ECG tracings

nurseprnRN, BSN, RN · Jan 9, 2015

The book they gave you in school on EKG basics, or the chapter in your med/surg text that talks about EKG basics would be a good place to start.

It's helpful to understand the derivation of the measurements behind those scary little boxes. This will make it easier to answer questions (your own and anyone else's) about what they mean.

The big boxes on an EKG tracing run under the pen at 300/boxes per minute. That means if there is one (regular) QRS in every box, the rate is...300/minute (ouch). If in every other box, then, that would be...300/2 = 150/minute. Every third box, 300/3 - 100/minute. One every 5 and a half boxes? 300/5.5 = 54.5 (we call this "55"). And so forth. If there is one every tenth box, the rate is 300/10 - 30/minute (ouch again).

Now, to measure intervals in the tracing that tell you how long it takes the electrical impulse in the heart to get from point A to point B (or, say, the SA node to the AV node, which is the PR interval, the impulse going through the atria), you count the little boxes. A little simple division (one big box = 1/300th of 60 seconds, so....) will get you the useful information that every big box is .20 seconds and so every little box (there are five in every big box) is 0.04 seconds.

So then if the PR starts at the beginning of one box and the QRS starts five little boxes later, that's 5 x .04 = .20 seconds (whew, normal). If the PR is four little boxes long, it's .16 seconds. If it's 8 little boxes long, the PR is .32 seconds (waaaaaay too long, 1st degree heart block by definition).

The distance between the beginning of the QRS and the end of the QRS tells you how long the impulse takes to get through the ventricles. It's usually around .08, about two little boxes wide. If you have a big honking wide weird looking QRS that takes a long time, that tells you that the conduction is not going through a nice normal pathway down through the right and left bundle branches the way it should, and is instead taking detours around infarcted areas OR the electrical impulse started somewhere entirely different from the AV node where it ought to have come from....a PVC, premature ventricular contraction.

Delayed conduction can be caused by any number of things (this is where your memory about drugs that affect conduction comes in).

Also, being able to measure PR intervals across a strip gives you useful information. What if they are different? Are they all randomly different? Are the Ps regular at rate X and the QRSs regular at rate Y, but there is no relationship between them? 3rd degree heart block (AV node is toast). Is there a normal PR on the first beat, a little longer on the next one, a little longer on the next one, and then there's a P right on time but no following QRS? This is one kind of 2nd degree block, where the AV node runs outta gas after a few conduction jobs and has to regroup before going back to work on the next cycle.

If there are no decent Ps to look at, just sort of a staticky baseline, and the QRSs are irregularly irregular, that's atrial fib. You know this because an organized atrial contraction would draw a nice P wave, and there aren't any, and the AV node isn't getting regular messages from above, so it does its thing irregularly.

Now, it's useful to know the difference between VT and VF.To understand this better, you have to understand cardiac conduction in general. This following section will have some repeats from above... if it doesn't lool familiar, then you didn't take the time to learn it. Go back.

Remember that an EKG shows you the path the electrical impulse takes as it travels through the heart. Take a look at the diagram of the normal conduction system. That will help you visualize better.

Most muscle cells cannot contract without some sort of electrical stimulus telling them to. Wouldn't it be a mess if all the muscles cells in, say, your thigh could depolarize and contract any old time, without your brain sending the impulse down to them? Cardiac muscle cells are a little different; they can generate their own little electric jolt and pass it along cell-to-cell to their neighbors IF the normal impulse doesn't come through the normal conduction pathway often enough. Remember that for later.

1)The normal impulse starts in some specialized cells in the sinoatrial (SA) node, a little patch of tissue that has the ability to do this by itself 'way up in the atria.

2) This impulse spreads thru conduction pathways in the atria, making the muscle cells contract as it goes, in a nice even pattern that empties the atria thru the tricuspid valve (right heart) and mitral valve (left heart) into the ventricles to give them something to do. That's diastole. This electricity looks like a nice round little bump, the P wave, on EKG.

3) There's a teeny pause while the impulse is gathered up in the atrioventricular (AV) node, then spreads in a nice pattern thru the ventricles, their muscle wringing in an orderly fashion, like a washcloth. (The electrical signature of this action is the QRS, the big spiky deflection on the EKG.) The pressure thus developed closes the mitral and tricuspid valves but opens the pulmonic valve (right side) and aortic valve (left side) and blood gets pushed into the pulmonary artery and aorta. That's systole, and we have...a blood pressure.

If the tissue at the AV node is on strike for some reason, like it's dead after infarct (good reason), when the impulse comes down to it from the atria, it's unable to pass it along to the ventricular conduction pathway, so there is no longer a nice P wave->QRS, P->QRS, P->QRS happening. After a bit the ventricles notice that they are not getting any direction from up above. They are big and strong, but not that smart, so they only get it together to generate their own contraction slowly after one of their cells takes it upon itself to contract. Because the impulse driving them does not come down that nice dedicated pathway but has to spread cell-to-cell from there, it takes longer and doesn't look like it knows where it's going, so the QRS is wider and funny-looking.

Now if you look at the tracing for this, you see a nice regular march of P waves, indicating the atria are working they way they are supposed to, and then, at a totally different rate and not playing nice and holding hands with their friends, the ventricles tooling along on their own, slower rate. It may be fairly regular but it won't have any relationship at all to the P waves. THAT's complete heart block (3rd degree AV block).

The question is, What's the difference between defibrillation and cardioversion?â€

I liked the answer that said, "A pt with afib is alive, but the pt with vfib is dead or almost there with an ETA of five minutes."

True enough. But I think that to help you answer your own question you need to be solid on the basics of normal cardiac cycle and the conduction system that makes it happen. Another reiteration:

1) teeny electrical impulse starts in the sinoatrial (SA) node, a little patch of tissue that has the ability to do this by itself 'way up in the atria.

2) impulse spreads thru conduction pathways in the atria, making the muscle cells contract as it goes, in a nice even pattern that empties the atria thru the tricuspid valve (right heart) and mitral valve (left heart) into the ventricles to give them something to do. That's diastole. This electricity looks like a nice round little bump, the P wave, on EKG.

3) Impulse is gathered up in the atrioventricular (AV) node, then spreads in a nice pattern thru the ventricles, their muscle wringing like a washcloth. (The electrical signature of this action is the QRS, the big spiky deflection on the EKG.) The pressure thus developed closes the mitral and tricuspid valves but opens the pulmonic valve (right side) and aortic valve (left side) and blood gets pushed into the pulmonary artery and aorta. That's systole, and we have...a blood pressure.

SO now can you see the diference between an atrial event and a ventricular one? They occur in different places. So their consequences are radically different.

Cardiac muscle is better off in terms of efficiency if it uses those organized conduction pathways to develop coordinated muscle contractions. But the conduction system can be stretched out too much, like it can be in mitral disease, because the atria have really high pressures in them (think: high-pressure systolic backflow thru the mitral valve if it doesn't close all the way OR higher pressures in the atria if the valves don't OPEN all the way when they should). Or it could lose some of its useful cells with an MI. Whatever. What happens then is that the individual cells all think they have to take over, and the atria becomes a quivering, uncoordinated mess. You no longer see a nice little round P wave, because there's no longer the nice organized flow thru the atria to make one. That's atrial fibrillation. Some people get a decrease in BP with this (this has more to do with how the ventricles behave with the varying amts of blood presented to them in "diastole", but I digress...), but blood continues to flow into the ventricles and so there is still some BP to make in systole :) .

VF is something else. As I mentioned above, the cardiac muscle cell has an interesting quality that no other muscle cell in the body has: it can, if conditions are right, contract on its own without an external stimulus. (To get an idea of how remarkable this is, imagine what would happen if all the muscle cells in, say, your thigh could do this without waiting for instruction from your CNS.)

Unsuccessfully treated VF is a terminal event, because a ventricle that is fibrillating is not circulating any blood out the aorta...and we all know what that means. VF on the EKG looks like a wiggly, squiggly line with small irregular points-- sorta like a very quiet EEG line. Nothing neat, nothing organized, nothing regular...because that's what the ventricle is doing: nothing neat, nothing organized, and nothing regular. All the cells are firing off in an uncoordinated fashion, and even if there are normal impulses coming thru the AV node the conduction system isn't working.

The way a defibrillator works is sorta like what happens in the old Western movie when the Sheriff finds an ugly, rowdy mob on the front porch of the jail. This is VF-- uncoordinated, unpredictable, and deadly. What does he do? He fires off his rifle, ka-BLAM! and this stops all the rabblerousing in its tracks so they can now listen to reason. Defibrillation makes all those rowdy cells discharge all at once, and while they're getting their breath back, so to speak, the normal conduction pattern can take up its work of making them orderly again. Well, we hope so, anyway. If other conditions are right (cell oxygenation, chemistries, cell wall integrity...) it will.

When you shock a fibrillating ventricle, that's called "defibrillation." When you shock a fibrillating atrium (in hopes of accomplishing the same thing: an end to chaos and a return to order) it's called "cardioversion," and has to be synchronized with the pt's own QRS (the machine does this for you, but you have to tell it to). This is because a jolt that lands in the wrong time in the ventricular conduction sequence can make for VT or VF itself, and you don't want to make extra work for yourself in this way :) .

I just love this stuff :)

kogepan · Jan 9, 2015

wow! above post is so informative. Thanks!