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, or the pacemaker of the heart. The SA node is located in the upper portion of the right atrium (Fig. 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. 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 re-entry 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, most sodium and potassium channels are located in the atria and ventricular muscle, and most calcium channels are located at the SA and AV nodes respectively. The activity of antiarrhythmic agents is based on these sites of action. For instance, calcium channel blockers such as verapamil will exert their main action at the SA and the AV nodes. Class I antiarrhythmic agents, such as procainamide are sodium channel blockers, exert their action mainly on the atrial and the ventricular tissue.

The electrocardiogram (ECG) complexes reflect the cardiac electrical activity. Electrical conduction of the heart is represented by waveforms on the ECG. The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization and the T wave represents ventricular repolarization (Fig. 7-2). The atrial contraction follows the P wave and the ventricular contraction follows the QRS complex. There are three key intervals that 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 less than 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.

A premature atrial complex (PAC) is an electrical impulse originating in the atria other than the sinus node. Premature atrial complexes often occur without apparent cause and symptoms. Commonly recognized clinical causes include the use of stimulants such as caffeine, tobacco, or alcohol.

The ECG criteria are:

Paroxysmal supraventricular tachycardia 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 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. Congestive 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:

Atrial fibrillation is a type of supraventricular arrhythmia defined as an extremely rapid and disorganized atrial activation (400–600 atrial bpm). This occurs when other ectopic foci in the atrium take over the role of the sinus node as the pacemaker. Such disorganized atrial contractions lead to a supraventricular impulse penetrating the AV conduction system in variable degrees, resulting in a totally irregular, often rapid ventricular rate. Because the AV node is composed of mostly slow conduction channels compared to the atrial tissue, which is composed of
mostly fast conduction channels, most of the supraventricular impulses are not conducted through the AV node. Therefore, although the atrial rates usually vary between 400 to 600 bpm, the ventricle responds at a considerably slower rate (120–180 bpm).

Atrial fibrillation is now believed to occur under certain distinct clinical circumstances:

The etiology of atrial fibrillation is categorized in Table 7-3 (Geraets & Kienzle, 1993).

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). This slower and regular atrial activity leads to a regular ventricular response and a pulse rate in dividends of 300 bpm (100 bpm for a 3:1 AV conduction, 150 bpm for a 2:1 AV conduction, and 300 bpm for a 1:1 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 CHF. Atrial fibrillation is usually categorized as paroxysmal or chronic and the management approaches are different. Atrial flutter, on the other hand, is an unstable rhythm and rarely remains chronic.

ECG criteria for atrial fibrillation are:

ECG criteria for atrial flutter are:

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. Sinus bradycardia is usually observed in athletes, most likely due to there 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.

Ventricular premature beats are ectopic ventricular beats that occur earlier than the normally expected beat and is often followed by a compensatory pause. VPBs may be uniform, arising from the same ectopic focus (unifocal), or multiform (multifocal), arising from two or more different ventricular sites. Patients experiencing VPBs may be asymptomatic or may complain of “skipping beats.” Depending on a patient’s ventricular function and the duration and frequency of the VPBs, a decrease in cardiac output may result. VPBs are more dangerous if they occur in the presence of heart disease. Possible cause of VPBs include digitalis toxicity, hypokalemia, hypocalcemia, and the use of caffeine and other stimulants.

The ECG criterion is a QRS interval that is wide and bizarre in morphology. While most VPBs are benign, certain forms of VPBs may be predictive of potentially serious arrhythmic events (eg, sustained VT). Potentially dangerous VPBs include:

Ventricular tachycardia is defined as premature ventricular complexes occurring in succession at a rate of more than 100 bpm. If sustained, cardiac output may drop drastically and the rhythm may deteriorate to VF. Common cardiac causes of VT include acute MI, coronary artery disease, rheumatic heart disease, and cardiomyopathy or heart failure. Other noncardiac causes include pulmonary embolism, electrolyte imbalance (eg, hypokalemia) and drug toxicity (eg, digitalis, procainamide, quinidine, and vasopressors such as epinephrine). If conscious, the patient may complain of palpitations, dizziness, and shortness of breath. Patients usually lose consciousness quickly if VT is rapid and sustained.

ECG criteria are:

Ventricular fibrillation is an arrhythmia marked by rapid, disorganized depolarizations of the ventricles and characterized by a lack of organized electrical impulse, conduction, and ventricular contractions. Patients at risk of developing VF include those with acute MI, untreated VT, electrolyte imbalance (hypokalemia and alkalosis, hyperkalemia and hypercalcemia), electric shock, and hypothermia. Patients are usually unconscious in this situation and there is an absence of pulse, heart sounds and blood pressure. ECG criteria are an indeterminate rate and a rapid and chaotic rhythm, with no pattern or regularity.

Torsades de pointes is a syndrome characterized by atypical polymorphic VT (the QRS polarity spiral around the isoelectric line) and a prolonged QT interval. Any condition that lead to prolonged QT intervals can precipitate torsades (see Table 7-2). Similar to VT, patients with torsades usually lose consciousness rapidly. If conscious, the patient may complain of palpitations, dizziness, chest pain, or shortness of breath.

ECG criteria are: