Hi,

It's most probably due to breathing at low frequency. If you perform spectral analysis of the RRIs you perhaps will see a peak at the frequency of breathing within the LF range. That's why in interpretation of HRV controlling for breathing can be helpful, either by paced breathing at HF range or just monitoring breathing and checking that breathing is within the HF range. Looking at other parameters of HRV in this case can also be helpful. I would expect a higher RMSSD, total power, and higher LF/HF ratio compared to other subjects !

Attached is a PSD of a case performing paced breathing at different frequencies and also uncontrolled breathing. Breathing frequency has a profound impact on PSD of the RRIs.

If you didn't monitor breathing still it may be possible to estimate breathing frequency using ECG by different methods generally called ECG-derived respiration (EDR). In some methods the band-pass filter used for the ECG recording is important. Kubios software will give you the EDR, though it may not be very accurate. Other method is based on respiratory-sinus arrhythmia.

Hi,

I agree with Ali's answer. It is actually a pretty common phenomenon in people who practice a lot of sport : their rest breathing frequency is very low and sometimes overlaps (partially or completely) with the low frequency components of the RR, thus leaving no high frequencies, and only one harmonic low frequency.

It is also the basic principle of cardiac coherence : synchronizing your breathing with the "Mayer waves" (low frequency component due to the baroreflex, at rest at least) by voluntarily lowering your breathing frequency around 0.1Hz is shown to be good for lowering stress for example.

Bad news is that in this case most indicators (like LF/HF) can't be interpreted like in a "normal" situation since they go completely out of hand (here your HF is about zero for example...).

Pierre

very important point by Pierre that in case that breathing frequency, completely or partially, is out of the HF range, the frequency domain of the HRV like the LF/HF ratio can no longer be interpreted same as when the breathing frequency is in the HF range.

Ali and Pierre, thank you very much. It makes a lot more sense now. You are correct Ali, spectral analysis shows that all of the variability is in the LF range. I guess since we didn't give specific breathing instructions this person might have been practicing calming breaths (since we told them they might be looking at mildly distressing photographs) just as Pierre has said. Another case of me not doing my homework properly and looking at best practice for HRV (sigh). On the bright side, this is a unique case in our dataset so we can afford to set this particular case aside, but I will be more mindful of breathing in the future, either controlling it or measuring it concurrently. Thank you both again!

Glad it could help !

Dear Adrianne

Yes, it seems this patient has a very strong respiratory sinus arrhythmia, that is, a strong modulation of the instantaneous HR by ventilation. It corresponds to just over 11.5 beats / cycle, or 0.086 cycles / beat. It is not possible for me to estimate it in Hz, as I don't have the absolute time for your plot, which you give in 'beats', but assuming a relatively high heart frequency it seems it is compatible with ventilation frequency.

By the way, if you control ventilation for this particular patient the modulation will continue or even get more marked.

Best wishes

Hi Fernando, thank you for your feedback. Would advise specific instructions for participants to "breathe normally", or should they be asked to breathe at a specific frequency?

I have read elsewhere (from Thayer and colleagues) that some HRV computations (such as RMSSD) are less affected by breathing. If so I hope we could use that for our analysis, although for this particular participant we might just need to set aside their data.

Dear Adrianne

When we inspirw the instantaneous heart rate increases. The mechanism is: the diaphragm goes down, reducing the thoracic pressure, so there is a relative 'vacuum' outside the atria, which admit a little more blood. In response, the heart beats more vigorously and faster. The opposite happens when we expire, with the heart beating more slowly. If you tell your subjects to breathe regularly (with some visual clue, for instance) then this modulation of the instantaneous heart rate becomes more marked. Here is a little text I wrote a while ago to explain this to my PhD students:

Bainbridge Reflex

An increase in atrial pressure (such as the one caused by an infusion of saline or blood or the momentary reduction of the thoracic pressure during normal inspiration) causes an increase in the heart rate. This is the so called  Bainbridge reflex. Atrial stretch receptors exist in both atria and are located in the junctions of the efferent veins and the atria. Ultimately the increased cardiac output will also produce an increase in arterial pressure and activate the baroreceptor reflex with an antagonistic action. The resulting heart rate will be a resultant of the effects of these two mechanisms (Berne and Levy, 1992).

 Respiratory Sinus Arrhythmia

Rhythmic variations of heart rate synchronous with respiration are observable in most normal individuals with the cycle length widening during inspiration and shortening during expiration. Both reflex and central factors play a role in the respiratory cardiac arrhythmia (or respiratory sinus arrhythmia). During inspiration the pressure in the chest cavity decreases facilitating venous return to the atria. This triggers the Bainbridge effect with the consequent increase in heart rate. Following that the ventricular output increases raising arterial pressure and triggering the baroreceptor reflex. Recordings of the activities of the sympathetic and parasympathetic nerves show that the sympathetic nerve is activated during inspiration while the vagus is activated during expiration. Since the clearance of the norepinephrine released by the sympathetic nerve endings is slow, the effect of these cyclic stimulations of the sympathetic system are damped by this low-pass filter action. On the other hand the release and clearance of acetylcholine released by the parasympathetic system are fast, therefore the rhythmic changes in heart rate caused by respiration are mostly attributed to the oscillations in vagal tone (Berne and Levy, 1992).

Now, for the advice you asked, it depends on what you want. If you want to see how marked is the RSA, then do instruct them to follow a metronome (timer) with their ventilation, if not, just tell them to breathe normally.

Best wishes

You might want to read ...

Variations in breathing patterns increase low frequency contents in HRV spectra

Article in Physiological Measurement 21(3):417-23 · September 2000

DOI: 10.1088/0967-3334/21/3/307 · Source: PubMed

...and the references they cite.

Ah, then the low frequency pattern of someone breathing very deeply and slowly is the result of the opposing actions of the Bainbridge and the Baroreflex, if I understand it correctly. And for normal breathing, that would more or less correspond with vagal tone, which means Thayer is probably right in saying normal breathing is not a problem for measuring high frequency HRV.

Thanks a bunch for the mini-lecture and also for the reference!

Hi Adrianne,

Respiratory parameters not only affects frequency domain indexes of HRV but also time domain indexes like RMSSD. Look at the attached picture from our study. Here NB is uncontrolled breathing and PB is paced breathing at 0.23 Hz (similar to breathing rate at baseline). SB0,5,10 are various slow breathing techniques. These conditions (except baseline) were while subjects breathed through a breathing circuit usually leading to higher tidal volume. Both breathing frequency and tidal volume affects HRV. The lower breathing frequency the higher RMSSD. Effects on frequency domain depend on the breathing frequency; BPV and HRV frequency exactly follows the breathing frequency. Therefore, if breathing frequency concentrate at HF you will see a peak in HF band. If breathing frequency concentrate in LF band, you will see a rise in LF power. Pay attention that this effect is more obvious when you look within-subject not between-subject. In some studies there has been no clear association between resting breathing frequency and HRV frequency domain indexes in healthy volunteers when they did between-subject comparisons (https://www.nature.com/articles/srep37212). But if you run a within-subject comparison, any significant change in respiration parameters (rate, depth) would affect all HRV indexes.

Any control over breathing requires using a visual or auditory cue and engagement of the subject with breathing protocol actively and continuously. The effect of this engagement on attention is large enough to reduce pain perception regardless of the breathing frequency (according to our study). Therefore, guided (paced) breathing even at natural individualized breathing frequency causes distraction. Paced breathing at natural breathing frequency does not have major impact on HRV indexes unless subjects do deeper breath with paced breathing. This can be controlled by appropriate instruction and training. Also, in very few subjects paced breathing may cause distress but this is rare.

Now the question is: can you control breathing during your study without interfering with the main task of your study? if yes, my suggestion is to control breathing by paced breathing at frequency of 12-15 breath/minute. Pay attention that even telling subjects to do "normal" breathing will shift their attention to their breathing and usually causes a decrease in respiratory rate. So, if control of breathing is possible, paced breathing is better than just instruction.

But, if control of breathing by paced breathing interferes with your study main task I would suggest to not do any control on breathing and even not explain subject to perform "normal" breathing. Just monitor it and then exclude those with breathing out of the HF band (they are few) and see if that affects your results. 

If you can provide more information about your study aims and steps I can be more helpful.

GL

Ali

Hmm, if RMSSD is indeed still vulnerable to effects of breathing, then I think my options are limited (at least for the data already collected). As you say, I will need to be vigilant regarding other cases of extreme LF in the HRV, but thankfully I have not seen anything as extreme as the Person X that I presented in this thread.

Our study is actually trying to correlate HRV and electrodermal signals at rest and during viewing of distressing pictures with psychometric measures of psychopathy, divergent thinking, and creative achievement. We inform them of the possibly distressing content of the pictures before hand since that is the ethical thing to do, which is probably why some of the participants were motivated to modify their breathing in anticipation.

I am aware that focus on breathing is a behavior that can be used to cope with stress, so if we implement controlled breathing it might actually mask the "normal" responses that we are wanting to see, so unless we can think of a way around that, controlled breathing might not be so attractive for us.

Adrianne,

I recommend to not control breathing by paced breathing or by instructing subjects to do "normal" breathing in this specific study. Our group at KU Leuven in multiple studies found that emotion induction for example by pictures affects respiration parameters. To mention some:

https://www.ncbi.nlm.nih.gov/pubmed/28315375

https://www.ncbi.nlm.nih.gov/pubmed/27404329

https://www.ncbi.nlm.nih.gov/pubmed/22634279

This is a natural psychophsyiological response to emotion involving the whole system and if you try to inhibit part of the system you would also manipulate other parts like the effects on autonomic activity since respiration parameters have profound effects on it.

To my opinion the best approach is to monitor respiration parameters like rate, tidal volume, EtCO2, along with autonomic indexes like HRV, EDR, etc. and then have a comprehensive look at the responses and interpret it as a whole. There are some analysis methods with two time series like the transfer function analysis by which you can evaluate the coupling between respiration and heart rate at different frequencies etc.. which provides information on cardiac vagal control by respiration and if it is affected by emotion.

Moreover, guided breathing shifts attention away from the task to breathing and affects your results.In some of our studies we even do not explain to the subjects about the respiratory belt and that we are monitoring their respiration. As you saw you had only one subjects with low breathing rate and even that case may have had low breathing rate at baseline and other conditions as well. I hope you did a within-subject design?

What you can do in future study is to explicitly ask subjects at the end of the study what strategy they used, if any, during picture viewing to cope with it and if they think it helped, as a qualitative step.

And regarding your current data, it is still possible to estimate respiratory rate based on the ECG signal and also based on HRV. In addition to HRV parameters, respiratory sinus arrhythmia can also be extracted from your data which would be helpful. And a very important note is that try to interpret your results by looking at all relevant HRV indexes, not to pick only those in line with your hypothesis.

GL

Ali