ventricular tachycardia is characterized by waveforms that change from beat to beat on ECG.
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A 45-year-old man with a history of myocardial infarction comes to the emergency department because of heart palpitations and sweating that began an hour ago. On arrival, the patient is alert but very disoriented. His temperature is 37°C (98.6°F), pulse is 172/min, respirations are 19/min, and blood pressure is 110/95 mm Hg. A rhythm strip is obtained en route and is shown below.The patient is admitted for treatment. After obtaining intravenous access, which of the following is the most appropriate next step in the treatment of this patient?
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.