Cardiac Arrhythmias

II. Cardiac Arrhythmias
A. Introduction
Bradyarrhythmias result from inadequate sinus nodal impulse production or from blocked impulse propagation, and usually are not cause for concern unless syncope or presyncope develops. Sustained atrial tachyarrhythmias usually permit adequate cardiac output and are less dangerous than sustained ventricular arrhythmias, which often cause collapse or death.
B. Atrial tachyarrhythmias
The atrial tachyarrhythmias can be classified into two subcategories: those that produce a regular cardiac rhythm and those that produce an irregular cardiac rhythm. In general, atrial tachyarrhythmias do not interfere with inter- or intraventricular conduction of the cardiac impulse, and therefore the QRS complex (which is generated from the ventricles) remains narrow in form. Occasionally, however, atrial arrhythmias cause aberrant ventricular conduction with a wide QRS complex, which may mimic arrhythmias of ventricular origin.




1. Regular atrial tachycardias
a. Sinus tachycardia. Sinus tachycardia represents an increase in the sinus rate (>100 bpm) and is usually secondary to some other disease process. In general, the physician should treat the condition that is causing the sinus tachycardia, not the tachycardia itself. However, in some patients, such as those with coronary artery disease, sinus tachycardia must be controlled to prevent myocardial ischemia. In this instance, خ²-blocking agents or calcium antagonists (either verapamil or diltiazem) may be effective in controlling heart rate.
b. Supraventricular tachycardia (SVT). The most common form of SVT is AV nodal reentry tachycardia (AVNRT).
(1) ECG identification. In SVT, the ECG shows regular, narrow QRS complexes without identifiable P waves at a rate of 150–200 bpm (Figure 1-2A).
(2) Therapy. AVNRT is due to re-entry within the compact AV node. Therapies that slow conduction or increase refractoriness usually succeed.
(a) Mechanical maneuvers such as carotid sinus massage and the Valsalva maneuver are often effective in terminating the arrhythmia. These are especially important because they can be self-administered by the patient prior to seeking medical assistance.
(b) Medical therapy. Intravenous (IV) adenosine is the medical treatment of choice. Less commonly used agents include verapamil or خ²-blockers.
c. Atrial flutter usually occurs in patients with antecedent heart disease, including coronary artery disease, pericarditis, valvular heart disease, and cardiomyopathy. Atrial flutter is characterized by an atrial rate of 220–400 bpm and is usually conducted to the ventricle with block so that the ventricular rate is a fraction of the atrial rate. Occasionally, atrial flutter may be conducted irregularly. Treatment is the same as for regular atrial flutter.
(1) ECG identification. As shown in Figure 1-2B, this arrhythmia produces a classic sawtooth pattern on the ECG. In this example, there is 4:1 AV block with an atrial rate of 300 bpm and a ventricular rate of 75 bpm.
(2) Therapy
(a) Although intravenous administration of digoxin, esmolol, or verapamil may be effective in converting the arrhythmia to normal sinus rhythm, conversion is less likely than
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in paroxysmal atrial tachycardia. Usually these medications control the ventricular response, which, in turn, helps maintain hemodynamic stability. Once the ventricular rate has slowed as a result of increased AV block (3:1 or 4:1 conduction), ibutilide or another antiarrhythmic agent can be administered to restore sinus rhythm.

FIGURE 1-2 Atrial tachycardias: A. Supraventricular tachycardia, B. Atrial flutter, C. Atrial fibrillation, D. Multifocal atrial tachycardia. (From Stein E. Rapid Analysis of Arrhythmias: A Self-Study Program. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999:91,66,68.)

(b) If medical therapy does not convert the patient to normal sinus rhythm, atrial flutter will usually self-convert over time, either to atrial fibrillation or to normal sinus rhythm.
(c) As in all arrhythmias, direct current (DC) cardioversion is necessary if the arrhythmia has already produced hemodynamic instability.
2. Irregular atrial tachycardias




a. Atrial fibrillation. Atrial fibrillation is an irregularly irregular arrhythmia in which there is no ordered contraction of the atria but, rather, multiple discoordinate wave fronts of depolarization that send a large number of irregular impulses to depolarize the AV node. The irregular impulses produce an irregular ventricular response, the rate of which depends on the number of impulses that are conducted through the AV node. Selected causes of atrial fibrillation include stress, fever, excessive alcohol intake, volume depletion, pericarditis, coronary artery disease, MI, pulmonary embolism, mitral valve disease, thyrotoxicosis, and idiopathic atrial fibrillation.
(1) ECG identification. An example of atrial fibrillation is shown in Figure 1-2C.
(2) Therapy
(a) If patients with atrial fibrillation are hemodynamically unstable or demonstrate an increase in angina pectoris or worsening of CHF, immediate DC synchronous cardioversion is indicated.
(b) If patients are hemodynamically stable, the physician should first focus on controlling the ventricular response to the atrial fibrillation by the intravenous administration of خ²-blockers, nondihydropyridine calcium channel blockers, or digoxin.
(c) In the absence of a contraindication, systemic anticoagulation should be instituted with unfractionated or low–molecular-weight heparin (LMWH). Oral warfarin should be started after heparin.
(d) Cardioversion can be considered immediately after a transesophageal echocardiogram, provided no intracardiac thrombus is visualized, or after 4–6 weeks of adequate oral anticoagulation with warfarin.
(e) In the absence of a reversible cause, long-term anticoagulation should be considered.
b. Multifocal atrial tachycardia. In this arrhythmia, there is synchronous atrial contraction, but the contraction arises from many sites in the atria, not from the sinus node. In the majority of cases of multifocal atrial tachycardia, patients have significant medical comorbidities.
(1) ECG identification. The multiple sites of origin of the atrial contraction produce many different P-wave configurations and different R-R intervals. At least three different P-wave morphologies are required to make this diagnosis (Figure 1-2D).
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(2) Therapy. Treatment is directed primarily at managing medical comorbidities. If these measures fail, خ²-blockers or nondihydropyridine calcium channel blockers may be useful in controlling the heart rate.
C. Bradyarrhythmias
Bradyarrhythmias occur when sinus node impulse generation is slowed or when normal sinus node impulses cannot be conducted to the ventricles because of AV nodal block or ventricular conducting system disease. In general, bradyarrhythmias are a cause for concern only when patients have become symptomatic with presyncope or syncope from the reduced cardiac output that the low heart rate produces. Medications such as خ²-blockers, nondihydropyridine calcium channel blockers, and digoxin may contribute to bradyarrhythmias.




1. Sinus bradycardia
a. Sinus bradycardia may be a physiologic and normal response to cardiovascular conditioning, as in trained athletes. In such cases, the arrhythmia is obviously a normal finding and requires no therapy. However, extreme sinus bradycardia (<>



D. Ventricular tachyarrhythmias
1. Types of ventricular arrhythmias (Figure 1-4)
a. Premature ventricular contraction (PVC). In this arrhythmia, heart beats arise directly from the ventricles, bypassing the specialized cardiac His-Purkinje conduction system.
(1) ECG identification
(a) Because the His-Purkinje system is bypassed, the QRS configuration is typically widened and bizarre in appearance.
(b) PVCs usually do not affect atrial depolarization, which proceeds normally and in dissociation with the PVC. Thus, the next sinus beat occurs at the same time it would have occurred if no PVC had been present. Accordingly, a full compensatory pause usually follows a PVC (Figure 1-4A). The normally occurring P wave is usually buried in the PVC–QRS complex.
(2) Therapy. Most isolated PVCs are benign and should not be treated.
b. Ventricular tachycardia is a regular rhythm that occurs paroxysmally and exceeds 120 bpm. AV dissociation, which causes the ventricular arrhythmia to proceed independently of the normal atrial rhythm, is the hallmark of the arrhythmia. During ventricular tachycardia, cardiac relaxation is impaired. This factor, together with loss of AV synchrony (i.e., loss of the atrial “kickâ€‌) and loss of the electrical coordination of the contraction by the His-Purkinje system, usually leads to severely reduced cardiac output, producing hypotension. Sustained ventricular tachycardia is usually a life-threatening arrhythmia that degenerates into ventricular fibrillation and death if untreated.
(1) Physical examination. In many cases of ventricular tachycardia, severe decompensation precludes performance of a detailed physical examination.
(a) If patients are relatively stable, physical diagnosis reveals AV dissociation, manifested by the appearance of cannon a waves in the neck veins. These waves occur intermittently when right atrial contraction occurs during ventricular contraction. Because the atrial blood cannot go forward against the closed tricuspid valve, backward flow produces a large bulge in the neck veins.

FIGURE 1-4 Ventricular arrhythmias. A. Premature ventricular contraction, B. Monomorphic ventricular tachycardia, C. Polymorphic ventricular tachycardia (torsades de pointes), D. Ventricular fibrillation. (From Stein E. Rapid Analysis of Arrhythmias: A Self-Study Program. 3rd ed. Philadelphia: Lippincott Williams & Wilkins, 1999:100,110–112.)

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(b) Variability in intensity of the S1, caused by variable positioning of atrial and ventricular contraction, can be auscultated.
(2) ECG identification (Figure 1-4B,C)
(a) The QRS complex is widened and bizarre in appearance because the arrhythmia does not use the specialized conducting system of the heart. Because the ventricles are operating independently of the atria, there is no constant relationship between the P wave and the QRS complex.
(b) The QRS complex may be monomorphic (i.e., of one shape), as shown in Figure 1-4B, or it may be polymorphic, as shown in Figure 1-4C. When the axis of a polymorphic arrhythmia appears to revolve about a central point and is associated with a prolonged QT interval, the arrhythmia is termed torsades de pointes.
(3) Therapy
(a) In hemodynamically unstable patients, DC cardioversion is urgently required.
(b) Stable patients with monomorphic ventricular tachycardia may be treated with IV amiodarone.
(c) Polymorphic ventricular tachycardia requires defibrillation. Common causes are ischemia, electrolyte abnormalities, and drugs that prolong the QT interval.
c. Ventricular fibrillation is characterized by a lack of ordered contraction of the ventricles; therefore, there is no cardiac output. Thus, ventricular fibrillation is synonymous with death unless conversion to an effective rhythm can be accomplished. The physician should begin cardiac resuscitation, including mechanical ventilation, cardiac compression, and drug and electrical therapy, immediately on recognizing the presence of ventricular fibrillation (Figure 1-4D).
2. Prevention and treatment of ventricular arrhythmias. Online Table 1-1 lists the current classification and some of the side effects of drugs currently available for long-term prevention of ventricular arrhythmias. Drug therapy is used when a patient has had symptomatic or sustained ventricular tachycardia or fibrillation. Today, insertion of an implantable cardiac defibrillator accompanies anti-arrhythmic agents in most cases of life-threatening arrhythmias. Some patients with heart failure symptoms and decreased left ventricular ejection faction may qualify for insertion of an implantable cardiac defibrillator for primary prevention of sudden cardiac death.




ONLINE TABLE 1-1 Antiarrhythmic Agents
Class Major Electrophysiologic
Properties Specific Agents Major Side Effects
Sodium channel Ia Inhibit rapid inward current Quinidine Proarrhythmia
Blockers Prolong repolarization Diarrhea
Procainamide Proarrhythmia
Lupus-like syndrome
Disopyramide Proarrhythmia
Congestive heart failure
Anticholinergic effects
Ib Inhibit rapid inward current Lidocaine CNS effects
Proarrhythmia
CNS effects
Accelerate repolarization Tocainide Neutropenia
Mexiletine CNS effects
Phenytoin CNS effects
Ic Inhibit rapid inward current Flecainide Congestive heart failure
Little effect on repolarization Proarrhythmia
خ²-blockers II Reduce ischemia Propranolol Bradycardia
Bronchospasm
Congestive heart failure
Reduce sympathetic arrhythmogenicity Acebutolol Congestive heart failure
Potassium channel III Prolong action potential duration Amiodarone Pulmonary fibrosis
blockers Hypo- and hyperthyroidism
Bretylium Orthostatic hypotension
Sotalol Proarrhythmia
Ibutilide Proarrhythmia
Calcium channel blockers IV Depress slow inward current Verapamil (atrial arrhythmias) Bradycardia
CNS, central nervous system.