Emergency Medicine

Managing Tachyarrhythmic Episodes

The authors outline a methodical approach to the patient who presents in a tachyarrhythmic state and discuss the identification and treatment of specific rhythm disturbances.

By Erik Snyder, MD, and Barry Knapp, MD, FACEP

Few emergencies require more immediate intervention than cardiac arrhythmias. It is crucial that physicians are prepared to evaluate and appropriately manage patients with this condition. In this article, we will present an approach to tachyarrhythmias in the acute care setting. Because tachycardia is such a broad clinical topic, we will focus on the keys to a methodical approach to tachyarrhythmias. We will also address treatment recommendations for specific tachyarrhythmias encountered in acute care and some pitfalls to avoid.

BASIC ELECTROPHYSIOLOGY

In a healthy heart, the sinoatrial (SA) node is a focus of pacemaking cells in the right atrium that triggers spontaneous depolarization across the heart at a rate between 60 and 90 times a minute in the average adult. From the SA node, an electrical signal travels to the atrial myocytes, inducing atrial contraction. When the electrical signal reaches the junction between the atria and ventricles, it is transmitted to the ventricles via a bundle of cells called the atrioventricular (AV) node. Once in the ventricle, the signal is carried down the ventricular septum in the bundle of His and then spread across the muscle by the Purkinje fibers.

Receptors in the SA and AV nodes receive parasympathetic input from the vagus nerve. Sympathetic input arrives from sympathetic nerve fibers and from catecholamines circulating throughout the body, released by the adrenal medulla. The rate at which the SA node fires and the speed and frequency at which the AV node conducts an electrical current are regulated by these inputs. The SA and AV nodes are also the sites of action of many cardiac pressors and antiarrhythmics.

Several tissues in the heart besides the SA node contain pacemaking cells. These cells have a slow intrinsic rate that is normally overridden by the faster SA node. When the SA node is diseased, these alternate pacemakers and even nonpacemaker myocardial cells can become ectopic pacemakers and drive arrhythmias.

Alterations in the pacemaking or conducting systems within the heart are the cause of most arrhythmias. These alterations can result from electrolyte imbalance, cardiac ischemia, cardiac medications (especially antiarrhythmics), hypoxia, and congenital abnormalities. Two primary mechanisms of arrhythmias are automatic ectopy and reentry. Reentrant sources can be within the atria, ventricle, AV and SA nodes, or through accessory pathways. Reentrant tachycardias, the most common cause of tachyarrhythmias, tend to begin and end abruptly. Ectopic-foci tachycardias tend to start gradually and can result from accelerated pacemaking cells (accelerated junctional rhythm) or diseased nonpacemaking cells.

INITIAL EVALUATION

Tachycardia is defined as depolarization of the heart at a rate of more than 100 beats per minute. All patients with tachycardia should have an intravenous line inserted and should be on a cardiac monitor. Analysis of the ECG will be central to patient evaluation. The clinician should always be prepared for defibrillation in the event that the patient decompensates, so all equipment needed for that procedure should be immediately accessible. Oxygen should be administered if hypoxia, a contributing factor in many disease processes, is suspected.

Unstable patients with tachyarrhythmia should be treated immediately with DC cardioversion. Treatment may be guided by advanced cardiac life support protocols. Sinus tachycardia is not a primary arrhythmia and is not treated with electrical shock.

History should focus on the onset and duration of symptoms, as well as on symptoms that may suggest a greater risk for decompensation such as syncope or chest pain. Underlying medical problems and disease history may provide critical clues. The patient's medications must also be carefully considered; these frequently suggest the patient's medical history and may be directly implicated in many arrhythmias.

Physical examination should initially assess for any signs of instability or airway compromise. Following this initial survey, a thorough physical examination should be performed, focusing on looking for clues to the disease process. Key findings would include signs of heart failure, pulmonary disease, metabolic derangements (such as thyrotoxicosis), illicit drug use, or vascular disease.

If bedside testing is available, rapid measurement of electrolytes is valuable. Otherwise, an electrolyte panel may be sent to the lab with other desired tests, and a portable chest x-ray should be obtained.

Patient presentation ranges from hemodynamic instability and near arrest to patients who have a tachyarrhythmia discovered incidentally during the evaluation of an unrelated complaint. Common presenting symptoms include chest pain, syncope or presyncope, palpitations, and dyspnea from heart failure. A tachyarrhythmia may be only one of the manifestations of a disease process such as thyrotoxicosis, drug overdose, or cardiac or pulmonary disease. Arrhythmias may be associated with ongoing cardiac ischemia, which should be considered in all patients.

NARROW- AND WIDE-COMPLEX TACHYCARDIAS

The key to treating an arrhythmia lies in knowing its etiology. Once you know where the rhythm originates, treatment can be directed at controlling the source. Although the physical exam and history can provide clues, the key diagnostic tool is the ECG. Tachyarrhythmias can be broken down into two main groups—narrow-complex and wide-complex. Narrow-complex tachycardias have a QRS of less than 120 milliseconds (or less than three of the smallest boxes). With rare exceptions, all narrow-complex tachycardias originate above the ventricle. A narrow QRS complex represents rapid conduction of the depolarizing signal to the ventricles. This occurs when the signal is transported through the AV node or originates high in the His bundle and travels in anterograde fashion through the His-Purkinje system. There will be a delay resulting in a wide QRS if the depolarization meets a block in the His-Purkinje system (a bundle branch block), the signal enters through an accessory pathway, or there is an ectopic ventricular source.

The sources from which narrow-complex tachycardias initiate are the SA node, atria, AV node reentry, and accessory pathways conducting anterograde through the AV node. The rate and the presence and location of the P wave are central to identifying narrow-complex tachycardias.

Wide-complex tachycardias have a QRS of more than 120 milliseconds. These rhythms are broken down into those originating from the ventricle and those that originate above the ventricle but are conducted by an abnormal path that causes the ventricle to take longer to depolarize.

IRREGULAR AND REGULAR RHYTHMS

Once it has been determined that a patient has a narrow-complex tachycardia, the specific arrhythmia needs to be identified to guide treatment. It is helpful initially to separate rhythms by whether they are regular or irregular. Irregular rhythms include atrial fibrillation, atrial flutter with variable block, multifocal atrial tachycardia, and frequent premature atrial contractions. Regular rhythms include sinus tachycardia, atrial tachycardia, atrial flutter with regular block, and paroxysmal supraventricular tachycardia (PSVT). Differentiating irregular and regular rhythms is done according to the rate and P-wave pattern and morphology.

Narrow-complex tachycardias have been classified in many ways as our understanding of these arrhythmias has grown. Most nonsinus narrow-complex tachycardias are reentrant in nature, with a circuit of depolarization driving the rhythm. These circuits may exist within the atrium, as with atrial fibrillation and atrial flutter, or across the AV septum, as in AV reentrant tachycardia and accessory pathways. Another type of tachyarrhythmia is driven by ectopic cells with automaticity; this group includes such rhythms as accelerated junctional rhythms and nonparoxysmal atrial tachycardia.

Adenosine is a valuable drug in treating narrow-complex tachycardia because it temporarily slows AV node conduction and can facilitate interpretation of the rhythm. It will also convert some rhythms. Adenosine should be used with caution in patients with severe asthma as it may precipitate bronchospasm.

Assessing for and treating any underlying disease process should always be part of every patient's care. For some narrow-complex tachycardias, this may be the primary mode of treatment. As noted, any patient with a decompensating arrhythmia should be treated with cardioversion.

ATRIAL FIBRILLATION WITH RAPID VENTRICULAR RESPONSE

This irregular rhythm results from multiple areas of atrial cells chaotically firing and contracting with intermittent transmission to the ventricle. This results in a narrow-complex tachycardia with no regular P waves but a fibrillatory baseline and an irregular rhythm (see ECG below). Patients with prolonged fibrillation are at risk for thrombus formation within the atria and embolic stroke with conversion. Therefore, rate control rather than conversion is the goal in patients whose atrial fibrillation is likely of more than 48 hours' duration. An exception would be an unstable patient who should be immediately cardioverted.

Atrial fibrillation. Chaotic atrial activity produces a narrow-complex tachycardia with no regular P waves.

All stable patients should initially be rate-controlled. Diltiazem, verapamil, or a beta blocker is first-line therapy in patients without heart failure. In patients with compromised left ventricular function, the agent of choice is digoxin or amiodarone because calcium channel blockers and beta blockers may worsen heart failure. Amiodarone carries the potential for cardioversion and takes longer to obtain rate control, but it also has milder hemodynamic effects. The risks and benefits of using these agents must be carefully considered, particularly in patients with an unknown duration of atrial fibrillation or a duration of more than 48 hours, because of the risk of thromboembolism. Patients who do not rapidly respond to pharmacologic rate control or who have heart failure or persistent angina should be electrically cardioverted.

Patients who have atrial fibrillation of less than 48 hours' duration may be considered for conversion once they are rate-controlled. A cardiology consultation early in a patient's treatment may be beneficial. Due to the hemodynamic effects and proarrhythmic potential of pharmacologic conversion, DC cardioversion should be the primary mode of conversion. In patients for whom DC cardioversion is not favorable, such as those who will not tolerate sedation or who do not convert with electricity, antiarrhythmics should be considered.

Multiple options exist for patients with normal left ventricular function, including ibutilide, flecainide, sotalol, procainamide, and high-dose amiodarone. Ibutilide may be the most effective agent, but it has the potential for inducing torsades de pointes. Potassium and magnesium levels should be measured and normalized prior to the use of ibutilide to reduce the risk of this complication. Amiodarone is preferred in patients with heart failure, again because of its milder effects on hemodynamics.

Any patient with atrial fibrillation of more than 48 hours' duration or of unknown duration should receive anticoagulant therapy. Cardioversion may be performed acutely in heparinized patients if atrial thrombus is ruled out by transesophageal echocardiography. Otherwise, standard recommendations are for three weeks of anticoagulation prior to cardioversion.

ATRIAL FLUTTER AND PSVT

Atrial flutter occurs as a regular atrial depolarization, classically at 300 beats per minute. The rate and regularity of conduction to the ventricles are variable. The P waves appear as a saw-tooth baseline, often best seen in lead II. With classic two-to-one conduction, every other P wave triggers a QRS, leading to a heart rate of 150, half the atrial rate (see ECG below). To avoid missing this diagnosis, atrial flutter should be considered any time a patient presents with a heart rate near 150. Treatment of atrial flutter should follow that for atrial fibrillation.

Atrial flutter. This rhythm looks like paroxysmal SVT but note the regular narrow-complex rate very close to 150. Indeed, when this rhythm was rate-controlled with diltiazem, it was shown to be atrial flutter.

Supraventricular tachycardia (SVT) is a broad term encompassing a variety of rapid narrow-complex tachycardias. It may be used to refer to paroxysmal reentrant tachycardias, atrial fibrillation, ectopic atrial tachycardias, or even sinus tachycardia. The term "paroxysmal supraventricular tachycardia" (see ECG below) is often used to group several reentrant rhythms that are managed acutely in a similar manner, including paroxysmal atrial tachycardia, AV nodal reentrant tachycardia, and accessory pathway tachycardias.

Paroxysmal supraventricular tachycardia. Note the extreme rate of 235 in this five-year-old patient.

The most common PSVT is AV nodal reentrant tachycardia, in which there are two pathways for conduction across the AV node, with variable refractory periods. If a depolarizing signal, such as an ectopic atrial beat, arrives while one path is open and the other is still in a refractory phase, it will travel down only the open pathway. However, if the refractory pathway is open when the signal reaches the ventricular side, it may conduct the signal retrograde and initiate a reentrant cycle. This whir of depolarization drives the rhythm. While there will be no P waves antecedent to the QRS, there may be retrograde P waves that may be hidden in the QRS or appear after it.

Another form of PSVT may occur via an accessory pathway of conductive tissue between the atria and ventricles that is present congenitally in some patients. A signal travels down the AV node or accessory pathway and then back up the opposite path to create a self-sustaining cycle. The P wave is usually buried within the QRS and is not visible.

In patients with an otherwise healthy heart, PSVT is usually well tolerated. In already compromised hearts, as in patients with poor left ventricular function, the tachyarrhythmia may precipitate heart failure.

Treatment is directed at slowing conduction through the AV node. First-line treatment in stable patients includes procedures to increase vagal tone, such as the Valsalva maneuver or carotid sinus massage. Intravenous adenosine should be administered next. If this does not work, a calcium channel blocker or beta blocker should be administered. If these fail, then electrical cardioversion should be tried or an antiarrhythmic administered. Because of the proarrhythmic potential of antiarrhythmics, it is prudent to first attempt electrical cardioversion. In refractory cases, the antiarrhythmics procainamide, amiodarone, sotalol, and other agents may be effective. In unstable patients, synchronized DC cardioversion should be tried. In healthy adult patients who respond to therapy, discharge with close follow-up may be reasonable.

ACCESSORY PATHWAY TACHYCARDIAS

Wolff-Parkinson-White (WPW) syndrome is the most common of the accessory pathway tachycardias. During normal sinus rhythm, some patients with WPW syndrome will have a normal ECG without conduction down the accessory pathway. Others will have pre-excitation with the classic features of the syndrome—a short PR interval, prolonged QRS, and a slurred upstroke on the QRS, called a delta wave (see ECG below).

Wolff-Parkinson-White syndrome. Though not currently in reentry, this ECG shows the classic features of WPW with a sinus rhythm. Note the wide QRS (136 ms), short PR interval (less than 120 ms), and slurred upstroke of the R wave (delta wave).

Symptomatic WPW syndrome most often presents with PSVT. The conduction may be orthodromic or antidromic. In orthodromic tachycardia, the anterograde conduction is via the AV node, and reentry is through the accessory pathway, leading to a normal QRS that appears identical to other cases of PSVT and is treated the same way. Antidromic tachycardia results when anterograde conduction is via the accessory pathway, causing a wide QRS that may be difficult to differentiate from ventricular tachycardia. Finally, 10% to 30% of cases of WPW syndrome may present as atrial fibrillation. If the syndrome is suspected and there is an irregular or antidromic pattern to the ECG reading, then all AV nodal blocking drugs are contraindicated because they may precipitate ventricular fibrillation. The treatment of choice is DC cardioversion. Other options include procainamide, ibutilide, and flecainide.

NONPAROXYSMAL ATRIAL TACHYCARDIA

Nonparoxysmal atrial tachycardia originates from an ectopic atrial focus of altered automaticity. Multifocal atrial tachycardia is a type of atrial tachycardia with more than one ectopic atrial source, resulting in at least three P-wave morphologies. Ectopic atrial tachycardias are usually secondary to an underlying process, and treatment is aimed at the primary disorder. Multifocal atrial tachycardia (see ECG below) is often secondary to pulmonary disease and may resolve with oxygen or some other treatment. Ectopic tachycardias do not respond to electrical cardioversion. Sinus tachycardia must be differentiated from other rhythms because it is not a primary arrhythmia but the heartÕs response to some stimulus. Some considerations include metabolic causes, an endocrine disorder (such as thyrotoxicosis), sympathetic stimuli (such as medications, stress, anxiety, or fear), hyperthermia, hypoxemia, anemia, and hypovolemia.

Multifocal atrial tachycardia. Note the regular narrow-complex tachycardia with multiple P-wave morphologies.

WIDE-COMPLEX TACHYCARDIAS

There are three primary types of wide-complex tachycardias: ventricular tachycardia, SVT conducted via an accessory pathway, and SVT with a bundle branch block. It is often very difficult to differentiate ventricular from supraventricular wide-complex tachycardias. A frequent misconception is that stable patients have an SVT and unstable patients have a ventricular tachycardia. It is true that ventricular tachycardia is more likely in stable patients, but whether or not the patient is stable should not be used to differentiate between these two rhythms.

A combination of clinical features may make a supraventricular or ventricular tachycardia more likely. For instance, a young patient (age 35 or younger) with no heart disease or with a history of SVT is much more likely to have SVT. A patient over 50 with a history of myocardial infarction is more likely to have ventricular tachycardia. An old ECG can be very useful in identifying a previous conduction defect, such as a bundle branch block, if it has the same morphology as the presenting rhythm. There are other specific ECG criteria that can help in the diagnosis. None of the criteria is perfect, however, and without frequent use it is difficult to apply them in the acute care setting.

Ventricular tachycardia (see ECG below) is the more common of the two rhythms. Because mistakenly treating a ventricular tachycardia as an aberrant supraventricular rhythm can be fatal, it is prudent to always treat a wide-complex tachycardia as ventricular tachycardia unless you are certain of a supraventricular origin.

Wide-complex tachycardia. This ECG is consistent with ventricular tachycardia.

Stable ventricular tachycardia or wide-complex tachycardia of uncertain origin may be treated by DC cardioversion or pharmacologic cardioversion. Appropriate medications for stable patients with wide-complex tachycardia of uncertain origin include amiodarone, procainamide, sotalol, and lidocaine. Amiodarone is preferred in patients with heart failure or left ventricular dysfunction. The most recent American College of Cardiology/American Heart Association/European Society of Cardiology practice guidelines published in the Journal of the American College of Cardiology (October 2003) gave lidocaine a IIb classification, which means that evidence and expert opinion are both weak and conflicting regarding its use. Lidocaine may be effective and is fast and easy to use, but it requires further study.

Calcium channel blockers are contraindicated in the treatment of ventricular tachycardia because they may cause immediate cardiovascular collapse. Adenosine has been used by some clinicians to help differentiate SVT from ventricular tachycardia; only SVT should be affected by this drug. This is generally not recommended, however, because of a lack of studies and also case reports of cardiovascular collapse with the use of adenosine for wide-complex tachycardias. If the origin of a wide-complex tachycardia is known to be an accessory pathway, treatment is as described for antidromic WPW syndrome. Known PSVT with conduction block is treated in the same way as narrow-complex PSVT.

VENTRICULAR FIBRILLATION AND TORSADES DE POINTES

Ventricular fibrillation has no QRS complexes. It is characterized by unorganized depolarization and contraction across the ventricle, leading to ineffective cardiac contractions. The ECG is a jagged pattern with no discrete P waves or QRS complexes. Defibrillation can be life-saving.

Torsades de pointes is a paroxysmal wide-complex tachycardia that must be considered separately from other ventricular tachycardias. It is usually a short burst of a wide ventricular tachycardia with its axis swinging around the baseline.

Two forms of torsades de pointes exist. One is rare and is secondary to catecholamine excess in patients with a congenital prolonged QT interval or in patients following a stroke or neck surgery. This form is treated with beta blockers. The majority of cases of torsades de pointes in adults are associated with bradycardia in the setting of a prolonged QT interval secondary to an electrolyte disturbance or medications. Treatment is repletion of electrolyte deficiencies (especially hypokalemia) and increasing the patient's heart rate to prevent recurrence of torsades de pointes. This may be done with isoproterenol or overdrive pacing. Additionally, 2 to 4 grams of magnesium intravenously may be useful. Unstable patients should receive unsynchronized electrical cardioversion.