What If Heart Beat Goes Fast Frequently And Qt And Pr Intervals Are Not Normal

The normal heartbeat is initiated by specialized cardiac cells (so-called pacemaker cells) located in the right atrium adjacent to its junction with the superior vena cava. These cells make up a specialized, albeit somewhat diffuse, region of the right atrium called the sinus node.

The rate and regularity of activity in the sinus node (the cardiac pacemaker) is determined by both the intrinsic firing rate (automaticity) of the cells within the node and the influence of extrinsic factors on these cells, including autonomic neural tone, electrolytes, and drugs. The usual range of resting sinus rate is 60-100 beats per minute (beats/min), although rates as low as 40 beats/min are common in fit individuals; most average adults have resting rates in the range of 60-70 beats/min. Bradycardia (slow heart beat) is a term used to refer to any heart rate less than 60 beats/min, and tachycardia (fast heart beat) describes heart rates greater than 100 beats/min.

Bradycardia is usually the result of either "sick sinus syndrome" (otherwise known as sinus node dysfunction) or atrioventricular conduction block (i.e., intermittent or permanent block of impulse transmission from the site of normal pacemaker activity in the atria through the specialized cardiac con-

From: Handbook of Cardiac Anatomy, Physiology, and Devices Edited by: P. A. Iaizzo © Humana Press Inc., Totowa, NJ

duction system to the ventricles). These conditions can be caused by either intrinsic disease of the pacemaker cell region or conduction system tissue or extrinsic factors such as drugs or autonomic system disturbances.

The mechanisms underlying tachycardia are more numerous and complex than those that cause bradycardia. Nevertheless, tachycardias can be classified as caused by abnormally rapid impulse initiation (i.e., abnormal automaticity from the sinus node region or other subsidiary or abnormal pacemaker sites) or abnormal impulse conduction (Table 1).

The term arrhythmia is mainly used to refer to disturbances of the normal heart rhythm. An exception to this rule is sinus arrhythmia, which refers to the healthy variation of the sinus rhythm associated with physiological alteration of neural influence on pacemaker automaticity. The most important cause of the sinus rhythm variation is the respiratory cycle, but other factors such as beat-to-beat changes in cardiac output (i.e., ventriculophasic sinus arrhythmia) may also contribute.

Although arrhythmias can occur in clinically normal hearts, they are more commonly associated with structural heart diseases. Myocardial ischemia is the most important of these diseases in the Western world, but other forms of cardiac dysfunction such as cardiomyopathies, valvular heart disease, and certain genetically determined disorders (e.g., long QT syndrome, Brugada syndrome) must also be considered. In certain

Table 1

Mechanisms of Tachycardias

❖ Abnormal impulse initiation

• Automaticity

• Enhanced normal automaticity, as seen in inappropriate sinus tachycardia and some idiopathic ventricular tachycardias

• Abnormal automaticity, as presumed to be the case in ectopic atrial tachycardia, accelerated junctional rhythm, and possibly certain idiopathic ventricular tachycardias

• Triggered activity

• Early after-depolarization, as presumed to be the case in torsades de pointes

• Delayed after-depolarization, as seen in digitalis-induced arrhythmias or presumed to occur in certain exercise-induced arrhythmias

❖ Abnormal impulse conduction

• Ectopic escape after block, such as junctional escape

• Unidirectional block and reentry

• Orderly reentry (macroreentry and microreentry)

• Random reentry, as seen in atrial fibrillation

• New concepts (reflection, phase 2 reentry, and anisotropic reentry)

regions of the world, infections remain an important cause of heart rhythm disturbance. Most important among these are rheumatic heart disease, common in the Far East, and Chagas disease in South America. In Western countries, myocarditis or pericarditis (most commonly of viral etiology) are occasionally associated with arrhythmias.

The clinical presentation of cardiac arrhythmias ranges from completely asymptomatic or inducing mild symptoms (palpitations and anxiety), to syncope and sudden cardiac death; the impact is largely dependent on arrhythmia-induced hemody-namic changes. The electrophysiological and hemodynamic consequences of a particular arrhythmia are primarily determined by the ventricular rate and duration, the site of origin, and the underlying cardiovascular status (i.e., severity of associated heart and vascular disease).

Many arrhythmias can be readily diagnosed from standard 12-lead electrocardiography (ECG). However, other diagnostic techniques are frequently required for a more precise diagnosis, including prolonged rhythm monitoring (an event monitor, Holter monitor, or implantable recorder) and electro-physiological testing. Exercise stress tests and signal-averaged ECGs may also be used in the assessment regarding the nature of an arrhythmia or susceptibility of the patient to elicit an arrhythmia. Other techniques (such as analysis of heart rate variability, baroreflex sensitivity, assessment of QT dispersion, T-wave alternans, and body surface potential mapping) have provided some useful research information, but their value in daily practice remains to be defined fully at this time.

The clinical goals in the treatment of arrhythmias are twofold: to alleviate symptoms for improved quality of life and to prolong survival. Pharmacological treatment has been the mainstay for the management of cardiac arrhythmias, although in recent years implantable devices and ablation have become increasingly important. Regarding antiarrhythmic drugs, many clinicians find it convenient to categorize them according to the Vaughn-Williams scheme. This classification is simple and has been widely used clinically because it offers a means to keep the principal pharmacological effects of drugs in mind (Table 2). A more comprehensive classification of antiarrhythmic drugs, called the Sicilian Gambit, was introduced in 1991 (1) and is based on a more widespread consideration of the cellular basis of drug actions. However, neither classification system offers much help in the treatment of specific arrhythmias. Selection of antiarrhythmic drugs for patients should be individualized based on their specific antiarrhythmic and proarrhythmic actions, the arrhythmia treated, and the nature and severity of any underlying heart diseases.

In patients with ischemia or left ventricular dysfunction of other etiologies, class I agents should be avoided because of their proarrhythmic risk. Class III drugs (i.e., amiodarone, dofetilide), on the other hand, appear to have a neutral effect on survival in these patients. It appears that p-blockers (class II) are the only drugs that have been proven to prolong survival in patients with structural heart disease. Nevertheless, nonpharmacological interventions, such as catheter ablation for supraventricular tachycardias and implantable cardio-verter-defibrillators for primary and secondary prevention of sudden cardiac death, are considered the treatments of choice in many clinical settings.

2. TACHYARRHYTHMIAS 2.1. Premature Complexes

Ectopic premature beats may originate from the atria, the atrioventricular junction, and the ventricles. Treatment of premature complexes is usually not necessary. If symptomatic, precipitating factors such as alcohol, tobacco, and caffeine should be identified and then eliminated. Although anxiolytic agents and p-blockers may be used in such cases, they are often problematic in terms of side effects. Other antiarrhythmic drugs may be used depending on the severity of symptoms and underlying cardiac disease, but avoidance of such drugs is the preferred strategy.

Table 2

Vaughn-Williams Classification "

❖ Class I: sodium channel blockers

• Class Ia: drugs that reduce Vmax (phase 0 upstroke of action potential) and prolong action potential duration, such as quinidine, procainamide, and disopyramide

• Class Ib: drugs that do not reduce Vmax and shorten action potential duration, such as lidocaine, mexiletine, and phenytoin

• Class Ic: drugs that predominantly slow conduction, moderately reduce Vmax, and minimally prolong refractoriness, such as flecainide, propafenone, and moricizine

❖ Class II: P-adrenergic receptor blockers

• P-blockers may be cardio- or p1-selective drugs such as atenolol, esmolol, and metoprolol or noncardioselective such as carvedilol, pindolol, and propranolol

• Some (acebutolol, bucindolol, and pindolol) exert intrinsic sympathomimetic activity

• Some have quinidinelike membrane-stabilizing activity (acebutolol, carvedilol, and propranolol)

• D-Sotalol has strong class III effects and has been regarded as a class III agent in many conditions

❖ Class III: potassium channel blockers that prolong refractoriness, such as amiodarone, bretylium, dofetilide, ibutilide, and sotalol; amiodarone has all the four class effects.

❖ Class IV: calcium channel blockers

• Dihydropyridine (almodipine and nefedipine)

• Nondihydropyridine drugs (diltiazem and verapamil)

"As discussed in the text, the utility of this classification in terms of selection of therapy is limited, but the groupings permit important toxicity issues to be more readily acknowledged, an important factor in choosing drugs for individual patients.

Prematuer Atrial Complex

2.1.1. Atrial Premature Complexes

Atrial premature complexes are recognized during the ECG exam as early P waves, with a P-wave morphology different from that of the sinus P wave (Fig. 1A). The premature P wave is often superposed in the preceding T wave; the T wave preceding a premature beat should be carefully compared to other T waves to see if there may be any buried P waves. Atrial premature complexes can conduct to the ventricles with a normal PR interval when atrioventricular junctions are not refractory or with prolonged PR intervals when atrioventricular junctions are in their relative refractory periods or blocked when atrio-ventricular junctions are in their effective refractory periods. They almost always enter into the sinus node region and reset the sinus cycle length, resulting in an incomplete compensatory pause (the sum of preatrial and postatrial premature complex intervals is less than that of two normal sinus PP intervals). Atrial premature complexes are frequently found in normal patients and are thus usually asymptomatic. Treatment is usually not necessary.

2.1.2. Multifocal Atrial Tachycardia

Multifocal atrial tachycardia, also called chaotic atrial tachycardia, is characterized by atrial rates between 100 and 130 beats/ min, with marked variations in P-wave morphology (arbitrarily defined as at least three P-wave contours). They often manifest as short bursts of tachycardia (Fig. 1D). Treatment is primarily directed toward underlying disorders and is followed by p-blockers if necessary. Verapamil (class IV) or amiodarone may be considered as a second-line therapy. Amiodarone may be predicted as the most effective drug in this setting, but its multiple side effects (particularly pulmonary effects) are of concern because many patients with multifocal atrial tachycardia already have significant underlying pulmonary problems.

2.1.3. Atrioventricular Junctional Premature Complexes

Atrioventricular junctional premature complexes are recognized on the ECG as normal QRS complexes without a preceding P wave (Fig. 1B). Retrograde P waves (inverted in leads II and III and aVF) may be seen after the QRS complexes. Such complexes are less common and often associated with drug intoxication and cardiac diseases. Most junctional beats have an incomplete compensatory pause. Occasionally, a junctional premature beat may fail to conduct to either the atria or the ventricle (concealed junctional beats), but results in usual refractoriness in the atrioventricular junction and blocks subsequent supraventricular beats.

2.1.4. Ventricular Premature Complexes

Ventricular premature complexes are recognized as wide and bizarre QRS complexes not preceded by P waves (Fig. 1C). They often fail to conduct retrogradely to the atria because of poor retrograde (i.e., ventriculoatrial) conduction properties in the diseased hearts of patients who most often manifest such complexes. Thus, ventricular premature complexes do not typically reset the sinus node, and they result in a fully compensatory pause (the sum of pre- and postatrial premature complex intervals equals that of two normal sinus PP intervals). Interpolated ventricular premature complexes do not influence the following sinus beats (i.e., their occurrence is timed so as not to impair the next sinus beat from reaching the ventricles at the expected moment).

They may occur singly, in patterns of bigeminy (sinus beat and ventricular premature complex alternating) and trigeminy (two sinus beats followed by a ventricular premature complex), or couplets or pairs (two consecutive ventricular premature complexes) and nonsustained ventricular tachycardia (arbitrarily defined as three or more consecutive ventricular premature complexes at a rate exceeding 100 beats/min). Their morphology may be monomorphic (uniform) or polymorphic (multiform).

Ventricular premature complexes often bear a fixed coupling interval (between the onset of ventricular premature complex and the onset of its preceding sinus QRS complex). When there is a protected ventricular ectopic focus, the focus is constantly firing without resetting by a sinus beat and thus results in ventricular parasystole. Ventricular parasystole can manifest with varying coupling intervals, whereas the interventricular premature complex intervals remain relatively fixed (i.e., variation <120 ms).

Importantly, the relationship of ventricular premature complexes to sudden cardiac death is poorly defined, but it has been suggested that frequent ventricular premature complexes (>5-10/min) are associated with an increased risk for sudden cardiac death. However, it has been reported that the suppression of ventricular premature complexes using antiarrhythmic drugs does not reduce the risk of sudden cardiac death in patients following myocardial infarction (2,3). At this time, treatment of ventricular premature complexes is primarily aimed at symptomatic alleviation rather than at prolongation of survival.

2.2. Sinus Tachycardias

2.2.1. Physiological Sinus Tachycardia

Physiological sinus tachycardia represents a normal response to a variety of physiological conditions (anxiety and exercise) and pathological stresses (fever, hypotension, thyrotoxicosis, hypoxemia, and congestive heart failure). Sinus tachycardia rarely exceeds 200 beats/min; it should not be treated for itself, but its causes must be explored (e.g., exercise, fever, anemia, hyperthyroidism), and some of these (e.g., fever, anemia, hyper-thyroidism) may require therapy.

2.2.2. Inappropriate Sinus Tachycardia

Inappropriate sinus tachycardia is characterized by an increased resting heart rate (>100 beats/min) and an exaggerated heart rate response to minimal stress, usually associated with markedly distressing symptoms (palpitations, fatigue, anxiety, and shortness of breath). The etiologies and underlying mechanisms are unclear. Care must be taken in diagnosing inappropriate sinus tachycardia to exclude secondary sinus tachycardia and to correlate symptoms with tachycardia. Electro-physiological study can be used to exclude atrial tachycardia located close to the sinus node. p-Blockers and calcium channel blockers can be used to treat inappropriate sinus tachycardia, although often with imperfect results. Radiofrequency modification of the sinus node may be considered if drug therapy fails.

2.3. Paroxysmal Supraventricular Tachycardias

Paroxysmal supraventricular tachycardias are a group of supraventricular tachycardias with sudden onset and termination. They are usually recurrent.

2.3.1. Sinus Nodal Reentry Tachycardia

Sinus nodal reentry tachycardia is relatively rare (accounting for approx 3% of all paroxysmal supraventricular tachycardias) and tends to occur mainly in older individuals with other manifestations of sinus node disease. The average rate of sinus nodal reentry tachycardia is 130-140 beats/min. Its P-wave morphology is identical, or very similar, to the sinus P wave. Vagal maneuvers can slow or terminate the tachycardia because it reenters within a region of the heart (i.e., the sinus node) that is heavily influenced by vagal (parasympathetic) nerve endings. Sinus nodal reentry tachycardia should be suspected in anxiety-related sinus tachycardia. p-Blockers and calcium channel blockers (e.g., verapamil, diltiazem) as well as ablation are considered treatment options.

2.3.2. Atrial Tachycardias

Atrial tachycardias, sometimes also called "primary" atrial tachycardias, refer to those tachyarrhythmias that arise in atrial

Refractoriness Nerve

Fig. 2. Schema of the typical atrioventricular nodal (AVN) reentry tachycardia. The atrioventricular node has a slow pathway (a) with short refractoriness and a fast pathway (P) with long refractoriness. (A) During sinus rhythm, the impulse conducts the ventricles through the fast pathway, yielding a normal PR interval. The impulse simultaneously goes down the slow pathway, but cannot conduct to the His bundle antegradely or retrogradely to the fast pathway because it is rendered refractory by the prior beat conducted in the fast pathway. (B) An atrial premature complex reaches the effective refractory period of the fast pathway and is blocked in the fast pathway. This atrial premature complex is able to conduct slowly down to the slow pathway, yielding a prolonged PR interval. The delay in conduction over the slow pathway gives rise to enough time for the fast pathway to recover and allow the impulse conducted from the slow pathway to continue over the fast pathway retrogradely to the atria, producing an atrial echo beat. At the same time, the returned impulse tries to conduct down over the slow pathway and fails because of unrecovered refractoriness of the slow pathway. (C) A sufficiently early atrial premature complex occurs, producing a similar echo beat as in Fig. 2B. However, the returned impulse is able to conduct down over the slow pathway, repeatedly producing another ventricular beat and atrial echo (i.e., supraventricular tachycardia, SVT). Reprinted from ref. 4 with permission. © 1993, Lippincott, Williams, and Wilkins.

Fig. 2. Schema of the typical atrioventricular nodal (AVN) reentry tachycardia. The atrioventricular node has a slow pathway (a) with short refractoriness and a fast pathway (P) with long refractoriness. (A) During sinus rhythm, the impulse conducts the ventricles through the fast pathway, yielding a normal PR interval. The impulse simultaneously goes down the slow pathway, but cannot conduct to the His bundle antegradely or retrogradely to the fast pathway because it is rendered refractory by the prior beat conducted in the fast pathway. (B) An atrial premature complex reaches the effective refractory period of the fast pathway and is blocked in the fast pathway. This atrial premature complex is able to conduct slowly down to the slow pathway, yielding a prolonged PR interval. The delay in conduction over the slow pathway gives rise to enough time for the fast pathway to recover and allow the impulse conducted from the slow pathway to continue over the fast pathway retrogradely to the atria, producing an atrial echo beat. At the same time, the returned impulse tries to conduct down over the slow pathway and fails because of unrecovered refractoriness of the slow pathway. (C) A sufficiently early atrial premature complex occurs, producing a similar echo beat as in Fig. 2B. However, the returned impulse is able to conduct down over the slow pathway, repeatedly producing another ventricular beat and atrial echo (i.e., supraventricular tachycardia, SVT). Reprinted from ref. 4 with permission. © 1993, Lippincott, Williams, and Wilkins.

tissue because of abnormal automaticity or reentry phenomenon. They are classified separately from sinus node reentry or atrioventricular nodal reentry (see Section 2.3.3.) despite the fact that these tachyarrhythmias also arise in the atria. A typical atrial tachycardia has an atrial rate of 150-200 beats/min with a P-wave morphology different from that of sinus P wave. Atrial tachycardia accounts for 5-10% of all paroxysmal supraventricular tachycardias. Atrioventricular block may develop without interrupting the tachycardia. Atrial tachycardia may be caused by automaticity or triggered activity as well as reentry.

Automatic atrial tachycardia has the following features:

1. It cannot be initiated or terminated by atrial stimulation.

2. The first P wave of the tachycardia is the same as the subsequent P waves of the tachycardia.

3. Its rate is often accelerated after initiation until stabilized (at 100-175 beats/min), the so-called warm-up phenomenon.

4. A premature atrial stimulation can reset automatic atrial tachycardia with full or incomplete compensatory pause, usually accompanied by a constant return cycle.

5. Overdrive suppression is a hallmark of automaticity. Both reentrant and automatic atrial tachycardia can be corrected by ablation therapy.

2.3.3. Atrioventricular Nodal Reentry Tachycardia

Atrioventricular nodal reentry tachycardia is the most common of paroxysmal supraventricular tachycardias (elicited in 50-65% of such patients) and usually presents as a narrow QRS complex with regular rates between 120 and 250 beats/min. In the absence of Wolff-Parkinson-White syndrome, atrioven-

tricular nodal reentry tachycardia and atrioventricular reentry tachycardia, using a concealed bypass tract, account for more than 90% of all paroxysmal supraventricular tachycardias.

A schematic representation of a typical atrioventricular nodal reentry circuit is shown in Fig. 2 (4). Retrograde P waves may be absent and buried in the QRS complexes or appear as distortions at the terminal parts of the QRS complex. Atrioventricular nodal reentry tachycardia can be reproducibly initiated and terminated by appropriately timed atrial extrastimuli; this is routinely done as part of the diagnostic electrophysiological catheter evaluation of patients in whom this arrhythmia is suspected. Atrial premature complexes that initiate atrioventricular nodal reentry tachycardia are usually associated with a prolonged PR interval.

In intracardiac recordings, the onset of atrioventricular nodal reentry tachycardia is almost always associated with a prolonged AH interval, which produces sufficient conduction delay in the so-called slow atrioventricular nodal pathway (Fig. 2) to ensure recovery of the fast pathway and permit it to conduct retrogradely back toward the atrium, thereby completing the reentry circuit. A critical balance between conduction delay and recovery of refractoriness is required to sustain the tachycardia. Simultaneous conduction to the ventricles in an antegrade direction and to the atria in a retrograde direction often leads to the buried P wave in the QRS complex. The RP interval is therefore less than 80-100 ms in atrioventricular nodal reentry tachycardia. In contrast, in atrioventricular reentry tachycardia, ventricles and atria are activated sequentially, and the RP interval is expected to be longer than 80 ms on ECGs.

Left Concealed Accessory Pathway

Fig. 3. (A) Atrioventricular reentry tachycardia using a left-sided concealed accessory pathway. (B) Left bundle branch block prolongs the tachycardia cycle length by 50 ms because of the conduction delay of the tachycardia circuit in the left ventricle. AVN, atrioventricular node; HB, His bundle; LA, left atrium; LBB, left bundle branch; LV, left ventricle; RA, right atrium; RBB, right bundle branch; RV, right ventricle. Reprinted from ref. 4 with permission. © 1993, Lippincott, Williams, and Wilkins.

Fig. 3. (A) Atrioventricular reentry tachycardia using a left-sided concealed accessory pathway. (B) Left bundle branch block prolongs the tachycardia cycle length by 50 ms because of the conduction delay of the tachycardia circuit in the left ventricle. AVN, atrioventricular node; HB, His bundle; LA, left atrium; LBB, left bundle branch; LV, left ventricle; RA, right atrium; RBB, right bundle branch; RV, right ventricle. Reprinted from ref. 4 with permission. © 1993, Lippincott, Williams, and Wilkins.

Acute treatment of atrioventricular nodal reentry tachycardia includes: (1) vagal maneuvers (e.g., carotid sinus massage, Valsalva maneuver); (2) adenosine injection; (3) administration of verapamil, diltiazem, and/or (4) ^-blockers; or electrical (direct current) cardio-version. Drugs used for longer term prevention of recurrences of atrioventricular nodal reentry tachycardia include digitalis (currently not often recommended because of low effectiveness), ^-blockers, calcium channel blockers, and class Ia and Ic antiarrhythmic drugs. However, the most important advance in the treatment of atrioventricular nodal reentry tachycardia is transcatheter ablation (principally of the "slow"-pathway region). Catheter ablation, in experienced hands, cures atrioventricular nodal reentry tachycardia in almost 100% of cases.

2.3.4. Atrioventricular Reentry Tachycardia Using Concealed Accessory Pathway

Accessory conduction pathways remaining from embryonic development of the heart can create the substrate for reentry paroxysmal supraventricular tachycardia. The most common form of accessory pathway connects the atria to the ventricle (i.e., an accessory atrioventricular connection). This connection is made up of working muscle tissue, but is so small it is usually invisible, even during cardiac surgery. When these connections conduct in the antegrade direction (i.e., from atrium to ventricle), they necessarily modify the QRS configuration, usually by virtue of earlier-than-expected activation of part of the ventricular muscle (i.e., preexcitation). The classic case is the "delta" wave observed at the onset of the QRS in Wolff-Parkinson-White syndrome.

In some cases, accessory connections only conduct in the retrograde direction (i.e., ventricle to atrium). In these cases, there can be no ECG footprint because ventricular preexcitation does not occur (thus the term "concealed" accessory connec tions). Nevertheless, because retrograde conduction can occur, a reentry tachycardia is possible. This form of accessory pathway most often occurs on the left side of the heart. Atrioventricular reentry tachycardias account for approx 30% of all paroxysmal supraventricular tachycardias.

The impulse circulates antegradely through the atrioventricular node and retrogradely through the concealed accessory pathway (Fig. 3) (4). Both the atria and ventricles are parts of the reentry circuit. Because atrial activation always follows ventricular activation, the P wave usually occurs after the QRS complexes (RP interval > 80 ms). Atrioventricular reentry tachycardia can be initiated and terminated by either atrial or ventricular extrastimuli. Even when the His bundle is refractory, a ventricular premature complex may be able to reset the atria through accessory pathways.

In contrast to the concentric atrial activation sequences in atrioventricular nodal reentry tachycardia, the atrial activation sequences in atrioventricular reentry tachycardia are eccentric when the accessory pathways are located away from atrio-ventricular node. Medical treatment of atrioventricular reentry tachycardia is similar to that of atrioventricular nodal reentry tachycardia.

Transcatheter ablation is highly effective for eliminating accessory atrioventricular connections. Utilized to correct the problem, mapping and ablation are currently effective in 9599% of cases.

2.3.5. Wolff-Parkinson-White Syndrome

When there are one or more accessory atrioventricular pathways or connections that conduct in the antegrade direction, the ventricles are preexcited to a varying degree as discussed in Section 2.3.4. The Wolff-Parkinson-White syndrome is applied when tachyarrhythmias occur in the setting of preexcitation. Tachycardias associated with this syndrome include: (1) orthodromic (antegradely through normal atrioventricular conduction system and retrogradely through atrioventricular accessory pathways); (2) antedromic (antegradely through atrioventri-cular accessory pathways and retrogradely through normal atrioventricular conduction system or another accessory connection); and (3) atrial flutter/fibrillation (activating the ventricles antegradely through both normal atrioventricular conduction system and atrioventricular accessory pathways), as well as other supraventricular tachycardias.

The ECG features of a typical atrioventricular connection (Fig. 4) are: (1) shortened PR intervals less than 120 ms during sinus rhythm, (2) widened QRS durations, and (3) presence of delta waves (a slurred, slowly rising onset of the QRS). The terminal QRS portion is usually normal; sometimes, it is associated with secondary ST-T changes.

In addition to typical atrioventricular pathways, other variants may exist, such as atriohisian, atriofascicular, nodofas-cicular, and nodoventricular fibers. Lown-Guang-Levine syndrome is applied to recurrent paroxysmal tachycardias (or atrial fibrillation) associated with a short PR interval and a normal QRS complex. Its presumed mechanisms include atriohisian fibers, preferential intranodal pathways or enhanced atrioven-tricular conduction, and posterior intranodal pathways or an anatomically small atrioventricular node.

Delta Waves Mahaim Fibers
Fig. 4. Wolff-Parkinson-White syndrome with a right posterior septal accessory pathway. See text for discussion.

Mahaim fibers were initially recognized as a nodoventricular bypass tract and now include atriofascicular, nodofascicular, nodoventricular, and fasciculoventricular fibers. The majority of these pathways are long right-sided atriofascicular or atrioventricular pathways between the lateral tricuspid and distal right bundle branch in the right ventricular free wall. These fibers almost represent a duplication of the atrioventricular node and are considered capable of only antegrade conduction. Therefore, only "preexcited tachycardia" can result from Mahaim fibers. Often, preexcitation is not initially apparent, but can be exposed by premature right atrial stimulation. The ECG tends to exhibit a left bundle branch block type of morphology with a leftward frontal axis similar to that associated with right ventricular apical pacing.

As a rule, accessory pathways conduct faster than the atrio-ventricular node, but have a longer refractory period and are therefore prone to conduction block at longer cycle lengths (e.g., a premature beat will tend to block at a longer coupling interval than is the case for the atrioventricular node). Furthermore, accessory pathways do not usually manifest decremen-tal conduction at faster pacing rates. An incessant form of supraventricular tachycardia has been recognized that is usually associated with a slow-conducting posteroseptal accessory pathway as its retrograde limb. The presence of an accessory pathway is not necessarily involved in the mechanism of tachycardia (a bystander). Atrioventricular echoes or atrioventricular reentry tachycardia may be present in 1520% of patients after successful ablation of accessory pathways.

It is estimated that 10-35% of patients with preexcitation experience atrial fibrillation at some point in their life times. In fact, atrial fibrillation and atrial flutter may be the presenting arrhythmias in up to 20% of patients with accessory atrioventricular pathways. In patients with Wolff-Parkinson-White syndrome, atrial tachyarrhythmias that conduct extremely rapidly (via the accessory pathway) to the ventricles may lead to syncope, ventricular fibrillation, or sudden cardiac death. A grossly irregular RR interval with widened QRS complexes and extremely rapid ventricular rates should immediately suggest the presence of antegrade accessory atrioventricular pathway conduction associated with atrial fibrillation (Fig. 5).

Patients with atrial fibrillation in the presence of an accessory pathway are at increased risk of developing ventricular fibrillation if the shortest preexcited RR interval during atrial fibrillation is less than 250 ms. Intravenous procainamide is the acute treatment of choice for hemodynamically stable preexcited atrial fibrillation. Intravenous atrioventricular nodal blocking agents, such as digoxin and verapamil, are con-traindicated in these patients because they may paradoxically enhance antegrade atrioventricular conduction via the accessory pathway conduction, resulting in hypotension or cardiac arrest. Patients who are hemodynamically unstable require immediate direct current cardioversion. As noted, it is likely that most episodes of atrial fibrillation may result from degeneration of orthodromic atrioventricular tachycardia (tachycardia-induced tachycardia). Successful ablation of the accessory atrioventricular pathway eliminates atrial fibrillation in most of these patients.

Radiofrequency ablation of the accessory pathway is the long-term (curative) treatment of choice for symptomatic patients with Wolff-Parkinson-White syndrome; it is safe and effective in more than 95-99% of patients.

Exame Psicotecnico

2.4. Atrial Flutter and Fibrillation

2.4.1. Atrial Flutter

Atrial flutter is characterized by an atrial rate between 250 and 350 beats/min, usually accompanied by 2:1 atrioventricular conduction and resulting in a ventricular rate of approx 150 beats/min. Classical flutter waves (F waves) are regular sawtoothlike atrial activity, most prominent in inferior leads and V1. Atypical F waves may manifest like atrial tachycardia, with a rate between 200 and 300 beats/min in surface ECG, particularly with antiarrhythmic drug therapy. Some atrial flutter may be terminated by rapid atrial pacing (type I atrial flutter) and may not be pace terminable (type II atrial flutter) (5). Although antiarrhythmic drugs may be useful to prevent recurrence of atrial flutter, they are less effective to convert to sinus rhythm. Direct current cardioversion is most effective for treatment of atrial flutter.

Typical atrial flutter is a macroreentrant rhythm confined to the right atrium. The tachycardia circulates around the atrium, but must pass through a relatively narrow isthmus of tissue between the inferior vena cava and the tricuspid valve annulus. Ablation creating conduction block in this isthmus is highly effective; as a result, typical atrial flutter can be easily ablated. Ablation is the treatment of choice in most of these patients. Although systemic embolization is less common in atrial flutter than in atrial fibrillation, anticoagulation in atrial flutter should follow the guidelines for the management of atrial fibrillation (6).

2.4.2. Atrial Fibrillation

Atrial fibrillation is an uncoordinated atrial tachyarrhythmia characterized on ECG by the absence of distinct P-waves before each QRS complex, the presence of rapid atrial oscillations (F-

waves), and variable RR intervals (Fig. 6). Paroxysmal atrial fibrillation is arbitrarily defined as lasting more than 2 min and less than 7 d and may be self-terminating in less than 48 h or persistent (lasting longer than 48 h). An episode of atrial fibrillation lasting longer than 7 d is termed chronic. If a number of attempts of cardioversion have failed or are not indicated in chronic forms (>1 yr), atrial fibrillation is regarded as permanent. When no history is available, the term recent or new onset is often used.

The incidence of atrial fibrillation is strongly age dependent, with a substantial increase of occurrences between the ages of 50 and 60 yr (6.2% in men and 4.8% in women 65 yr or older). In addition to age, other common cardiac precursors include a history of congestive heart failure, valvular heart disease, hypertension, and coronary artery disease. Yet, rheumatic heart disease, together with overt heart failure, is considered as the most powerful predictor for atrial fibrillation. Atrial fibrillation is also common following acute myocardial infarction (10%) or cardiac surgery (~35%), which is usually self-limited. Noncardiac precursors include thyrotoxicosis and pulmonary pathology leading to hypoxemia. Lone atrial fibrillation is said to be present when the tachyarrhythmia occurs in the absence of underlying structural heart disease or transient precipitating factors.

The mechanisms underlying atrial fibrillation include multiple-wavelet reentry and focal-enhanced automaticity. The atrial rate during atrial fibrillation ranges from 350 to 600 beats/min. Because of concealed atrioventricular nodal penetration and subsequent variable degrees of atrioventricular block, the characteristic irregularly irregular ventricular rate is usually between 100 and 160 beats/min in untreated patients with normal atrioventricular conduction properties. Both

Cardiac Cycle Atrial Fibrillation
Fig. 6. Atrial fibrillation. See text for discussion.

branches of the autonomic nervous system can be involved in the initiation, maintenance, and termination of atrial fibrillation (vagally mediated atrial fibrillation and adrenergically mediated atrial fibrillation). Aberrant conduction may occur when a long ventricular cycle is followed by a short cycle (Ashman phenomenon). Atrial fibrillation itself modifies atrial electrical properties in a way that promotes the occurrence and maintenance of the arrhythmia, a process identified as atrial electrical remodeling.

The major adverse clinical consequences of atrial fibrillation include palpitations, impaired cardiac function, and an increased potential for thromboembolism. Physical findings include an irregularly irregular ventricular rhythm, variations in the intensity of the first heart sound, and the absence of a waves in the jugular venous pulse. A peripheral pulse deficit (pulse rate less than heart rate) is often noted during a fast ventricular response. Patients with continuous rapid ventricular rates for a prolonged period are at risk of developing a tachycardia-induced cardiomyopathy.

The ultimate goal of therapies for atrial fibrillation is improvement of symptoms, that is, reduction of atrial fibrillation-associated morbidity and improvement in prognosis. The three basic tenets of therapy for atrial fibrillation are: (1) control of ventricular rate response; (2) restoration and maintenance of sinus rhythm; and (3) prevention of thromboembolism.

A resting ventricular rate under 90 beats/min and ventricular rates between 90 and 115 beats/min during moderate exercise are considered optimal. Commonly used drugs for rate control include p-blockers, calcium channel blockers, and digoxin. In general, sinus rhythm is preferable to atrial fibrillation, as long as it can be achieved and maintained with relative safety.

Approximately 50% of patients with recent onset of atrial fibrillation will convert spontaneously to sinus rhythm within 48 h. Potential precipitating factors should be sought and treated. Sinus rhythm can normally be restored in such cases, either pharmacologically or electrically. Class Ia, Ic, and III antiarrhythmic drugs all have the potential to restore sinus rhythm. Flecainide is a good choice for patients without coronary artery disease or significant left ventricular dysfunction; otherwise, class III agents should be used. Ibutilide and dofetilide have been shown to be effective in the treatment of atrial fibrillation and atrial flutter, particularly in atrial fibrillation following cardiac surgery or for patients in whom direct current cardioversion is not ideal. Approximately 50% of such patients remain in sinus rhythm when treated with various class I and III drugs (6 mo to 3 yr).

Single- or dual-site atrial pacing may also be useful for prevention of recurrence of paroxysmal atrial fibrillation. Implant-able atrial defibrillators have been introduced for treatment of recurrent atrial fibrillation. The surgical Maze procedure and catheter ablation may also be considered in refractory patients.

For elective cardioversion of atrial fibrillation lasting longer than 48 h, patients should be anticoagulated for 3-4 weeks before and after cardioversion regardless of their risk of embolization. Transesophageal echocardiography combined with short-term heparin infusion has gained acceptance as an alternative rapid preparation for direct current cardioversion. However, postcardioversion atrial stunning may create a favorable milieu for thrombogenesis, and embolization may occur despite a negative transesophageal echocardio-graphy. Hence, adequate anticoagulation is pivotal in preventing spontaneous embolism in patients with atrial fibrillation.

What Ventricular Fibrillation
Fig. 7. (A) Ventricular tachycardia, (B) ventricular flutter, (C) ventricular fibrillation, and (D) torsades de pointes. See text for discussion.

Table 3

Recommendations for Anticoagulation Therapy in Atrial Fibrillation by the American College of Chest Physicians

Table 3

Recommendations for Anticoagulation Therapy in Atrial Fibrillation by the American College of Chest Physicians


No risk factors

With any high-risk factors

< 65 years



65-75 years



> 75 years



Source: Modified from ref. 7.

Source: Modified from ref. 7.

In addition to rheumatic mitral valve disease and prosthetic valves (mechanical or tissue valves), major risk factors of embolization in nonvalvular atrial fibrillation include: (1) a prior history of ischemic stroke (or transient ischemic attack); (2) congestive heart failure or left ventricular dysfunction (ejection fraction < 35%); (3) advanced age (>65-75 yr old); (4) hypertension; (5) coronary artery disease (particularly myocardial infarction); (6) diabetes; (7) left atrial thrombus; (8) thyrotoxicosis; (9) increased left atrial size (>50 mm); and/or (10) left atrial mechanical dysfunction. Atrial fibrillation patients with any risk factors as listed should be treated with warfarin to achieve an INR (international normalized ratio) of 2.0-3.0 (target INR 2.5) (Table 3) (7). Anticoagulation therapy reduces stroke risk by 68% (4.5 vs 1.4%), yet the major concern with anticoagulation therapy is bleeding, especially in elderly pa tients (>75 yr old) or when the patient's INR is greater than 4.0. A complete guideline for management of atrial fibrillation was published in October 2001 (6).

2.5. Ventricular Tachyarrhythmias 2.5.1. Ventricular Tachycardias

Although ventricular tachycardias can occur in a clinically normal heart, they generally accompany some form of structural heart disease; this is particularly true for patients with prior myocardial infarction. A fixed substrate, such as an old infarct scar, is most often responsible for episodes of recurrent monomorphic ventricular tachycardia. Yet, acute ischemia may play an even more important role in the pathogenesis of polymorphic ventricular tachycardia or ventricular fibrillation.

Ventricular tachycardia is characterized on an ECG by a wide QRS complex tachycardia at a rate of more than 100 beats/ min (Fig. 7). Like ventricular premature complexes, ventricular tachycardias can be monomorphic (Fig. 7A) or polymorphic.

Sustained ventricular tachycardia is defined as ventricular tachycardia persisting more than 30 s or requiring termination because of hemodynamic compromise. Nonsustained ventricular tachycardia refers to ventricular tachycardia lasting longer than 3 consecutive beats but less than 30 s. Bidirectional ventricular tachycardia is defined as ventricular tachycardia that shows an alternation in QRS amplitude and axis.

The key marker of ventricular tachycardia on an ECG is ventricular atrial dissociation. Capture and fusion beats also support the diagnosis of ventricular tachycardia; sustained ventricular tachycardia is almost always symptomatic. Nevertheless, the presentation, prognosis, and management of ventricular tachycardia largely depend on the underlying cardiovascular state.

Procainamide and amiodarone are commonly administered for the acute termination of ventricular tachycardia. Yet, an implantable cardioverter-defibrillator, with and without amiodarone, is the most established long-term therapy for ventricular tachycardia. In some cases, ablation provides a cure for normal heart ventricular tachycardia, bundle branch reentry ventricular tachycardia, and selected ischemic ventricular tachycardia. However, as left ventricular function is more severely impaired, it may be prudent to place an implantable cardioverter-defibrillator, even after an apparently successful ablation.

2.5.2. Ventricular Flutter and Ventricular Fibrillation

Electrocardiographically, ventricular flutter (Fig. 7B) usually appears as a "sine wave" with a rate between 150 and 300 beats/min. It is impossible to assign a specific morphology to these oscillations. Ventricular fibrillation (Fig. 7C) is recognized by grossly irregular undulations of varying amplitudes, contours, and rates, which are often preceded by a rapid repetitive sequence of ventricular tachycardia. Spontaneous conversion of ventricular fibrillation to sinus rhythm is rare. Prevention of sudden cardiac death in these patients predominantly depends on implantable cardioverter-defibrillators.

2.5.3. Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm can be regarded as a type of slow ventricular tachycardia with a rate between 60 and 110 beats/min, usually occurring in acute myocardial infarction, particularly during perfusion. Because the rhythm is usually transient and rarely causes significant hemodynamic compromise, treatment is rarely required.

2.5.4. Torsade de Pointes

When polymorphic ventricular tachycardia occurs in the presence of prolonged QT intervals (congenital or required), it is termed torsade de pointes. It is often preceded by ventricular premature complexes with a long-short sequence (Fig. 7D). Torsade de pointes often has multiple episodes causing recurrent syncope and may generate into ventricular fibrillation, leading to death. Identification of torsades de pointes has important therapeutic implications because its treatment is completely different from that of common polymorphic ventricular tachycardia. Magnesium, pacing, and isoproterenol can be used to treat torsades de pointes if required. Left cervicothoracic sympathectomy has been proposed as a form of therapy for torsades de pointes in patients with congenital long QT syndrome.

2.5.5. Nonparoxysmal Junctional Tachycardia

A nonparoxysmal junctional tachycardia rhythm is recognized by a QRS complex identical to that of sinus rhythm at a rate between 70 and 130 beats/min, usually associated with a warm-up period at its onset. This type of tachycardia frequently results from conditions that produce enhanced automaticity or triggered activity in the atrioventricular junction, such as inferior acute myocardial infarction, digitalis intoxication, and postvalve surgery. Treatment should be directed toward the underlying diseases.

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