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 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 atrium, creating the P wave on an ECG. And when the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles.

From the atrium, electrical activity goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down; this is the PR interval on an ECG. This pause allows the atria to contract while the ventricles fill with blood. From the AV node, the depolarization wave goes through the Bundle of His, then the right and left branches of the Bundle, and finally through the Purkinje fibers, which deliver the current to the right and left ventricles, causing them to depolarize.

This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations, and it’s represented by the QRS complex on an ECG. 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 pause 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 congenital heart disease, being assigned female at birth, and young or 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 a 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 nonsustained, slower ventricular response may be asymptomatic except for occasional palpitations. In contrast, with sustained, rapid ventricular response, clients often present with palpitations, chest pain, anxiety, weakness, shortness of breath, and syncope or hypotension can also occur.

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.