Sinus Bradycardia and Sinus Node Dysfunction

Sinus bradycardia is generally defined as periods of sinus rhythm with rates less than 60 beats per minute. In the absence of symptoms, it usually is benign and requires no treatment. Sinus bradycardia is common in young adults (particularly the physically fit). Nocturnal rates of 35 to 40 beats per minute and pauses during sleep of 2 seconds or longer are not uncommon. Sinus arrhythmia (Fig. 31.1) is a normal variant in which there are respirophasic changes in the RR interval on electrocardiogram (ECG) (prolongation of RR intervals during expiration).

Sinus bradycardia may also be a manifestation of certain pathologic conditions such as increased intracranial pressure, oculocardiac reflex after ophthalmologic surgery, cervical and mediastinal tumors, hypothyroidism, hypothermia, gram-negative sepsis, Chagas’ disease, depression, and anorexia nervosa. Sinus bradycardia is often seen after cardiac transplantation. Beta blockers, parasympathomimetic agents, calcium antagonists, amiodarone, and lithium commonly produce sinus bradycardia. Digoxin, in therapeutic doses, usually does not markedly affect the sinus node and is relatively safe to use in patients with SND.² Sinus bradycardia complicates 10% to 15% of acute myocardial infarctions and is most common with inferior infarcts. It also may be seen after successful thrombolysis. In the absence of hemodynamic compromise, it is associated with a more favorable prognosis than sinus tachycardia.³

Short-term pharmacologic enhancement of the sinus rate may be accomplished using atropine, catecholamines, or theophylline. Isoproterenol should be avoided in patients with ischemic heart disease and hypertrophic cardiomyopathy. No safe, reliable drug is available for long-term management of sinus bradycardia. Temporary pacing may suffice when the underlying condition is reversible. Permanent pacing should be employed to alleviate persistent bradycardia and symptoms.

Sinus bradycardia (with or without AV block) may occur during periods of autonomic instability. Examples include carotid hypersensitivity and neurocardiogenic syncope. These syndromes have cardioinhibitory (bradycardic), vasodepressor (vasodilatory), and mixed forms. Permanent pacing (which must include the ability to pace the right ventricle for heart block) is a well-established therapy for cardioinhibitory carotid sinus hypersensitivity. Neurocardiogenic syncope generally is a benign condition that usually can be managed without permanent pacemaker therapy. However, treatment for patients with frequent and severe cardioinhibitory spells, especially those in whom asystolic periods exceeding 5 seconds can be demonstrated clinically or during head-up tilt table testing, may include palliative pacemaker therapy.⁴

SND may manifest in a variety of ways, including persistent sinus bradycardia, sinus pause or arrest, sinoatrial (SA) exit block, and the bradycardia-tachycardia syndrome.

SA exit block occurs when an impulse from the sinus node is not conducted to the surrounding atrium. First-degree SA exit block results from intranodal conduction delay and is not manifest on surface ECG. Complete (third-degree) SA exit block will manifest as sinus arrest. Only second-degree SA exit block is uniquely manifest on surface ECG.

Type I second-degree SA exit block is characterized by progressive PP interval shortening before pauses that are less than two PP cycles in duration. In type II second-degree SA exit block, pauses are exact multiples of the basic PP interval. SA exit block usually is transient and often is reversible. Its presence should prompt a search for underlying causes such as enhanced vagal tone, acute myocarditis or infarction, or drug effect (as from digitalis).

Symptomatic SND virtually always requires permanent pacing. Patients with concomitant supraventricular tachycardias may require supplemental antiarrhythmic therapy. Drug therapy may aggravate the bradycardia and in many instances should be initiated after device placement. Catheter ablation may palliate or eliminate the tachyarrhythmia.

Atrioventricular Block

The various forms of heart block are disturbances of impulse conduction. Heart block may be transient or permanent. The following paragraphs focus on disturbances of AV conduction.

In reality, first-degree AV block involves no AV block at all but is due to delayed conduction from the atria to the ventricles. Every atrial impulse is conducted to the ventricles in a delayed fashion such that the PR interval is greater than 200 ms. If the QRS complex on the surface echocardiogram is narrow, the delay nearly always is in the AV node. In the presence of a wide QRS complex, the delay may be in either the AV node or the His-Purkinje system.

Second-degree AV block is classified as Mobitz type I (Wenckebach), Mobitz type II, 2 : 1 AV block, or high-degree AV block. In Mobitz I (Wenckebach) block, PP intervals are constant, with gradual PR prolongation before failure of impulse conduction (nonconducted P wave) (Fig. 31.2). Although classic Wenckebach block involves simultaneous shortening of successive RR intervals before AV block, atypical alternations in RR intervals actually are more common. In younger people, Mobitz I AV block with normal QRS complexes generally is benign and does not progress to more advanced AV conduction disturbances. In older patients, the prognosis may be similar to that with Mobitz II block. Mobitz I second-degree AV block may accompany inferior myocardial infarction. The condition is benign, with a favorable prognosis, in the absence of hemodynamic compromise. The conduction disturbance usually is transient, and permanent pacing is not required.

Mobitz II AV block is characterized by sudden failure of atrial impulse conduction without prior PR prolongation (Fig. 31.3). This form of AV block frequently heralds development of complete AV block and Adams-Stokes syncope. Mobitz II second-degree AV block in the setting of anterior infarction is associated with pump failure and high mortality rates. Survivors should receive permanent pacemakers.

In general, the surface ECG allows the clinician to localize the site of AV block without the use of invasive electrophysiologic testing. Mobitz type I AV block with a narrow QRS almost always occurs at the AV node. Rarely, Mobitz I second-degree AV block may have an intra-His location. Mobitz I AV block with wide QRS complexes may occur in either the AV node or the His-Purkinje system. Mobitz II second-degree AV block (particularly in the presence of wide QRS complexes) localizes to the His-Purkinje system.

In general, atropine improves AV nodal conduction and carotid massage worsens it. These interventions typically have the opposite effect when AV block occurs in the His-Purkinje system. Atropine increases both atrial and ventricular rates in AV nodal block. Likewise, exercise (increased endogenous catecholamines) may reduce the extent of block. Precipitation of second-degree, high-grade, or complete AV block during exercise strongly suggests an infranodal site of block.

It is important to remember a few general rules to avoid common ECG misinterpretations of second-degree AV block. The 2 : 1 form of AV block may be nodal or infranodal. 2 : 1 block associated with narrow QRS complexes generally results from AV nodal block (Fig. 31.4). Wide QRS complexes are compatible with block in either the AV node or His-Purkinje system. If more than one P wave is not conducted to the ventricle, the term high-grade AV block is used (Fig. 31.5).

Complete AV block is diagnosed by the presence of independent atrial and ventricular activity on the ECG where the atrial rate is faster than the ventricular rate. When the atrial rhythm is sinus, AV dissociation is present, with the sinus rate exceeding the ventricular rate. The PP interval is constant. The RR interval is constant. The PR interval is variable in a random, nonrecurring pattern (Fig. 31.6). Complete AV block may also be present during all varieties of atrial tachycardia.

Complete AV block proximal to the His bundle results in a narrow QRS complex escape rhythm with rates of 50 to 60 beats per minute. Complete intra-His block may also result in a narrow QRS escape rhythm with ventricular rates less than or equal to 45 beats per minute.

Acquired complete AV block most commonly occurs distal to the His bundle, usually is secondary to a trifasicular conduction disturbance, is potentially life-threatening, and generally is irreversible. A wide QRS escape rhythm with ventricular rates less than 40 beats per minute is the rule. An exception is seen in the setting of inferior infarction, in which recovery of complete (narrow QRS) AV nodal block occurs in greater than 90% of patients (time to recovery 30 minutes to 16 days).⁵

Drug toxicity, coronary artery disease, and degenerative disease of the conduction system are the most common causes of AV block in adults. Surgery, electrolyte disturbances (such as hyperkalemia), endocarditis, myocarditis (Lyme carditis), tumors, myxedema, rheumatoid nodules, Chagas’ disease, calcific aortic stenosis, polymyositis, amyloidosis, sarcoidosis, scleroderma, and vagotonic reflexes all may result in AV block. In truth, the number of factors and conditions that may result in AV block is nearly endless. “Hypervagal” responses (carotid hypersensitivity, neurocardiogenic syncope) may produce transient AV block (see later).³

Congenital complete AV block results from separation of the atrial musculature from the conduction system, or from nodoventricular disconnection. Mortality rate is highest in neonates, diminishes during childhood and adolescence, and then increases later in life. Patients may be asymptomatic for many years. It is difficult to predict prognosis in individual patients. Persistent ventricular rates less than 50 beats per minute correlate with the development of symptoms and syncope. Symptomatic patients and those patients with left ventricular dilatation should receive permanent pacemakers.

No reliable long-term pharmacotherapy exists for AV block. Transient AV nodal block may be managed with atropine. Infranodal block may be managed with (carefully titrated) isoproterenol until temporary or permanent pacing is established.

Junctional Rhythm

When the sinus node does not depolarize the atrium for any reason (high vagal tone, SND), the cells near the AV junction (AV node, His bundle) may take over as the active pacemaker. Retrograde activation of the atrium, commonly manifest as negative P waves in the inferior leads (II, III, aVF), may be seen (Fig. 31.7). If the junctional rhythm goes faster than 60 beats per minute, it is termed an accelerated junctional rhythm. This is a common manifestation of digitalis toxicity.

Vagally Mediated Sinus Arrest, Bradycardia, and Heart Block

The most common cause of nonconducted P waves during telemetry or Holter recordings is bradycardia-associated AV block. This manifests as sudden (usually nocturnal) block of one or more P waves with or without antecedent PR prolongation. This phenomenon is characterized by PP prolongation before AV block and is the result of transient increases in vagal tone. Vagally mediated sinus arrest, bradycardia, and heart block often occur in the intensive care unit (ICU) setting as a result of suctioning, gagging, femoral vessel compression (for hemostasis), and a variety of other triggers (Box 31.1). Vagal stimulation may lower blood pressure with or without significant bradycardia. Bradyarrhythmias and hypotension usually resolve when vagal stimulation ceases. Persistent bradycardia or hypotension mediated by vagal tone may require placing the patient in the Trendelenburg position, temporary saline infusion, or intravenous administration of atropine to fully resolve the episode.

Overview

Tachyarrhythmias often occur in critically ill patients. Conditions such as hypoxemia, electrolyte imbalance, catecholamine excess (endogenous and exogenous), and other metabolic disturbances predispose patients (with or without preexisting arrhythmic substrates) to tachyarrhythmias. Intensivists must be prepared for acute management of supraventricular tachycardia. Knowledge of arrhythmia mechanisms, appropriate choices for acute pharmacotherapy, and indications for urgent or emergent direct current cardioversion are requisite.⁶ We will discuss the mechanisms of supraventricular tachyarrhythmias, give an ECG-guided approach to their diagnosis, and cover specific treatments for these dysrrhythmias (pharmacologic and catheter ablation).

The substrate for most supraventricular tachycardias is present before ICU admission. Notable exceptions include atrial fibrillation (and flutter) after open-heart surgery and multifocal atrial tachycardia (MAT) (which may be transient, requiring no chronic therapy). Conditions such as hypoxemia, electrolyte imbalance, catecholamine excess (endogenous and exogenous), and other metabolic disturbances predispose patients (with or without preexisting arrhythmic substrates) to tachyarrhythmias.

Premature Atrial Contractions

Premature atrial, junctional, or ventricular beats are common in patients with or without structural heart disease and rarely result in significant alteration of cardiac output. They may occur as a result of enhanced sympathetic tone, metabolic stress, pericarditis, or direct mechanical irritation (as occurs with intracardiac catheters) and may result from the stimulant effects of caffeine, alcohol, intravenous inotropic support, or illicit drugs (such as cocaine). Atrial premature beats may be associated with aberrant conduction and confused with premature ventricular beats, or they may block in the AV node, creating a pause that may be confused with sinus arrest or SA exit block. Atrial premature beats may initiate reentrant supraventricular tachycardias or atrial fibrillation. Premature atrial contractions rarely require treatment, unless they trigger sustained supraventricular tachyarrhythmias.

Paroxysmal Supraventricular Tachycardia

Five types of paroxysmal supraventricular tachycardia (PSVT) are recognized: (1) AV nodal reentry tachycardia (AVNRT); (2) AV reentrant tachycardia (AVRT); (3) intra-atrial reentry; (4) automatic atrial; and (5) sinus node reentry. First-line chronic therapy for most supraventricular tachycardias is catheter ablation. The following discussion of therapy will be limited to acute pharmacologic management.

AVNRT is by far the most common and in the past accounted for 50% to 60% of PSVTs evaluated at referral centers.⁷ The precise reentrant circuit is not defined; however, it is clear that the anterior and posterior AV nodal approaches and the perinodal atrial tissue are involved. In 76% to 90% of cases, antegrade conduction proceeds along the posterior (slow) AV nodal approach (pathway) and retrograde conduction along the anterior (fast) AV nodal pathway.^7,8 This is slow-fast AVNRT. Because retrograde conduction is so rapid, atrial and ventricular activation are virtually simultaneous. P waves are usually not visible on the surface ECG or may appear in the terminal portion of the QRS complex (pseudo R′ in lead V₁ or pseudo-S waves in the inferior leads). Atrial contraction on a closed AV valve may produce neck pounding.⁹ Less common (so-called “unusual”) variants (fast-slow, slow-slow, and slow–sort of slow) of AV nodal reentry also exist.⁸

AVNRT usually manifests after the age of 20 years⁸ and is more common in women than in men. The typical heart rate in AVNRT ranges from 150 to 250 beats per minute. Palpitations, lightheadedness, and near-syncope may accompany an episode. True syncope is unusual. Neck pounding (see previously) is virtually pathognomonic,⁸ but its absence does not exclude AVNRT.

Before catheter-based cures became routine, AVRT was the next most common (accounting for 30%) PSVT mechanism.⁷ AVRT (also commonly referred to as orthodromic tachycardia) manifests (on average) at a somewhat earlier age than that typical for AVNRT. The antegrade limb of the circuit proceeds down the normal AV nodal His-Purkinje system. The retrograde limb uses an accessory pathway that usually is located along the mitral or tricuspid valve annulus. Because the accessory pathway conducts in only retrograde fashion, it is concealed (not seen on surface ECG).

Because AVRT proceeds normally antegradely, the QRS complex is generally narrow. The AVRT reentry circuit travels antegradely through the AV node and His-Purkinje system to the ventricles before retrograde activation of the atria occurs via the bypass tract. The extra time taken to travel by way of the ventricles creates a longer RP interval during tachycardia compared with that seen in AVNRT. Because AVNRT and AVRT activate periannular atrial tissue first, P waves (if visible on surface ECG) will be negative in the inferior leads. Upright P waves in these leads indicate atrial (or sinus) tachycardia. AVRT tends to go faster than AVNRT and is more prone to manifest with QRS alternans or left bundle branch block (LBBB) aberrancy.10,11 A decrease in tachycardia rate on development of bundle branch block ipsilateral to the pathway is characteristic of AVRT. AV block is unusual during AVNRT and excludes the diagnosis of AVRT (which requires both atrial and ventricular participation). The presence of AV block strongly suggests the diagnosis of atrial tachycardia.

In the past, intra-atrial reentry, automatic atrial tachycardia, and sinus nodal reentry accounted for the remaining 8% to 10% of PSVTs.⁷ Sinus node reentry rarely occurs as an isolated phenomenon.¹²

Approximately 50% of patients with intra-atrial reentry have evidence of structural heart disease.¹³ This tachycardia is particularly prone to develop after surgery for congenital cardiac anomalies. Reentry occurs around structural barriers, such as suture lines. In patients without clear-cut structural disease, subtle changes such as scarring and fibrosis provide the substrate for reentry. Automatic atrial tachycardias occur along the crista terminalis, near the ostium of the coronary sinus, along the tricuspid and mitral annulus, in both atrial appendages, and within or in close proximity to the pulmonary veins. Automatic atrial tachycardias are exquisitely sensitive to catecholamines. Although these tachycardias may manifest in the absence of structural heart disease or obvious precipitants, they also are commonly associated with chronic lung disease, pneumonia, myocardial (atrial) infarction, and acute alcoholic binges. Amphetamine or cocaine abuse also may precipitate automatic atrial tachyarrhythmias.

Reentrant atrial tachycardias tend to be paroxysmal, whereas automatic forms are more likely to be incessant. In both, atrial rates less than 200 beats per minute are characteristic. Persistent elevation of the ventricular rate may result in a (reversible) tachycardia-mediated cardiomyopathy.

As noted, the presence of AV block during tachycardia provides strong evidence that the rhythm disturbance is atrial in origin. Negative P waves are not helpful in differentiating atrial tachycardia from AVNRT or AVRT. An inferior P wave axis with a negative P in lead I is diagnostic of left atrial tachycardia. An inferior P axis, a positive P in lead I, and a P wave morphology different from sinus rhythm can result only from atrial tachycardia.

Sinus node reentry may occur within the sinus node, the perinodal atrial tissue, or both. Although the mechanism may be difficult to prove clinically, most investigators agree that the P wave may be nearly identical to sinus rhythm, suggesting that the reentrant exit point may differ slightly from sinus pacemaker beats. Average rates generally are 130 to 140 beats per minute (range 80 to 200).

Approach to Paroxysmal Supraventricular Tachycardia Therapy

Acute management of PSVT should begin with attempts to slow or (transiently) interrupt AV nodal conduction. Vagal maneuvers (such as carotid sinus massage or Valsalva) may be tried first. Adenosine is the initial drug of choice for acute management of PSVT. An initial intravenous dose of 6 mg may be followed (2 minutes) later by 6 mg (if necessary), and 12 mg may be given (2 minutes) later if 6 mg is unsuccessful.

Adenosine should terminate more than 90% of AVNRT and AVRT. This agent also is effective in sinus node reentry. Adenosine also may terminate automatic atrial tachycardias, particularly those originating near the crista terminalis, where vagal innervation is rich. Termination may be transient because of adenosine’s short half-life (10 seconds).

Intravenous verapamil (5 to 10 mg is injected over a period of 30 seconds, followed by an additional 5 mg, if necessary, after a 5- to 10-minute interval) or diltiazem (0.25 mg/kg, followed by an additional dose of 0.35 mg/kg, if necessary, after a 15-minute interval) usually is effective for PSVT termination when adenosine fails. AV block without arrhythmia termination (again) suggests the diagnosis of atrial tachycardia. Because of their longer half-lives, intravenous calcium channel blockers also may be effective for treatment of prompt tachycardia recurrence after initial success with adenosine.

Automatic atrial tachycardia is difficult to manage with pharmacotherapy. Precipitants should be treated or eliminated whenever possible. Beta blockers may slow atrial rate but rarely restore sinus rhythm. Adenosine may produce sinus rhythm; however, tachycardia may resume as soon as the drug is metabolized.¹⁴ Vagal maneuvers may produce AV block but do not terminate these arrhythmias. Clinical successes have been obtained with class IC agents and amiodarone. Flecainide should be avoided in patients with coronary artery disease or significant left ventricular dysfunction. Intravenous flecainide is not available in the United States (see later). Amiodarone is available for intravenous administration. Intravenous amiodarone may result in hypotension (vasodilation) but usually does not exacerbate heart failure or cause proarrhythmia in the setting of preexisting left ventricular dysfunction.

Sinus node reentry may respond to vagal maneuvers, adenosine, verapamil, and digitalis (relatively slow onset of action limits acute application). Acute management of intra-atrial reentry is similar to that for atrial fibrillation in the absence of antegrade accessory pathway conduction (see later). Emergent or urgent direct current cardioversion is indicated when PSVT results in angina pectoris, congestive heart failure (CHF), or hypotension. Techniques for and limitations of direct current cardioversion are discussed later in the chapter. Automatic tachycardias (including MAT) do not respond to direct current cardioversion.

Wolff-Parkinson-White Syndrome and Its Variants

The ECG pattern of Wolff-Parkinson-White syndrome (see “Electrocardiographic Patterns Intensivists Should Recognize”), short PR interval with preexcitation (delta wave), has a reported prevalence of 0.1% to 0.3% in the general population. It is twice as common in men as in women.

Classic Wolff-Parkinson-White syndrome occurs when the accessory AV pathway is capable of bidirectional conduction (AV and ventriculoatrial). Symptomatic presentation usually is during the teenage years or early adulthood. Pregnancy may exacerbate symptoms. The most common tachycardia is AV reentry (down the AV node and His-Purkinje system, up the bypass tract), identical to AVRT involving a concealed bypass tract. Approximately 25% of patients with a Wolff-Parkinson-White ECG pattern are incapable of retrograde conduction via the accessory pathway (and therefore do not have orthodromic AVRT). Asymptomatic patients generally have a benign prognosis; however, the initial presentation may be ventricular fibrillation (see later).¹⁵

Accessory pathways generally have conduction properties similar to those of myocardium. Decremental conduction, (AV conduction delay or block) which is characteristic of the AV node, is uncommon. Pathways may therefore be capable of very rapid antegrade (AV) conduction. In these instances, atrial fibrillation may be associated with irregular wide QRS tachycardia and ventricular rates in excess of 300 beats per minute (Fig. 31.8). Syncope or SCD (degeneration to ventricular fibrillation) may ensue. Intravenous ibutilide (1 mg infused over 10 minutes; a second 1-mg dose may be given by infusion after a 10-minute wait, if necessary) also blocks antegrade accessory pathway conduction and is more likely to terminate acute episodes of atrial fibrillation or flutter (see later).¹⁶

Regular wide QRS tachycardia in patients with Wolff-Parkinson-White syndrome may have any of several mechanisms. Aberrancy resulting from right or LBBB (fixed or functional) may occur during orthodromic AVRT. As noted, bundle branch block ipsilateral to the accessory pathway may slow the tachycardia rate.

Antidromic tachycardia occurs when antegrade conduction proceeds via a free-wall accessory pathway, and retrograde conduction occurs over the normal His-Purkinje–AV nodal route. The ventricles are activated eccentrically beginning at the insertion of the accessory pathway. The resulting maximally preexcited wide QRS rhythm may be difficult to distinguish from ventricular tachycardia.

Although accessory pathways may be located anywhere along the AV groove, two variants with characteristic locations deserve mention. Paroxysmal junctional reciprocating tachycardia (PJRT) is a form of AV reentry that may be nearly incessant. The antegrade limb of the circuit is the normal AV conduction system. The retrograde limb is a concealed, decrementally conducting accessory pathway usually located posteroseptally. As noted earlier, incessant tachycardia may result in a tachycardia-mediated cardiomyopathy.

Atriofascicular pathways (Mahaim fibers) connect the right atrium and the right bundle branch. During sinus rhythm, preexcitation is minimal or absent. Typical Mahaim reentry travels antegradely down the bypass tract and retrogradely through the normal conduction system (usually beginning with the right bundle branch). A regular wide QRS typical LBBB pattern is seen.¹⁷ These pathways conduct antegrade in a decremental fashion (retrograde accessory pathway conduction is absent) and occur much less frequently than typical AV accessory pathways. Patients with atriofascicular fibers frequently have multiple accessory pathways or AVNRT.^15,18

Nonparoxysmal Atrioventricular Junctional Tachycardia, Paroxysmal Atrial Tachycardia with Block, and Automatic Atrioventricular Junctional Tachycardia

Nonparoxysmal AV junctional tachycardia occurs primarily in the setting of digitalis toxicity. It also is associated with cardiac surgery, myocardial infarction, and rheumatic fever. Hypokalemia may cause or exacerbate this arrhythmia. Sympathetic stimulation increases the tachycardia rate.

Digitalis toxicity also may precipitate atrial tachycardia (so-called paroxysmal atrial tachycardia with block) (Fig. 31.9). This tachycardia usually is managed by withholding digoxin and administering potassium. Lidocaine, phenytoin, and digoxin-specific antigen-binding fragments also may be used.

Automatic AV junctional tachycardia, also known (particularly in pediatrics) as junctional ectopic tachycardia, primarily affects children and infants. It often is incessant. In patients without congenital heart disease, it may manifest as a tachycardia-mediated cardiomyopathy.

This tachyarrhythmia results in marked hemodynamic deterioration after corrective surgery for congenital heart disease. It generally appears within 12 hours postoperatively and terminates within a few days if the patient survives. Digitalis, beta blockers, and class IA antiarrhythmics are ineffective in children. Amiodarone (which may suppress tachycardia or control its rate) should be administered when rates less than 150 beats per minute cannot be achieved by other means.²¹ In adults, beta blockade may successfully control the rate. Adult automatic AV junctional tachycardia may be difficult to manage medically (Fig. 31.10). Recent reports suggest that catheter ablation can eliminate tachycardia while preserving AV conduction.^22–24

Multifocal Atrial Tachycardia

MAT is an automatic tachyarrhythmia. It is characterized by three or more morphologically distinct (nonsinus) P waves, atrial rates of 100 to 130 beats per minute, and variable AV block (Fig. 31.11).

MAT is commonly associated with respiratory disease and CHF. It has been reported in patients with cancer, lactic acidosis, pulmonary emboli, renal disease, and infection. Hypoxemia frequently is present. MAT may be exacerbated by digitalis or theophylline toxicity, hypokalemia, hypomagnesemia, and hyponatremia. These precipitants usually do not result in MAT if respiratory decompensation is absent. Although MAT is (in general) an uncommon arrhythmia, it is relatively common in the critical care setting. Treatment of MAT usually is directed at elimination of the underlying precipitants. Metoprolol (used cautiously when bronchospasm is present) or verapamil may provide (atrial and ventricular) rate control and occasionally restore sinus rhythm.25,26 Potassium and magnesium supplements may help suppress MAT. Amiodarone has also been useful in restoring sinus rhythm. MAT may, superficially, resemble atrial fibrillation. Careful examination of a 12-lead ECG may be required to distinguish between these two entities. Differentiation is important for proper patient management. As noted, MAT does not respond to direct current cardioversion and is not amenable to catheter ablation.

Sinus Tachycardia

Sinus tachycardia usually is a normal reflex response to changes in physiologic, pharmacologic, or pathophysiologic stimuli such as exercise, emotional upset, fever, hemodynamic or respiratory compromise, anemia, thyrotoxicosis, poor physical conditioning, sympathomimetic or vagolytic agents, and abnormal hemoglobins.²⁷ The resulting increase in cardiac output usually is beneficial. Heart rate generally does not exceed 180 beats per minute, except in young patients, who may achieve rates higher than 200 beats per minute during vigorous exercise.³ Tachycardia resolves when conditions return to baseline. The differential diagnosis for sinus tachycardia is presented in Table 31.1.

Sinus tachycardia is often present in ICU patients and sometimes is difficult to distinguish from other supraventricular tachycardias. When observed over time, sinus tachycardia will change its rate, with gradual acceleration and gradual deceleration. The P wave morphology of sinus tachycardia should be upright in leads I, II, aVF, and V₄ to V₆. Sinus tachycardia may slow transiently with vagal maneuvers or intravenous adenosine. If adenosine administration produces AV block, the P wave morphology can be clearly seen if a 12-lead ECG is run in rhythm strip mode. A negative P wave in (any of) leads I, II, aVF, and V₄ to V₆ excludes sinus tachycardia. P waves that are negative in lead I suggest a left atrial origin. Differentiation of “high” right atrial tachycardia waves from sinus tachycardia is more difficult. P-wave amplitude in the inferior leads may increase (normally) during sinus tachycardia. Comparison of the 12-lead P-wave morphology with that on an older 12-lead ECG tracing (if obtainable) when the patient was clearly in normal sinus rhythm may not result in an exact match.

Atrial Flutter

Although the precise reentrant circuit is unknown, typical atrial flutter traverses (with either counterclockwise or clockwise rotation) through an isthmus formed by the inferior vena cava, tricuspid valve, eustachian ridge, and coronary sinus ostia. Counterclockwise rotation is more common and results in negative “flutter” waves in ECG leads II, III, aVF, and V₆. Atrial activity in lead V₁ is positively directed. Clockwise atrial flutter produces oppositely directed flutter waves in these leads. Atrial rates generally range between 250 and 350 beats per minute; however, slower rates may be seen in the presence of specific pharmacotherapy (which slows conduction within the circuit) or marked right atrial enlargement (presumably caused by a larger circuit).²⁸ Atrial flutter usually manifests with 2 : 1 AV block and ventricular rates of approximately 150 beats per minute.

Pharmacotherapy for (typical and atypical) atrial flutter is similar to that outlined for atrial fibrillation. Special care must be taken to avoid inadvertent precipitation of 1 : 1 AV conduction and subsequent hemodynamic deterioration. Radiofrequency ablation is first-line curative therapy for typical atrial flutter.

Atrial Fibrillation

Atrial fibrillation is the most important sustained supraventricular arrhythmia both in frequency and in potential for long-term sequelae. Atrial fibrillation and atrial flutter frequently coexist. More than 2 million people in the United States suffer from atrial fibrillation and this number is expected to rise as the population ages. The frequency of this arrhythmia increases dramatically after the age of 60.

Atrial fibrillation most often is associated with structural cardiac (diffuse atrial) disease. Unlike in typical atrial flutter, left atrial enlargement is more important than right atrial enlargement in the pathogenesis of atrial fibrillation.²⁹ The chaotic ECG appearance of this arrhythmia usually is the result of shifting reentrant circuits (multiple wavelet hypotheses). Atrial fibrillation may have focal triggers (usually in one or more pulmonary veins).³⁰ Causes of atrial fibrillation are listed in Box 31.2.

Arrhythmogenesis

Reentry is the most common mechanism for sustained ventricular arrhythmias. Three conditions are required for reentry. The first is the presence of two anatomically contiguous pathways separated by a central region of inexcitable tissue. Second, there must be unidirectional block in one of the pathways. Third, a zone of slow conduction also must be present to allow recovery and excitation of the region of block. Such conditions may be anatomically defined (as in the border zone of an old myocardial infarction scar) or result from functional disturbances in conduction and refractoriness.

Enhanced automaticity results in spontaneous impulse formation in cells that otherwise do not exhibit pacemaker activity. Diseased cardiac tissue is particularly susceptible to development of enhanced automaticity. This may result in rates faster than the normal pacemaker activity of the sinus node. Automatic cells (in the AV node, the His-Purkinje system, or the ventricles) may usurp the sinus node by means of enhanced automaticity if their depolarization is accelerated by drugs, sympathetic activity, or metabolic disturbances.

Triggered activity occurs when oscillations in membrane potential (called afterdepolarizations) reach the threshold for action potential formation, resulting in abnormal impulse formation. Early afterdepolarizations (EADs) result from delayed inactivation of inward ion currents during the plateau phase of the action potential. EADs appear to be important in the genesis of torsades de pointes (see later). Delayed afterdepolarizations (DADs) result from increased intracellular calcium. Digitalis toxicity is the classic example of DAD-induced triggered activity. Digitalis inhibits the Na⁺-K⁺ pump, thereby increasing intracellular Na⁺, which in turn increases intracellular Ca²⁺ via the Na⁺-Ca²⁺ exchange current.⁷⁹ Idiopathic outflow tract ventricular tachycardia may also result from DADs (cyclic AMP-mediated triggered activity).⁸⁰

Metabolic Disturbances and Ischemia

Metabolic disturbances and ischemia are common in the critically ill. Patients may suffer from (synergistic or opposing) effects of multiple abnormalities. In the presence of partial predispositions, arrhythmias may not develop until patients are exposed to factors resulting in enhanced automaticity, delayed conduction, or changes in refractoriness.

Hypokalemia delays repolarization and prolongs action potential duration. This may lead to EADs and triggered arrhythmias. Hypomagnesemia and hypokalemia often coexist. Each is associated with QT prolongation and torsades de pointes. Repletion of Mg²⁺ is an important adjunct to the management of hypokalemia. Hypermagnesemia usually is not associated with arrhythmogenesis.

Hyperkalemia suppresses automaticity and slows conduction. The earliest ECG sign is peaked T waves. At high levels (usually 7.0 mEq/L or greater), marked QRS widening (sine wave morphology) may be seen, followed by cardiac arrest. Patients with renal insufficiency may be particularly susceptible. Cardiac effects of severe hyperkalemia may be lethal and require prompt intervention. The most rapid means of countering cardiac toxicity is intravenous administration of 10% calcium chloride. The ECG should be monitored to ensure that signs of hyperkalemia have been reversed. Calcium chloride, although effective emergently, does not lower serum potassium.

Sodium bicarbonate (usual dose 44 to 88 mEq) reduces serum potassium. Regular insulin (10 units) will result in redistribution of K⁺ from the extracellular to the intracellular space but does not lower total body potassium stores. Insulin should be followed by 50 mL of 50% glucose.

Further treatment of hyperkalemia involves removal of potassium from the body. The most common method is administration of the cation-exchange resin sodium polystyrene sulfonate (Kayexalate). The usual dose is 50 g given two or three times daily. The most effective means of reducing body potassium is dialysis. Care must be taken to avoid precipitous reduction, especially in patients taking digitalis glycosides.⁸¹ ECG patterns associated with electrolyte and metabolic disturbances are discussed in more detail later in this chapter.

Myocardial ischemia, from coronary artery disease, hemodynamic deterioration, or hypoxemia, can produce a variety of electrophysiologic effects. Acid-base disturbances and exogenous or endogenous catecholamines also can predispose affected patients to ventricular (often polymorphic) arrhythmias. The role of the sympathetic nervous system in arrhythmogenesis and electrical storm cannot be overemphasized.79,82,83 Reentry, enhanced automaticity, and triggered activity may all be provoked.

In the absence of QT prolongation, ischemia is the most common cause of polymorphic ventricular tachycardia. Polymorphic ventricular tachycardia/ventricular fibrillation in the early phase (less than 48 hours) of an acute myocardial infarction does not require additional evaluation or treatment. Late polymorphic ventricular tachycardia/ventricular fibrillation complicating myocardial infarction usually occurs when severe heart failure or cardiogenic shock also has been problematic. The initial prognosis usually is determined by hemodynamic recovery rather than arrhythmias.

Ischemia is also a common cause of polymorphic ventricular tachycardia/ventricular fibrillation in the absence of acute infarction. A reduction in or withdrawal of catecholamines should be tried. Beta blockers should be titrated to tolerance. Intra-aortic balloon counterpulsation and acute revascularization should be considered. Pharmacologic therapy with amiodarone may be useful.

Differential Diagnosis of Wide QRS Tachycardia

Wide complex tachycardia (WCT) may be supraventricular or ventricular in origin. Evaluation of WCT remains a common dilemma for clinicians. Numerous algorithms aid in arriving at the correct diagnosis. Unfortunately they are difficult to remember and an overreliance on algorithms may prevent clinicians from understanding the underlying arrhythmic mechanisms. Presence of AV dissociation is diagnostic of ventricular tachycardia. In general, supraventricular tachycardia with aberrancy will manifest with a typical bundle branch block pattern, whereas ventricular tachycardia will have more “bizarre” QRS complexes. Preexcited supraventricular tachycardias may be impossible to distinguish from ventricular tachycardia using ECG criteria alone. Algorithms (with good sensitivity and specificity) to help distinguish supraventricular tachycardia from ventricular tachycardia are summarized in Table 31.3.⁸³

Approach to Ventricular Arrhythmias in the Critically Ill

New ventricular arrhythmias warrant an assessment of electrolytes, oxygenation, and acid-base status. Routine measurement of cardiac enzymes is not mandatory with the onset of each arrhythmia. The QT interval should be checked via 12-lead ECG. The 12-lead ECG also is useful in distinguishing monomorphic from polymorphic ventricular tachycardia. Dislodgement of intravascular catheters may result in mechanically induced arrhythmias. Catheter position may be confirmed by x-ray examination or fluoroscopy.

A comprehensive discussion of advanced cardiovascular life support (ACLS) is beyond the scope of this chapter. Current recommendations for management of adult cardiac arrest are discussed in Chapter 1 of this book and are summarized in recently published ACLS guidelines.⁸⁴

Specific Ventricular Arrhythmias

The occurrence of premature ventricular contractions (PVCs) and nonsustained ventricular arrhythmias in the ICU generally has little immediate importance. Reduction or withdrawal of exogenous catecholamines and elimination of metabolic disturbances often will decrease the frequency and severity of nonsustained ventricular tachycardia (NSVT). Acute antiarrhythmic drug therapy is rarely required unless symptoms of hemodynamic compromise occur.

The approach to NSVT that persists after recovery from acute illness depends on the underlying cardiac substrate. Asymptomatic persons without structural disease require no therapy. Patients with reduced left ventricular function (less than or equal to 35%) should be evaluated for ICD therapy.85–87 Amiodarone, which has a neutral effect on mortality rates, may be used to suppress symptomatic NSVT in patients with significant structural heart disease.⁸⁵

Acute management of sustained monomorphic ventricular tachycardia depends primarily on its hemodynamic stability. Unstable tachycardia should be treated promptly with direct current cardioversion. Stable arrhythmias may be treated with intravenous amiodarone or beta blockers. Although lidocaine remains an option, the International Cardiopulmonary Resuscitation (CPR) guidelines no longer recommend lidocaine as a first-line agent. Antitachycardia pacing may be considered in patients with transvenous or epicardial pacing leads. If these modalities are unsuccessful (or arrhythmia acceleration occurs), direct current cardioversion can be used to restore sinus rhythm. Electrical storm is defined as ventricular tachycardia or ventricular fibrillation occurring more than twice in 24 hours, usually requiring electrical cardioversion or defibrillation.⁸⁸ Although data are limited, beta blockade in conjunction with amiodarone appears to be the most effective therapy for electrical storm.^82,88

Because the arrhythmic substrate usually is fixed (most commonly, coronary artery disease and prior myocardial infarction), recurrence rates may remain high even after elimination of “reversible” causes.89,90 Although no definite guidelines exist in the presence of reversible causes, an ICD should be strongly considered in patients with left ventricular dysfunction (if comorbidity is not prohibitive). Electrophysiologic testing may be useful in patients with coronary artery disease but is much less reliable in patients with nonischemic cardiomyopathy.

Bundle branch reentry has been reported to account for up to 6% of the cases of monomorphic ventricular tachycardia.⁹¹ This percentage may rise to 40% to 50% in patients with idiopathic dilated cardiomyopathy.⁹² It has been our clinical experience that this arrhythmia is far less frequent. Nevertheless, bundle branch reentry should be considered in patients with marked left ventricular dysfunction (especially nonischemic), intraventricular conduction defects, and wide QRS tachycardia. It may appear after valve replacement surgery. The tachycardia circuit typically uses the right bundle branch as its antegrade limb and the left bundle branch as its retrograde limb. Tachycardia therefore manifests with classic LBBB morphology. Diagnosis and treatment may be accomplished during a single invasive electrophysiology session. The right bundle branch is easily ablated during sinus rhythm, permitting tachycardia cure without detailed mapping during hemodynamically unstable arrhythmias.^93,94 Although the postablation prognosis has been said to be favorable for patients with isolated bundle branch reentry, patients with residual inducible or spontaneous ventricular tachycardia should be offered ICD therapy. Patients with significant residual infranodal conduction delay (His-ventricular rates longer than 90 ms) after ablation should be considered for permanent pacing (usually with an ICD). It is appropriate to implant an ICD after ablation in patients with heart failure and ejection fractions less than 35%.

Optimal long-term management of patients with structural heart disease and sustained monomorphic ventricular tachycardia is to implant an ICD.95,96 Hemodynamic stability does not predict a better long-term outcome.⁹⁵ Ablation generally is regarded as palliative and is used primarily to reduce shock frequency in patients with recurrent ventricular tachycardias.⁹⁷ However, substrate-based catheter ablation may reduce the ICD therapies in post-myocardial infarction patients who received ICDs for secondary prevention.⁹⁸

The risk of recurrent polymorphic ventricular tachycardia/ventricular fibrillation is high, and the long-term prognosis is poor. Most patients, particularly those with left ventricular dysfunction, should have an ICD implanted if no contraindications exist. Idiopathic ventricular fibrillation may respond to catheter ablation if a single PVC focus (usually from the Purkinje system or the right ventricular outflow tract) is the consistent trigger.99,100 Coronary artery spasm may result in ventricular fibrillation caused by myocardial ischemia. Recognition of this uncommon cause of cardiac arrest is critical. Ideal treatment for patients with coronary spasm and associated ventricular arrhythmias remains controversial. Titration of calcium channel blocker dose to prevent ergonovine-induced spasm eliminated arrhythmia in one small series.¹⁰¹ Despite optimal medical therapy (nitrates and calcium channel blockers), this patient subgroup falls into a high-risk category of vasospastic angina and appears to be at greater risk for sudden death. Concomitant ICD implantation has been advocated to reduce this risk.¹⁰²

Less Common Substrates

Serious ventricular arrhythmias are uncommon in the absence of significant left ventricular dysfunction. A few specific entities should be readily recognized by the intensivist.

Electrolyte, Endocrine, and Metabolic Abnormalities

Electrolyte and metabolic abnormalities may affect cardiac depolarization or repolarization. The ECG may be the first clue that an electrolyte or metabolic abnormality is present.

Hyperkalemia is frequent in the critically ill, in particular in patients with impaired renal function. As the serum potassium increases, the ECG follows a characteristic stepwise pattern of derangement. The first sign of hyperkalemia on ECG is peaked T waves. Although there is no universal definition of “peaked,” we agree with the definition of T waves greater than 10 mm in the precordium and 6 mm in the limb leads.¹⁷⁵ In addition to being peaked, the T waves typically appear narrow. At a potassium level of greater than 6.0 mmol/L, T-wave peaking is pronounced, the P wave will begin to lose amplitude, and the QRS complex begins to widen. At potassium levels greater than 7 mmol/L the P wave is no longer visible and QRS widening progresses. The ensuing ECG pattern is known as sinoventricular rhythm (Fig. 31.18).¹⁷⁶ Sine waves may become present as the widened QRS complex blends into the T wave (Fig. 31.19).¹⁷⁷ An abnormal ECG may be the initial sign of dangerous hyperkalemia and therapy should begin immediately to eliminate the hyperkalemia and stabilize the heart (calcium gluconate infusion).

Hypokalemia also results in characteristic ECG changes. The hallmark of hypokalemia is the U wave, an additional wave seen after the T wave (Fig. 31.20). As the hypokalemia becomes more severe, the U wave increases in amplitude, and T-wave amplitude will decrease. Eventually, the T wave and the U wave may fuse, giving the appearance of a widened T wave. This creates a prolonged QT interval, which may result in torsades de pointes. The risk of hypokalemia-induced arrhythmia is increased in patients receiving digitalis and during myocardial ischemia.¹⁷⁸

Hypomagnesemia is usually associated with potassium depletion. ECG abnormalities seen are produced by hypokalemia. Hypermagnesemia is uncommon and usually associated with renal failure. Observed ECG changes result from concomitant electrolyte disturbances (hyperkalemia and hypocalcemia).¹⁷⁸

The principal electrocardiographic feature of hypercalcemia is a shortening of the QT interval (Fig. 31.21).¹⁷⁶ This finding is not associated with arrhythmias. In contrast, patients with the rare SQTS have a QTc interval less than 360 ms (typically <300 ms) and a high risk of sudden death due to ventricular fibrillation (Fig. 31.22).¹⁷⁹ Patients often have permanent or paroxysmal atrial fibrillation and occasionally manifest depression of the PR interval. Tall, peaked T waves without flat ST segments and impaired rate-dependent QT shortening has been recorded.¹⁸⁰ SQTS appears to be inherited in an autosomal dominant pattern.

The principal finding in hypocalcemia is a prolongation of the QT interval. It should be noted that, unlike in hypokalemia, the T wave is normal sized and QT interval prolongation results from lengthening of the ST segment, not a broadening of the T wave due to fusion with a U wave. In severe hypocalcemia, PR and QRS intervals are frequently prolonged (Fig. 31.23).¹⁷⁶ Second-degree or third-degree AV block has been reported. J waves (see later) have occasionally been reported.¹⁷⁸

In addition to electrolyte abnormalities, metabolic derangements can cause characteristic ECG findings. Hypothermia, both from accidental exposure as well as therapeutic cooling after cardiac arrest, has classic findings on ECG (Fig. 31.24).¹⁸¹ As the core body temperature drops below 32° C, conduction becomes slower with slower sinus rates, prolonged PR and QT intervals, as well as junctional rhythms.¹⁸² The finding of an Osborn or J wave is a hallmark of hypothermia. This wave appears as an upward deflection at the terminal portion of the R wave, before the J point. Additionally, the ECG baseline may have artifact or oscillations from shivering. Though classically associated with hypothermia, the Osborn wave may also be a sign of other conditions such as sepsis and diabetic ketoacidosis (which can be hypothermic conditions) as well as normothermic conditions such as neurologic insults and hypercalcemia.¹⁸³

Hypothyroidism characteristically shows slowing of conduction and often has sinus bradycardia, low voltage, and prolonged PR and QT intervals as well as intraventricular conduction delays. Hyperthyroidism may cause sinus tachycardia and premature atrial complexes or may precipitate atrial fibrillation.

Brugada Pattern

As mentioned earlier, the Brugada syndrome is characterized by an inherited disorder of sodium channels. Brugada pattern is characterized on the ECG by RBBB (complete or incomplete) morphology and abnormal repolarization characterized by ST-segment elevation in leads V₁ to V₃. Three distinct patterns have been identified. Type 1 features a “coved” type ST segment (more than 2 mm) elevation and a negative T wave. Type 2 features a “saddleback” ST-T configuration, recognized by two notches in the T wave. Type 3 can have a coved or saddleback morphology. This configuration is less specific for Brugada syndrome (Fig. 31.25).¹⁸⁴ A patient with any of the Brugada patterns and a history of cardiac arrest, syncope, or ventricular tachycardia should have an ICD implanted, as there is no effective drug therapy for this disease. It is not recommended that asymptomatic patients with the Brugada pattern on ECG receive a defibrillator, and clinical monitoring is advised instead. Should a patient suffer from electrical storm, isoproterenol is considered useful.¹³²

Long QT Syndromes

As mentioned previously, the congenital long QT syndrome is associated with SCD due to torsades de pointes. The three most common inherited forms (LQT1, LQT2, and LQT3) represent 75% of the inherited long QT syndrome. Each one of those subtypes has a specific mutation and an activity in which the arrhythmia (and hence syncope or cardiac arrest) is triggered. LQT1 is associated with events during exertion, LQT2 is associated with events occurring after hearing a sudden loud noise, and LQT3 is associated with events at rest or sleep. There are also ECG patterns associated with each of those three variants, though it should be noted that the clinical scenario will often correlate better than the ECG pattern to the specific gene mutation. The LQT1 has a broad T wave, the LQT2 has a bifid T wave, and the LQT3 has a long isoelectric segment and a narrow T wave. The LQT3 pattern appears somewhat similar to the ECG seen in hypocalcemia (Fig. 31.26).¹⁸⁵

More commonly, however, intensivists will see patients with transient prolongations in their QT interval due to their illness, ingestion of medications, or antiarrhythmic drugs. These patients need to be monitored carefully for the development of torsades de pointes. In addition, an alternation in T wave amplitude can be seen. This is referred to as T wave alternans and represents a harbinger of worsening arrhythmias (Fig. 31.27). Dramatic QT prolongation and T wave stroke may occur after cardiovascular accident.

Torsades de Pointes

The term torsades or torsades de pointes refers to a polymorphic ventricular tachycardia that appears to rotate around a horizontal axis, hence the name (from the French “twisting of the points”) (Figs. 31.28 and 31.29).³⁴ The term torsades de pointes should be used only in the setting of the ventricular tachycardia seen with a prolonged QT interval (either acquired or congenital). It is important to differentiate this rhythm from other types of polymorphic ventricular tachycardia (as seen in ischemia) because the management is different. Urgent management of acquired long QT prolongation and torsades de pointes is typically intravenous magnesium sulfate and defibrillation for hemodynamic instability. As mentioned previously, isoproterenol and temporary pacing increase ventricular rates, shorten QT intervals, and help prevent recurrent arrhythmias until the effects of the offending agent diminish. Torsades de pointes is often initiated by a short-long-short sequence of a premature ventricular beat (short segment) followed by a compensatory pause (long segment). The long delay from the compensatory pause delays repolarization. As a result, the QT segment is prolonged after the compensatory pause, and it is more likely that the next depolarization will occur when the ventricle is vulnerable (R on T phenomenon).

Wolf-Parkinson-White Pattern

As described previously, patients with Wolff-Parkinson-White syndrome can present in sinus rhythm or during an arrhythmia. There are three classic ECG patterns in this disorder depending on the patient’s presenting rhythm. Patients in sinus rhythm with activation of the ventricle by both the normal AV node and His-Purkinje system as well as by the accessory pathway will have a fusion beat on their ECG. This beat manifests as a delta wave and short PR interval as part of the ventricle is activated (preexcited) by the accessory pathway (Fig. 31.30). Patients with Wolff-Parkinson-White pattern in sinus rhythm are asymptomatic and usually come to attention when presenting for other reasons, after an arrhythmia has broken, or on a routine ECG that incidentally detects the abnormality. T-wave inversion may develop after accessory pathway ablation (Fig. 31.31). This is a transient, reversible, repolariztion phenomenon and does not reflect myocardial ischemia.

Patients with an accessory pathway often present for the first time when they have palpitations. More often, the patients will present with an AVRT. In orthodromic AVRT, the conduction travels down the normal conduction system and retrograde up the accessory pathway. The QRS will be narrow (unless there is a preexisting or rate-related bundle branch block) and the delta wave will no longer be visible (the ventricle is entirely activated by the normal conduction pathway). In antidromic AVRT, the conduction will proceed antegrade down the accessory pathway and retrograde up the normal conduction system. There will be a wide complex regular tachycardia (maximal preexcitation).

Atrial fibrillation in a patient with Wolff-Parkinson-White must be recognized as it requires specific treatment, which is different from other forms of atrial fibrillation. The ECG shows an irregular rhythm with a delta wave. The ventricle is again being depolarized from both normal pathway as well as the accessory pathway. As mentioned earlier, AV nodal blocking agents, which are the mainstay of treatment in most cases of atrial fibrillation, may facilitate conduction down the accessory pathway. Decremental conduction (like the AV node) is rare in these accessory pathways and atrial fibrillation may be conducted very rapidly to the ventricles. There is a concern for triggering ventricular tachycardia or fibrillation, so drug therapies include ibutilide (which blocks the accessory pathway) or amiodarone (which blocks both the AV node and the accessory pathway). Additionally, both of these medications can convert atrial fibrillation back to sinus rhythm.

Arrhythmogenic Right Ventricular Dysplasia

In patients with ARVD, inverted T waves may be noted in the right precordial leads (V₁, V₂, and V₃). In addition, an upward deflection, called an epsilon, may be seen just after the QRS complex and is due to late right ventricular activation (Fig 31.32).¹⁸⁶ In addition, the QRS duration will be prolonged, often with a complete or incomplete RBBB pattern. The ECG may be the initial clue to this disease. Ventricular tachycardia with a LBBB-like morphology (right ventricular origin) is often precipitated by catecholamines (e.g., exercise).

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