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. If the next deflection is upward, or positive,
then it’s called the R wave. If, though, the first wave after the p-wave
is upwards, instead, or positive, you basically skip the Q and just called it an R wave. 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

43 thoughts on “Premature Ventricular Contraction – causes, symptoms, diagnosis, treatment, pathology”

  1. My patient recently presented with ventricular bigeminy? recorded on ECG and he complaint of lightheadednes. On pulse palpation and heart ascultation concordant rate at 48 bpm ….so what doesn't mean ?

  2. just like all your videos , Short And Clear And the best information in the easiest way , seriously you are a gift may god bless osmosis

  3. Thank you. I just went to the ER and they told me this is what I have then sent me home. This explains what is going on. At least now I understand better what's happening to me. So yeah, thanks for that.

  4. Had a catheter ablation 3 days ago, the only regret I have is, why didn't I get it sooner, I feel great, I can see the quality of my life changing for the better.

  5. Ive had PVCs for 18 months off and on. One PVC every 20 -60 sec. Tried to figure it out on my own because doctors dont know jack and would say they are benign or would try to prescribe some BP meds. Something that feels like PVCs are not benign!

    Started off taking 400-600 mg of potassium a day, 200mg with each meal, and it help a little. Bumped it up to 900 mg a day, 300mg with each meal and the PVCs are mostly gone! Will probably bump it up again to 1200mg a day.

    Alcohol, caffeine, or a heavy meal speed up the blood flow and the potassium is filtered out/depleted more quickly.

    Look for more nutrient rich foods with lots of potassium.

    I AM NOT A DOCTOR SO BE CAREFUL WITH POTASSIUM. There is a lethal dose and you should research the problems from taking too much.

    Also i am outside all day, everyday so i sweat a lot. Dont eat many veggies. I say this just to portray my lifestyle.


  6. Quick question! Shouldn't the ectopic focal point @6:10 be drawn at the left ventricle since the "R" is so large (based on what you mentioned earlier)? Am I missing something, or was it just drawn inaccurate to move on with the next lesson? Thanks in advance!

  7. I had wpw syndrome, and had ablation procedure and now it's gone the ecg is normal now. However, I still have some extrasystoles and my cardiologist says and shouts at me, to stop getting stressed and have anxiety and also to watch my food. They are mostly have to do with lifestyle 95%

  8. Guys your videos are amazing! But please change you Prime plans as it is very expensive for us students. It would be a lot easier to pay monthly than the whole year at once. 🙁

  9. I have read in guyton that AV node allows unidirectional conduction , so how can depolarising wave enter from ventricle to atria?

  10. Very helpful. Please read. I had been having PVC's for a few weeks, but didn't know what they were. I was under some pretty aggressive stress in life and drank a lot of coffee at the time. My wife finally took me to the ER when I almost fainted in the kitchen one morning. I was in the hospital for 2 days while they ran tests, including that damn treadmill. Happy to say that we've downsized life. We moved, I quit that job and calmed things w-a-y down. Also switched to decaf. 🙁 Anyway, thank you very much for putting this together. I'm no doctor, but I try really hard to find education for things that go wrong. This was the best one for PVC's that I've found.

  11. How do you know when PVCs are dangerous? I have an electronic blood pressure monitor that also tracks my heart rate. Sometimes it’ll say that I have an irregular heartbeat. I take my blood pressure again and then I start to worry. I was diagnosed with PVCs a couple of years ago and my doctor said it was nothing to worry about. Other than feeling lightheaded sometimes, I don’t really have any symptoms. I also have low blood pressure.

  12. I was diagnosed with PVCs about 12 years ago. The doctors put me on 25mg of beta blockers, Atenolol which I take at bedtime. I'm fit, exercise very regularly, don't smoke. I still get the odd skip now and then but they no longer bother me.

  13. Great explanation. Kudos
    But you forgot the Roemheld syndrome or gastro-cardiac syndrome as a cause.
    It isn't only anxiety, mineral (electrolyte) imbalance, thyroid issue.

  14. I have those and i had a catheter ablation at 2015 and 2017 for WPW treatment which i was born with it. My cardiologist has seen all those premature beats,although they don't pose any risk like he said they are SUPER ANNOYING,which can make you get scared.

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