UNIT II: CARDIOVASCULAR CONDITIONS

CHAPTER 7

Arrhythmia

Judy Cheng, PharmD, MPH, BCPS, CHFN, FCCP

An arrhythmia is defined as a disturbance of cardiac electrical conduction. The synchronous interaction between the electrical and the mechanical properties of the heart is important if the heart is to function properly and maintain adequate blood supply and perfusion to other vital body organs. The management of arrhythmias continues to evolve as results of many landmark studies are published.

With the original discovery of surface electrocardiography (ECG) and the availability of intracardiac recordings and programmed cardiac stimulation, there is considerable insight into cardiac electrophysiology. This technology has allowed for sophisticated classification of many arrhythmias.

Cardiac arrhythmias can be broadly classified into two groups: supraventricular (originating above the ventricle) and ventricular (originating from the ventricle) arrhythmias. Common supraventricular arrhythmias include atrial fibrillation, atrial flutter, paroxysmal supraventricular tachycardia (PSVT), sinus tachycardia, and bradycardia. Atrial fibrillation is probably the most common sustained cardiac arrhythmia encountered in primary care practice. The prevalence of atrial fibrillation increases with increasing age and the presence of structural heart disease. Atrial fibrillation is the major cause of stroke, especially in the elderly. Ventricular arrhythmias include premature ventricular contractions (PVCs), monomorphic and polymorphic (such as torsades de pointes) ventricular tachycardia (VT), and ventricular fibrillation (VF).

Multiple antiarrhythmic agents are available for management of these disorders. Unfortunately, many problems are associated with these agents, proarrhythmia being the most significant because it has a potential effect on patient mortality. Fortunately, technical advances have been made in the development of nondrug therapies. Some examples include radiofrequency ablation, the internal cardioverter/defibrillator, and pacemakers.

This chapter discusses the pathophysiology and management of arrhythmias in a primary care setting, with an emphasis on long-term management to prevent complications such as life-threatening ventricular arrhythmias, heart failure, or thromboembolic events.

ANATOMY, PHYSIOLOGY, AND PATHOLOGY

Cardiac Electrical Condition Pathway

The heart is an organ that is capable of producing an intrinsic electrical rhythm and has automaticity. This rhythm may be modified by the autonomic nervous system (sympathetic and parasympathetic nervous systems). In normal cardiac conduction, the electrical activity begins in the sinoatrial (SA) node, known as the pacemaker of the heart. The SA node is located in the upper portion of the right atrium (Figure 7.1).

In adults, the SA node fires at a regular rate of 60 to 100 beats per minute (bpm), which is defined as the normal sinus rhythm (NSR). Following discharge of the SA node, the electrical impulse is conducted through the right atrium, to the left atrium, then to the atrioventricular (AV) node (Figure 7.1). The impulse continues to conduct through the AV node, with a momentary delay, then to the bundle branches. From the bundle branches, the electrical activity is carried to the ventricular muscle by networks of Purkinje fibers. In abnormal cardiac conduction, enhanced automaticity and formation of reentry circuits at certain foci of the heart (either SA node or other latent pacemakers) may lead to tachycardia.

Electrical impulses are capable of conduction through ion channels. The major ion channels include sodium and potassium channels (fast conduction channels), as well as calcium channels (slow conduction channels). They are labeled as fast and slow conduction channels based on the speed of ion influx and efflux. These conduction channels are distributed throughout the myocardium. However, the atrial and ventricular tissue has more sodium and potassium channels compared to calcium channels, and the SA node and the AV node have more calcium channels relative to sodium and potassium channels. Therefore, calcium channel blockers such as verapamil will demonstrate more pharmacological activity at the SA and the AV nodes, as these nodes are where more calcium channels are located. Class I and III antiarrhythmic agents, such as procainamide and amiodarone, are sodium channel blockers and potassium channel blockers, which demonstrate more pharmacological activity in the atrial and ventricular tissue.

The ECG complexes reflect the cardiac electrical activity. Waveforms on the ECG represent electrical conduction of the heart, the P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization (Figure 7.2). The atrial contraction follows the P wave and the ventricular contraction follows the QRS complex. Three key intervals play an important part in ECG interpretation. The PR interval, normally 0.12 to 0.20 seconds in duration, represents the travel of electrical impulse from the SA node through the AV node. A prolongation of the PR interval indicates a delay in AV nodal conduction, known as first-degree heart block. The QRS interval, normally <0.12 seconds in duration, represents the time required for the ventricle to depolarize. Prolongation of the QRS interval may indicate ventricular hypertrophy (it takes longer for a thicker piece of muscle to depolarize) or a defect in the conduction of the Purkinje fibers. The QT interval, normally 0.4 seconds or less, represents the time necessary for ventricular depolarization and repolarization. Prolongation of the QT interval (>0.5 seconds) indicates prolongation of the relative refractory period. During this phenomenon, the ventricles are especially vulnerable to extra stimuli. This increases the risk of developing life-threatening arrhythmias such as torsades de pointes.

Pathophysiology

The mechanisms of tachyarrhythmias (both supraventricular and ventricular) have been classified into two general categories: those resulting from an abnormal impulse generation and those resulting from an abnormal impulse conduction or reentrant tachycardia.

Reentry tachycardia involves indefinite propagation of the impulse and continued activation of previously refractory tissue. Three conduction requirements must be fulfilled for the formation of a viable reentrant focus: There must exist two pathways for impulse conduction with an area of unidirectional block (prolonged refractoriness) and slow conductions in the other pathway.

Different precipitating factors of automaticity and reentry may lead to different types of bradyarrhythmias or tachyarrhythmias. Bradycardia is usually due to sick sinus or AV nodal conduction delay or blockade. Classifications of cardiac arrhythmias are summarized in Table 7.1. Pathophysiology of some of the more clinically significant arrhythmias is discussed in greater detail later in this chapter.

SUPRAVENTRICULAR ARRHYTHMIA

Atrial Fibrillation and Atrial Flutter

In atrial fibrillation, reentry circuits are formed when the atrium is being stretched or disturbed. They take over the SA node and become multiple independent pacemakers of the heart. All of these pacemakers beating independently result in an overall atrial rate of 400 to 600 bpm. In atrial flutter, the mechanism is similar except that there is one instead of multiple reentry circuits.

Paroxysmal Supraventricular Tachycardia

PSVTs include those arrhythmias caused by AV nodal reentry, SA nodal reentry, and intra-atrial reentry. AV nodal reentry is by far the most common form of PSVT. Lown–Ganong–Levine (LGL) syndrome is an example of AV nodal reentry PSVT. Wolff–Parkinson–White (WPW) syndrome is another type of PSVT that involves both the AV node (slow conduction pathway) and an extra nodal AV connection (accessory fast conduction pathway). PSVT types that involve an accessory pathway may be the more common orthodromic (down AV node, up accessory pathway, which usually presents with a narrow/normal QRS interval on ECG), or the less common antidromic (down accessory pathway, up AV node, usually with a wide QRS interval on ECG).

VENTRICULAR ARRHYTHMIAS

Ventricular Tachycardia

VT is defined as three or more repetitive PVCs, occurring at a rate >100 bpm. VT can be subdivided into two major types: monomorphic VT, which has a consistent QRS morphology; and polymorphic VT, which has varying QRS morphology. VT may occur acutely as a result of metabolic abnormalities; electrolyte abnormalities such as hypokalemia or ischemia; organic heart disease such as heart failure or left ventricular aneurysm; or drug toxicities such as digoxin overdose. VT, if sustained for a prolonged period of time, can lead to hemodynamic collapse. Immediate treatment is required.

Torsades de Pointes

Torsades de pointes is a rapid form of polymorphic VT associated with delayed ventricular repolarization (prolonged QT intervals). Table 7.2 lists the common causes of torsades de pointes.

Ventricular Fibrillation

VF is an electrical anarchy of the ventricle, resulting in no blood pressure or cardiac output. VF is a medical emergency that requires advanced cardiac life support measures. VF is often preceded by VT. VF occurs most commonly in patients with ischemic heart disease, WPW, and (less commonly) mitral valve prolapse.

AV, atrioventricular.

EPIDEMIOLOGY

The most common type of arrhythmia, other than atrial and ventricular premature contraction (which most people will experience during their lifetime), is atrial fibrillation. It is estimated that by the year 2050, 16 millions Americans will have atrial fibrillation (Lloyd-Jones et al., 2004). Heart failure and rheumatic heart disease were the most powerful predictive precursors for atrial fibrillation, with relative risk in excess of sixfold. Hypertension, a history of cerebrovascular disease, diabetes, and left ventricular hypertrophy were also found to be significantly associated with atrial fibrillation.

The clinical importance of atrial fibrillation, other than its difficult-to-tolerate signs and symptoms, such as palpitations, dizziness, and fatigue, is its relation to a mortality rate double that of control subjects. Much of the morbidity and mortality related to atrial fibrillation is caused by stroke (Wolf et al., 1991). This is because atrial fibrillation creates turbulent flow in the cardiac chambers, promoting the formation of thrombi. Such thrombi, when dislodged from the cardiac chambers, may eventually lodge in another organ and lead to a thromboembolic event. Other morbidity and mortality related to atrial fibrillation include heart failure. Without thromboprophylaxis, the risk of ischemic stroke in patients with nonrheumatic atrial fibrillation is approximately 5% per year (Wolf et al., 1991). For ventricular arrhythmias, the incidence of sudden cardiac death varied from <200,000 to 450,000 annually based on whether the patients also have coronary heart disease (Zipes et al., 2006).

DIAGNOSTIC CRITERIA

Supraventricular Arrhythmias

PREMATURE ATRIAL COMPLEXES

A premature atrial complex (PAC) is an electrical impulse originating in the atria outside of the SA node. PACs often occur without apparent cause or symptoms.

Commonly recognized clinical causes include the use of stimulants such as caffeine, tobacco, or alcohol. The ECG criteria are:

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA

PSVT is a clinical syndrome characterized by repeated episodes of atrial tachycardia with an abrupt onset (preceded frequently by a premature atrial contraction), lasting from a few seconds to many hours. They usually end abruptly and often can be terminated by vagal maneuvers. Possible causes of PSVT include physical and psychological stress, hypoxia, hypokalemia, and excessive use of caffeine or other stimulants. Primary cardiac causes include myocardial infarction (MI), congenital heart disease, and cardiomyopathy. Other causes include digitalis toxicity and chronic pulmonary disease. Patients may feel a sudden rapid palpitation and severe anxiety. Heart failure, angina, and shock may occur as a result of a decreased cardiac output and an increased need for myocardial oxygen, if the tachyarrhythmia is persistent.

The ECG criteria are:

LGL Syndrome • LGL, one type of PSVT, is usually benign unless debilitating tachyarrhythmias occur. ECG criteria are normal except that PR intervals are abnormally short but constant.

The etiology of atrial fibrillation is categorized in Table 7.3 (Benjamin et al., 1994).

Any situation that leads to an increase in atrial mass, atrial dilatation (in fluid overload states), myocardial injury (in coronary artery disease), increased vagal tone, or any other disturbance to the atria (open heart surgery) increases the risk of developing atrial fibrillation.

Atrial flutter is another form of supraventricular arrhythmia. Atrial flutter occurs less frequently than atrial fibrillation but has similar precipitating factors, consequences, and approach to treatment. This arrhythmia is characterized by rapid but regular atrial activation (250–350 bpm). The ventricular rate is determined by AV nodal conduction and is some dividend of the atrial rate. For example, for an atrial rate of 300 bpm, the ventricular rate would be 100 bpm for a 3:1 AV conduction, 150 bpm for a 2:1 AV conduction, and 300 bpm for a 1:1 AV conduction. Atrial flutter usually occurs in conjunction with atrial fibrillation; in this situation, the ventricular rate will be irregular.

Symptoms of atrial fibrillation and atrial flutter are similar. Patients often present complaining of palpitation, dizziness, fatigue, and dyspnea, especially if they have a rapid ventricular rate. Patients with a relatively slower ventricular rate may be asymptomatic. A prolonged uncontrolled ventricular rate may lead to cardiac decompensation or heart failure. Atrial fibrillation is usually categorized as paroxysmal or chronic and the management approaches are different. Atrial flutter, in contrast, is an unstable rhythm and rarely remains chronic.

ECG criteria for atrial fibrillation are:

ECG criteria for atrial flutter are:

BRADYARRHYTHMIAS AND HEART BLOCK

Bradyarrhythmia usually refers to sinus bradycardia. Sinus bradycardia is an arrhythmia where the sinus rate is below 60 bpm and all impulses come from the SA node. The morphology of the ECG is normal except a demonstration of a very slow ventricular rate. Sinus bradycardia is usually observed in athletes, most likely due to their increase in vagal tone. It is also noted during sleep, elevation of intracranial pressure, and situations with increased vagal tone such as straining of stool, vomiting, intubation, sick sinus syndrome, and hypothyroidism. Certain medications, such as beta-blockers, calcium channel blockers, and adenosine, may also induce sinus bradycardia.

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