This is written from my personal experience and based on my own web research.

I’ve experienced PVCs for at least the last decade. During that time I’ve spent months having 5-10,000 PVC per day, every single day. I’ve also spent months where I’ve lost count of the number of days between feeling even a single PVC. I can only estimate that my heart has kicked out millions of PVCs since I first experienced them. I mention all this to explain that when it comes to premature heart contractions, I’ve built up a substantial body of work. I know what they feel like, where I feel them and how strong they are.

But in December 2008 I began having what felt like small explosions in my chest. They felt like they originated in the same place as my PVCs - my heart. Only it felt like someone had placed a firecracker inside of my chest and lit it.

And as quickly as one would appear, it would disappear, and leave me wondering what the hell had just happened, and if I should be calling a doctor.

As many of you do, I Googled. And I Googled. I was fortunate in that I was able to capture one of these “explosions” during an event monitoring, which helped to put my mind at ease but also presented me with more questions that needed answers.

Because I’m not a doctor and I don’t have access to text and other professionals in the field, I had to reach my own conclusion: I was having esophageal spasms.

If you look at the ecg tracing above from my event monitoring in early 2009, you’ll see several negative spikes in the highlighted green area.  You’ll also notice that the large positive spikes, the QRS complexes of my heartbeat, are unchanged during this time.  No difference in heart rate, no change QRS adjustments because of an early beat.

Clearly this ECG is showing an electrochemical discharge, but not one inside the chambers of my heart, because heart rate was completely unaffected.

Through the process of elimination and a careful review of my symptoms, it appears that esophageal spasms are the most likely cause of these explosion sensations in my chest, which is great news because while they can stop me in my tracks, they aren’t dangerous.

So if you’re feeling something similar, you may be experiencing the same thing as I was, which is anything but the end of the world and the end of you.

I did find one reference study worth noting, but it involved people already suffering from some form of angina and/or coronary artery disease.  So bear that in mind when you read about the study.

-Jeff

How an Understanding of Ventricular Escape Beats Puts PVCs Into Perspective

A ventricular escape beat is a spontaneous contraction of your heart’s ventricles, initiated by ectopic pacemaker cells in the ventricles instead of the usual method, which is initiation by the sinoatrial node transmitting an electrochemical signal through the atria to the atrioventricular (AV) node, then on to the ventricles, which contract and perfuse blood throughout your body.

In conditions such as AV block, where the regular electrical impulse from the atria is not transmitted to the ventricles (signaling them to contract), a backup mechanism in the ventricles initiates to maintain perfusion of blood through the body and maintain life.

This backup mechanism, called the ventricular escape beat, is initiated by ectopic pacemaker cells within the ventricles.  If it’s longer than a few beats it’s considered a ventricular escape rhythm, or idioventricular rhythm. This cluster of ectopic cells is actually keeping the heart’s owner alive! Because these independent cells aren’t located in the usual place, conduction of the electrical signal isn’t as efficient as when the signal comes from the AV node. It also doesn’t occur at the same frequency as the atrial contractions.  On an EKG an escape beat is recognized by a QRSd that is greater than .12 seconds, and a wave form that is wider and less spiked than the wave form of normal depolarization.

These pacemaker cells have a lower electrical threshold before initiating a contraction, and when AV node stimulation has not occurred within a certain amount of time, the ectopic pacemaker cells initiate ventricular contraction. In other words, these easily excited cells in the heart jump into action if it’s been too long since the last heartbeat.

Compare that to what happens with a premature ventricular contraction (PVC), right. With a PVC there’s also a cluster of ectopic cells trying to act as a pacemaker. The QRSd also tends to be greater than .12 seconds as the signal transmits through the ventricles.

Unlike an escape beat, the cluster of cells (focus) initiating this impulse didn’t wait to see if a signal was coming from the AV node. In fact, this focus just waited long enough for the ventricles to re-polarize before it made the ventricles contract again.

Like an escape beat, the R wave morphology (shape) looks nothing like a normal QRS complex, and whether the PVC results in a good, mechanical contraction depends on where the focus is located and how the signal spreads through the ventricles.

But it can be seen and hopefully understood how your heart’s original design included a backup system that makes use of easily excited ventricular cells to force ventricular contractions, much in the same way your PVCs are generated.

QRSd stands for QRS duration, which is a measure of the length of time from the start of the Q wave in the QRS complex to the end of the S wave.

Measuring this duration can provide clues as to what a potential heart rhythm problem might be.

Normal QRSd

The parameters for normal QRS duration have been defined as between 60ms (milliseconds) and 100ms. ^[1] “Normal” has also been defined as less than 120ms.^[2] Generally a QRSd between 100ms and 120ms indicates that the electrical impulses are not spreading through the ventricles as quickly as they should, which can be a sign of partial bundle branch block, fascicular block or a nonspecific intraventricular conduction delay (IVCD).   A QRSd greater than 120ms is indicative of complete bundle branch block, and the patient’s heart is likely conducting electrical impulses through ventricular muscle to compensate.^[3]
“Poor R wave progression” is often the notation seen on ECGs that show a prolonged QRSd.

References