The maximum increase in heart rate of 1 sec in sinus rhythm, registered us with spiroarteriokardiorhythmography was 10 beats / s (on rapid deep breathing)

It depends on what kind of stimulus you are delivering. I've seen step decreases in rate with intense reflex vagal activation in rats from 285 bpm to 124 bpm in a single beat (~330 bpm/sec) (unpublished). Don't know if it is relevant but a paper in Circulation (Moya & Brignole 2001) shows very rapid decreases in HR for tilt-positive syncope patients. 

you will find the answer in borst AJP 1982 243 H676-81. According to this paper in healthy volunteers, the HR increases from circa 60 to circa 100 bpmin over 1-2 s, presumably secondary to cardiac parasympathetic withdrawal.

in our experience marathon runners are able to increase HR from 35 to 70 within 1-2 s upon standing.

apparently I cannot copy the fig 1 into research gate so you will have to go to the library :)

Thank you all for your answers and paper suggestions.

I should point out too that we're looking specifically at the human heart, and the subjects are being exposed to artificial gravity in a short arm human centrifuge.  

borst is in humans. with respect to artificial gravity, I have no answer. But you may look under convertino va : he has published a lot on re-entry and prevention of re-entry syncope. You may find food for thought in his papers. I add this ref so that you can orient yourself in the literature : Convertino VA, AJP 1991 260 R570-5. from there you will manage :)

L.

Heart rate is driven by the electrochemical discharges originating in the sinoatrial node and propagated through atrial tissue contraction to the atrioventricular node, and then into the Purkinje fibers grouped into the bundles of His for distribution of the electrochemical discharge into the ventricles. To make a long story short, let us take the example of atrial fibrillation, in which the length of one cardiac (i.e., ventricular) cycle can easily be twice or half of the preceding one, and are scattered randomly in time by variable (refractory) blockage by the atrioventricular node of the intrinsic 360 or so atrial beats per minute from fibrillation. That is, as an electrically controlled phenomenon, (ventricular)  heart rate can and sometimes does literally turn on a dime. A patient in atrial flutter, for example, can have a run of 90 beats per minute for several minutes and change during a single heart beat to 120 beats per minute. Consequently, changes in heart rate can be abrupt or gradual, and the rate of change of heart rate is not stable. For example, premature ventricular contractions (PVCs) are quite common. I realize that the question pertains to a particular stressor, and requires a physiologic as opposed to pathophysiolgic response. However, the question asked is a conundrum. There is no such thing as a normal response to an abnormal stimulus. First, we mush establish that the stimulus is in some way "normal." The easiest way to do that is to establish that the response to the stimulus predictably agrees with the stimulus. For a stimulus consisting of a rate of change of stress in time, the response within the physiologic range would be a rate of change of heart rate in time that agrees statistically with that rate of change of stress, where lag time is considered.

Thank you very much for your input.

During our experiment where the subjects went through a predefined gravitational force profile with a caudal fluid shift and a resulting activated baroreceptor reflex, we found a corresponding, aka. "normal" physiological reaction of the heart rate as well as the systemic vascular resistance as an attempt to maintain a constant mean arterial pressure. While examining our findings we did so in relation to the magnitude of the external stimulus and so expected a higher increase in HR and SVR during high G-force phases where the fluid shift is respectively stronger. However several subjects showed a tendency to present frequent peaks in their HR recordings (jumps of about 20-50 bpm in a second) within a phase (while G-force was constant). While we have been trying to conceptualize whether if such abrupt changes are at all physiologically possible (which with the arrhythmia references it is now clear to me that it is) to develop a strategy to eliminate possible artefacts, we may need to alter our approach a little bit and evaluate these peaks in relation to the stimulus. 

Some people suffer from paroxysmal atrial tachycardia as a response to stress. This can be triggered, for example, from standing up from a crouch too suddenly, and appears to fit with your description.

Carl Wesolowski's observations (paroxysmal atrial tachycardia upon standing) and your observations (changes in HR circa 20-50 bpm within one beat within a centrifuge a constant gravity) are quite in line with what borst (AJP 1982) observed. We observed changes in RR from 800 to 2000 ms within one beat (Gratadour, Anesthesiology 1997, 87, 1359-67, fig 4) during syncope. So what you observe is perfectly in line with what others do observe.

The next question is artifact : is this sinus rythm or not. It all depend what you want to do with your data : do you restrict yourself to sinus rythm ? would you be happy to consider a bout of paroxysmal atrial fibrillation lasting a couple of beats as suggested by Carl Wesolowski ?

Best. L.

Cardiovagal motor outflow will also be reduced during inspiration (one of the reasons for respiratory sinus arrhythmia) so HR can increase for a few beats even during intense baroreflex activation. Any correlation between these beats of high rate and respiration? 

Hi,

A bit more information would make this easier to answer.  

You didn't indicate, but I assume you are referring to human heart rate changes.

Also not known, are you considering only normal beats or looking at arrhythmias, such as PVCs?  Are you considering adults, neonatal, or fetal heart rate changes?  What sort of external stimulation (drugs, exercise, emotion, etc) are being considered.

Here are some things to consider:

Asking about the beat interval change "within a second" would perhaps be better asked, "what is the maximum rate of change in the beat-to-beat interval" because one only obtains a sample on each heart beat.  There is a different maximum if you are truly considering the maximum variation from one beat to the next vs the sustained heart rate change.    For example, with exercise as the forcing function, HR may increase at a rate of 165 beats/minute (see link for elliptical ramp image), but there are in this plot beat-to-beat variations at a higher rate.

With POTS, "average" patients see increases of about 3 bpm/minute.(see wikipedia link, https://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome) when they change their position from supine to upright; however, some patients say their HR can double or even triple in a few seconds.  See Dysautonomia Information Network Forums link.  http://forums.dinet.org/index.php?/topic/14754-speed-of-pulse-increase-with-standing/

Fetal heart rates change rapidly with each contraction from the mother, 10 bpm/10seconds is common.  From a statistical sense, if 10 bpm/10 seconds is common, then one should assume a rate change much greater than this.

Drugs, such as epinephrine (adrenaline) can change the heart rate rapidly.

https://en.wikipedia.org/wiki/Postural_orthostatic_tachycardia_syndrome

https://canute1.files.wordpress.com/2010/07/ellipticalramp18jul2009.jpg

http://forums.dinet.org/index.php?/topic/14754-speed-of-pulse-increase-with-standing

In case of a cardiac disorder (arrhythmia), HR can change very fast – RRI, in terms of HR, can change by 50 – 100 BPM for one heart beat. For normal health condition, HR may also change very fast, for example, when one breathes at rate of ~6 time/min, HR can change (increase or decrease) by 6 – 8 BPM per second, i.e., by 360 – 480 BPM.

Thank you again for all your answers.

I had pointed out earlier but that answer remains on the previous page now. We're looking specifically at the human heart and the subjects consist of young adults with no history of cardiovascular disease. We measured changes in their cardiovascular parameters as a response to exposure to artificial gravity in varying intensities in a short-arm-human-centrifuge.

Our HR data at the moment is only in bpm with presumed sinus rhythm. If we took a further look into the raw 3-canal-ECG data the probability of running into such supraventricular arrhythmias is certainly there. It will have to be discussed in our group whether if these should be taken into account in case there are any. During my studies I have encountered several predominantly female patients with such arrhythmia that presented themselves with corresponding symptoms such as dizziness, headache, fatigue. These are similar to that of a sudden foot-ward fluid shift, which we induced with the centrifuge. It has to be pointed out here that subjects, who were symptomatic or presyncopic were eliminated. I am not aware though whether if paroxysmal atrial fibrillation can occur isolated in a single beat asymptomatically, and if yes, what is the likelihood that this is the case with almost half of our subjects, who were chosen randomly. It is definitely a point that requires reevaluation.

Thanks for bringing attention to the influence of breathing, Jesse. This is definitely a factor we have considered after we noticed regular oscillations in the polynomial of the bpm data, that had a higher frequency during a G-force increase, where a respiratory rate increase would be expected. Unfortunately we don't have real time respiratory rate measurements but we did not consider a connection between respiration and the singular HR peaks since we did not see a time correlation between the peaks and the more respiration-related seeming oscillations.