Approach to Supraventricular Tachycardia - SVT


Supraventricular Tachycardia

I would like to share with you about SVTs, or supraventricular tachycardia, today. I'll be focusing on the pathophysiology, ECG features, and the management of SVT today. So this is a brief outline of the lecture today. I will be going through the definition of SVTs, followed by a brief classification of tachyarrhythmias, the pathophysiology behind it all, ECG features, and management principles of SVTs. I will round off the lecture with a clinical scenario related to the topic. This lecture is meant to be a basic introduction to SVTs, and is by all means not exhaustive. So without further ado, let us begin. Supraventricular tachycardias are defined as narrow complex tachycardias where the point of stimulation arises from above the bundle branches. There are many types of SVTs, as will be shown in the next slide, and some are more common than the others.

 However, in our local context, it is used interchangeably with proximal supraventricular tachycardias, which make up a majority of the SVTs. The three main features of proximal supraventricular tachycardia are that they are regular and have narrow complexes, which means that the QRS complex is less than 120 milliseconds, and that it is a tachycardia with rates usually around 150 beats per minute and above. This is a simple flow chart showing the classification of tachyarrhythmias. Tachyarrhythmias can be divided into narrow and broad complex tachycardias. Broad complex tachycardias are not in the scope of this lecture. Narrow complex tachycardias are further divided into regular and irregular. Atrial flutter and atrial fibrillation will be covered as part of a series of lectures under cardiology. I'll be focusing on AVRT and AVNRT in this lecture. The basic mechanism of SVTs fall into three main categories-- namely, re-entrant dysrhythmias, abnormal automaticity, and triggered dysrhythmias. Of these three, re-entry is by far the most common encountered mechanism. This slide demonstrates the mechanism of re-entrant dysrhythmias.

For a re-entrant circuit to propagate, there must be two functional anatomic pathways that differ in their speed of conduction of impulses and the speed of recovery. Let's name them beta track and alpha track. The beta track is a fast conducting and slow recovery track. This type of conduction pathway is the normal conduction pathway through the AV node. On the other hand, the alpha track is a slow conducting, but fast recovery, pathway-- the direct opposite of the beta track. Let's look at figure A. Normal conduction goes down to the two different tracks. As the beta track is fast conducting, it conducts the signal to the ventricles before the alpha track. A re-entrant circuit is precipitated by a premature atrial complex, which is an atrial conduction that comes earlier than usual. This finds a slow recovery beta track refractory from the previous beat, as represented in diagram B by a black rectangle. Thus, the signal is conducted down the slow conducting alpha track. Because the alpha track conducts signals slowly, by the time it reaches the ventricle, the fast recovery beta track is no longer refractory. It is ready to conduct signals again. The signal is then conducted retrogradely up the beta track. On reaching the HON, the first recovery alpha track is no longer refractory, and thus conducts the signal down the alpha track again, and the cycle repeats itself. Thus, the reentry loop is established.

There are two types of paroxysmal SVTs-- AVNRT and AVRT. AVNRT stands for atrial ventricular nodal reentrant tachycardia. It makes up about 60% of SVTs, and is the commonest type of SVT. The other type is AVRT, which stands for atrioventricular reentry tachycardia, which makes up about 30% of SVTs. AVRTs are associated with accessory pathways. An example is the Wolf-Parkinson-White syndrome. This is a 12-lead ECG showing an AVNRT. Typically, a regular narrow complex tachycardia is seen. The ECG features of AVNRT as shown previously are that often narrow complex regular tachycardia with no P wave seen prior to the QRS complexes. The P waves are usually buried within the QRS complexes, and are not seen in the ECG. But this is not always the case. The rate is fixed, and does not undergo variations as compared to sinus tachycardia, where the rate demonstrates gradual variations over time in response to etiology and interventions. Now this is a 12-lead ECG showing an AVRT. Notice that although it also shows a regular narrow complex tachycardia, there are retrograde P waves seen after the QRS complex, best seen in the inferior leads here. The ECG features of AVRT as described previously are that of a narrow complex regular tachycardia with no P waves seen prior to the QRS complexes. However, a P wave may be seen retrograde to the QRS complex, but this may not be seen always. Thus, it is difficult to tell AVRT apart from AVNRT based on the ECG alone. Definitive diagnosis can only be obtained on electrophysiology studies-- in the cardiac catheterization lab. But treatment of AVNRT and AVRT are the same. So in the emergency setting, it is not that crucial to differentiate between the two, but more importantly to recognize it as a SVT. So know that we have diagnosed a patient with SVT, how do we treat the patient. These are the management principles for SVT-- first, we assess the patient for hemodynamic stability; and based on that, treat the rhythm; followed lastly by disposition of the patient. Just a word of caution-- SVTs are generally relatively benign arrhythmias, and a large portion of patients present with little or no hemodynamic compromise. If your patient presents with what looks like SVT with hemodynamic compromise, please have a high degree of suspicion that it might not be SVT-- but rather, another tachyarrhythmia like fast AF, and sometimes fast AF with rapid ventricular rates may look like SVTs on ECG. So, when first presented with a patient with an SVT, the first thing to do is to examine the patient and determine if the patient is hemodynamically stable. Take a set of parameters, listen to the basis of the lungs, look at the JVP.

If the patient is hypotensive, has altered mental state, is tachypneic, has basal crackles and a raised JVP, or has any other sign of cardiopulmonary compromise, treat as for hemodynamically unstable SVT. Proceed to sedate the patient and administer synchronized cardioversion starting at 50 joules and increasing the energy level if unsuccessful. The goal of therapy, be it via electrical means or via pharmacological means, is to disrupt the reentrant circuit by blocking conduction in either limb of the circuit. This will result in a return to normal conduction and normal sinus rhythm. If, on clinical examination, the patient is hemodynamically stable, then vagal maneuvers or pharmacological therapies can be used first. If all else fails, we'll just have to fall back on synchronized cardioversion. Vagal maneuvers include the Valsava maneuver and the carotid sinus massage. Be very cautious when doing a carotid sinus massage in patients who are more than 60 years of age and has a history of diabetes mellitus, hypertension, ischemic heart disease, transient ischemic attacks, and strokes. These patients are at risk of having carotid plaques, which could be dislodged during a carotid sinus massage, resulting in a stroke. Do bear in mind that the absence of a murmur on auscultation of the carotid arteries does not mean that no carotid stenosis and plaques are present. In such patients, it will be wise to choose the Valsava maneuvers over carotid sinus massage. For carotid sinus massage, it is done with the patient lying down. At the level of the cricoid cartilage, drop a line 90 degrees down to the lateral neck till the carotid pulse is felt. Then press down firmly against the spinous processes and proceed to massage site to site. If vagal maneuvers fail, then proceed to pharmacological methods for chemical cardioversion. Atrial ventricular nodal blocking agents like adenosine, and calcium channel blockers like verapamil or diltiazem work at the AV node to break the reentrant circuit by blocking the limb of the circuit that is in the AV node.

Adenosine is the most commonly used agent, and I will elaborate more about it in my next slide. Agents that block the accessory pathway preferentially, like procainamide, can be used, especially in antidromic conduction in Wolf-Parkinson-White syndrome, or WPW, where the use of AV nodal blocking agents are contraindicated. This will be elaborated more in the WPW lecture as part of the cardiology series. Other agents, like amiodarone, can also be used if the usual therapies fail. Just a little bit more about adenosine-- it is the most commonly used drug to abort SVTs. One of the reason it is particularly favored is because of its fast onset and very short half life of less than 10 seconds. It is given as a fast bolus by a large peripheral cannula in the cubital fossa followed immediately by a saline flush. We usually start by giving IV 6 mg bolus followed by a 12 mg bolus if the first dose is unsuccessful, and another 12 mg bolus if the second dose is unsuccessful. If it is still unsuccessful after three doses of adenosine, other pharmacological agents can be used-- or if all else fails, synchronized cardioversion. The ECGs should also be reviewed to ensure that it is not another rhythm that is the cause of the tachycardia. Lastly, not only is it adenosine therapeutic, It can also be diagnostic. It slows down the AV node enough to bring up faster waves in atrial flutter, thus revealing the diagnosis as that of atrial flutter with a two is to one block rather than that of SVT in such situations.

After successful cardioversion to normal sinus rhythm, the patient is then observe in the emergency department for a period of about two to four hours to ensure that the activity does not recur and that the patient is stable and well before discharge. A repeat ECG should also be obtained to ensure that the patient is in normal sinus rhythm. A follow-up with the cardiologist for further electrophysiological studies, and ablation if need be, should be arranged before discharge from the emergency department. The patient should also be educated about his or her condition, and taught how to recognize it and what to do when experiencing the palpitations again. Prior to discharge, patients should be also taught how to do a Valsava maneuver or to perform the carotid sinus massage when similar symptoms arise again. All patients should be cautioned to return to the emergency department if the palpitations and symptoms persist despite vagal maneuvers. So we've come to the end of the presentation. These are the take home messages-- remember, synchronized cardioversion for all unstable patients with SVT; do refer patients with SVT to the cardiologist for electrophysiology studies on discharge from the emergency department; and most importantly, please educate the patient. Please teach the patient how to perform the vagal maneuvers, and what to do if the vagal maneuvers does not work, prior to the patient leaving the emergency department. With that, I'd like to thank you all for your kind attention, and have a nice day.