17.1: Introduction to Dysrhythmias

Learning Objectives

By the end of this section, you should be able to:

• 17.1.1 Describe specific cardiac dysrhythmias and their significance to cardiac function.
• 17.1.2 Discuss the principles of managing dysrhythmias to improve cardiac functioning.

Dysrhythmias

Dysrhythmias, also known as arrhythmias, occur when there is abnormal automaticity (spontaneous impulse generation) or abnormal conduction that results in a problem with the heart rate and/or rhythm. Medications address dysrhythmias by manipulating the electrolytes and other receptors involved in the cardiac conduction system to either treat the manifestations of the underlying arrhythmia or restore a normal heart rate, suppress the dysrhythmia, and thus restore normal sinus rhythm in a process known as cardioversion. When cardioversion is accomplished via drug administration, may be referred to as chemical cardioversion.

Dysrhythmias can be classified in multiple ways. One way is according to the ventricular contraction rate, or heart rate. A heart rate less than 60 beats per minute is considered bradycardia. Bradycardia can occur due to the SA node incorrectly pacing too slowly or to the AV node conducting incorrectly, leading to AV block. Bradycardia can lead to problems because it decreases cardiac output, which is affected by both stroke volume and heart rate. A heart rate greater than 100 beats per minute is called tachycardia. Tachycardia can further be categorized as supraventricular tachycardia (the stimulus physically originates above the ventricle but not from the sinus node) or ventricular tachycardia (the origin of the stimulus is physically located in the ventricle). Tachycardia is problematic because at very high heart rates, the ventricles do not have enough time to fill with an adequate amount of blood in between contractions. Thus, the stroke volume and cardiac output are both decreased. Tachycardia also increases the workload of the heart and can lead to a type of heart failure called tachycardia-induced cardiomyopathy.

Sinus Bradycardia

In sinus bradycardia, although the heart rate is less than 60 beats per minute, the rhythm is regular, and the SA node acts as the pacemaker for the heart. Aside from the slow heart rate, there is no other problem with conduction. On an ECG, every P wave is followed by a QRS complex, which is followed by a T wave.

Sinus Tachycardia

In sinus tachycardia, although the heart rate exceeds 100 beats per minute, the rhythm is regular, and the SA node acts as the pacemaker for the heart. Aside from the rapid heart rate, there is no other problem with conduction. Every P wave is followed by a QRS complex, which is followed by a T wave. Sinus tachycardia is often caused by exercise, pain, stress, anxiety, or dehydration.

Atrial Fibrillation

Atrial fibrillation is described as an irregularly irregular rhythm in which multiple areas of the atria generate spontaneous impulses such that the atria quiver at 400–600 beats per minute. Only some of the impulses are conducted through the AV node, resulting in a variable ventricular contraction rate or heart rate. When the heart rate is high, it is called atrial fibrillation with rapid ventricular response. Because the atria are quivering because so many impulses are being formed, the individual’s ECG will show no distinguishable P waves; however, the baseline will appear wavy due to the presence of “fibrillatory” waves (Figure 17.2).

There are two overall strategies for treating atrial fibrillation: rhythm control and rate control. The aim of rhythm control is to cardiovert and then maintain normal sinus rhythm. Rate control is a strategy that allows the client’s rhythm to remain in atrial fibrillation but slows the rate of conduction through the AV node, thereby slowing the ventricular rate/heart rate.

Atrial Flutter

Atrial flutter is a dysrhythmia closely related to atrial fibrillation. The atria quiver at rates of 250–400 beats per minute. As with atrial fibrillation, abnormal impulses are generated in the atria. Commonly, there is 2:1 conduction through the AV node, meaning that for every two impulses from the atria, one conducts through the AV node and leads to ventricular contraction. This process commonly leads to a ventricular rate of approximately 150 beats per minute (assuming an average atrial rate of 300 beats per minute). It is noteworthy that the conduction is not always 2:1; it may be 3:1, 4:1, or 5:1. As in atrial fibrillation, there are no typical P waves on the ECG of a client with atrial flutter. Instead, there are “flutter waves” in a characteristic sawtooth pattern between QRS complexes.

Premature Ventricular Contraction

A premature ventricular contraction (PVC) represents the ventricle contracting earlier than it should during the cardiac cycle due to a spontaneous impulse from the Purkinje fibers (rather than from an impulse carried from the SA node).

Ventricular Tachycardia

When multiple PVCs occur consecutively, it is known as ventricular tachycardia. Sustained ventricular tachycardia (lasting more than 30 seconds) can be serious and cause hemodynamic compromise necessitating advanced cardiac life support. Ventricular tachycardia can occur due to abnormalities of electrolytes such as magnesium or potassium or to myocardial ischemia (oxygen deprivation in the heart muscle). It can devolve into ventricular fibrillation, described next. On an ECG, ventricular tachycardia has multiple wide QRS complexes (Figure 17.2). Torsade de pointes is a dangerous ventricular tachycardia associated with medications that prolong the QT interval (the time it takes the heart to contract and recover).

Ventricular Fibrillation

Ventricular fibrillation is a medical emergency that necessitates advanced cardiac life support (ACLS). This is another ventricular arrhythmia, meaning it originates from spontaneous impulses from the Purkinje fibers (rather than from an impulse carried from the SA node), causing the ventricles to quiver erratically rather than pump, which, in turn, causes cardiac arrest. On an ECG, ventricular fibrillation appears as multiple and varied wide complexes, without any pattern or discernable P waves, QRS complexes, or T waves (Figure 17.2).

Table 17.1 Vaughan Williams Classification of Antidysrhythmic Drugs

Special Considerations

Older Adults

The risk of being diagnosed with dysrhythmia skyrockets after age 60. Not only does the risk for dysrhythmias increase, but older adults have a higher risk for concomitant disease states that interfere with the action of antidysrhythmic drugs. For example, beta-adrenergic blockers, quinidine, and procainamide can exacerbate the postural hypotension that is particularly prevalent in older adults, leading to falls. Clients with heart failure (who are usually older adults) can experience exacerbation of their underlying condition when treated with flecainide or sotalol. Furthermore, older clients are more likely to be on multiple medications, increasing the likelihood of experiencing drug interactions. Age-related decreases in metabolic processing and excretion of drugs can increase antidysrhythmic plasma levels, putting these individuals at higher risk for adverse effects. Thus, antidysrhythmic drugs require extra vigilance to prevent harm in the older adult population.

(Source: Curtis et al., 2018)

Special Considerations

Pediatrics

Pediatric clients may experience arrhythmias that must be treated with antidysrhythmic therapy. Some of this use is off-label. Off-label prescription drug use means that the drug may not be specifically approved for a particular client or diagnosis, but health care providers may choose to use the drug anyway because the potential benefit outweighs the potential risks. In these circumstances, drug dosing and administration may not be standardized. The nurse should consult institutional protocols to avoid medication errors, especially overdoses.

(Source: Oeffl et al., 2023)