Ventricular tachycardia

Definitions & Key takeaways

Ventricular tachycardia is a type of tachycardia, or a rapid heartbeat that arises from improper electrical activity of the heart presenting as a rapid heart rhythm that starts in the ventricles. There are two main types of ventricular tachycardia: monomorphic, and polymorphic ventricular tachycardias.

In monomorphic ventricular tachycardia, all the beats look the same because the impulse is either being generated from increased automaticity of a single point in either the left or the right ventricle, or due to a reentry circuit within the ventricle. Polymorphic ventricular tachycardia, on the other hand, is most commonly caused by abnormalities of ventricular muscle repolarization. Ventricular tachycardia is a potentially life-threatening arrhythmia because it can cause low blood pressure and may lead to ventricular fibrillation, asystole, and sudden death. Ventricular tachycardia ranges between 100 and 250 bpm.

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Ventricular refers to the bottom chambers of the heart, the right and left ventricles, as opposed to the top chambers, the right and left atria.
Tachycardia refers to a fast heart rate. Typically, a fast or “tachycardic” heart rate is considered anything above one hundred beats per minute.
But ventricular tachycardia’s different than, say, a fast heart rate from exercising, which is called as “sinus tachycardia”.
Normally, the electrical signals that generates each heart beat starts in the right atrium, at the sinus node, also known as the sinoatrial node or the SA node, if the rate goes over 100 bpm and originates in the SA node, it’d be considered sinus tachycardia, which is totally normal.
Sometimes though, heartbeats can become abnormal if that electrical signal doesn’t start in the SA node...and starts in the ventricles instead.
Premature Ventricular Contractions (or PVCs) are single beats originating from the lower chambers. Any time there are more than 3 beats like this in a row then it’s defined as ventricular tachycardia.
Ventricular tachycardia, sometimes called V-tach or VT, can cause the heart rate to get above 100 beats per minute, which can be extremely dangerous and lead to sudden cardiac death...but hold on, how can that happen?
It’s not like while we exercise we’re risking sudden cardiac death, right? Well, even though we say tachycardia is anything above 100 beats per minute, most patients with ventricular tachycardia experience heart rates as high as 250 beats per minute.
250 beats per minute means the heart’s beating over four times per second, and when the chambers are pumping that fast, they don’t have enough time to even fill with blood, so the heart is furiously pumping out just tablespoons of blood to your body (and most importantly—your brain), which is just not enough.
If this happens, a person can have symptoms of not having enough perfusion to their tissues like chest pain, fainting, dizziness, or shortness of breath—it can even cause sudden death.
Now there are essentially two ways an electrical signal can start in a ventricle, either the signal’s focal, or it’s reentrant.
Focal V-tach is where a specific area of the ventricle has abnormal automaticity. The automaticity rate is the frequency at which a cell sends out a signal, so for pacemaker cells in the SA node the rate is between about 60 and 100 signals per minute, resulting in 60 to 100 beats per minute, let’s just say 60 beats per minute, so one beat every second.
Some specialized pacemaker cells in the ventricles also have this ability, they’re just usually a lot slower, about 30 beats per minute, or one beat every two seconds.
So in most cases, the SA node fires ‘em off a lot faster, sending electrical waves throughout the atria and ventricles, and not giving the ventricular pacemaker cells a chance to ever have just 2 seconds of peace which is what they need before they fire at a rate of 30 bpm.
For example, say all the other pacemaker cells stopped suddenly, after two seconds, the ventricular cells would initiate a signal, right?
Alright, now if a certain area of ventricular tissue gets stressed or irritated in some way, the ventricular pacemaker cells might start firing at higher rates, and essentially flip roles with the SA node, firing so fast that the pacemaker cells in the SA node don’t get a chance to fire, and at this point the heartbeat is being driven by the ventricles.
This “stress” might be triggered by things like certain medications, illicit drugs such as methamphetamine or cocaine, electrolyte imbalances, and ischemia to the ventricular muscle.
More commonly, though, the V-tach is actually reentrant as opposed to focal. So if we take a closer look at the cardiomyocytes, or heart muscles cells, instead of the pacemaker cells, these can be stressed in a similar way as well, which might change a couple of their properties, including how fast they relay or conduct the signal to the next cell, as well as how long their refractory period is.
Now the refractory period is this period right after conducting a signal, where the cells can’t conduct another signal. To help explain this, let’s say this myocardial tissue on side A conducts really fast, so the electrical signal zips through, but it takes a long time to be able to conduct again, in other words it has a long refractory period.
The other side (side B) is the exact opposite, so slow conduction, short refractory period. Now this isn’t entirely unusual, since the heart naturally can have tissue with different properties.
But let’s say that this tissue becomes damaged and some of these cells actually die, like with a heart attack. Well now you’ll get some scar tissue, which really can’t conduct the signal as well, and sometimes this can create a sort of split pathway, where it goes around the scar, and meets back up on the other side.
And with these conditions met, it’s possible that a reentrant circuit develops. K so if one signal comes through, that’s fine.
Because on side A, the wave makes it around first and goes on to the rest of the ventricle and contracts the ventricle, but it also starts up the other path, and sort of runs into the other, slower wave, called a unidirectional block.
Now side A goes into its long refractory period, while side B goes into its short refractory period, so basically side B comes out of refractory first.
If another signal comes early, while side B’s ready but side A’s not ready and is still in refractory it’ll be stopped on the A side right?
But moved down Side B. If, by the time the signal makes it down the slow Side B, Side A is now out of refractory, the signal can re-enter the circuit, essentially moving up Side A.
It then gets back to the top of Side A, and then goes down the Side B again, which comes down and then goes back up. This can happen again and again.
And every time you go around, you get a ventricular contraction, or a heartbeat! And this is what can lead to a reentrant ventricular tachycardia.
Now the type of ventricular tachycardia is diagnosed via electrocardiogram, or ECG. ECG’s measure the electrical activity of the heart via electrodes that are placed on the skin.
A normal ECG looks something like this, with characteristic waves PQRST (and sometimes U). This big guy in the middle, the QRS complex, represents the depolarization (and therefore the contraction) of the ventricular muscle fibers.
During ventricular tachycardia, you’ll typically see something like this. Each of these represents a ventricular contraction.
When they all look the same, it’s called monomorphic, since it just has one morphology, or one form. This is typically the case for reentrant circuits, since it’s just that one single spot where everything’s starting from.
It’s also the case for focal VTs where one group of cells is responsible. Sometimes the VT can be polymorphic, though, meaning the shape changes from beat to beat because the signal’s originating from different points in the ventricles.
Polymorphic VT might happen when multiple areas of pacemaker cells become irritated and develop increased automaticity rates, like from severe hypoxia, for example.
Having V-tach is really dangerous and can develop into another dangerous rhythm Ventricular fibrillation, both of these require immediate medical attention.
VT is treated with cardioversion, either drug cardioversion or electrical cardioversion. Drug cardioversion involves a drug treatment that aims to lower the heart rate back to a normal rhythm.
Electrical cardioversion, on the other hand, uses an electrical pulse of energy delivered to the heart, that is synchronized with the fast rate to be delivered on the R-wave, which is this peak of the QRS complex; this is done to try and avoid delivering it during a vulnerable period on the T wave, in which the electrical cardioversion could induce ventricular fibrillation.
Sometimes patients might have a radiofrequency catheter ablation, where radiofrequency waves are used to heat up and destroy the tissue that’s causing the irregular heartbeat, which can essentially cure certain tachycardias.
Sometimes, patients prone to having bouts of ventricular tachycardia will be surgically implanted with a small device capable of delivering electrical cardioversion, called an implantable cardioverter-defibrillator, or ICD.