Afib and Oxygen Desaturations - looking for cause and effect

Please excuse this newbie question, I'm sure it's been discussed before but I just can't find the relationship I'm looking for.

I'm anticipating to find that an Afib episode may cause oxygen desaturations.

Now, I'm not questioning that the reverse relationship,that of lowered blood oxygen saturation, may be a trigger for an Afib episode, that apparently is an accepted notion and is the potential mechanism for suggesting that sleep apnea may trigger Afib.

Context (for those who might be inclined to indulge me further):
My wife, who has been medically treated for paraoxsimal Afib for over 10 years (current assessment of burden is 3%) was told to get a sleep study by her electro-physiologist to rule out that sleep apnea was causing her Afib.

The sleep study, which was a home sleep study (no eeg) was begun uneventfully but about a half hour into the 7 hour study she had an Afib episode that persisted for about 3-4 hours.
The sleep tech that read the device, reported correctly that the patient had an episode of Afib and reported the time (which was obvious on the pulse rate graph). Also reported was that she experienced 74 oxygen desaturations. (It turns out that 72 of the desaturations (less than 90% PO2) occurred during the Afib episode.

So the sleep doctor, seemingly based largely on the desaturations, concluded that she required CPAP treatment, and right away.

We have been unsucceesful with suggesting to the Dr that the sleep study was flawed, in that it did not represent her normal sleep. Another sleep study, conducted when she is not having a Afib episode (recall that her 14 day EKG pegged her Afib burden at 3%) would be more representative.

So I'm trying to obtain information (if there be any) that a patient in Afib is likely to exhibit Afib caused oxygen desaturations.


On the other hand, I may be entirely WRONG !. if so that is useful information also.
Thanks for listening

I think you're engaging in wishful thinking. Afib might cause a slight drop in O2 sats but nothing like under 90%. Two or three percentage points I could believe, but not all the way down to <90%. I've been in afib hundreds of times with rates ranging from 180 to 250, and my O2 sats always remained perfectly normal. As an EMT I've seen dozens of others in afib and I've never observed a reduction in SpO2 unless they also had other issues such as asthma or COPD.

When you see O2 sats dropping that low it's either because the patient isn't moving air adequately or they're unable to absorb it effectively. It's not a pumping problem unless we're talking about someone in cardiac arrest. (And even then a person in arrest won't be breathing, so it's still an air movement problem.)

It's extremely unlikely the sleep study was flawed. (How would that even happen?) Your wife needs CPAP. It's the apnea causing the afib -- which it's well known to do -- not the other way around. Get her on CPAP and I predict she'll experience many fewer afib episodes.

Thanks for the reply Carey,
The wife did start APAP therapy in October '21 with no observable change in the frequency or duration of her Afib episodes. Her AHI has dropped from the study value of 11 to approximately 3-4.
They say a picture is worth a thousand words, so here is the pulse/saturation graph from her sleep study.

She started the study a ~2230 and promptly fell asleep, at 2300 she was awakened by the vague chest pains and "palpitations" that she has experienced over her 10 years of Afib. She struggled trying to sleep while this Afib episode continued, but she reported never being able to get to sleep for several hours, finally she fell to sleep and then stated her day at 0600. Her normal heart rate while sleeping is about 40-50 bpm, her normal nocturnal saturation level is 92-93.

I suggest that the study is flawed because the AHI was evaluated over the entirety of the 7.5 hours, when it is more representative to say that the last 2.5 hours are representative of her normal breathing. (Recall that I said that her 14 day Holter exhibited a 3% Afib burden, which I interpret as saying that during the 14 days of continuous monitoring she demonstrated Afib only 3% of the time)

Anyway here is the pulse/saturation graph.

I can see why you think the afib is responsible from that chart, but notice that she had no dips below 90% for over an hour between about 2:15 and 3:30 despite still being in afib, and also notice that she had three dips below 90% later when she was in NSR. How do you explain those last three dips?

Incidentally, posting an image here won't work because we don't allocate disk space for photo storage. That's expensive overhead because the space used just increases perpetually, and after 23 years we would be hosting a LOT of images by now.

I can only see the chart by right clicking the icon and choosing "copy image link" and then going there. In the future, instead of inserting an image in your post, insert a link to the image. For those who want to see it, the image is at https://imgur.com/a/SsktaHD

Thanks for the heads up on images.

Regrading the three dips while appearing to be in NSR --- I'd venture you would not accept "normal variation" seeing as how her usual saturation (measured independently of this session is 92-93), so a 5 percent temporary drop is not so alarming.

But that's neither here nor there, because if the study is scored only on the period in NSR, her AHI is 2.8 well in the normative range.

If the total period (10:45p to 6;00a) is scored her AHI is 11,

In a nutshell, that is why I think the sleep study is distorted (probably better word than flawed).

But back to my original thought.

Is a consequence of an Afib episode a depressed cardiac output, (consequently less blood being delivered to the lungs)?

If I understand you correctly, you are saying no, that Afib does not impact cardiac output (volume of blood per second). Or am I misunderstanding you?

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Searching9
If I understand you correctly, you are saying no, that Afib does not impact cardiac output (volume of blood per second). Or am I misunderstanding you?

Yes, afib can reduce cardiac output, but not by much. The key point here is that reducing cardiac output doesn't reduce O2 sats unless the reduction is quite severe (severe as in life threatening). You might be pumping a little less blood, but the O2 saturation levels of that blood won't change. As I said in my previous post, reduced O2 sats means you're either not moving a sufficient amount of air or your lungs aren't exchanging O2 adequately. Respiratory function determines O2 sats, not cardiac function.

And if afib is the cause of the reduced O2 sats, what about the periods from about 11:00 to 12:00 and 2:15 to 3:30? For over two hours her O2 sats remained above 90 despite being in afib. If reduced cardiac output was the cause, it would have been consistent across the entire afib episode. In fact, if that were the cause I don't think you'd see dips; it would drop below 90 and stay there until she was back in NSR. If you have a chart showing her level of sleep, I would bet you'll find those low O2 levels correlate consistently with periods of REM sleep because... she has sleep apnea. The sleep study proves it and I don't think it's flawed or distorted.

Not the message you wanted to hear, I know, but based on my medical training and personal experiences, I think your wife has sleep apnea and afib. The apnea may be the root cause of the afib, but no matter if it is or not, treating it will improve her afib in the long run. She'll probably also feel better during the day. Most people I know who use CPAP wouldn't consider going without it.

OK, I had thought I had read some where or another that Afib may be responsible for a reduction in cardiac output by as much as 30%.

The rest of this is sidebar:
Now, does she have sleep apnea, well that's a matter of degree. After 7 months she still claims to feel no change during the day, so subjectively her Pap therapy isn't doing anything. From an Afib standpoint her Afib burden after 7 months remains at 2-3% - the same as it was prior to Pap treatment. Technically, with a co-morbidity, she just qualifies (under AASM standards) for treatment. (in fact her sleep doc's first progress notes called for "no treatment at this time". Her EP then called the sleep doc who then changed his mind and ordered a PaP machine.)

Without her knowing when I would do it, I reset her PaP pressure to a constant lowest pressure the PAP machine is capable of (4cm). I ran that experiment for 4 days to see if her AHI would change in comparison to the maximum treated pressure she had been using which ranged about 8 to10 cm. There was no change in AHI over a four day observation period.

On a different topic entirely.... I'd like to ask the community about their experiences using a HR smart watch to monitor and suggest possible Afib episodes..... Do I start a new topic or stay in this thread?

Many thanks,

I don't know where you read about a 30% decrease in cardiac output from afib but that's wrong in an otherwise healthy person. Perhaps it was something discussing patients with other serious cardiac issues? Because 30% would make afib a debilitating, life-threatening disease, which it isn't. Heck, 30% would put many of us immediately into heart failure, and that just doesn't happen with "lone" afib.

As for smart watches, instead of asking I recommend using the search feature first to see what's already been posted. Smart watches and similar devices have been discussed here at length many, many times. Searching for 'Apple Watch' would probably be the quickest way to find the discussions you're looking for.

But if you were going to ask a question like that, please start a new topic. Always start a new topic when you jump from one subject to another.

Actually I finally found the reference (re reduced cardiac output);
From the abstract:

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The presence of chronic or paroxysmal atrial fibrillation places the patient at increased risk for embolic stroke and/or death. When atrial fibrillation develops, there is loss of the atrial transport factor ("atrial kick"), with consequent decrease of cardiac output. Stroke output declines by 20-30% in normal individuals with loss of atrial kick; the decline in stroke output is considerably larger in patients with heart disease.

Atrial Fibrillation

I will continue to review some of the smart watch commentary, though it seems like most folks are looking for a portable, wearable, recording EKG, that's not really my focus.

I was always under the assumption that when I was in afib, my cardiac output was reduced (as I recall, one of my Drs. told me this). Plus, that was consistent with my increased respiratory demand when climbing stairs, walking fast or doing any type of exercise while in afib. I had over 200 episodes of afib and tried a few times to do my regular exercise program when in afib, but it flat didn't work because of oxygen debt. Below is old study, finding that it is true. I looked for more current studies and didn't find much, but the suggestion was often stated that afib does reduce cardiac output, but that it can be compensated for by a higher heart rate. When I was in afib without rate control meds, my heart rate was 180. Going for a jog and expecting my heart rate to go up to compensate for the reduced cardiac output is nuts.

The resting cardiac output was estimated in 30 patients with atrial fibrillation before and after
attempted direct current conversion. An increase in output and stroke volume was noted in the
20 patients in whom sinus rhythm was established. The mean increase in output was 53 per cent.
This increase appears to be independent of drugs. No significant change in the cardiac output
was noted in 10 patients in whom direct conversion failed. When, after successful conversion,
atrial fibrillation recurred cardiac output fell to pre-conversion levels.

https://heart.bmj.com/content/heartjnl/27/5/719.full.pdf

My experience mirrors Ken's. I've had afib for just shy of 18 years. In the first four months, I had a 2 1/2 month episode. During that time I could clearly see the effect of the lowered cardiac output during exercise. After that long episode, I rarely do exercise during afib, I primarily am relatively sedentary till I convert, as conversion is my goal. However, regarding the original post, I would hypothesize this reduced cardiac output would likely not be noticed when at rest. Its effect would be experienced during material exertion. In other words, it would limit your top end, not decrease SpO2 during rest.

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GeorgeN
However, regarding the original post, I would hypothesize this reduced cardiac output would likely not be noticed when at rest. Its effect would be experienced during material exertion. In other words, it would limit your top end, not decrease SpO2 during rest.

The medical studies cited above are silent on if the patients observed were at rest or were undergoing material exertion.
I could be wrong, but I'd have suspected that if the patients were being stressed by exertion, the study would say that.
(But my suspicions have been known to be wrong occasionally!)

Quote
Searching9
The medical studies cited above are silent on if the patients observed were at rest or were undergoing material exertion.
I could be wrong, but I'd have suspected that if the patients were being stressed by exertion, the study would say that.
(But my suspicions have been known to be wrong occasionally!)

I'm not saying that the decrease in stroke volume doesn't exist at rest, just that it doesn't matter. Think if you crimped the fuel line on car, at idle, you would not notice, but when you floor it you would. Back 18 years ago, if I was sedentary, my in afib heart rate was ~80 BPM. Now I was decent condition and my NSR heart rate would have been in the 40's or 50's at rest. I recall my first ever afib episode, I strapped on a heart rate monitor walked down to my basement and back up. My heart rate coming up the stairs was 145. I'd been training for a race that topped out at 14,100', so in NSR I would have expected to have my heart rate at 80 or at most 90 going up the stairs. The increased heart rate was to make up for the lower stroke volume. I didn't have an SpO2 monitor at the time, but would not have expected it to have changed at rest.

I have a graph of a recording SpO2 monitor that I happened to be wearing when an episode started and I converted it in three minutes with an exhaled breath hold (meaning I exhale all the air from my lungs and then hold it out). If you look at the second graph in this post you will see that there is no drop in SpO2 from the afib till the end of the breath hold. Note that I live at 5,500' elevation, so normal SpO2 is a bit lower: 94-95%. The drop into the low 80's was due to the breath hold. I do breath holds like this in NSR on many days and I intentionally drop the SpO2 to 70% or lower on s several minute breath hold.