Premature ventricular contraction
Definitions & Key takeaways
Premature ventricular contractions are abnormal heartbeats that originate in the ventricles and show up as tall and wide QRS complexes on an ECG. They occur when an extra beat is initiated by Purkinje fibers in the ventricles rather than by the sinoatrial node, the normal heartbeat initiator. PVCs are usually asymptomatic, but when they're a sign of an underlying disorder, treatment including a radiofrequency ablation may be necessary.
The heart has two lower chambers, called the ventricles, so a premature ventricular contraction is when the ventricles contract earlier than normal in the cardiac cycle.
This happens because an abnormal contraction signal, called a depolarization, originates from somewhere in the ventricles rather than coming from the pacemaker cells.
So, if we simplify this heart a little bit, normally, the sinoatrial node or SA node sends an electrical signal that propagates out through the walls of the heart and contracts both upper chambers.
Then that signal moves to the atrioventricular node or AV node, where the signal is delayed for a split second, and then goes down into the ventricles or lower chambers where it moves down the bundle of His and into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well.
So, in a healthy heart the upper chambers contract first, then shortly after, the lower chambers contract. On an electrocardiogram or ECG which measures the electrical activity of the heart via electrodes that are placed on the skin.
The atrial depolarization, and therefore it’s contraction, is seen as a p-wave, the ventricular contraction is seen as a QRS complex, and the ventricular repolarization, and therefore it’s relaxation, is seen as a T-wave.
This empty space here is called the PR segment, and it corresponds to the pause in the AV node, and this one is called the ST segment, and it corresponds to the interval between ventricular depolarization and repolarization, and this one is called the TP segment, which represents the heart’s quiet time when the cells are finished repolarizing and are ready for another signal.
Now, if we just look at the QRS complex, which normally lasts less than 100 milliseconds or 2-and-a-half little boxes, it’s usually made up of three smaller waves, also called deflections.
If the first wave after the p-wave is downwards, or negative, it’s called a Q wave - which you can remember by the letter Q having a downward tail.
Finally, any downward deflection after the R wave is called the S wave. Now, the interesting thing is that in addition to the pacemaker cells in the SA node, cells in the AV node, Bundle of His, and the Purkinje fibers, all have the ability to generate an electrical potential.
Those last three are called latent pacemakers, and they have slower depolarization rates—which is the rate at which they fire off electrical signals—and they get slower as you move further down.
Let’s use this bar to visualize the SA node’s depolarization rate, which is the fastest, and then each one below is slightly slower.
Notice that each time the SA node fires, it resets all the slower ones, and this is exactly how it works. If, for example, the SA node stopped altogether, then the AV node would take over at it’s slightly slower pace.
Now, though, let’s say you have a ventricular ectopic focus somewhere in the ventricles, which is a cell or area of tissue that sends off an early depolarization wave, before even the SA node gets to fire.
This is what leads to a premature ventricular contraction, or PVC. One cause of a latent pacemaker cell or cardiac muscle cell depolarizing early is it gets enhanced automaticity which might result from irritating stressors like electrolyte imbalances, drugs like cocaine or methamphetamines, ischemic damage like a heart attack, or anything that increases sympathetic activity, like anxiety.
Ectopic beats can also have “triggered activity” which is where cells depolarize early. The exact mechanism here, though, is unclear, but it might be due an ion channel dysfunction that leads to an unexpected change in the membrane potential during or right after repolarization.
When a cell depolarization happens during ventricular repolarization, it’s called an early-afterdepolarization, and if it happens after repolarization is finished, it’s called a delayed-afterdepolarization.
A final type of ventricular ectopic focus is a reentrant loop, where a depolarization wave encounters tissue that doesn’t depolarize - which can be something like scar tissue after a heart attack - and as a result the wave starts going around and around that tissue - forming what’s called a reentrant loop.
A reentrant loop basically starts sending out depolarization waves to the rest of the heart tissue each time the wave goes around.
If the ectopic focus originates in the right ventricle, the wave will depolarize the right ventricle first and then the left ventricle, and this produces a QRS complex that looks like a left bundle branch block.
If the ectopic focus originates in the left ventricle, the wave will depolarizing the left ventricle first and then the right ventricle, which produces a QRS complex that looks like a right bundle branch block.
Now, lead V1 on an ECG measures a depolarization wave that moves towards the right ventricle. So, when an ectopic focus originates in the left ventricle, and moves towards the right ventricle, the V1 lead shows a large positive complex, with a dominating R wave.
When an ectopic focus originates in the right ventricle, and then moves towards the left ventricle, the V1 lead shows a large negative complex, with a dominating S wave.
Regardless of the originating ventricle, a premature ventricular contraction often has an abnormal T wave since the timing and direction of repolarization will be abnormal as well.
Alright, so let’s say this heart’s cruising along at about 60 bpm, which means that there’s 1 second between p waves and QRS complexes.
All the sudden an ectopic focus in the ventricles fires off, which contracts the ventricles, and that wave of depolarization tries to travel up to the atrium, but since this happens so close to the previous depolarization, the atrium’s still in its refractory period so the wave gets stopped at the AV node.
A split second later, the ventricle enters its refractory period. Since the sinus node’s going at 1 second per beat, and it’s out of refractory, it fires off a signal and the atria contracts and you get another P wave, which is right on schedule.
But this time the opposite thing happens, and the ventricle’s in refractory so it doesn’t contract! K, now both relax and come out of refractory, and exactly one second later, the sinus node sends another signal and the atrium contracts as it should, and then everything carries on as per usual.
This situation is called a compensatory pause, which is defined as having a normal sinus complex landing exactly 2 times the normal sinus interval, which was 1 second, so 1 times 2 equals 2 seconds.
What ends up happening here is there’s this big long pause between ventricular contractions, greater than the sinus interval.
Longer time between contractions means more ventricular filling, which means the heart contracts with greater strength, which can be felt as a palpitation.
Alright, now let’s run a slightly different scenario, one where the PVC comes a little bit later, after the atrium comes out of refractory.
In this case the wave of depolarization makes it into the atrium and depolarizes the atrium, including the sinus node, so essentially the sinus node resets about 4.4 boxes from the last, or 0.88 seconds.
In this case, after being depolarized the sinus node waits its 1 second, and then sends another signal and again we carry on as normal.
This time we call this a noncompensatory pause, because the sinus complex lands less than 2x the normal sinus interval. And this is how you could tell if the PVC depolarized the atrium or not.
A ventricular ectopic focus can fire at different points in the cardiac cycle, which we can look at using the ECG. First off, it might happen during a P-wave, which can get completely lost in the QRS complex, but can sometimes be seen if you search for it.
Next, the ectopic beat could happen during the PR segment, and because the ectopic depolarization happens relatively slowly, oftentimes, it will combine with the normal depolarization wave coming down the ventricular conduction system, resulting in a ventricular fusion beat.
These can appear lots of different ways depending on where the two depolarization waves meet each other. Early after-depolarizations might start during the ST segment or even during the T-wave, which is called R-on-T phenomenon.
This used to be considered an ominous sign of an impending dangerous arrhythmia, but recent studies show that this is a bit more unclear than once thought.
Sometimes premature ventricular contractions can keep happening rather than being isolated events. For example, ventricular bigeminy is when a premature ventricular contraction consistently comes after each normal cardiac cycle.
Ventricular trigeminy, on the other hand, is when one consistently comes after every two normal cardiac cycles. Also, you might have multiple ectopic foci PVCs, producing different appearing QRS complexes on a single rhythm strip.
Now, most people with premature ventricular contractions don’t notice them, but if they keep occurring they can cause lightheadedness because of less blood getting delivered to the brain.
In rare situations, an ectopic focus can trigger ventricular tachycardia or even ventricular fibrillation, which are more serious arrhythmias where the ventricles beat too quickly to fill up with an adequate amount of blood.
The diagnosis of a premature ventricular contraction is based on the ECG, but sometimes a Holter monitor - which is like a continuous ECG monitor used over a few days - is needed to capture the event.
Typically, premature ventricular contractions don’t need treatment, and if there is an obvious cause like a medication or use of a substance, then stopping that typically resolves the issue.
If the premature ventricular contractions keep happening or cause palpitations, they can be treated with beta blockers or calcium channel blockers, both of which prevent the heart from beating too strongly.
If an ectopic focus is triggering ventricular arrhythmias, radiofrequency ablation can be done, which is where radiofrequency waves are used to destroy the tissue that’s causing the ectopic heartbeat.
Alright, as a quick recap - Premature ventricular contractions are abnormal heartbeats that originate in the ventricles, and show up as tall and wide QRS complexes on an ECG.
They can be caused by abnormal automaticity, reentry, or a triggered afterdepolarization. They’re usually asymptomatic, but when they’re a sign of an underlying disorder, treatment including a radiofrequency ablation may be necessary.
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