Science topic

Heart Rate - Science topic

The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Questions related to Heart Rate
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Heart rate is a simple clinical parameter. However, it varies with respiration and autonomic sympatho-vagal balance. A huge number of studies has evidenced usefulness of heart rate variability for diagnosing (diabetic neuropathy, sick sinus syndrome, OSAS) or prognosing (myocardial infarction, heart failure, stroke etc.) reasons. As yet, HR is usually reported in many clinical trials, while HRV is not. Does HRV really mean nothing?
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Sorry if I insert here such my suggestion.
I am not here to outline you the importance of the HRV current studies and I have not to remember you that the current linear or non linear methodologies are not completely satisfactory. Of course every day we find papers published also in valuable international journals that continue to use standard linear indexes and FFT or DFT for their clinical investigations and conclusions. Non linear methodologies have their valuable content also if currently they still do not find a continuous clinical appreciation. Usually three bands are considered in the frequency domain , as you well know, the VLF, the LF , and the HF for short 5-6 minutes recording. We need to remain in this framework, we need to use such bands for our estimations but my modest opinion is that the basic methodology as well as the physiological setting need to be advanced. This is the reason because we have studied for several years a new method, called the CZF method. We have verified, however, that such method, although of great interest, results of difficult interpretation for some clinicians. Consequently we have elaborated a new method, the new CZF version , that , in addition to the rigour of the previous formulation , gives results that give immediate clinical interpretation.
The method as well the software for your experimentation are given in our site www.saistmp.com Consequently I invite all you to visit the site and go to use such new method in your experimental as well as clinical conditions and verify directly its interest. The present software is the primary elaboration. Within a brief time we will give the complete version responding to all the formulation of the method. All the researchers that , at this time, will result using currently such new CZF method will receive obviously automatically the updates.
A final question. We have experienced the method on a large number of subjects and in some different pathological conditions. Consequently don’t hesitate to contact me if you need help, suggestions, questions, previous results that may help you in your use of the method (stmp@saistmp.com)
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I am looking for a device to track HR without the risk of injury (by using the watch) or degrading the material.
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Hi Diogo,
Here is one to consider:
Could give some interesting data for football.
Thanks, 
Jamie 
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A good review is: KOTCHEN T A 2011, Hypertension 58; 522.
I personally think that the cuff measurement of BP is antiquated and should be replaced by a technique that takes into account an individual's perfusion of essential organs & cardiac function, which means one size does not fit all. But inherent conservatism of clinical medicine, insurance companies, & drug manufacturers will probably prevail. Last I heard we were all trying to be 115 systolic.
So the short answer is: nobody discovered it..
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I have to compare one of these parameter to HRV in my experiment. I am not sure which one to pick. In my experiment, subjects will be introduced to two different stressors- cognitive (stroop test) and emotional while using a driving simulator.
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Hi Asha,
IN reality:
HRV records both RR and HR fluctuations of the individual. There is no question of picking one. both are already a part of HRV.
If you can measure the Galvanic skin resistance along with pupillary diameter in response to  stress, it might give you more accurate results.
HRV can be used as a starting parameter. good topic to do research on. socially relevant and we need more evidence this field.
 pros,
easily recordable with portable instruments
repeated recordings possible
analysis like HRV, pulse RV,  arterial stiffness
respiratory rate along with depth and characteristic analysis is also possible
Cons
Not a very reliable results or comparable parameter. 
Both HR and RR are bound to be varying in all types of stress.
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I want to monitor Heart rate and other physiological parameters of a Driver in real life situations in different environment (Day/Night) using non-contact systems ( like camera). What are the main things to be considered ?
Your valuable thinking/ suggestions are appreciable. 
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As far as I'm aware skin tone proved to be somewhat of a stumbling block in the way of camera-based technology.
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I am interested in using vagal tone (i.e., variability in heart rate between inhalation and exhalation) as an outcome measure for psycho-social interventions. I believe there is some disagreement about what constitutes a valid measure of vagal tone. I would appreciate any information on whether there is a standardized method for measuring it, and, if so, does it require highly specialized instruments? Thank you.
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Dear Desiree
I have been active in this field for over 30 years. Vagal tone is not "variability in heart rate between inhalation and exhalation"; the latter is termed respiratory sinus arrhythmia (RSA) and under very specific conditions  may sometimes reflect, or be a marker of, cardiac vagal tone. Cardiac vagal tone--on the other hand--is defined as the magnitude of mean heart rate change from one condition to another (e.g. rest to different levels of physical exertion or to pharmacological blockade of parasympathetic control) that is a specific consequence of parasympathetic effects. Obviously the two phenomena are not equivalent: Resipratory sinus arrhythmia is an inherently phasic (not tonic) phenomenon (heart rate shifting rhythmically from inspiration to expiration).  Cardiac vagal tone characterizes the average effect of vagal influences upon heart rate during a particular duration of time. Changes in breathing frequency can have dramatic effects upon magnitude of RSA without any effects upon cardiac vagal tone. There are also other conditions in which the two phenomena do not change proportionally to each other: e.g. sometimes when sympathetic activity substantially changes; or when efferent vagal traffic to the heart is blocked by chemicals before it can reach the sinus atrial node; or probably when vagal discharge is so great that the  vagal traffic saturates the sinus atrial node leading to profound slowing of heart rate during both inspiration and expiration. These effects are rather clearly shown in the autonomic cardiovascular physiological literature but fail to be acknowledged in much of the psychological or psychophysiological publications. Thus it is plain wrong to believe that RSAis vagal tone. There is really so much evidence that is often systematically ignored by psychologists working in the field.
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Premise 1: Neurogenic bradycardia and RSA are mediated by different branches of the vagus and need not respond in concert.
Premise 2: Neurogenic bradycardia associated with orienting is a phylogenetic vestigial relic of the reptilian brain and is mediated by the dorsal motor nucleus (DMNX).
Premise 3: Withdrawal of cardiac vagal tone through Nucleus Ambiguus (NA) mechanisms is a mammalian adaptation to select novelty in the environment while coping with the need to maintain metabolic output and continuous social communication.
(From Porges SW (2013) Polvagal Theory. NY: Norton)
The current evolutionary vagal evidence indicates that neither Premises 2 nor 3 are accurate. Also 1) there is a confluence of evidence regarding Premise 1 showing that the DMNX  may only manifest vagal effects upon heart rate under conditions of severe physiological respiratory distress (and even this is not very well documented), 2) Porges provides  merely very indirect findings to support his hypothesis (and his Figure 2.3 of  the time course of putative DMNX-stimulated bradycardia in a single anesthetized rabbit shows much too rapid onset and offset for the heart rate drop to be a response of the unmyelinated DMNX vagal fibers [which should have a much more gradual onset and offset than shown because slow conduction time of these fibers prevent sudden changes]), and 3) no mention is made by Porges of earlier findings that indicate that the DMNX is not implicated in normal vagal control of heart rate.
Nevertheless, perhaps there are strands of direct evidence of which I am unaware? In any case, polvagal conjectures have become very popular in psychology, psychophysiology and therapy literature. It seems, therefore, high time to critically assess the value of Stephen Porges' ideas in this area.
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Dear Emily,
If you mean that myths can affect people's lives, I have no problem with that. I also agree that is probably what has inflated the popularity of the polyvagal speculations. Wampold, in his work, makes a very convincing case that improvements in psychological wellbeing don't rely very much at all upon the method (or, perhaps, ritual would be a better word) chosen: improvement has more to do with having some ritual one believes in, a practitioner of it who seems competent to the client, a joint plan and goals, and maybe most importantly an atmosphere of trust and compassion.
However, my problem is that the ritual becomes conflated with science in this case, and the scientific aspect is used to sell the approach, when all the scientific evidence speaks against the speculations. There are, I hope you will agree, multiple myths that could be invoked to explain the various conditions to which you allude. Why not construct an explanation (myth) more consistent with what we know? That would provide, in my opinion, a much healthier approach for the therapy (i.e. ritual), as well as the societal acceptance of it, in the long run. Right now, what might happen to a client who has gone through a therapy with a polyvagal explanation (and who believes in "science" as the new religion) when they eventually read that in the New York Times that the polyvagal ideas have been thoroughly debunked? What happens to the credibility among scientists of a potentially helpful therapy (ritual) when the underlying scientific premises are thoroughly falsified, as seems to be happening. I don't think that is good for anyone. And I strongly believe one could adjust the vagal myth, employing autonomic explanations that have been around for at least a century before the polyvagal speculations were suggested. That is all I am trying to get at.
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If we look at the relationship between cardiac output and heart rate, we see that without the influence of the autonomic nervous system the CO would decrease at higher frequencies due to a respectively shorter diastole and insufficient atrial filling, but positive initropy and chronotropy mostly go hand in hand without one having to be sacrificed thanks to the sympathetic nervous system, such as during exercise, orthostasis or a fight or flight response. I'm wondering if a HR increase without sympathetic activation is physiologically or pathologically possible, and if yes does it make sense (at higher frequencies this would mean a decrease in CO)? 
I ran into the information that mild exercise can stimulate a decrease in vagal tone, allowing heart rate to increase without SNS activation. At lower frequencies (< ~80 bpm) a HR increase causes a linear CO increase, so it makes sense for this to happen during mild activity. But I ran into this without a paper/author reference or a source. Does a decrease in vagal tone without SNS activation really occur?
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Another avenue you might pursue is the heart rate response of the transplanted heart, which has lost both parasympathetic and sympathetic innervation. As already intimated, the resting heart rate is dominated more by a parasympathetic (vagal) brake than sympathetic output. A transplanted heart generally has a resting rate +/- 20 bpm higher than normal. And as you have noted the initial heart rate response in exercise (unless being pursued by a bear?!) is probably due to reduced vagal tone. 
There are internal mechanisms within the heart associated with changes in rate (in either direction) Rapid atrial filling of the denervated heart is associated with an increase in rate, possibly via stretch stimulation of conducting tissue, and rapid decrease in atrial filling is associated with a decrease in heart rate. Someone is bound to mention the Bezold Jarisch reflex (forgive the spelling if wrong) if I don't, which is a (paradoxical?) slowing of the heart following sudden emptying but this may be a local cholinergic reflex associated with ischaemia.
Another area of interest would be heart rate changes associated with the rapid onset of high spinal anaesthesia, which takes out the traffic from the sypathetic chain, but leaves the vagal input intact. One would expect this to result in a bradycardia, which can occur and is quite common particularly in the elderly, but in pregnant patients the commonest immediate response is a tachycardia, perhaps due to rapid reduction in venous return.
a fascinating and time-consuming question. good luck!
Chris
PS don't try the bear experiment!
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Partial heart block - this is when the electrical impulses are delayed or stopped. The heart does not beat regularly.
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A sort of algorithm/guideline and individualized therapy, based on etiology and level/extent/site of complications has been described, as delineated hereunder:
I- Approach consideration and immediate response:
Treatment of third-degree AV block is based on the level of the block. A common misconception of an inexperienced clinician is to gauge a patient’s stability according to the heart rate and blood pressure rather than according to the symptoms and level of the block.
An asymptomatic patient with inferior wall myocardial infarction (MI) causing complete heart block at the atrioventricular node (AVN) level and a heart rate of 35 beats/min is at very little immediate risk. A patient in the acute phase of an anterior wall MI with intermittent distal high-grade block is at immediate danger of impending asystole and requires immediate preparation for pacing of some kind, even though the heart rate between asystolic episodes might be 90 beats/min.
The first, and sometimes most important, medical treatment for heart block is the withdrawal of any potentially aggravating or causative medications. Many antihypertensive, antianginal, antiarrhythmic, and heart failure medications cause AV block that resolves after withdrawal of the offending agent.
II- Initial Management Considerations:
All patients should be rapidly transported to the nearest available facility, receiving advanced life support (ACLS) with continuous cardiac monitoring, as per local protocols. In all patients, oxygen should be administered and intravenous (IV) access established. Maneuvers likely to increase vagal tone (eg, Valsalva maneuvers, painful stimuli) should be avoided. Atropine can be administered but should be given cautiously.
Treatment in the emergency department (ED) should continue that already established in the prehospital setting, which includes administering oxygen, maintenance of an IV line, frequent monitoring of blood pressure, and continuous cardiac monitoring. Transcutaneous pacing pads should be applied and tested, if this has not already been done.
III- Atropine?? Isoproterenol ?? and Transcutaneous/Transvenous Pacing: Caveats and individualization therapy apply:
Hemodynamically unstable patients may be treated with atropine. This should be done with a degree of caution. The goal of atropine therapy is to improve conduction through the AVN by reducing vagal tone via receptor blockade. Atropine often improves the ventricular rate if the site of block is in the AVN. Peak increase in heart rate occurs in 2-4 minutes after IV administration; half-life is 2-3 hours.
However, if the block is in the His bundle, atropine may lead to an increased atrial rate, and a greater degree of block can occur with a slower ventricular rate. Atropine is unlikely to be successful in wide-complex bradyarrhythmias where the level of the block is below the level of the AVN.
Hemodynamically unstable patients may be treated with atropine. This should be done with a degree of caution. The goal of atropine therapy is to improve conduction through the AVN by reducing vagal tone via receptor blockade. Atropine often improves the ventricular rate if the site of block is in the AVN. Peak increase in heart rate occurs in 2-4 minutes after IV administration; half-life is 2-3 hours.
However, if the block is in the His bundle, atropine may lead to an increased atrial rate, and a greater degree of block can occur with a slower ventricular rate. Atropine is unlikely to be successful in wide-complex bradyarrhythmias where the level of the block is below the level of the AVN.
In addition, care should be taken in administering atropine to a patient with a suspected acute MI, in that the resulting vagolysis leads to unopposed sympathetic stimulation, which can cause increased ventricular irritability and potentially dangerous ventricular arrhythmias. Furthermore, atropine is ineffective in patients with a denervated heart (eg, those patients who have undergone a cardiac transplant procedure).
Similarly, isoproterenol may be attempted to accelerate a ventricular escape rhythm with a low probability for efficacy and the same concerns in patients with suspected acute MI. Isoproterenol is more likely to facilitate conduction with a distal level of block, but patients with a block at the distal level are more likely to have a contraindication, such as active ischemic heart disease. Isoproterenol should only be used as a temporary measure until more definitive and less risky treatments (eg, transvenous pacing) can be arranged.
Once the patient has been stabilized, a decision must be made regarding permanent pacemaker implantation. The admitting cardiologist will determine the need for and timing of permanent pacemaker implantation.
IV- Pacemaker Implantation for Acquired AV Block in Adults
Unless the heart block is due to a medication that can be discontinued or an infectious process that can be effectively treated, most patients with acquired complete heart block should receive a permanent pacemaker or an ICD (if a high risk of sudden cardiac death exists on the basis of severe left ventricular dysfunction or other criteria).
Pacemaker Implantation for Chronic Bifascicular Block
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I'm wondering if there is a limit of absolute increase in bpm within a second. We're trying to decide whether if a +10bpm/sec, ex. 60bpm to 70, is within physiological limits, and if yes what about +15, +20bpm/sec etc., if this is a realistic acceleration given that an external change causes this HR elevation. The same applies for HR decrease.
Paper suggestions or opinions to what is physiologically possible are all appreciated!
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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. 
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Specifically: Deceleration of left ventricular contraction during systole produces an expansion pressure wave (pressure drop) just before valve closure. Is it conceivable that (under possibly pathological condition) the timing of the expansion wave may modulate the radial pulse pressure wave form (incident and reflected wave) into a type-C pressure wave form (wave forms according to Murgo et al. and Nichols et al.)? Is it possible that a pathological condition may thereby produce a radial waveform which is typically associated with a healthy CV system? Has anybody made such observation in practice?
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Interesting- low ventricle end systolic pressure wont occur unless there is an ambient arterial bp which is also general low - so it should be encouraging  to you how this model is seeing the low bp condition to be a property of  healthy / fit subjects. 
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Regards
I need to define some values for:
  • Ambient temperature
  • Body temperature
  • Altitude
  • Humidity
  • Air pollution
  • Wind Chill
Where the value in each of the previous influencing factor starts to affect the heart rates number. (Say at 32 degrees Celsius of ambient temperature the heart rate will start to rise above resting heart rate average for a certain person).
I need to know minimums and maximums in each influencing factor.
Thank you a lot. 
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Autonomic control of heart rate can be a useful marker to know the human response to exercise.
Are there are any works which like a experiment design have used it as a training load parameter and reference to design training program? 
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The parameters to be analyzed in my research are
pNN50
RMSSD
SDSD
NN50
HF
LF
VLF
Can you explain if it is worth to buy Polar RS800CX to get practical recording or Suunto t6 HRM?
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I work with Kubios Software. If you transfer your data in a .txt file it would be working.
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Have you done any studies on heart rate variability?Could You suggest heart rate variability (HRV) monitor device and software that are validated and could be used for research?
Thank You.
How can scientists age gracefully, and keep our flexibility, mobility, independence; physical and psychological health and well-being?
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All of us are concerned about quality of life even as we age.  What are the exercises that could improve quality of life, a healthy metabolism and reduce resting heart rate?  (Besides ourselves, we also have family members who are aging and we are the care providers.) Please provide research papers that are relevant.  Thanks.
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"The power of positive thinking is vital for maintaining happiness, good health and longevity." - Eraldo Banovac
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In pulmonary CT angiography, different protocols are applied with different contrast volumes. However, if we know the physiological average amount of CM that fills the pulmonary artery down to the tertiary branches, we can do good exam.
In timing the scan, we need to exclude the CM-filled SVC and the left side of the heart in order to avoid artifacts. So knowing the physiological CM volume on average patient and adjusting the scan time given the size of the chest, and heart rate, a good timing of pulmonary angiography can be performed.
One more technical factor is calculating the scan time in testing bolus technique. This method ensures a maximum concentration of CM in the pulmonary trunk. But giving that we start the scan in the caudo-cranial direction, the CM may be not maximum by the time PA is scanned. It is said that 5 seconds should be added to the time to peak, I don't understand why 5 second? In fact, rationally some seconds should be deducted from the time to peak because this time is consumed by scanning the chest from the base till it reaches the pulmonary artery.
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We use test bolus with ROI in pulmonary trunk and add 2 secs to peak time as delay. Then 30 ml are sufficient for CTPA (on Flash the scan of thorax takes about 3 secs), but aorta is "empty" . However there are plenty of possibilities.  
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.
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If you are interested in the correlation and not in humans in particular, you can correlate mean heart rate and survival in different animal species (elephants, whales, humans, rats and so on). The correlation is very nice.
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I am interesting The effect of environmental condition (salinity, heavy metal, t0, pH, ...) change on the heart rate of Bivalvia (hard clam) ?. I hope that I combine with the expert to study in Viet Nam. Thank you !.
My publish: 
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short or long term prognosis
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Thanks Dr/ Thomas W Weiss but You did not get me. I'm asking about heart rate recovery after the exercise stress  Test. that is calculated after one min in the recovery stage of  exercise. Normally it is more than 12 beats. if less than 12 it indicates some sort of autonomic dysfunction with bad prognosis in stable IHD  . but till now we didn't have a study to determine the prognosis post PCI.
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It seems that the use of IV short action GLP1 in pre surgical diabetics, may decrease the patients heart rate... any idea Why?
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While GLP-1 agonists are documented to exhibit sympathomimetic activity,  the bradycardia you observed may be due to GLP- 1 agonists inhibiting glucagon release, which is the same effect that beta blockade exerts - sympatholytic activity - (beta blockers can cause hypoglycemia because of this). Thus, I would question whether this is a synergistic effect of beta blocker use in such patients, particularly since continuation of beta blockers are preoperatively encouraged .
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Heart rate and AF association?
Do agents blocking AV node or SA node predipose patients to the AF?
Ivabradin use and AFare associated or not with each other?
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I think Dr. Sachdeva has given a complete answer and patient need to be observed periodically.
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electrical cardioversion, synchronised direct current dc shock, direct current cardioversion
Are the 3 terms above interchangeable?  
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Those terms are quite often used interchangeably for a synchronized shock.  I think it depends on the audience.  It's easier to tell patients they are having an electrical cardioverson.  There are of course pharmacologic (e.g. ibutilide) carvioversions and spontaneous (e.g. while giving diltiazem) cardioversions.  In my cardioversion notes I usually say "synchronized shock of 200J". I think the main thing is to be clear on is that the indication for the shock wasn't defibrillation of VF or a polymorphic VT (as you can use synchronized shocks for monomorphic VT).
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I am especially interested in HRV, HR and respiration rate. Even better if it’s in context to driving simulation. 
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Hi Asha,
The following systematic review could be a useful resource:
I also can refer you to following articles that assessed stress in drivers:
  • Detecting Stress During Real-World Driving Tasks Using Physiological Sensors
  • Impact of Mental Stress on Heart Rate Asymmetry
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I need to have access to "raw data" and the accuracy of this during physical activities is important to me. Any kind of help would be much appreciated.
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A wearable PPG device used "during activity" is a recipe for tears. These are fairly sensitive to movement artifacts, and the adaptive filter will be going crazy at any activity faster than a slow walk. Does it absolutely have to be a PPG? Could you use, for instance, a Holter monitor or similar?
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Research shows (e.g. Shalev et al., 1998; Orr et al., 2008) that people diagnosed with posttraumatic stress disorder (PTSD) had significanly higher heart rates in the ER and at 1 week (but not 1 and 4 months) post-trauma than those who were resilient to PTSD. A high percentage of people with mild traumatic brain injury (mTBI) also develop PTSD. Do those people brought into the ER for head trauma who later develop PTSD show elevated heart rates compared with the heart rate of mTBI patients who do not develop PTSD?
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Hi Gina,
Great to see this direction in your research! The only comment I would make to your query is that injury to the insular cortex and cerebellum often is a consequence to TBI, partially directly through indirect perfusion changes by middle cerebral artery alterations to injury, partially through direct trauma to the lateral skull, and to the cerebellum, from direct trauma, including damage to projecting fibers from the trauma. Those areas are especially affected by chronic irritants, such as hypoxia from obstructive sleep apnea, perhaps operating through alterations in the blood brain barrier caused by OSA. The right insula is badly hit in OSA and heart failure. Momentary changes in the BBB should not be overlooked in acute injury as well. The reason the insula is important is, of course, the significant role that it plays in regulating the baroreflex and heart rate, well documented by Oppenheimer, Henderson, and ourselves. Stroke injury to the right insula is typically followed by myocardial infarctions two weeks later, probably as a consequence of increased sympathetic tone. The cerebellar role is also important for transient changes to heart rate, because of its dampening role in modulating blood pressure through its fastigial nuclei; the incredible sensitivity of the cerebellar Purkinje neurons and the climbing fibers to injury have substantial potential to modify overall sympathetic tone, and thus, heart rate. That area also possesses substantial plasticity, so that recovery is eminently possible. A very complex story, and a very interesting one.
Ron
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We have used the equivital SEM-EQ-02-SEM-007 in our lab to record ECG in order to calculate heart rate variabilty. So far we have had massive artifact problems (mainly caused by movement) which we never got rid of completely. What is more, these artifacts occur eventhough our participants do not really move a lot, because they are sedentary throughout all of our experiments.
I would like to know wether this is a common problem with Equivital products or if this is just a malfunction of some sort in our equipment.
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I evaluated the SEM-EQ-02 a while back and cannot confirm that there is a general problem with their data quality, meaning with their recording equipment itself.
The recordings were much more noise and artifact prone than I am used to, but I would attribute this to the use of the chest belt with the 2 built-in electrode patches which can never give as good and stable a signal as good chest ECG electrodes can.
Also, the chest belt seemed to be more of a "mediator" than a "stabilizer" of movements and yes, there were plenty of corresponding artifacts.
However, the real show stopper was that the ECG is only recorded at 256 Hz, which is WAY to low a frequency for any type of valid/reliable HRV analysis.
All in all I was not very impressed with what looked like a brilliant package at first.
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Is it better to use Signal Processing Cup 2015 or PhysioNet dataset for getting photoplethysomograph signal for motion artifact removal application ?
SPcup data provides 2-channel ppg with simultaneous ecg and acceleration data whereas physionet only provides single channel ppg.
PS links are provided for both datasets.
physionet data
SP cup 2015 data
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It depends ... the SP cup dataset is rather limited (you'll certainly find more PPG data on PhysioNet), but that could also be an advantage.
Arguably, what speaks in favour of the SP cup dataset is that it is also provides you some information on the performed activities causing the artifacts. Furthermore, it has been rather heavily used in the literature (so it's certainly a good dataset to use for comparing your method with others). On the other hand, most papers using the SP cup data should be interpreted with caution (see e.g. the paper by Temko from last year for some remarks on that).
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I conducted an experiment which involved collecting Photoplethysmogram (PPG) data of participants with sampling rate of 128 Hz. After removing artifacts and noises, I converted PPG to heart rate (BPM). This study is related to capturing PPG from healthy participants in a flexible experiment setting when they were walking in streets.
First of all, is it possible for heart rate based on BPM (which by definition looks like it should be calculated based on the number of beats per minute) to show values of BPM for 128 data points per second? In other words, is it right to convert PPG to HR, point by point?
Second, assuming that I did everything correct up to this point, can I calculate sample entropy for this data set (with the resolution of 128 Hz)? I saw in the literature that sample entropy is usable on Heart Rates based on BPM, but I'm not sure If I can use it right now or not because, I'm seeing some strange and extreme numbers like 34 in some instances of my data set for BPM. Of course, these strange numbers are not for a whole minute and they are present for less than a second. 
Any kind of help would be greatly appreciated.
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Hi Mohammad
There are a number of factors to consider. The sampling rate of 128Hz  is easily above what is required. The lowest sampling rate required is determined by Nyquists sampling theory, which is essentially 2 x the bandwidth of the data being sampled. For heart rates the bandwidth is roughly 3Hz (0.5Hz = 30bpm and 3.5Hz= 210bpm) so the Nyquist frequency would be 6Hz - this is the lowest sampling rate that could be used.
So sampling rate should not be a problem for you. The other thing to think about is conversion of the input signal, which is roughly a sine wave, to numbers - essentially you are measuring the distance between peaks (in time) and then converting to rate in bpm. This needs to be accurate, but also take into consideration any noise in the input signal.
If you are interested in heart rate change, then averaging beat to beat data over a given time (5, 10 or 30 seconds) will help to eliminate noise and artefact.
Extremes such as 34bpm may be real on a single beat to beat measurement, but you need to be careful when interpreting their significance.
Hope this is helpful
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I am looking to purchase a reliable heart rate monitor for research use. Despite the obvious quality of Polar HR equipment (I used Polar team in my previous institution), the majority of the new monitors appear only to have software for use on a mobile phone (e.g. Polar H7). I am concerned about the limitation of this software to allow detailed analysis of the data collected.
I would be keen to hear opinions on good (i.e. valid, reliable) heart rate monitors that connect to software that allows detailed analysis of a session (i.e. mean HR, peak HR, analysis of HR within different time periods).
I have already had a trawl around Research Gate and seen some interesting information, but these mainly relate to HR monitors for specific HRV measurements. I would be using the device to record HR during short and long duration exercise tests (i.e. max tests, performance tests).
Thanks!
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Hi Bryan,
We now use FirstBeat for our Team stuff. They have been excellent (much better than Polar). May be worth checking out their website for individual monitoring solutions.
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I am looking to run a feasibility study that involves the need to collect heart rate information in adult rats. We have considered telemetry setups, but we do not have the equipment, nor the time for extensive surgeries when we are primarily interested in heart rate only (and perhaps breathing). What methods might work that are minimally invasive and also cost effective? Any suggestions would be very helpful- thanks!
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Dear Jennifer, if you can measure one, probably sleeping rat, I can imagine getting heart rate from cage vibrations. 
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Smart Watches can be used to monitor the heart rates especially for elderly people. Kindly share your experiences regard:
1- Quality, brands
2- Accuracy of data
3- Real-time
4- Pros and Cons
Elderly peope deserve to be supported and provided with the quality of life. Therefore, dont hestiate to share what you have......... Little things can make alot. 
 I appreciate your time and effort in advance. 
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I know that autonomic physiological functions such as heart rate, or blood pressure are affected by activities we make (that are controlled by CNS) e.g., when we run(motor activity) , the heart rate becomes faster.... 
But I need a scientific explanation showing the relationship or the influence of the CNS on the ANS in terms of innervation maybe, or physiological organs involved. 
Thank you 
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For my study, we are collecting 24-48hr heart rate recordings and are interested in calculating RSA for this data. Are there any R packages or free online programs that will calculate RSA from our data? We have the R-R intervals and respiration rate available to us.
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Hello Isabelle,
I guess, what you are looking for, can be found in  "R Heart Rate Variability (RHRV)" project.
Regards.
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I'm trying to understand how to link PsychoPy to LabChart (AD Instrumte' data acquisition software), in order to get PsychoPy to write down event-related time stamps (events' start and end) on HR and SC data.
Do you have any idea?
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This could help: https://forum.adinstruments.com/viewtopic.php?t=522#p1381 But the mentioned COM interface does not seam to be documented. You could pose your question in this forum.
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I'm looking specifically at RMSSD. Kubios needs a minimum of 30". I need to analyse periods of 15" to 20".
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If your recordings are short (and not too many) you might even 'program' it in a spreadsheet like Excel or Quattro Pro.
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In one of my studies I want to monitor HRV at two instances on a typical working day. Considering obtrusiveness, I want the protocol to be as short as possible. Preferably below 5 minutes. However, I've been having trouble finding a suitable measurement protocol. I hope you can provide me with some suggestions or references. Thanks in advance!
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Hi Sander,
1- It is not necessary to measure HRV in resting position, it all depends on your main question; are you going to measure resting HRV, then it must be in resting position after about 10 minutes of rest for 5 minutes and here is a guideline: http://www.ncbi.nlm.nih.gov/pubmed/8598068.
Of course the guideline is old and many questions remained unanswered such as if it's necessary to do paced breathing etc.... (I would recommend paced breathing of course)
2- When you have ~ 5 min recording then it's not ultra-short it's enough for most of the HRV measures. An ultra-short HRV means something below 1-2 min for example 10-30 seconds in that situation the best measures are time domain measures; such as RMSSD, SDNN. Pay attention that for frequency domain measures you need at least 5 minutes of recording according to the above guideline. 2 minutes may also be enough but not recommended.
3- You can use available free software such as Kubios for HRV analyses (it also provides you possibility of beat correction) but you need at least 30 seconds of recording for each sample. If you insert a sample of less than 30 second in Kubios it still gives you the HRV measures but if you insert a long sample in Kubios you cannot select less than 30 second of the sample for analyses.
4- If you are doing research I strongly recommend you to not rely on any commercial device that only give you the HRV. Always look for those devices that give you the raw ECG signal (and not PPG signal) as you always need to correct the beats. Even few wrongly detected beats can considerably deviate the HRV measures. Also, the device must have a sampling rate of at least 200-500 Hz not lower, according to the guideline.
Good luck !
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We are looking at the behavioral patterns of cardiovascular parameters such as HR, CO, TPR, MAP i.e. whether if they tend to increase, decrease or stay relatively constant. What defined methods do you know that can be used to describe such changes?
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Thank you for your answer, Erik Dietrichs. I probably should have given more details in the question description. The experiment including 24 subjects on a short arm human centrifuge already took place and the data has been collected non-invasively via 3-lead-ECG and Finometer finger cuffs for continuous BP monitorization. My question was more regarding properly describing the behavior of the parameter curves. So far we have been experimenting with their slopes but we're looking for alternative methods.
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Technical question - has anyone used Polar Team2 and Polar TeamPro systems during (pool) swimming? A few research papers suggest you can, but details are brief and water resistance is unclear on manufacturers web resources...planning a study but don't want to fry our system!
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Hello, Daniel,
We used Polar Team Pro system in our experiment, but recorded data did not look good - there were unexpected pauses in HR records. Then we utilised Polar S 810 (each athlete had got individual item) and the records were clear.
With best regards,
Grzegorz Bielec
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I have a cohort study of an elderly population (45-85 years old) and I found in opposite to many others that sdnn is increasing with age, the cutpoint could be about 70 years. It seems to could be explained with an additional quadratic term in regression, but I wonder if any other colleagues have similar results?
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Dear Frank,
Perhaps you might be interested to read the work “Pikkujämsä SM et al. Cardiac interbeat interval dynamics from childhood to senescence : comparison of conventional and new measures based on fractals and chaos theory. Circulation. 1999 Jul 27;100(4):393-9”.
These charts I found there. On the chart clearly show that SDNN decreases with aging.
My own limited data in LF power spectra shows a similar picture.
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From my understanding, under increased metabolic demand, heart rate (HR) and respiratory rate (RR) increase (i.e. they are positively correlated). Is this always true?
1. Is there any metabolic situation where HR would increase but RR would not (no correlation)?
2. Is there any metabolic situation where HR would increase and RR would decrease (HR and RR are negatively correlated)?
Kindest regards,
Onkar Marway
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No they are not always positively correllated. The example that comes to mind is respiratory failure in COPD. as the condition deteriorates ant the level of  consciousness decreases the respiratioy rate decreases  but there is usually a significant tachycardia. The same happens in many other conditions in which the respiratory failure  progresses initially respiratory rate increases initially but if the condition is not reversed reduced respiratory rate occurs initially wiith tachycardia. If untreated brady cardia occurs and low respiratory rate with low pulse rate often signals  omminent cardiac arrest if untreated.
Hope this  helps
Richard
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I started my PhD study about stress and daily activity and I need to find appropriate device for long measurements (+24). I've found two interesting devices so far: E4 wristband produced by Empatica (https://www.empatica.com/e4-wristband) and BioHarness 3 by Zephyr (http://www.zephyranywhere.com/products/bioharness-3). Did you use one of them during your studies? How do you assess their quality? Or maybe did you use something another? 
I'm interested in measuring such signals as: EDA, heart rate and motion. Thank you for each proposition of device and your opinion.
Mateusz Soliński
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You can see also our work on the E4 validation:
Our results are slightly different from those of Matthijs Noordzij as we found no visual ressemblance between wrist and finger SC, and we found accurate HRV metrics compared to ECG only in motion- and stress-free conditions. Having an adaptation period (e.g., 1 min) before the recording intervals of interest seems to increase the measurement accuracy.
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I came along quite some papers in the field of biosignal processing which first apply a low-pass or bandpass filter to the recorded signals (to remove high frequency sensor noise, etc.) prior to spectral estimation. 
Does this make sense? If I know that for instance the heart rate is between 30 bmp and 200 bmp, why would I not just compute the power spectral density and then look for the max in that very window?
Wouldn't a frequency selective filters skew the estimate (due to roll off  and ripples in the pass band)?
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The only reason I can think of, where you might want to do this, would be if you knew there was a strong interfering sinusoid, at a frequency in between two DFT frequency bins. Without pre-filtering, the energy due to this interferer would spread over all nearby DFT bins, and might mask/hide weaker signals of interest there. You may gain something if you designed a notch filter to remove the interferer, before doing your spectrum estimation. But yes, the filter may also adversely affect signals of interest.  
But you could do the filtering in the frequency domain anyway, after you have computed the spectrum.
In general I would say that your intuition is correct - just look at the band of interest and don't bother filtering.      
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What is the best way to calculate the sympathetic influence during a short-term (3 minute) HRV-measurement based on time-domain measurements. At the moment I am using the rMSSD for the parasympathetic influence and the equation rMSSD/SDNN for the sympathetic influence, yet I experience that this is not the most ideal method. Any thoughts on this?
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3 minutes might be enough to resolve some frequencies (it is incorrect to say these can't be resolved - they can, but there is a relationship such that the reliability/volatility of your measurement will increase as your observed frequency decreases).
But your main problem is much more straightforward - there is no method to adequately resolve cardiac sympathetic outflow from time-domain RR intervals.
However, as luck would have it, you're at Vrije - and a team at your university has commercialised a good impedance cardiograph. Which having used, I can recommend thoroughly.
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any explanation for arrhythmia (irregularly irregular rhythm) in a child with TB lymphadenitis without pericarditis/myocarditis/pericardial effusion and normal echo finding.. while not on ATT or any other arrhythmogenic drugs....
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 Isolated peripheral tuberculous lymphadenopathy is usually due to reactivation of disease at a site seeded hematogenously during primary tuberculosis (TB) infection, perhaps years earlier].
It has been postulated that cervical tuberculous lymphadenitis occurs as a result of TB infection involving the tonsils, adenoids, and Waldeyer's ring, leading to cervical lymphadenopathy. Abdominal tuberculous lymphadenopathy may occur via ingestion of sputum or milk infected with Mycobacterium tuberculosis or M. bovis.
Though most cases of tuberculous lymphadenitis occur in the setting of reactivation of latent infection, miliary dissemination with prominent lymph node involvement in the setting of primary infection can also occur.
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What will happen to the pressure in the ball (image shown) with four different types of pumping mechanics? Can it be related with heart rate and blood pressure, so that the influence of heart rate and strength of cardiac contraction be seriously taken into account in understanding individual-specific blood pressure?
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Looks like you have diagrammed a classic "windkessel". The pressure in the balloon should increase if the balloon's outlet is closed ( analogous to isovolumic contraction). Open up the  balloon outlet's per Johns suggestion and pressure will rise when pump  volume delivery rate exceeds ejection rate (the strong ejection phase)- and balloon pressure will fall  when ejection rate exceeds  pump delivery rate (weak ejection)
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Hello.
I use Brainvision analyzer to analyze ERP data, and lately I've started to collect ECG in parallel to the EEG recording, in order to see the correlation between some ERP components and HR related measures (Specifically - the heart rate deceleration seems like a good candidate, as it is event related, but I'm also thinking about using HRV in an event-related style, if it's possible). I have some experience with using Analyzer for ERP analyses, and I was wondering whether anyone has any advise on how to use Analyzer to detect R-R intervals, and to analyze related measures.
Thanks a lot,
Isaac.
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For interbeat interval phasic analysis (heart rate stimulus-evoked responses) and also HRV, you may also consider using my free matlab toolbox called KARDIA. Feel free to contact for details.
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Like an open db for affective computing 
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The Mahnob-HCI database for affect recognition. I worked with this database for several papers related to emotion recognition.
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Hi,
I am interesting to find the answer to a question related to using Kubios (in particular it would be good to get advice from Mika Tawvainen who created the software but if anyone knows anything about this software I would very much appreciate your help). 
I want to remove artifacts from some collected HRT and HRV data. My other colleagues have suggested that only automatic filters can be applied to parts of the data. However, the User's guide of Kubios seems to suggest you can remove artifacts manually. 
If this is so am I correct in understanding that this can only be done using the ECG data but not the RR interval data displayed on the Kubios data browser?
If this is the case as well, is it right to assume that in order to manually remove artifacts you would want to find data points on the RR interval data browser that seem like artifacts (e.g., they spike up very quickly and suddenly) and then find the corresponding part on the ECG data display and add a marker which would remove the data point so that it is not included as an R wave in the RR interval data browser. By doing this all the artifacts that seems like real R waves will be removed from the data resulting in "clean data" as free from artifacts as it is possible to get it.
If this is all correct then I would assume my colleagues were not aware of a manual function to remove artifacts (i.e., they just used the automatic low, medium and high level artifact corrections) because their data did not have the ECG information which I underestand is required to manual remove artifacts. 
It would be great if corrections can be made to my understanding where required.
Many thanks,
Victor
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I have used Kubios with great success. Yet, I purely used it for analysis, not for R wave detection. I used other (Clampfit or custom) software that detected the R wave, and thus RR interval. I was able to manually remove artifacts as well as RR intervals that were more than 2 standard deviations from the mean RR. I exported it as a text file that I loaded into Kubios.
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dV/dtmax is used to describe the maximal conduction velocity. Similarly, dP/dtmax is defined as the maximal rate of rise of (usually) left ventricular pressure. Is there a similar term in use which defines the temporal rate/velocity at which heart rate increases?
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In practice I'm not aware of a dHR/dt. One might use intrinsic heart rate and match or correlate this with heart rate variability parameters. 
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I am trying to compute directly a spectrum from the so called event series. Which is a series of Dirac impulses allocated at the times of R waves in an ECG.
I know that it is possible to low pass filter the series and get an evenly sampled representation of the HRV which can be easily analyzed. I am using this approach already but I would like to compute the spectrum (spectrum of counts) also directly from the unevenly sampled Dirac impulse series.
Can anyone suggest an algorithm for this?
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I've used sometimes a simple approach, though probably could be some more better or more efficient. Assuming that you have a sum of delayed deltas in time, with unit area, you can build its spectrum as the sum of frequency exponentials (with exponent coefficient given by the delay-time of each impulse, according to continuous-time Fourier Transform of a delayed delta). As far as this is complex, you should just sample in frequency (for getting discrete-Fourier) and take the modulus. Alternatively, you could be thinking in using Lomb periodogram (just for comparing HRV interpolated, spectrum of counts and Lomb, and see the similar and the difference). More sophisticated non-uniform interpolation and spectrum algorithms exist, which are seldom used in HRV.
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I'm using kubios to analyze r-r intervals and it looks fine to me. However just few papers in the literature used kubios for Hrv.
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Thank you all for the kind words about Kubios. We are working hard to make Kubios even better, including also the pre-processing steps like R-wave detection and artifact correction. Just few days ago, we released the a new version of Kubios (ver. 2.2) which is now available also for Mac OSX and includes support for Garmin FIT files. Of course there are many things that could be improved and sometimes I hope that I would have more time to give for Kubios.
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Hi. We need measure some physiological indicators to could have a correlation between behavior and physiology.
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Just as an add to the gentlemen above there are also some options becoming more popular like Kaha and Indus on the market for telemetry and are worth looking into as well.
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When supervising phase II cardiac rehabilitation patients, we control the intensity using Watts on an exercise bike and Heart Rate HR. Some patients when completing their program are above their target HR calculated at their initial exercise test. Most of them are recovering from valve or artery replacement. In wich case should one prohibit going above the target HR?
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Hi Alexandra!
It is difficult to determine the optimal training intensity. It depends on patients (former physical activity, LV function, risk of arrhythmia, what kind of operation, etc.).
The training pulse can be useful, if there is a preserved chronotopic reserve. However, most of patients take beta blocker or other heart lowering drugs. In this cases it is better to determine the training intensity according to work intensity (watts) or according to Borg scale.
The training pulse is only a rough calculation. In the same patients it can be lower (if he is a starter, has no experience with exercise) or higher. So do not worry about higher than predetermined training pulse if it is well tolerated (Borg 13-14).
But be careful with patients after aortic repair. I do have bad experiences. In these patients the training should be limited (mostly to avoid blood pressure elevation above 150/90 mmHg).
 Best wishes:
Attila
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When I do analysis by taking an average of cardiovascular parameters every five second during inspiration and the same thing during expiration. I am finding a delay between blood pressure response than heart rate and cardiac output. This make me confused when the respiration starts and ends. So, I do not know what should I do.
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We captured the raw data of the maternal heart rate as part of another study, but would like to analyze it later to determine possible associations with pregnancy outcome.
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Maternal HRV is a convinient instrument to evaluate regulatory balance that could promote control of hemodynamics. Variability (oscillations) of maternal hemodynamic processes spreads its influence through placental barrier and provide fetomaternal cooperation. Maternal sinus respiratory arrhythmia is the most valuable oscillator in the system of "mother-placenta-fetus".
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It is known that when performing fractal analysis of R-R intervals in HRV we often are subject to consider different situations: white noise, time dependence at all scales, and statistically self similar series'. It should be interesting to discuss these cases and possible clinical implications.
It may be interesting also to visit our site www.saistmp.com and our new methodology on HRV
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Specifically in teenagers.
So far I've only found a job to address the issue specifically but is rather old:
Antel, J., & Cumming, G. R. (1969). Effect of emotional stimulation on exercise heart rate. Research Quarterly. American Association for Health Physical Education and Recreation, 40(1), 6–10. doi:10.1080/10671188.1969.10616635
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Association between heart rate variability and fluctuations in resting-state functional connectivity
Catie Chang, Coraline D. Metzger, Gary H. Glover, Jeff H. Duyn, Hans-Jochen Heinze, Martin Walter
Neuroimage. 2013 March; 68: 93–104
Heart Rate Variability Response to Alcohol, Placebo, and Emotional Picture Cue Challenges: Effects of 0.1 Hz Stimulation
Evgeny G. Vaschillo, Marsha E. Bates, Bronya Vaschillo, Paul Lehrer, Tomoko Udo, Eun Young Mun, Suchismita Ray
Psychophysiology. Author manuscript; available in PMC 2010 October 26.
Recovery of heart rate variability and ventricular repolarization indices following exercise
Marc K. Lahiri, Alexandru Chicos, Dan Bergner, Jason Ng, Smirti Banthia, Norman C. Wang, Haris Subačius, Alan H. Kadish, Jeffrey J. Goldberger
Ann Noninvasive Electrocardiol. 2013
Autonomic nervous system reactivity to positive and negative mood induction: The role of acute psychological responses and frontal electrocortical activity
Willem J. Kop, Stephen J. Synowski, Miranda E. Newell, Louis A. Schmidt, Shari R. Waldstein, Nathan A. Fox
Biol Psychol. 2011 March; 86(3): 230–238.
Music in the exercise domain: a review and synthesis (Part I)
Costas I. Karageorghis, David-Lee Priest
Int Rev Sport Exerc Psychol. 2012 March; 5(1): 44–66.
Heart Rate Recovery after Cognitive Challenge is Preserved with Age
Olga V. Shcheslavskaya, Matthew M. Burg, Paula S. McKinley, Joseph E. Schwartz, William Gerin, Carol D. Ryff, Maxine Weinstein, Teresa E. Seeman, Richard P. Sloan
Psychosom Med. 2010 February; 72(2): 128–133
Here are some papers to get you started. Good luck!
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It is well known that in Heart Rate Variability - HRV analysis the use of linear and non linear methodologies is suggested. Sometimes, some methods also enable us to evaluate fractal features. Does anyone have any indications of what it means to find fractal dimension whose counterpart is a) white noise, b) time-dependent at all scales, c) statistically self-similar behaviour? What about clinical implications?
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I recommend the review article by Bravi and Seely:
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May we use a proper method for estimation of variability by HRV
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starting with yesterday the software has been updated with new entries. Please E-mail directly to me elio.conte@fastwebenet.it if you have questions.
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Or, in other words, are the methods 3 & 4 used in the article "2nd VT from HRV: valid when the upper body is involved?" using the PSD of FFT or the PSD of Autoregressive Model to divede the extended HF in the refered 2 components? I found this article highly interesting and useful. Thank you very much.
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Dear colleagues , please I apologize if I insert me in such discussion with a new information.
Dear Colleagues,
I am not here to outline you the importance of the HRV current studies and I have not to remember you that the current linear or non linear methodologies are not completely satisfactory. Of course every day we find papers published also in valuable international journals that continue to use standard linear indexes and FFT or DFT for their clinical investigations and conclusions. Non linear methodologies have their valuable content also if currently they still do not find a continuous clinical appreciation. Usually three bands are considered in the frequency domain , as you well know, the VLF, the LF , and the HF for short 5-6 minutes recording. We need to remain in this framework, we need to use such bands for our estimations but my modest opinion is that the basic methodology as well as the physiological setting need to be advanced. This is the reason because we have studied for several years a new method, called the CZF method. We have verified, however, that such method, although of great interest, results of difficult interpretation for some clinicians. Consequently we have elaborated a new method, the new CZF version , that , in addition to the rigour of the previous formulation , gives results that give immediate clinical interpretation.
The method as well the software for your experimentation are given in our site www.saistmp.com Consequently I invite all you to visit the site and go to use such new method in your experimental as well as clinical conditions and verify directly its interest. The present software is the primary elaboration. Within a brief time we will give the complete version responding to all the formulation of the method. All the researchers that , at this time, will result using currently such new CZF method will receive obviously automatically the updates.
A final question. We have experienced the method on a large number of subjects and in some different pathological conditions. Consequently don’t hesitate to contact me if you need help, suggestions, questions, previous results that may help you in your use of the method.
Sorry once again but it seems important for our studies
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Kenyans are dominating long distance races. Why are Manipur's long distance runners lagging behind?
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In the cardiovascular rehabilitation centre I work, we conduct aerobic exercise on recumbent bicycles, controlling heart rate. We also lead gym sessions that consist in dynamic global movements and analytic muscle reinforcement but don't monitor heart rate. Would it be preferable to control intensity during gym by measuring HR?
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Hi there
It's an interesting dilemma. I no longer work in this field but when I did we used to avoid using HR to monitor exercise for a couple of reasons-
1. Many patients were on medications such as beta-blockers which artificially limit HR and make it unsuitable for guaging exercise intensity
2. The purpose of the rehabilitation sessions in Phase 2 was to enable and equip patients to self-monitor their activity and symptoms in the general community. If they are to successfully exercise out of the gym environment you don;t want them reliant on external monitoring or a number (HR) but on knowing their own body's response to activity and how that feels.
The only time we would use HR would be to show people (who weren't beta-blocked) that when they were feeling this level of exertion (using a Borg RPE scale) then their heart was doing a particular HR. Again, a tool to reinforce the idea that they need to listen to their body.
Of course I agree with Ankush above that you need to have appropriate safeguards in place- just don;t lose sight of the goals of Phase 2 CR!
I'd be interested in any counterpoints to this view.
Regards
David
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I'm looking for these kind of databases to apply some data mining approaches! Thanks.
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Sylvio, I did some research on google scholar and found one person in Brazil that seems to have the type of database you need. His name is Diogo Simões Fonseca, and his email is: diogo.simoes@peb.ufrj.br
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ie. If I would like to see the influence of static magnetic field at 1.5T or 3T to HRV, How long should I record? And which parameters could best satisfy the short-term HRV analysis?
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In 1996, the European Society of Cardiology and the North American Society of Pacing and Elec- trophysiology organized a Task Force to develop appropriate standards for HRV measurement. Over the years these recommendations resulted in a wide array of interpretations by different researchers using HRV quantification. Today many published articles using HRV claim adherence to these general guidelines and recommendations by the Task Force. However, although the recommended sampling time (tachogram length) for short-term HRV analysis is 5 minutes, numerous studies employ different time windows. For example 2 minutes, 3 minutes, 5 minutes, 10 minutes, and 15 minutes. In addition, recordings are often done without an initial standard resting period for reaching homeostatic equilibrium, thus violat ing the stationary prerequisite. More info available in the following article: Importance of Tachogram Length and Period of Recording during Noninvasive Investigation of the Autonomic Nervous System Ann Noninvasive Electrocardiol 2011;16(2):131–139
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With reference to the energy pathways, blood lactate levels, heart rate, distance run, dominant energy systems used, specific examples of when energy systems would be used?
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Thomas, look for work from the group of Jens Bangsbo and Peter Krustrup. They did many studies on this topic, including muscle biopsies.
Particularly this paper:
this one:
and this one:
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I'm in search of articles referring to the different classifications of HR intensity zones.
Optimally I want to use the participants VD and RCP points to identify their zones, but I saw that some articles refer to the % of the maximal heart rate (example <65% = Low intensity or >85 = High intensity) etc...
Any help would be appreciated*
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It is a good idea to use scientific methods, especially the heart rate (since there have developed many app software in cell phone markets), to prescribe and classify the exercise intensity for the general population. Although Conconi et al. had proposed the concept of heart rate deflection point to take the place of traditional concepts, e.g., the anaerobic threshold, lactate threshold etc. [1], it seems not a valid method to assess the anaerobic threshold [3]. In our experiences, it is difficult to define the heart rate deflection point in most of health participants during the incremental exercise test.
To my knowledge, some researchers [2, 4, 5] attempted to use the heart rate variability threshold to find out the possible method to assess the anaerobic threshold. However, we need more works on this topic.
If the purpose is only for prescribing the exercise intensity for sedentary adults, I recommend you to read the book: ACSM’s Guidelines for Exercise Testing and Prescription (http://www.acsm.org/about-acsm/media-room/news-releases/2013/03/13/acsm-to-preview-9th-edition-of-exercise-guidelines) for gathering more available and reasonable information. You may also use the formula (206.9 – 0.67*age) to calculate the maximum heart rate, and then use the Karvonen formula to set the intensity zone (http://en.wikipedia.org/wiki/Heart_rate; http://www.brianmac.co.uk/hrm1.htm).
1. Bodner ME, Rhodes EC. A review of the concept of the heart rate deflection point. Sports Med. 2000 Jul;30(1):31-46.
2. Boettger S, Puta C, Yeragani VK, Donath L, Müller HJ, Gabriel HH, Bär KJ. Heart rate variability, QT variability, and electrodermal activity during exercise. Med Sci Sports Exerc. 2010 Mar;42(3):443-8.
3. Bourgois J, Coorevits P, Danneels L, Witvrouw E, Cambier D, Vrijens J. Validity of the heart rate deflection point as a predictor of lactate threshold concepts during cycling. J Strength Cond Res. 2004 Aug;18(3):498-503.
4. Karapetian GK, Engels HJ, Gretebeck KA, Gretebeck RJ. Effect of caffeine on LT, VT and HRVT. Int J Sports Med. 2012 Jul;33(7):507-13.
5. Michele RD, Gatta G, Leo AD, Cortesi M, Andina F, Tam E, Boit MD, Merni F. Estimation of the anaerobic threshold from heart rate variability in an incremental swimming test. J Strength Cond Res. 2012 Nov;26(11):3059-66.
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Heartrate monitor should be able detect small chances in heart rate variation. I found one called bodyguard 2, but I'm uncertain if it is accurate enough. Any suggestions?
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Well, there are some important things to consider:
Do you want to record ECG raw signal or InterBeatIntervals (IBI, also called RR). The first let you do your own ECG artefact correction and you may hand edit for missed heart beats etc. The latter does this within the small IBI motor and he formulas are often not published by the producer of the device.
Your sampling rate should be at 1000Hz,
What shall the participant be able to do with that device? Does it need to be e.g. waterproof?
Will wet electrodes hold for 3 days "wet"? Consider that some participants get skin irritations from long term recordings.
Can you shave chest hair to attach electrodes if necessary? (ethics) or do you need to use a chest belt.
What software would you like to use to process your raw ECG or IBI files? Can you export those recordings to other software containing the FULL information (e.g. ECG & Accelerometer data).
Can the other software you may use read the format generated by the device?
Shall the device store the data on the recorder, or on a SD-card or on a watch (like polar does).
Is the device validated within the population desired?
Beside Suunto & Polar, you have CamNtech (Actiheart), Movisens, first beat (body hard), mega electronics (eMotion), Neurocor (fitness observer) to name the one i know of and have some experience with.
Hope this helps you to make your decision!
Marc
How we can calculate the duration of heart rate zones of Edwards training load in a well-determined period of the session ??
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Edwards TL
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Imagery and sports
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Hello Laurent,
I have used covert sensitization (verbal aversion therapy) to reprogram alcohol dependent patients’ responses to their imagined alcohol drinking experiences. Prior to treatment these imagined drinking experiences typically stimulate alcohol cravings. Repealed pairings of the imaginary drinking with verbally induced nausea short of emesis usually renders the images aversive to the extent that they can induce abstinence-facilitating conditioned nausea responses. GSR was a sensitive and reliable psychophysiological indicator of conditioned nausea, which also was validated by patients’ self-reports and other behavioral indices.   You can view the GSR responses that accompany conditioned nausea acquisition in Elkins (1980), which can be downloaded as the 5th featured publication on my ResearchGate Profile page. Additional information can be found in my answer to Gerald Pohler’s GSR question.
I have no experience using GSR with emotionally neutral imagery but expect that for GSR to be of value the imagery will have to elicit some degree of negative or positive emotional reactivity.
I hope that this will be helpful.
Take care,
Ralph Elkins
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I know that heart rate tends to be increased among those with chronic insomnia, and that impaired parasympathetic tone has been linked to insomnia, but can't seem to find any evidence that there is a relationship between insomnia and heart rate recovery (which is an indicator of parasympathetic tone). Any information or thoughts?
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Thanks, Dieter. I also am not aware of any studies that look at this (obviously!!). The article by Spiegelhalder does provide some interesting background, and contributes significantly to the theoretical framework of my study.
Maurice - a study by Jolly et al. (2011) looked at the prognostic value of HRR among patients in cardiac rehabilitation. Indeed, they found that abnormal HRR (usually considered to be less than or equal to 12bpm) was predictive of all cause mortality. Numerous studies have also found that abnormal HRR has been shown to predict mortality. What is interesting is that I can find an abundance of literature on the prognostic value of HRR (and resting HR for that matter), and on the effects of insomnia on the heart - it is considered to be a risk factor for the development of cardiovascular disease and for myocardial infarction - but can't seem to find any research that links HRR values to Insomnia.
My current research (we are just in the process of collecting data) is hoping to provide this link. I'll be looking at resting HR and HRR in cardiac rehabilitation patients at entry and exit exercise stress tests. It is very similar to what Jolly and his colleagues did, but will be adding in symptoms of Insomnia (using the insomnia severity index). I'm hoping to find that elevated ISI scores will be associated with lower HRR. Further, I'm hoping that a positive change in ISI scores over the 3 month cardiac rehabilitation program will be associated with an increase in HRR at exit exercise stress testing. Symptoms of insomnia are extremely common among the cardiac rehabilitation population, so it should be interesting to see what comes of this.
Does anyone have any thoughts, or maybe some more information?
Affect of music on heart rate
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The effect of music on heart rate
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The heart rate variability and the inspiration rate are closely related. What is the reason and is there any coherence to it?
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Hello Andrews,
can you be more specific regarding the question. Do you consider influence of respiration rate on HRV or just inspiration part of breathing?
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I am having tough time to simulate heart rate monitor using proteus. All the components are available except LTH 1550-01 IR diode photo transistor pair. Can anyone help me find this component in the proteus software or rather suggest another component that will work just like LTH 1550-01 IR diode photo transistor pair? The circuit diagram is as shown in the attachment below.
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Hi!
To test the circuit You may place ex. voltage-controlled-current-source (VCCS) in place of reflexive optocoupler. Gain for VCCS you may get from device datasheet. Functionally You could test whole the circuit except setting the operation point with potentiometer R14.
With this testing setup control voltage would correspond to "amount" of reflected light from finger. i.e. voltage waveform that models reflected light must be created. 
Best Regards!
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I am analizing the heart rate of both gender referees during a basketball championship. Curiously the female referees HR was lower in each quarter than males contrary to scientific publications.
Somebody know why could occur this situation?
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Firstly, Brian thank you for the paper.
Regarding Hamish that says, I have these data and I have seen only differences between gender along the match in Moderate (55 - 69% HRmax) and Light (35-54% HRmax) intensity; showing lower values in females than males.
On the other hand I have only the final score but seem this score did not influence in HR in general because each match is judge by 3 referees and in this champisonsish never coincident 3 females referees.
I think this differences in HR are psychological aspects more than physiological, but I don´t know how demonstrate this with the data that I have (HR, total result of match, HR intensity, body composition and RPE).
By the way, The RPE did not show differences between gender.
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I am using a Polar bluetooth H7 with a link up to Polar beat, which works without problems in dry conditions. Once the sensor is immersed in water, a signal interuption occurs, and heart rate monitoring ceases to function. How does one then monitor heart rate underwater via bluetooth Polar sensor? Polar states that using the heart rate sensor in combination with the watch should work, however, in our lab, that has not seem to work either. Is it possible to go cableless while monitoring heart rate underwater, or is the solution good old EKG cables?
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Principally any Polar heart rate monitors using either one a T31 coded chest strap or a regular Wearlink chest strap will work and then the Suunto Memory belt and that is it. Those are the only ways I know of to get continual heart rate while swim training. The Swimovate Poolmate swim watch is a great solution for counting laps and strokes
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Julian Treasure, author of Sound Business and chairman of The Sound Agency comes across the problem often."We experience every space in five senses so it's strange that architects design just for the eyes," he says. "Sound in a space affects us profoundly. It changes our heart rate, breathing, hormone secretion, brain waves, it affects our emotions and our cognition." His research suggests that trying to perform knowledge-based tasks in a space in which other people's conversations are clearly audible is difficult. "Productivity can be degraded by up to two thirds," he says
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This is a good question with many possible answers.
Traditionally, the ideal place to study (as a student) is in a quiet corner of a library.   The sounds one hears in a good library are almost nil, except of movement of chairs in sitting down or getting up and the turn of pages or movement of books.   In that library atmosphere there really is not much else one can do except study, do research, even one is clicking away on a laptop.
This same library atmosphere also pervades many research laboratories, where intense concentration is needed to carry out experiments and tabulate results.
But then the quiet of a library is swapped for a music-filled atmosphere by some researchers.   Somehow different sorts of music work wonders for some who find the background sounds appealing and stimulating while doing research.
I know of a story of a mathematician who made a major discovery in algebraic topology while lying on a beach in Chile, just soaking up the sunshine, listening to the waves roliing  up and down the Chilean shoreline, and realizing that the a spherical shape volume as large as the sun can be mapped into a matchbox.
The old saying applies here: One person's pleasure is another person's poison.
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My works involve monitoring of QT and RR interval in albino rats. Due to lack of telemetry system I need to anethatise the animal prior to ECG recording. I seek for a robust anesthetic agent that would impart least impact on the heart rate, RR and QT interval. Kindly advise.
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Etomidate (Hypnomidate) could be your drug of choice. It is a carboxylated imidazole anesthetic with minimal myocardial depressive effect. It was found to be a potent, short-acting and heart rate usually stays unchanged. Incidence of apnaea is also very low.
(ED50 = 0.57 mg/kg)
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Reduction in heart rate using anti-hypertensive drugs should be or should not be a therapeutic target among hypertensives free of overt cardiovascular disease?
Use of beta-blockers or CCB for hypertensives to reduce heart rate or none of them?
Is there a must or should for physicians to reduce heart rate below a known level in hypertension?
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What is the other factors and / or anthropometric data except age, BMI ,Height, Weight... Can Influence Maximal Heart rate? Because the all these factors represent only 45 percent?
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In the 60 through 90 all over the western world a large number of studies have been performed, among other reasons also to obtain normal values from reference populations, as it is clearly obvious that normal values for people from Norway or The Netherlands cannot be applied in India and vice versa.
One of many theses on this subject is from H.W.W.Weeda Maximal Exercise Tests in 331 Male Employees.
I have participated as a medical student in another similar trial,
In these studies healthy volunteers were exercised to their personel limits while an ECG registration and repeated bloodpressure measurements were taken. In addition continuous bloodgas and or oxygen-uptake and or carbondioxide  in the expirated air were assessed.
In fact, other than exhaustion, signs of ischaemia on the ECG, CO2-retention, arythmia on the ECG, extreme systolic hypertension, tension drop there were no well defined stopping limits that were routinely applied.
So what investigators ended up with is tables with heart rates obtained versus various other parameters. There is no clear cut universally valid endpoint for what is the maximum heartrate other than the observation that 'the investigator got away with it' without observing ischaemia or other ominous signs.
So actually there is a real scarcety of data on people who have exercised beyond the point considered unsafe [i.e. 2 mm ST segment depression / downsloping ST-segments].
Given this fact no clear cut statistical method can be applied. Far too few subjects have gone 'over the edge'.
This lack of solid endpoint definition and relatively few hard endpoints and the very subjective nature of the criterium 'exhaustion' makes this a hard one for statistical analyses. This is not straight forward
What we do have is the best possible body of accumulated experience that has resulted in a report.
And even when you read that full report [ref 2] you will find that they do not have a simple simple universal criterium, nor a single well defined statistical method. It is all just 'descriptive data' and some consensus among experts. There exists no golden standard for methodology for this.
The American College of Cardiologists/American Heart Association has published an authorative paper every couple of years about the criteria they recommend for various types of stress testing. Read the full report, not just the executive summary.
The indications to terminate exercise testing:
Absolute indications
•Drop in systolic blood pressure of >10 mm Hg from baselinebloodpressure despite an increase in workload, when accompanied by other evidence of ischemia
•Moderate to severe angina
•Increasing nervous system symptoms (eg, ataxia, dizziness, ornear-syncope)
•Signs of poor perfusion (cyanosis or pallor)
•Technical difficulties in monitoring ECG or systolic bloodpressure
•Subject’s desire to stop
•Sustained ventricular tachycardia
•ST elevation (≥1.0 mm) in leads without diagnostic Q-waves(other than V1 or aVR)
Relative indications
•Drop in systolic blood pressure of (≥10 mm Hg from baselineblood pressure despite an increase in workload, in the absence of other evidence of ischemia
•ST or QRS changes such as excessive ST depression (>2 mm ofhorizontal or downsloping ST-segment depression) or marked axis shift
•Arrhythmias other than sustained ventricular tachycardia, includingmultifocal PVCs, triplets of PVCs, supraventricular tachycardia, heart block, or bradyarrhythmias
•Fatigue, shortness of breath, wheezing, leg cramps, or claudication
•Development of bundle-branch block or IVCD that cannot bedistinguished from ventricular tachycardia
•Increasing chest pain
•Hypertensive response*
As you might have noticed: the maximum heart-rate is not one of them.
Usually the criterium for heart rate in  sustained ventricular tachycardia is substantially higher than the values in tables used in sports medicine
For several of the above criteria, explanations other than coronary artery disease can be found.
I'll give a single example:
A patient with long standing mild hyperthyreoidism and otherwise good health is likely to tolerate higher heart frequencies than an average individual with otherwise equal profile.
If you have not tested all of your subjects for this, you may judge that the maximum heart rate can be taken higher than judged from truly healthy subjects alone.
So best advise: look in literature and see what is generally accepted
stick to that method. There is no Holy Grail to be found, no superior methodology. anyhow it will all remain descriptive.
Know what your results are going to be used for and adjust to the frame of reference of your prospective users.  The maximum heart rate criterium is ill-defined and best avoided.
It is stated on page 5 of reference 2:  Although exercise testing is commonly terminated when subjects reach an arbitrary percentage of predicted maximum heartrate, it should be recognized that other end points are strongly preferred.
Ref -1- Circulation 2000 volume 102 pages 1726-1738
ACP/ACC/AHA Task Force Statement on Clinical competence in Exercise Testing
Ref -2- Gibbons RJ, Balady GJ, Bricker JT, Chaitman BR, Fletcher GF,
Froelicher VF, Mark DB, McCallister BD, Mooss AN, O'Reilly MG, Winters
WL Jr. ACC/AHA 2002 guideline update for exercise testing: a report of the
American College of Cardiology/American Heart Association Task Force on
Practice Guidelines (Committee on Exercise Testing). 2002.
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Is, for example, a correlation of a peak in the HF-Frequency band of HRV and the mean respiration rate with the same frequency a reliable measure for respiration/heart rate coherence? In Case of HRV-Biofeedback with a strong peak at about 0,1 Hz (although in the LF-band) it seems quite obvious.
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Excellent answer by David Eddie. I would only suggest to consider a very good device to collect RR samples as only few beats lost (or extasistolic beats) can deeply influence the spectrum coherence.
1) of course "istantaneous RR  length (hence vatiability) is modulatae by respiration
2) It is possible and already described in literature (se as examples papers by Luciano Benrardi  in the late 90s). It could be pleonastic to remind you that the frequency respiration will coincide with HRV at 01 Hz only when respiratory acts are 6 per min. But in my experience it is not so easy to drive the respiration at this frequency in non well motivated patients,. Hence the cross correlation betwwen RF and HRV spectrums during free respiration is the best way to understand the relationship between the cited physiological acts.
Good luck
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Hello,
I am looking for data sets generated by pulse measuring devices that are suitable for TCM diagnosis. Does anyone know of any such data available online or of any hospital / practitioner that could provide such data?
Thank you.
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The Korea Institute of Oriental Medicine (KIOM) does research into computerized pulse diagnosis and pulse wave analysis systems.
The Institute's website is here http://www.kiom.re.kr/eng/index.jsp
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Hi, everyone, I found that both respiratory disturbance index (RDI) and micro-arousal index (MI) have significantly positive correlations with nighttime high frequency band power (HFpower) of HRV, and with very low frequency peak. HFpower mainly reflects parasympathetic activation, and very low frequency peak mainly relates to thermoregulation and hormones. What are the possible reasons for these phenomenons? Thank you very much!
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Thank you very much for your great help, Tatyana.
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I work on shoulder blade EMG signals and have problem with filtering heart rate noise. Has anybody experienced this? If so, what code did you use in order to filter this noise?
The attached file is a sample of a 13-channel EMG signal, which channel number 1,2,4,5 &6 have heart rate artifact. I want to filter this heart rate noise and have a pure muscle activity signal.
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you can use this: (I attached data.txt and a sample result)
clear all
close all
clc
data=importdata('data.txt');
signal=data(:,5)'; % choose a channel, channel 5 for example
plot(signal)
signal_out=signal*0;
for i=100:100:size(data,1)-300
s=signal(i-99:i+100);
e_s=sum(s.^2);
if e_s< 50000 %% you can change these thresholds for different channels
signal_out(i-99:i+100)=s*.01+signal_out(i-99:i+100);
elseif e_s< 100000
signal_out(i-99:i+100)=s*.1+signal_out(i-99:i+100);
else
signal_out(i-99:i+100)=s*.95+signal_out(i-99:i+100);
end
end
figure, plot(signal_out,'r')
%% you can save signal_out 
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My research lab is currently in search of an alternative to Polar RS800CX watches to collect heart rate with R-R and future HRV analyses. The BioNomadix looks like a viable option, but I want to know if anyone has used the ECG-ECG module. What's your experience with it? What were participants doing while wearing it?  Any feedback is appreciated!
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Hi Dear
Today I find new scientific email that answered to any question you can contact with helptoresearchers@gmail.com
Regards  
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In a field situation how to measure heart rate, SPO2, temperature, Blood pressure telemetrically?
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CorScience Multiparameter Sensor MP-10 will fit your needs. As far as I know it offers blood pressure, heart rate, oxygen saturation, 6 or 12 channel ECG. Not sure about temperature. It also has Bluetooth capabilities so that it can interact with your mobile phone for telemedical purposes. 
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Inappropriate sinus tachycardia is a rare form of nonparoxysmal atrial tachycardia characterized by persistent elevation of heart rate (HR) due to an apparent sinus mechanism disproportional to the physiologic demand.The underlying pathological basis is incompletely understood, likely multifactorial, and complex. Inappropriate sinus tachycardia is characterized by persistent and disproportional elevation of heart rate. Ivabradine has been successfully used in some patients.
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It is def. worth trynig since ivabradine has relatively low incidence of side effects and is well tolerated by majority of patients. There are some studies with short-term positive results but long-term efficacy is not known. In addition, there are also no RCT I am aware of. 
I recommend this editorial from JACC: http://content.onlinejacc.org/article.aspx?articleid=1358180 to broaden the horizon.
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I am searching for a device to measure ECG and EDA. Ideally the device should be worn on the wrist or the arm. I prefer not to use chest band or similar. 
Thanks,
Davide
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You're going to have to be more specific about what you're trying to do, because I'm not sure there's a device that actually fulfills those precise specifications. I'll lay this out in points for simplicity:
* ECGs need a dipole, so a single-point arm or wrist device - if it exists at all - would be pretty weak. Wrist and finger devices typically are photoplethysmographic.
* If you are trying to measure any kind of episodic EDA response, you want a palmar (or foot) device. If EDA is going into a model of physical or metabolic activity, that's probably less important.
And the devices...
* Pulse oximeters, as stated, can indeed do HR monitoring from the finger or wrist. They are also prone to movement errors, and the different and various commercial versions will probably not give you much access to the pulse-to-pulse interval. Which you probably need. Consequently, they are not ideal for ambulatory monitoring, two-handed tasks and work fairly badly in some environments.
* Bitalino is great hardware - I just ordered one myself off their Kickstarter - and can be modified to do more or less whatever you want. However, you will need at least some basic biomedical engineering skills to make it work, and you will have to build it yourself.
* Movisens I haven't used but the hardware has a good reputation. The heart rate monitor is chest strap, from memory, which you don't want. If I was measuring ambulatory SCR, though, I would choose a device very similar to their EDA-sensor, which is a great build - electrodes around the thenar eminence, wrist mounted... good stuff.
Basically, we need a lot more information about what you want to do - time frame, participants, posture and movement, task content (if any), and most importantly the measures you want from the raw heart and skin c. data in the first place. There are probably 50 suitable and relatively low-cost devices that do some version of what you want to do here, and there are new builds every month as the technology is now very accessible.
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1. protects cells during stress, hypoxia
2. anti inflammatory
3. decreases heart rate and drops bp
4. caffeine is opposite to adenosine so basically calms the brain
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I have heart rate data of an athlete when he was running 35 minutes on a treadmill. 
The data were observed every 5s. For time series analysis purposes, how can I  convert heart beat time series data? Is this correct for time series analysis?
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Saba, if your data were recorded with spaces of 5s, you need first to do like Parth Shah told you, ok? Then you can create a column of values and insert them in Kubios, ok?
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I'm looking for an alternative method for vo2 max testing due to time constraints on my experiment. Any journal articles to read regarding resting heart rate at predicting vo2 max would be appreciated.
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Mark, do not trust any method that can assess VO2max without the person work out. The evaluation of resting HR does not allow that the VO2max can be calculated indirectly because many factors affect the values of HR at rest, therefore invalidating your data or your value of VO2max. You can use submaximal tests that allow, by inference, that VO2max can be established. They are more reliable, but even so, the real value of VO2max can only get in maximum dynamic effort.
y
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Multiple algorithms are proposed to retrieve ppg from mobile video. Though most of them are good enough for heart rate detection, more complex vitals are difficult to estimate. How can we get a ppg signal from mobile phone, retaining finer signal details?
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yes, we have this for Andriod based smartphone.
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I am new to physiological measurements and am struggling with what seems to be the worst software manual on the planet!
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I would highly recommend  you to puzzle out the properties of the studied characteristics. And only then deal with whatever software. Otherwise, you can get good looking but useless results. E.g., take a look at these old but  very useful articles:
1.  Akselrod S, Gordon D, Madwed JB, et al. 1985 Hemodynamic regulation:
investigation by spectral analysis. Am J Physiol 249:H867-875.
2. "Heart rate variability: standards of measurement...", Circulation. 1996 Mar 1;93(5):1043 - 65. 
If you have any specific questions, don't hesitate to ask.
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We are testing a new simulator and need data about pathological heart rate in adults and children.
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^^ Many databases w. arrhythmia, fib, etc.
Not sure about children.
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I would like to know if it is valid to calculate the heart rate variability of a  70 years old subject with sinus arrhythmia? 
Thank you in advance
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Hi dear colleague,
The heart rate variability is a method that quantifies the difference between successive sinus heart beats. So, the basic asumption of this method is that the individual has a preserved sinus rhythm. Since your subject present some arrhythmias, you will not be able to detect if his heart rate variability is promoted by the autonomic nervous system or by the arrhythmias.
You can try exclude the ectopic heart beats and then interpolate the missing data, before the analysis of HRV. However,  if the amount of such arrhythmias is too large, your analysis will be compromised.
Why don't you try to assess other indexes of autonomic function in your subject ? A simple way would be to quantify the heart rate recovery after a single session of exercise.
I hope my answer can help you. 
Tiago
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Hello there! Can anyone recommend online courses for Matlab? I want to learn how to process physiological data (HR, RSA and SCR with Biopac equipment) in MATLAB. Which company/course would suit this best? I found that MathWorks have many courses online, but I am not sure which ones to take. I would be very grateful for any advice! Thanks!
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Thanks so much Saman! Very helpful!! :)
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as compared to healthy people in a similar way as what can be observed at rest?
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 It all depends what level of exertion is being performed. Resting tachycardia and a more or less fixed heart rate are characteristic of long standing diabetic autonomic neuropathy with vagal involvement. impairment.
See: Ewing DJ, Clarke BF. Diabetic autonomic neuropathy: present insights and future prospects. Diabetes Care. 1986; 9: 648–665.
If there is significant cardiac autonomic neuropathy, this will impair exercise tolerance and actually lowers maximal heart rate.
See: Vinik, A. I., and D. Ziegler: Diabetic cardiovascular autonomic neuropathy. Circulation 115 (3):387–397, 2007
Among people with diabetic autonomic neuropathy, I would suggest the modified Borg Scale of perceived exertion at a level of 2-3/10 for physical activity for the exercise prescription. However, before prescribing exercise among those with diabetes and autonomic neuropathy, a cardiovascular stress test should be performed, first.
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General anesthetic dose of Ketamine - 80mg/kg & Xylazine - 10mg/kg will affect heart rate of rat? anyone will experienced ECG recording using this anesthetic combination and how much heart rate would observed? 
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Hi,
General anesthesia with Ketamine+Xylazine decreased strongly heart rate in rats, mice, rabbits and other animals.You can find the information about the effects of this type of anesthesia on heart rate in rats in the study conducted by Olson ME et al. (see attached file).
Yours sincerely,
Jin Bo Su
---------------------------------------------
Jin Bo Su, Ph.D.
INSERM U955 EQUIPE 3
ENVA, BATIMENT FERRANDO
7 AVENUE DU GENERAL DE GAULLE
94700 MAISONS-ALFORT
France
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swimming
heart rate measurement
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Many thanks for the reply Ricardo.