predicated on altering conduction in one or both limbs of the reentry circuit.

Classification of Antidysrhythmic Drugs

Medications used to treat dysrhythmias are classified into four major categories on the basis of their electrophysiologic effects (Box 79-1). Other agents fall outside this classification system and are discussed separately.

Class I agents exert their major effects on the fast Na+ channels, resulting in membrane stabilization. The subclasses IA, IB, and IC are distinguished on the basis of differential effects on depolarization, repolarization, and conduction. Class II agents are the beta-adrenergic antagonists, which depress SA node automaticity and slow AV node conduction. Beta-blockers can also suppress conduction in ischemic myocardial tissue. Class III agents prolong repolarization and refractory period duration, predominantly via their effects on K+ channels. Class IV agents are the Ca2+ channel blockers, which slow conduction through the AV node and suppress other calcium-dependent dysrhythmias. Other agents important in the emergency treatment of dysrhythmias include magnesium sulfate, digitalis, and adenosine.

All antidysrhythmics can cause “prodysrhythmic effects.” This occurs most often in patients with existing structural heart disease and in patients receiving new or higher doses of antidysrhythmic agents. The class I and III agents are associated with prodysrhythmic effects in up to 15% of patients.1,2

Class IA Agents

Class IA agents slow conduction through the atria, AV node, and His-Purkinje system and suppress conduction via accessory pathways. Class IA agents also exhibit anticholinergic and mild negative inotropic effects, with procainamide having the least effect on contractility. Procainamide is the most commonly used class IA agent in the emergency treatment of ventricular and supraventricular dysrhythmias. Intravenous procainamide is administered at a rate of 20 to 30 mg/min in stable patients until the dysrhythmia is terminated, hypotension occurs, or the QRS complex widens (to 50% of the pretreatment width), or up to a total dose of 18 to 20 mg/kg (12 mg/kg if congestive heart failure is present). The peripheral vasodilatory effects cause the hypotension, and the risk of prodysrhythmia is approximately 5%.

Class IC Agents

The class IC agents profoundly slow depolarization and conduction and have pronounced antidysrhythmic properties.1,2 Up to 15% of patients treated with class IC agents experience new or increased ventricular dysrhythmias. Class IC agents are approved only for oral use in the United States.

Class II Agents

Class II agents suppress SA node automaticity and slow conduction through the AV node. Because of their effect on AV node conduction, class II agents are well suited to control the ventricular rate in patients with atrial fibrillation and flutter. Beta-blockers can terminate AV nodal reentrant tachycardias (AVNRTs). In the setting of acute myocardial ischemia, beta-blockers play a role in preventing ventricular dysrhythmias.

Side effects of beta-blockers include bronchospasm, bradycardia, hypotension, and heart failure. All beta-blockers are active at both beta1 and beta2 receptors (Table 79-2) to varying degrees. Those with more prominent beta1 effects are said to be cardioselective. Relative contraindications to the use of beta-blockers include asthma or chronic obstructive lung disease, advanced congestive heart failure, and third-trimester pregnancy. Beta-blockers should not be used in patients with preexisting bradycardia or heart block beyond first-degree. Intravenous beta-blockers should be used cautiously in conjunction with calcium channel blockers because of the risk of additive side effects. Acute side effects of beta-blockers include bronchospasm, heart failure, excessive bradycardia, and hypotension.


Amiodarone is approved for the treatment of both ventricular and supraventricular dysrhythmias. In addition to features in common with all class III agents, amiodarone has numerous other effects, including actions that are similar to those of class IA, class II, and class IV agents.

The serum half-life of amiodarone is 25 hours after a single intravenous dose and up to 50 days during long-term oral use. Because of the unusual pharmacokinetics, oral regimens vary widely. The acute side effects of amiodarone are primarily limited to hypotension, bradycardia, and heart failure (Box 79-2). There is an additive risk of bradycardia and hypotension when amiodarone is used in conjunction with calcium channel or beta-adrenergic blockers. Rates of prodysrhythmia are relatively low (1-3%). Long-term amiodarone use, however, is associated with significant extracardiac side effects, including irreversible lung and thyroid disease. Amiodarone alters the pharmacokinetics of numerous other drugs, including digoxin and warfarin.

Class IV Agents

Class IV agents block the slow Ca2+ channels, slowing conduction within the AV node and suppressing the SA node to a lesser degree. Like beta-blockers, their primary use is in patients with SVTs. Of the two commonly used class IV agents, diltiazem is more frequently used for ventricular rate control in patients with atrial fibrillation or flutter.

All class IV agents are associated with peripheral vasodilation. Verapamil has the least effect on peripheral vascular tone, and diltiazem has an effect between that of verapamil and purely peripherally acting calcium channel blockers, such as nifedipine. In the acute setting, intravenous calcium salts (1 g slow intravenous delivery) can attenuate peripheral vasodilatory effects. Class IV drugs should not be used in patients with second- or third-degree AV block and should be used with close monitoring in those with first-degree block.

Miscellaneous Agents


Digitalis compounds have a variety of effects on myocardial cells. Digoxin inhibits the ATP-dependent Na+-K+ exchange pump, increasing intracellular Na+ concentrations and decreasing intracellular K+ concentrations. The resultant increase in intracellular Ca2+ concentration accounts for the positive inotropic effects of digitalis. Digoxin can behave as an excitant, a depressant, or both. Excitant effects of digoxin have to do with enhanced automaticity and triggered activity, particularly at high therapeutic or toxic doses. At the same time, digoxin slows AV node conduction at therapeutic doses via lengthening of the refractory period.

Digoxin (0.25-0.5 mg IV) can control the ventricular rate in patients with SVTs, including atrial fibrillation and atrial flutter. Because of its delayed onset of action and narrow therapeutic window, however, digitalis is not a first-line agent for emergency therapy. It is not true that digoxin promotes conversion to a sinus rhythm any more than other rate-controlling agents.9

Side effects of digoxin are listed in Box 79-3 and are aggravated by hypokalemia, hypercalcemia, hypomagnesemia, increased catecholamines, and acid-base disturbances. Digoxin overdose therapy is covered elsewhere.


Adenosine is a naturally occurring purine nucleoside used for the termination of narrow-complex tachydysrhythmias. Administered as an intravenous bolus, adenosine causes an abrupt slowing of AV conduction in both anterograde and retrograde pathways. Adenosine usually has an onset of action of 5 to 20 seconds and a duration of effect of 30 to 40 seconds. Except in rare cases of catecholamine-induced ventricular dysrhythmias, adenosine has little or no effect on infranodal conduction. For this reason, adenosine is often used as a diagnostic agent in patients with wide-complex tachydysrhythmias when the cause is unclear.1012 An initial dose of 6 mg as a rapid bolus for adults weighing 50 kg or greater is recommended, with flush through a large peripheral vein. If no response is seen within 1 to 2 minutes, the second dose is doubled (12 mg) and administered. If no effect is seen after a final 12-mg dose, the rhythm should be reassessed and another agent used. Pediatric doses are 0.05 mg/kg initially with doubling at similar intervals up to a total dose of 0.25 mg/kg. Side effects coincide with the onset of clinical effects and occur in up to a third of patients but are usually minor. These include flushing, dyspnea, chest pressure, nausea, headache, dizziness, transient bradycardia or heart block, and hypotension (seen rarely, from the vasodilatory properties). These side effects usually resolve rapidly without treatment, although many patients are intensely uncomfortable for a short period. Asystole can occur but is usually transient though unsettling to those observing.

Because of its short duration of action, adenosine is not an effective rate control agent for atrial fibrillation or flutter, although it can help unmask these rhythms when not apparent on the initial surface ECG. Similarly, some narrow-complex tachydysrhythmias that terminate with adenosine will recur later given the short duration of action.

Approach to Dysrhythmia Recognition and Management

Dysrhythmias are classified according to their electrophysiologic origin, ECG appearance, and underlying ventricular rate. Although overlap exists, the following categorization is useful:

Classically, the approach to any specific dysrhythmias is defined on the basis of the clinical stability. Unstable patients demonstrate evidence of severe or multiple end-organ features of hypoperfusion, such as altered sensorium, respiratory distress, hypotension, syncope, or chest pain suggestive of myocardial ischemia. Stable patients may be asymptomatic or have mild symptoms, such as light-headedness, dyspnea on exertion, palpitations, or mild anxiety. In practice, clinical stability is a continuum; in the absence of profound altered sensorium or hypotension, a clear line distinguishing stable and unstable patients is often not present.

It is important to consider whether a dysrhythmia is the cause or an effect of a clinical presentation; for example, rapid atrial fibrillation may be causing hypotension or resulting from profound volume depletion. Failure to consider the clinical situation can lead to an inappropriate focus on diagnosing and treating the rhythm to the detriment of the patient. With recognition of this need to incorporate the overall clinical picture, treatment of those with a dysrhythmia and clear instability is empirical and assumes the rhythm is the cause, whereas stable patients can be approached in a more systematic and thoughtful manner to identify the cause and choose the most appropriate therapy.

Initial Assessment of Stable Patients

The approach to the patient with a stable dysrhythmia begins with gathering evidence from the history, physical examination, 12-lead ECG, and a rhythm strip. The nature of any symptoms, including the timing, velocity of onset (gradual vs. abrupt), and duration, is important. For the patient with “palpitations,” questions about the rate and regularity of the heartbeat are often asked, but having the patient tap out the rhythm with a finger can often be more valuable. Inquiring about precipitating events and associated symptoms such as dizziness, chest pain, dyspnea, or syncope is critical to understanding the context of any dysrhythmia. The past history—of rhythm disturbances or a prior history of ischemic or structural heart disease—and a thorough medication history are essential. For example, a new and symptomatic wide-complex tachycardia in a patient with known ischemic heart disease is much more often VT than a supraventricular event. Occasionally the family history can be helpful, particularly if there are first-degree relatives with a history of dysrhythmia, unexplained syncope, or sudden death—all of which suggest an inherited disorder such as an accessory pathway or Brugada’s syndrome.

Aside from palpating the pulse and listening to the heart sounds, the physical examination should focus on detecting subtle evidence of end-organ hypoperfusion or clues to an underlying cause of the dysrhythmia (e.g., heart failure). Palpating the pulse for several minutes while asking the patient to report any symptoms can be helpful in detecting pauses, extrasystoles, or brief runs of tachycardia. This technique can be enhanced by observing the patient’s rhythm on a continuous cardiac monitor.

The 12-lead ECG is essential for evaluation of any patient with a suspected dysrhythmia. Use of a single ECG lead is often adequate for diagnosis, but multiple leads are often required to detect such things as the presence or absence of P waves (often best seen in inferior leads or V1-2; Fig. 79-7), the relationship between P waves and QRS complexes, prolongation of the QRS and QT interval, and evidence of ischemia or prior myocardial infarction (Box 79-4). For certain conditions, such as Brugada’s syndrome, the 12-lead ECG together with a history of syncope is diagnostic.