CPAP causing major EKG changes

[Rialaigh]

I have looked through my books a bit and browsed google some and am still fuzzy on the physiological process by which the extra pressure that CPAP can cause on the heart can cause electrical changes on the EKG, massive ones at that. Below is several 4 leads and 12 leads with some patient information, I am curious on your thoughts on what is going on...

57 year old female, history of cardiac problems, implanted A-V pacemaker, COPD, and CHF. Lung sounds are minimally wet and from description of patient upon arrival this seems to be more COPD exacerbation than CHF. No edema noted in lower extremities. Patient GCS 15 upon arrival breathing 24-28 times a minute, very shallow, with a pulse ox on home O2 of 84% while resting.

Initial vitals
BP 226/140
HR 81
Respirations 24-28
O2 84% on home O2 while resting



First 4 lead and 12 lead were obtained at the same time (within 30 seconds).
CPAP was placed 1-3 minutes after EKG obtained. 5-7 on the pressure
Second 4 lead and 12 lead were obtained 7 minutes later.


Patients work of breathing and O2 sat Improved dramatically shortly after placement of CPAP. Patient was comfortable upon arrival to hospital.


So Im wondering about these EKG changes and the process by which this occurs...and how worried do I need to be when I see this...

In order,
First 4 lead
First 12 lead

7 Minutes later

Repeat 4 lead
Repeat 12 lead

 

[Brandon O]

Are they so massive? If we ignore the rhythm strips it's not so dramatic.

 

[04_edge]

I am not an expert on pacemakers, but heres my opinion. The initial ECG has a p wave for every QRS, the rate is regular, and the complex is narrow, it is a sinus rhythm. I am not too familiar with lifepacks, but i am assuming the arrows are supposed to mark pacer spikes? The second ECG is not as clear, however the rate is faster, and is ventricular in origin. My bet would be that it is a demand pacemaker and in the second ECG the pt is being paced from the ventricles. I have not personally seen CPap have an effect on an ECG. In this case, unless the pt has a change in condition, the ECG change would be of little concern to me.

 

[paradoxicalmotion]

I second 04_edge's post.

In the first set of strips, the patient had no native atrial activity, and was being paced at a rate of 80.

In the second set, the patient's atria started doing their job (at a rate of 96), and just the ventricles were now being paced.

I could be totally wrong. I've always been terrible with paced rhythms.

 

[sdadam]

Are they so massive? If we ignore the rhythm strips it's not so dramatic.

I'm with Brandon on this one.

These ECG's read identically, just like the monitor says. Remember that reading an ECG is not about pattern recognition. Just because the patterns of the tracings don't look like the same thing doesn't mean that the ECG's don't read the same.

First off, rhythm strips are not for morphology interpretation. Monitors have a different filtering and amplification algorithm for the rhythm display and the diagnostic 12 Lead. The rhythm strip is the "Non Diagnostic Mode", that's why it takes a moment to process a 12 lead. Can you sometimes see nice big tombstones on lead II? Sure, but even someone with the worst, blurriest vision can point out a huge mountain on the horizon, they can't tell you if it's snow capped though. That's an apt analogy, the rhythm strip is literally a lower resolution than the 12 lead.

If we compare the two 12 leads they are identical, if of different overall voltages, including a non-diagnostic tracing in v1 and v2 as well as aVL on the second. When you look at them side by side the morphology is the same, the center of each complex has just been pulled up or down respectively. The increase in amplitude is due to the 12 Lead warming up.

Ok, that was a joke, sorry. When I learned about this from my preceptor he told me a story about a 12 Lead class he was once in where a medic asked the instructor;

"Why does it sometimes take five or so minutes for my ECG to 'warm up' and the artifact to go away and the tracing be clear?"

Everyone looked at her like she was crazy, but it's true. Not that the 12 Lead warms up, but the gel on the electrodes is water soluble. We put the electrodes on the "skin" but really the outermost or "horny" layer of the skin is extremely hydrophobic, while just under it the dermis is extremely hydrophilic. The electrode gel at first only comes into contact with the "horny" layer made up of sebum, oils, and dead dermal cells among other non-living stuff. This isn't enough impedance to completely keep the ECG from seeing the electrical signals of the heart but it is enough to dampen them. That's why you have lower voltage in your first 12 Lead. After three to five minutes the electrode gel has dissolved much of the water soluble materials and seeped down to come into more complete contact with the dermis and thereby the patients total body water compartment, where all the electrical activity happens. Now you have a much clearer picture but you are seeing a lot more artifact, which is to be expected. Additionally I would guess the second 12 Lead was done with more general movement of the patient? Maybe in the back while driving? We lost diagnostic tracings completely on V1, V2, and aVL, so maybe the electrodes aren't adhering well? Are the electrode on the extremities? You always want the electrodes on the shoulders and chest.

For further proof of this you have to look only as far as the stress test lab. Those cats get awesome 12 leads on people on freaking stairmasters and I have my medic students tell me the artifact from the road is too much to overcome.... Something is up. The trick turned out to be super fine grit sandpaper made by 3M. I asked a cardio tech. friend about it and he said they sand the skin down so it's slightly red and raw before putting the electrode on. Bam, near perfect ECG's (chest and abdomen, no extremities! ECG's literally can't see extremities, it's a mathmaticall sphere and you're just putting the "camera" further away.) Always shave off all hair and the I use a damp 4x4 to rub the spot raw. I haven't been able to convince anyone to buy my sandpaper yet, but someday.

With the 12 leads above they read identically, if we were evaluating them for ischemia / infarct (we have a paced rhythm so we're going to use the scarbosa(sp?) criteria) we get a negative assessment for signs of ACS in both ECG's, and in the leads we can compare (v3 for example) that have diagnostic tracings both times the read according to the scarbosa(sp?) criteria is pretty much without change.

Anyway, like Brandon brought up in order to discuss this someone is going to have to point out how the 12 Leads are different other than overall amplitude.

What interested me more in your post was that you seem to know, or have been taught that it would be normal for CPAP to induce ECG changes. I haven't ever read that, could you provide a source that talks about that happening? I'm not convinced that it couldn't but I can't really talk about it without knowing more about it, I couldn't turn up much on google either.

Electrophysiology is one of my favorite topics so I'll say what I THINK might be how it should work, but I'm kind of hoping I'm wrong here cause this sounds interesting.

CPAP should not, in an otherwise healthy heart induce any ECG changes that are not secondary to the possible increased oxygenation of the heart. It is well documented however in research on Obesity Hypoventilation Syndrome / Sleep Apnea that CPAP is capable of eliminating transient ST changes associated with hypoventilation induced hypoxia. So where I come out of it is; although it is documented that CPAP could enact ECG changes in relation to restoring oxygenation to the heart thereby directly relieving ischemia and it's corresponding ECG changes, we wouldn't expect any change in an ECG not related to that relieved ischemia. I just can't think of an electrophysiologic mechanism by which we would expect CPAP to cause primary ECG changes.

 

[Brandon O]

Not thinking about the specific patient, but spitballing a couple versions of how CPAP could affect the ECG:

1. Mechanical changes in the size, impedance, and orientation of the thorax.
2. Decreased preload due to increased intrathoracic pressure. You could argue for various changes from this, some contradictory.

I bet there's been something published. But I gotta run.

 

[ricardoj]

sdadam, on your sandpaper point, the "paper" that many electrodes come stuck to in the packaging have a thin line, typically black, on the backside that is a sandpaper of sorts. Not the greatest and not much surface area to it, but it can certainly help out in a pinch.

 

[sdadam]

Not thinking about the specific patient, but spitballing a couple versions of how CPAP could affect the ECG:

1. Mechanical changes in the size, impedance, and orientation of the thorax.
2. Decreased preload due to increased intrathoracic pressure. You could argue for various changes from this, some contradictory.

I bet there's been something published. But I gotta run.

For sure, I was thinking about the structural changes and pressure changes as well, but everything I could think of would be contradictory in this ECG so although probably there, I think they are completely over written by the changes due to the effects above (described in my other post) and any minor morphological changes are non-diagnostic.

I tried to find a study on anything regarding resistance of a body, positive pressure ventilation, and ECG changes. But the only research that I could find had to do with CPAP relieving hypo-ventilation and thereby relieving ischemia. It wouldn't be hard to test this, it would be hard to come up with a mechanism but you could set up a pretty simply study and with <$100 in commercial electrical equipment record the thoracic impedance of normal PT's and then PT's under different levels of positive pressure ventilation. At this point I didn't even find any references to a mechanism or discussion in bioelectomagnetic or electrophysiologic publications that overlaps with this. I didn't look THAT hard, but I feel like I would have come across something, I'm relatively familiar with the state of electrophysiology, I don't think it's been studied. You could probably pretty easily get published if you did the study and found an interesting difference. It's then up to smarter people than me to theorize the mechanism and prove it.

sdadam, on your sandpaper point, the "paper" that many electrodes come stuck to in the packaging have a thin line, typically black, on the backside that is a sandpaper of sorts. Not the greatest and not much surface area to it, but it can certainly help out in a pinch.

That's sick, I haven't ever heard of that! I'm going to look into it and see if we can get those! Thanks!

 

[ricardoj]

That's the blue "sandpaper" strip

 

[CANMAN]

I'm with Brandon on this one.

These ECG's read identically, just like the monitor says. Remember that reading an ECG is not about pattern recognition. Just because the patterns of the tracings don't look like the same thing doesn't mean that the ECG's don't read the same.

First off, rhythm strips are not for morphology interpretation. Monitors have a different filtering and amplification algorithm for the rhythm display and the diagnostic 12 Lead. The rhythm strip is the "Non Diagnostic Mode", that's why it takes a moment to process a 12 lead. Can you sometimes see nice big tombstones on lead II? Sure, but even someone with the worst, blurriest vision can point out a huge mountain on the horizon, they can't tell you if it's snow capped though. That's an apt analogy, the rhythm strip is literally a lower resolution than the 12 lead.

If we compare the two 12 leads they are identical, if of different overall voltages, including a non-diagnostic tracing in v1 and v2 as well as aVL on the second. When you look at them side by side the morphology is the same, the center of each complex has just been pulled up or down respectively. The increase in amplitude is due to the 12 Lead warming up.

Ok, that was a joke, sorry. When I learned about this from my preceptor he told me a story about a 12 Lead class he was once in where a medic asked the instructor;

"Why does it sometimes take five or so minutes for my ECG to 'warm up' and the artifact to go away and the tracing be clear?"

Everyone looked at her like she was crazy, but it's true. Not that the 12 Lead warms up, but the gel on the electrodes is water soluble. We put the electrodes on the "skin" but really the outermost or "horny" layer of the skin is extremely hydrophobic, while just under it the dermis is extremely hydrophilic. The electrode gel at first only comes into contact with the "horny" layer made up of sebum, oils, and dead dermal cells among other non-living stuff. This isn't enough impedance to completely keep the ECG from seeing the electrical signals of the heart but it is enough to dampen them. That's why you have lower voltage in your first 12 Lead. After three to five minutes the electrode gel has dissolved much of the water soluble materials and seeped down to come into more complete contact with the dermis and thereby the patients total body water compartment, where all the electrical activity happens. Now you have a much clearer picture but you are seeing a lot more artifact, which is to be expected. Additionally I would guess the second 12 Lead was done with more general movement of the patient? Maybe in the back while driving? We lost diagnostic tracings completely on V1, V2, and aVL, so maybe the electrodes aren't adhering well? Are the electrode on the extremities? You always want the electrodes on the shoulders and chest.

For further proof of this you have to look only as far as the stress test lab. Those cats get awesome 12 leads on people on freaking stairmasters and I have my medic students tell me the artifact from the road is too much to overcome.... Something is up. The trick turned out to be super fine grit sandpaper made by 3M. I asked a cardio tech. friend about it and he said they sand the skin down so it's slightly red and raw before putting the electrode on. Bam, near perfect ECG's (chest and abdomen, no extremities! ECG's literally can't see extremities, it's a mathmaticall sphere and you're just putting the "camera" further away.) Always shave off all hair and the I use a damp 4x4 to rub the spot raw. I haven't been able to convince anyone to buy my sandpaper yet, but someday.

With the 12 leads above they read identically, if we were evaluating them for ischemia / infarct (we have a paced rhythm so we're going to use the scarbosa(sp?) criteria) we get a negative assessment for signs of ACS in both ECG's, and in the leads we can compare (v3 for example) that have diagnostic tracings both times the read according to the scarbosa(sp?) criteria is pretty much without change.

Anyway, like Brandon brought up in order to discuss this someone is going to have to point out how the 12 Leads are different other than overall amplitude.

What interested me more in your post was that you seem to know, or have been taught that it would be normal for CPAP to induce ECG changes. I haven't ever read that, could you provide a source that talks about that happening? I'm not convinced that it couldn't but I can't really talk about it without knowing more about it, I couldn't turn up much on google either.

Electrophysiology is one of my favorite topics so I'll say what I THINK might be how it should work, but I'm kind of hoping I'm wrong here cause this sounds interesting.

CPAP should not, in an otherwise healthy heart induce any ECG changes that are not secondary to the possible increased oxygenation of the heart. It is well documented however in research on Obesity Hypoventilation Syndrome / Sleep Apnea that CPAP is capable of eliminating transient ST changes associated with hypoventilation induced hypoxia. So where I come out of it is; although it is documented that CPAP could enact ECG changes in relation to restoring oxygenation to the heart thereby directly relieving ischemia and it's corresponding ECG changes, we wouldn't expect any change in an ECG not related to that relieved ischemia. I just can't think of an electrophysiologic mechanism by which we would expect CPAP to cause primary ECG changes.

Excellent reply/post!

 

[Christopher]

A few notes:

1. First 12-Lead shows definite Atrial pacing, with a relatively narrow complex ventricular response. Differentials include: A-V sequential with a programmed AV-delay set at ~240 ms (perhaps found as part of a search algorithm in the pacemaker), A-pacing with a long AV-delay and intrinsic V-response.

2. Second 12-Lead shows definite A-V pacing without question. Of note the PRi has shortened considerably, perhaps in response to the rate increase turning off whatever programmed A-V delay setting was present. There was also a 15 bpm jump in rate, which going back to ECG1 may mean that there was a different degree of conduction block in the ventricles.

3. A BiV pacemaker may explain some of the differences in morphology, perhaps with the initial ECG representing fusion of intrinsic and extrinsic conduction.

The 40Hz filter cuts out most of the pacer spike amplitude making it difficult to say for certain. The full 150Hz response would have made it a bit easier to see the spikes.