Arrhythmias - Supraventricular tachycardia (SVT): Nursing

Supraventricular tachycardia, or SVT for short, is an arrhythmia where the heart beats faster than normal, meaning over 100 bpm, but most clients with SVT have a heart rate between 151 and 220 bpm. The cause of the tachyarrhythmia must originate from above the ventricles, and this could be from the myocytes of the atrium or part of the heart’s conduction system. The most common type is called paroxysmal SVT, or PST where there’s sporadic attacks that start and stop suddenly.

Now, the cardiac conduction system is made up of specialized myocardial cells that can create and transport electrical potential, also called an action potential. These cells have many special features, including automaticity, meaning that they can generate an impulse, excitability, which is the ability to respond to a stimulus by creating an electrical impulse, conductivity meaning they can carry the impulse to other cells, and contractility, which is the ability to shorten the length of their fibers, causing a contraction.

Alright, now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart. Then, the impulse is conducted through the atria, causing depolarization and creating the P wave on an ECG. When the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles. From the atria, the impulse goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down. The interval from the atrial depolarization to just before ventricular depolarization is the PR interval on an ECG. This delay allows the atria to contract while the ventricles fill with blood. From the AV node, the impulse goes through the Bundle of His, then to the right and left bundle branches, and finally through the Purkinje fibers, which deliver the impulse to the right and left ventricles, causing them to depolarize, and is represented by the QRS complex on an ECG.

This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the phase between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles.

Now, the main cause of paroxysmal SVT is an abnormal circuit in the heart’s conduction system that allows electrical impulses to loop back in on themselves, and this is called reentry. One type is called atrioventricular reentrant tachycardia, or AVRT, where there’s an accessory pathway, meaning another path for the electrical impulse to go from the atria to the ventricles. One type of AVRT is Wolff-Parkinson-White syndrome in which a client has a congenital accessory pathway. On the other hand, atrioventricular nodal reentrant tachycardia, or AVNRT, is the more common cause of paroxysmal SVT and this is where the reentry occurs in or near the AV node. In rare cases there are also paroxysmal SVT that originate from an atopic focus in the atrial tissue and this is called focal atrial tachycardia. This means parts of the atrium that can generate impulses on their own independent of the SA node.

Risk factors for supraventricular tachycardia include heart disease like coronary artery disease and congenital heart disease; digoxin toxicity; and advanced age. Other risk factors include hyperthyroidism, as well as anxiety, stress, stimulant drugs, like cocaine or methamphetamine, and excessive alcohol, caffeine or tobacco consumption.

Now, the pathology of paroxysmal SVT starts with a reentrant loop, meaning electrical activity is literally trapped in a circular electric racetrack, altering normal conduction. So, with AVRT, the electrical signal from the SA node goes through the atrium to the AV node, then it travels through the Purkinje fibers throughout the ventricles like normal. However, the accessory pathway allows the impulse to go back up to the atrium, causing the cycle to repeat itself before the next impulse from the SA node. The reentrant loop is little different with AVNRT. So, there are two branches coming from the AV node, forming a loop. In branch 1, the impulse travels at a normal speed, but in branch 2, the impulse travels slower. The impulse from the SA node reaches the AV node and goes down both pathways. It rushes through pathway 1 and causes ventricular contraction, but it also goes up pathway two, and causes the atrium to contract again, leading to a cycle

In both cases there’s now a cycle independent of the SA node, meaning it can pretty much run itself now and with each cycle, this can trigger an atrial and a ventricular contraction. Usually, paroxysmal supraventricular tachycardia starts abruptly, lasts for a few minutes, and also ends abruptly, without causing serious complications. However, with prolonged episodes, clients can develop hemodynamic instability. Finally, frequent untreated episodes of supraventricular tachycardia can weaken the heart muscle, causing heart failure.

Clients with SVT can have varied clinical manifestations depending on the duration of SVT and the rate of ventricular response. Clients with a non-sustained, slower ventricular response may be asymptomatic except for occasional palpitations.

In contrast, with sustained, rapid ventricular response, clients often present with palpitations, and clinical manifestations of decreased cardiac output, such as chest pain, anxiety, weakness, shortness of breath, and syncope or hypotension.

The diagnosis of SVT starts with the client's history and physical assessment, followed by cardiac monitoring using an electrocardiogram or a Holter monitor, which is basically a portable ECG that records for a 24-hour period.

So, on the ECG, the heart rate is typically between 151 to 220 beats/min, and the rhythm can be regular or slightly irregular. Of note, P waves can be abnormally shaped or hidden in the preceding T wave, and as a consequence, PR intervals can be shortened or difficult to measure. The QRS complex is typically normal or narrow.

Alright, now, no treatment is needed for healthy clients when SVT stops on its own, and no causes necessitate further treatment. In contrast, symptomatic clients who are hemodynamically unstable should be treated with electrical synchronized cardioversion with a defibrillator. For a stable client with sustained SVT with a rapid ventricular response, vagal maneuvers like carotid sinus massage and Valsalva maneuvers are typically started.

At the same time, they are usually given medications, like IV adenosine for an acute episode or AV nodal blocking agents like beta and calcium channel blockers. For recurrent SVT, radiofrequency catheter ablation is often used to destroy the tissue causing the recurrent loop or the ectopic focus.

Alright, now let’s talk about the nursing care you’ll provide for a client with SVT. Your priority goal of care is to assist in restoring a normal sinus rhythm.

As you assist in restoring normal sinus rhythm during an episode of SVT, initiate continuous cardiac monitoring, and assess your client to determine if they are hemodynamically stable. Assess their vital signs and check for symptoms of decreased cardiac output. Report dizziness, hypotension, chest pain, tachypnea, or shortness of breath to the healthcare provider. Administer supplemental oxygen and prepare your client for synchronized cardioversion. Then, work with the other members of the healthcare team to address the underlying cause of the arrhythmia.