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Premature ventricular contraction

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Premature ventricular contraction

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Premature ventricular contraction

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A 55-year-old man comes to his cardiologist for a followup visit. He denies cardiac symptoms, though his EKG shows a ventricular fusion beat. Which of the following is the most likely potential cause of this patient’s fusion beat?

Transcript

Content Reviewers:

Rishi Desai, MD, MPH

The heart has two lower chambers, called the ventricles, and 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 normally, the sinoatrial, or SA, node sends an electrical signal called a depolarization that propagates out through the walls of the heart and causes both upper chambers to contract. Then, that signal moves to the atrioventricular, or AV, node, where it’s delayed for a split second. Then, the signal travels down into the ventricles, or lower chambers, where it moves down the bundle of His into the left and right bundle branches and into each ventricle’s Purkinje fibers, causing them to contract as well. This trip is called a depolarization wave, and in a healthy heart, it makes sure that the upper chambers contract before 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 its contraction are seen as a P-wave, the ventricular contraction is seen as a QRS complex, and the ventricular repolarization and its relaxation are seen as a T-wave.

This empty space is called the PR segment, and it corresponds to the pause in the AV node. This one is called the ST segment, and it corresponds to the interval between ventricular depolarization and repolarization. Finally, this one is called the TP segment, which represents the heart’s quiet time, which happens 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, and a way to remember that is by thinking that the letter Q has a downward tail. If the next deflection is upward, or positive, then it’s called the R-wave. However, if the first wave after the P-wave is upwards, or positive, instead, 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 these depolarization rates get slower as you move further down the heart. 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. If, for example, the SA node stopped firing action potentials altogether, then the AV node would take over at its slightly slower pace. Now, though, let’s say you have an ectopic focus, which is a cell or area of tissue that sends off an early depolarization wave before even the SA node gets to fire, somewhere in the ventricles. This is what leads to a premature ventricular contraction, or PVC.

A latent pacemaker cell or cardiac muscle cell could depolarize early if it experiences 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 be caused by triggered activity, which is when cells depolarize early. The exact mechanism here 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 the depolarization 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 could happen in scar tissue after a heart. The wave starts going around and around that tissue, forming 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 depolarization wave will depolarize the right ventricle first and then the left ventricle. 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, and this 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 because the timing and direction of repolarization will be abnormal as well.