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EP Procedures - Arrhythmia Induction

Arrhythmia Induction

          Earlier in this document, we discussed how the fastest rhythm was the one that would control the heart.  By using this knowledge, physicians can "take control" of the heart and set up various conditions that help in determining if an arrhythmia may be possible. By pacing at a rate that exceeds the patient's intrinsic rate, the operator takes control of the properties of depolarization. Once that has been achieved, it is possible to introduce early stimuli to determine how the heart will respond. This process is known as induction.

          Induction is the heart of electrophysiology studies. All the previous testing we have done checks for different forms of delays within the conduction system. With induction, we move away from the slow paced world of blocks and enter into the fast paced world of tachycardias. Here is where the fun starts.

          To fully understand how induction works, you should first read the section on automatic and reentry arrhythmias. I will assume that you have already done this and I will move forward into induction protocols. The type of induction you utilize is often dependent upon what type of arrhythmia you suspect the patient may have. While reentry tachycardias are usually triggered using extra stimuli, automatic tachycardias are more easily initiated using burst pacing. The majority of arrhythmias you will encounter will be caused by reentry, so most induction will be done using extra stimulus. In this section I will discuss some of the various pacing protocols we use in our lab.

          Before we actually look at the process of induction, there are a few terms you will need to be familiar with.

Pacing train: A series of pacing stimuli delivered at either constant or variable pacing rates.
S1: The S indicates a stimulus. The 1 indicates the first interval used in a pacing train. For example, if you deliver two or more pacing signals at a constant rate, the interval between them would be your S1 interval, or your pacing cycle length.
S2: This refers to the second interval used in a pacing train. If you deliver 5 paced beats at 500ms and a 6th stimulus at 320ms, the S2 interval would be 320ms. This pacing train would be described as 500/320.
S3 & S4: Each time you add a different cycle length, you are adding a new S to the pacing train. In essence, each new pacing interval is labeled as a new stimulus or "S". In induction protocols, it is rare that you will exceed S4.

          When a patient presents to our lab with an unknown tachycardia or with a diagnosis of SVT, we will usually start with our basic setup. This means we place one quadrapolar Josephson diagnostic catheter into the right atrium and one quadrapolar CRD2 diagnostic catheter in the HIS bundle region. After we have completed the preliminary tests, we will start atrial induction. The pacing protocol we use starts with an S1 interval of 600ms and an S2 that is at least 60ms higher than the documented wenckebach interval. It is very common for us to start at 600/400. Note that if the patients heart rate is above 100bpm, (100bpm = 600ms), you will need to start at a faster cycle length for S1. If we encounter this problem, we will usually start with an S1 of 500.

          Once stimulation has begun, the S2 interval is decreased by 10 to 20ms for each new pacing train. The stimulator we use is fully computerized and the S2 interval is programmed to decrease by 10ms automatically. Each new pacing train is programmed to begin after a 4 second rest period. As each train occurs, we observe and document certain events. If the AH interval increases by at least 50ms from one train to the next, this may indicate what is called an "AH Jump". When this occurs, it is, in most cases, considered to be evidence of dual AV node physiology. For more details on this, please see EP Lab/Arrhythmias/AVNRT. We also document the point where the pacing interval does not conduct through the AV node to the ventricles. This is called the AV Node Effective Refractory Period, or AVNERP. If there is evidence of atrial tachycardia, we may continue to decrement the S2 interval until the pacing signal no longer causes the atrium to contract. This is known as the Atrial Effective Refractory Period, or AERP.

          Keep in mind that besides documenting these intervals, you are also trying to induce the patient's arrhythmia. Keep a close eye on the response to every pacing train and be ready to turn off the stimulator if a tachycardia occurs. When this happens, you will want to record the entire duration of the arrhythmia. If your system has automatic record for stimulation trains and high heart rate, you simply need to let the system record the event for you. Make sure you take a quick glance and verify that recording is on, especially during the tachycardia. Even if you have pressed the record button, you need to be certain you didn't double trigger the button and thus turn the recorder off an instant after it was turned on.

          After the S2 has become refractory, we stop the stimulator and increase the S2 to at least 20ms above the AVNERP. In cases where dual AV node physiology has been documented, you may find it handy to set your S2 to at least 20ms above the point where the AH jump occurred. This point is called the fast pathway effective refractory period, or FPERP.After the S2 is reprogrammed, and extra stimulus, or S3 is added to the pacing train. The S3 interval is started at the same point the S2 originated. Once the stimulator has been reprogrammed, stimulation begins again. You will need to keep an eye out to make sure that all the stimuli are capturing the myocardium. If there is dual AV node physiology,. the time it takes to conduct down the slow pathway may cause the AV node to be refractory when you try and add the S3 signal. This is why it is sometimes easier to set your S2 above the FPERP. If starting the S2 at 20ms above the FPERP, you may need to try repeated pacing trains with the S2 being gradually increased until all the extra stimuli capture appropriately.

          Once everything is set with both S2 and S3, induction is started once again with the S2 being held constant and the S3 being decreased in steps. This process continues until S3 becomes refractory or until tachycardia is initiated. If S3 becomes refractory without a tachycardia occurring, then an S4 signal is usually added. The same process is repeated until S4 no longer conducts or tachycardia is triggered.

          If S4 is reaches its refractory point without a tachycardia being initiated, the S1 interval may be decreased and the entire process repeated. We will usually decrease the S1 to 400ms, though this is decided on a case by case basis. Once the entire process has been repeated at the lower cycle length, we may try burst pacing, especially if there has been indications that there may be an atrial tachycardia present. The protocols we use for burst pacing are considerably more simple than the ones used for reentry. The stimulator is set to pace at 300ms in the right atrium. Pacing is initiated for 10 to 30 seconds while we closely observe the atrial channels. If we start to see indications of extra atrial activity, the stimulator is turned off immediately. If, however, nothing happens after pacing at 300ms, the cycle length is decreased by 20ms and the process repeated. For burst pacing protocols, we will not pace below 200ms.

Ventricular Stimulation

  It seems pretty simple to think that when you do atrial stimulation, you will be trying to induce some form of supraventricular tachycardia. It would also seem to follow that when you are doing induction in the ventricle, you would be trying to trigger some form of ventricular tachycardia. While that is true a portion of the time, it is by no means the only reason you perform ventricular induction. A wide variety of arrhythmias may be initiated while pacing in the ventricle. It is possible to see several types of SVT including AV node reentry, AV reentry and even atrial fibrillation during ventricular pacing. At first this may seem a bit strange, but as you learn more about the mechanisms of arrhythmias, you will find that ventricular induction of SVT is actually fairly common.

          The primary reason that pacing the ventricle can cause SVT is that many forms of supraventricular tachycardias rely on retrograde conduction either through the AV node, or along an accessory pathway. There are even forms of AVRT that can not be visualized unless ventricular pacing is utilized. These AVRTs use what are known as concealed pathways. Pathways of this type do not show on a standard electrocardiogram. The familiar delta wave that many of us associate with WPW is absent along with the ventricular preexcitation that it heralds. But throw a PVC into the rhythm, and you may have an instant SVT on your hands. For these reasons, it is important to know what to look for when performing ventricular induction.

          The process of induction in the ventricle is the same as that which is used in the atrium. Pacing trains with progressive extra stimuli are used until the refractory periods are found. Which refractory periods you are looking for depends entirely on what type of arrhythmia you suspect the patient has. It is always possible to trigger VT using ventricular induction, but if you are looking for some form of SVT, you need to pay close attention to the retrograde atrial signals. The coronary sinus and HIS catheters can make this a fairly simple task as they both display atrial and ventricular signals on each channel.

          When the patient presents with suspected ventricular arrhythmias, the extra stimuli are decreased until the ventricle becomes refractory and no V signal occurs with pacing. If you are looking for SVT, keep an eye on the retrograde conduction. When the ventricular stimulus stops conducting up to the atrium, you have reached the retrograde AVNERP. In this case, the pacing protocol is complete and extra stimuli are not usually added. If SVT does develop, the relationship between the ventricular signal and the retrograde atrial signal is key in diagnosing the origin of the tachycardia. A shorter VA interval, usually under 70ms, is a strong indicator of AV node reentry. A more prolonged VA interval points towards AV reentry tachycardia through a bypass tract. Note that patients with retrograde conduction through a bypass tract have a higher incidence of atrial fibrillation. If atrial fib occurs while you are doing ventricular stimulation, give strong consideration to the possibility of a concealed bypass tract.

           While uncovering SVT by pacing the ventricles is a useful tool, the main reason you perform ventricular pacing is to induce ventricular tachycardia or ventricular fibrillation. When this is your goal, the extra stimuli is decreased until tachycardia is induced, the pacing interval reaches 200ms or until the ventricle becomes refractory. This point is called the VERP, or ventricular effective refractory period. If you are wondering why the pacing interval should not be decreased below 200ms, then you are in the same boat I was several years ago. When I first started in electrophysiology, I learned a great deal from Dr. Thampi John. Dr. John, whom I consider a good friend, was responsible for the strong growth our program has seen over the past several years. Much of what I have written here is knowledge that I originally learned form him. When we were doing ventricular stimulation, I asked him why we stopped decrementing the extra stimuli at 200ms. His response was, "You can put anyone into V fib if you push them hard enough. But if you do it like that, it is garbage, it has no clinical significance." So, when I reach 200ms, I stop pacing, add the next extra stimuli and begin again.

          If the pacing protocols are completed through S4 using two S1 cycle lengths, the ventricular catheter is often repositioned to the Right Ventricular Outflow Track, (RVOT), and induction is started over again. Once the process of pacing the RVOT has been completed using the standard protocols, isuprel may be given to enhance cardiac conduction. Note that isuprel should be used very carefully, if at all, in patients with known or suspected coronary artery disease. As a cardiac stimulant, isuprel may increase blood pressure and cause vasoconstriction. If the choice is made to use isuprel, the entire process of ventricular stimulation may be repeated starting in the RVOT and concluding in the right ventricular apex. If the pacing protocols are completed without induction of an arrhythmia, the test results are considered to be negative.

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