Skip to content

Ventricular tachycardia

Videos

Notes

Cardiovascular system

Pathology

Vascular disorders
Congenital heart defects
Cardiac arrhythmias
Valvular disorders
Cardiomyopathies
Heart failure
Cardiac infections
Pericardial disorders
Cardiac tumors
Cardiovascular system pathology review

Assessments
Ventricular tachycardia

Flashcards

0 / 13 complete

Questions

0 / 2 complete
High Yield Notes
9 pages
Flashcards

Ventricular tachycardia

13 flashcards
Questions

USMLE® Step 1 style questions USMLE

2 questions
Preview

A 24-year-old male presents to the emergency department after a witnessed syncopal episode. The patient’s parents report they had just finished dinner when their son spontaneously passed out. The patient does not recall the event and had no prodromal features. He is otherwise healthy and does not take any medications, use alcohol, tobacco, or illicit substances. Vital signs are within normal limits, and physical examination is unremarkable. Electrocardiogram is demonstrated below:


Image reproduced from Wikimedia Commons  

If left untreated this patient is at risk for which of the following complications?  

Memory Anchors and Partner Content
External References
Transcript

Content Reviewers:

Rishi Desai, MD, MPH

Contributors:

Tanner Marshall, MS

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 tachycardic, or fast, heart rate is considered anything above 100 beats per minute, or bpm. However, ventricular tachycardia is different than a fast heart rate from exercising, which is called sinus tachycardia.

Normally, the electrical signals that generate each heartbeat start in the right atrium at the sinus node, which is also known as the sinoatrial node, or the SA node. If the rate goes over 100 bpm and originates in the SA node, it’s considered sinus tachycardia, which is totally normal.

However, heartbeats can become abnormal if the electrical signals don’t start in the SA node, but start in the ventricles instead. Premature Ventricular Contractions, or PVCs, are single beats originating from the lower chambers. Any time there are more than three 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 rise above 100 beats per minute, which can be extremely dangerous and lead to sudden cardiac death.

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 mean that the heart is beating over four times per second. 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 only tablespoons of blood to your body, and most importantly, to your brain, which is just not enough. If this happens, a person can have symptoms from not having enough perfusion to their tissues, such as 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 is focal, or it’s reentrant. Focal V-tach happens when 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 the 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, making about 30 beats per minute, or one beat every two seconds. So, in most cases, the SA node fires signals off a lot faster, which sends electrical waves throughout the atria and ventricles. This doesn’t give the ventricular pacemaker cells a chance to ever have just two seconds of peace, which is what they need before they fire at a rate of 30 bpm.

For example, imagine all the other pacemaker cells stopped suddenly. After two seconds, the ventricular cells would initiate a signal, right? 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. They 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; at this point, the heartbeat is being driven by the ventricles. This stress might be triggered by: certain medications; illicit drugs, such as methamphetamine or cocaine; electrolyte imbalances; and ischemia to the ventricular muscle.

However, it’s more common for V-tach to be reentrant, as opposed to focal. So, let’s take a closer look at the cardiomyocytes, or heart muscles cells, instead of the pacemaker cells. These can be stressed in a similar way, which might change a couple of their properties, including how fast they relay, or conduct the signal to the next cell, and how long their refractory period is. Now, the refractory period is the period right after conducting a signal when the cells can’t conduct another signal.

All right, to help explain this, let’s say the myocardial tissue on side A conducts really fast, so the electrical signal zips through; however, it takes a long time to be able to conduct again. In other words, it has a long refractory period. The other side, or side B, is the exact opposite; it has slow conduction and a short refractory period. Now, this isn’t entirely unusual, since the heart can naturally 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. Sometimes, this can create a sort of split pathway, where it goes around the scar and meets back up on the other side.

Under these conditions, it’s possible that a reentrant circuit develops. Okay, if one signal comes through, that’s fine. On side A, the wave makes it around first and goes on to the rest of the ventricle, and contracts the ventricle. It also starts up the other path, and sort of runs into the other, slower wave, which is called a unidirectional block.

Summary
Ventricular tachycardia is a type of tachycardia, or a rapid heart beat that arises from improper electrical activity of the heart presenting as a rapid heart rhythm, that starts in the ventricles. 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. This 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.