Cardiovascular Physiology - Science topic
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Questions related to Cardiovascular Physiology
Pulse oximetry is now the standard way to measure oxygen saturation, however in certain situations, it losses its efficacy (e.g. patients in shock who have become vasoconstricted). Are there alternative methods to measuring oxygen saturation besides the gold standard which is the arterial blood gas?
Slow breathing, usually at frequency of 0.1 Hz, is a method of relaxation and supposed to increase parasympathetic activity. Heart rate variability is used as a marker for autonomic response to such intervention. In the frequency domain of HRV analysis, the HF power is considered as a marker of vagal modulation of cardiac activity, the LF power for sympathetic influence with parasympathetic component, and LF:HF ratio as sympatho-vagal balance, though with controversy.
There is a concern about how to interpret frequency domain of the HRV analysis if respiration frequency is variable (not controlled). For example, as showed in the attached file, while time domain analysis of HRV indicates increased vagal activity in response to slow breathing (increase in SDNN, RMSSD, NN50, and pNN50), the frequency domain is complex; LF (and LFnu) and the LF:HF ratio are higher in slow breathing compared with normal breathing and also compared with breathing at frequency of 0.2 Hz. Also, HF is not significantly different between slow breathing and breathing with frequency of 0.2 Hz while HFnu is lower in slow breathing.
How frequency domain of HRV must be interpreted when the intervention itself is changing the frequency of respiration? Is the time domain a better analysis of autonomic response in such case?
According to some studies, very hard water can have effects on cardiovascular physiology (Rubenowitz-Lundin and Hiscock, 2005). Other studies have not shown an association or have found a lack of association (Miyake and Iki, 2004). The link between water hardness and cardiovascular disease is not clear from studies. Are there studies that manage to clearly determine the link that exists between them now?
Can I use EDPVR to characterize LV compliance if I get that EDPVR from PV loop at steady state, without loading change? What are the limitation of this indice?
In an experimental study we tested various breathing exercises and monitored respiratory flow, beat-to-beat blood pressure, and heart rate. We developed MATLAB script for baroreflex analysis based on the sequence method and the result was interesting.
Now, we want to compare breathing exercises regarding the magnitude and phase of transfer between respiration -> blood pressure, respiration -> heart rate, and blood pressure -> heart rate using transfer function analysis.
I appreciate if someone with experience in such analysis can help us with a MATLAB script.
I am going to induce acute myocardial infarction in rats by LAD ligation. As you know, the mortality rate in this model is usually high. What should I do to reduce the casualties?
I would be very grateful if you could give me some advice.
Slow breathing increases fluctuation of blood pressure over the breathing cycle which is followed by the larger amplitude of respiratory-sinus arrhythmia. One main mechanism is the baroreflex. In our study on slow breathing we found that although blood pressure variability stays more or less the same over 3 minutes of slow breathing, RSA decreases over time.
Can this be due to habituation of the baroreflex?
Dear All, I am trying to apply data mining and machine learning techniques in diabetes prediction. Therefore, I need more data.
I understand that, there is a Pima indian and UCI database. But this not enough, what i need.
The required data can be
e.g., Age, sex, glucose, LDL, HDL, BMI, HbA1C and other variables and short and long term outcome of the subject. Outcome can be defined by good and poor outcome.The poor outcome can be chronic disease or CVD.
I would like to collaborate.
Your cooperation will be highly acknowledged.
Waiting to hearing from you.
I am going to treat the myocardial infarction rats with spironolactone for 8 weeks/56 days. As you know, there are several ways to administer this drug, such as oral (gavage and mixed in rat chow), intraperitoneal and subcutaneous injection. We currently cannot mix it with rat chow.
Which technique do you think is more prior?
How to make the solution of it? Can we make the solution with physiological serum?
Your advice and suggestions will be much appreciated and welcomed.
The fibrotic response after a myocardial infarction (MI) can be classified into two types of fibrosis:
1-Replacement or reparative fibrosis at the infarcted area (scar formation)
2- Reactive fibrosis outside the infarcted area usually after the replacement fibrosis
The replacement fibrosis or fibrosis healing phase (takes 4 to 6 weeks post MI) is a pivotal process to prevent the rupturing of the ventricular wall after an ischemic insult. However, is it wrong if we disrupt this process?
I would be grateful if you could give me anything about this topic.
Does stroke volume and diastolic BP have a positive linear correlation?
Given greater pre-load and thus end-diastolic volume is it expected that diastolic BP would be reduced?
I am going to induce acute myocardial infarction in rats by LAD ligation. I want to know what protocol is most suitable for getting to the heart.
Thoracotomy or lateral thoracotomy?
I would be very grateful if you could give me some advice.
The video of your surgeries will also be very helpful.
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.
In reporting systemic vascular resistance measurements, one can use mmHg/min/L, dyn/sec/cm5, or pascals per second/cm2. Is there a general consensus from the field of applied physiology or medical physiology as to which one to use? There seems to be a varied use of SVR units used amongst different publications. Any suggestions would be greatly appreciated.
These devices have been around for a while now. Is there a consensus on the best way to do this, for low-cost/low-power computers and digitizers (e.g. wearable consumer tech)? I'm mainly interested in the digital signal processing involved.
In one of our studies on the effect of various breathing exercises on Vagal activity and Baroreflex Sensitivity, subjects performed uncontrolled breathing, paced breathing at 0.23 Hz, and paced breathing at 0.1 Hz.
In spectral analysis of both HR and BP based on FFT (attached picture), in addition to the peaks in the spectrum around the breathing frequency there are also other peaks (2nd harmonics) in both blood pressure and heart rate variability spectrum. What is the origin of these harmonics? are they because of the FFT method and has no physiological origins?
How could I have information about blood flow restriction training and cardiovascular function adaptations?
Can overemphasize on high intensity intermittent exercise (HIIT) in a training protocol lead to micro trauma to the cardiac muscle due to the micro-ischemia caused by intense exercise over a longer period of time (5-10 years)?
Some researchers from Russia (Victor Seluyanov) have proposed that the lack of inclusion of steady-state long duration continuous exercise for improving eccentric hypertrophy of the heart and overemphasize on HIIT training methods for improving aerobic power could lead to micro damages to the heart muscle over a longer period of time and therefore cause sudden cardiac failure or heart attack in healthy physically active asymptomatic population.
Victor Seluyanov, Russian professor in sports biochemistry states that:
a) Heart training is important to deliver enough O2 to muscles
b) Training with pulse higher than 180 bpm promotes D-type heart growth. Eventually, it results in myocardial degradation (dystrophy) and is one of the major causes of death and debilitation in high ranking endurance athletes. Prolonged training with 120-150bpm promotes L-type growth which is healthy and safe.
For those who understand Russian I'd recommend this video regarding sambo training: https://youtu.be/n7c352NSDUk
Other references on Victor Seluyanov's work:
In respiratory research a breathing apparatus consisting of mouthpiece, filter, Pneumotachometer, and non-rebreathing valves plus some connectors are usually used. Although a non-rebreathing valve is used to reduce dead space, each of these devices has its own dead space. Though small, adding together they build a relatively large dead space sometimes. What is the max acceptable dead space in a breathing apparatus, for a study including healthy adults?
I am looking if there is any novel technique that allows you to calculate the myocardial oxygen consumption. I know the double product (systolic pressure X cardiac frequency) but I would like to know if there are any other methods.
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!
We have cleaned the system thoroughly, prepared new buffers and used the control rats. However, the problem remains the same.
I would like to analyse the additive predictive value of a biomarker over an old model in development of stroke using NRI.
I was wondering:
1. Is it possible to calculate NRI in SPSS?
2. I know that NRI tries to identify how a new model can reclassify subjects (in my example as having stroke or not). Is it possible to calculate NRI for a model with no binary outcomes (e.g. low, medium and high risks)?
Thanks in advance.
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)?
Cardiovascular physiology is the field of interest.....
Any institute having expertise in analytical techniques of HPLC and MS on methylated protein studies
Anyone who is doing work on cardiac tissue and if anyone doing it on cardiomyocytes too?
I am interesting to do some studies together if someone wants.
I have calculated Framingham risk score in my cohort (Hispanic farm workers) with mean age 35.3±9.4, and I would like to compare my results with Hispanic population of similar age. Do you have this kind of results?
EHRA scores are used to discriminate symptoms severity when patients feel they are in AF. However, patients still complain of disabling symptoms when they are in constant sinus rhythm post AF ablation. What is the validity of using EHRA score post procedural when the patient's general condition due to other comorbidities is restricted (arthritis, COPD, asthma, etc) while they are in sinus rhythm all the time?
How much LBNP is equivalent to 1G, 2G and 3G? Does "equivalent" mean that the two activate the same cardiovascular response intensity or is there a defined objective way of converting one to the other?
Most of the longitudinal studies on the cardiac adaptation to exercise training seems to report on wall thickening and moderate increase in internal ventricular diameter at best, with some notable exceptions, e.g.:
Any observations and considerations how to effectively induce "physiological" ventricular chamber expansion are welcomed. Also are speculations/hypotheses on the means to induce longitudinal (apex to valves) left ventricular enlargement.
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?
We are currently trying to implement filters for hemodynamic data collected from a centrifuge run with human subjects. Given this, we are looking for expert opinions on what are the acceptable standard deviations for the following parameters under mild/moderate +G challenges:
Heart rate, Mean Arterial pressure, Cardiac Index, Systemic vascular resistance index (mmHg please), and stroke volume index. The subjects are all healthy individuals, and all data was recorded during 1/2 +Gz levels.
Thank you in advance for any and all feedback/article recommendations.
In our experiment we observed that hemodynamic adaptation pattern correlated with BMI and BSA separately, but stronger so with their quotient (BMI/BSA), which we have called the BMI/BSA-Index.
Has anyone encountered such a term before?
Any opinions on introducing such an index?
There appears to be a low dose therapeutic window for alpha lipoic acid in both schizophrenia and ischemia reperfusion. Could disturbances in glutathione homeostasis, either through increased synthesis or reduced degradation be a factor? The half-life for both alpha lipoic acid and glutathione is very short.
I want to correlate changes in temperature with cardiovascular related diseases. There are too many confounding factors. Kindly help
Deterioration of renal function with significant reduction in GFR following treatment with beta blockers have been outlined in clinical practice and experimental research (vide Wilkinson 1982). The beneficial role of dopamine have also been acknowledged, but clinical evidences about the effects of some specific beta blockers are conflicting, i.e., nadolol, propranolol etc. So what's the current guideline of beta blocker usage in patients who have moderate renal impairment?
Epstein M, Oster JR. Beta blockers and renal function: a reappraisal. J Clin Hypertens 1985; 1: 85-99.
I am looking for theory Information about angiotensin II receptors and about their genes, PDF or electronic books. Can you help me?
The literature shows that myocardial antioxidant capacity, cardiac Heat Shock Porteins, Nitric Oxide, ATP-dependent potassium channel function, and opioid system activation are related to this, but also turns it inconclusive in some original articles or systematic reviews.
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?
Atheromatous plaques are commonly seen in the coronaries, carotids and aorta. Despite sharing the same risk factors only certain sites are predisposed. Even in the same individual, despite similar blood vessel size, hemodynamic stress and blood flow patterns, plaques are often unilateral and seem to spare vessels sharing similar stress.
Why this variation?
In my country (Spain) our degree (Sport Science) is not legally regulated and we are not considered by law as a health profession. For previous reason, we cannot work as exercise physiologists.
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?
Would it be possible to make RR Interval longer by increasing the concentration of extracellular calcium?
The parameters to be analyzed in my research are
Can you explain if it is worth to buy Polar RS800CX to get practical recording or Suunto t6 HRM?
I did an experiment wherein I periodically add increasing levels of calcium (contained in a ringer's solution) to a frog's heart. I noticed that the interval between each successive beat increases (becomes more longer) as I add calcium (from 4mmol/L to 10mmol/L in concentration). Furthermore, in 10mmol/L, beat skipping becomes noticeable. However, when I searched for literatures regarding hypercalcemia, they said that the interval between each beat becomes shorter which is entirely opposite of what I've observed in a frog's heart. What could be a possible explanation for this?
Pocholo Luis Mendiola
I am looking for as accurately as possible method of counting the number of human breaths per minute (repiration rate) in the LabChart software.
Option which are proposed by LabChart software (cylic measurment → Preset → Respiration - Respiratory belt with SD = 0.9) fails to find all of the breaths (there are no marks for about 30% peaks of breaths).
It seems to me that much more precise are such option like:
- General - Spikey shape with SD = 2.5 SD
- Sine shape with SD = 2.0 SD
Are there any guidelines for the size of standard deviations which should I use? Can I use Spikey shape or Sine shape method?
I would be very grateful for any help!
Any one who can working on exercise physiology or doing research in cardiovascular physiology can answer the question.
Let's say a person undertakes a program of high-intensity interval training (HIIT) on an exercise bike, with a heart-rate monitor, in a gym. This program involves 30 min sessions every day. The objective of each session is to reach the maximum achievable heart rate at the end of the 30 min period. By 'maximum achievable' I mean the rate at which a highly motivated individual is able to reach (while being yelled at by a trainer, for instance). I think this limit is effectively determined by the person's ability to tolerate pain/discomfort - it would be around say 85% of a person's 'maximum' heart rate, which is determined using the 220-age_in_years rule-of-thumb. At this limit the person is a 'mess' (lost all inhibition, sweating profusely, short of breath, grunting involuntarily, etc.).
My question is - How would this 'maximum achievable' rate change as the program progresses and as the person (who is already reasonably fit) becomes fitter? Would it increase or decrease? And what determines this discomfort/pain threshold anyway, if it is not heart rate? Furthermore, what is the significance of the 'maximum' heart rate if it is not reachable/achievable in reality?
Thanks in advance for your help.
LV overload leading to non-compaction. Needs some info on how LV remodeling after being overloaded may result in non compaction.
I want to know about the is the approx frequency and amplitude of S1 and S2 sounds of normal human heart beat.
Looking to find normal ranges for carotic flow velocities, via dopller ultrasound.
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?
I've found various different paper which used I/R protocols in H9c2 cells to bring those cells into apoptosis, but none worked in my lab so far. Additionally, I've found none where they tested the anti-apoptotic effect of insulin after/during I/R in vitro.
Hope you can help me
I need to collect data about the changing autonomic nervous system after precise manipulation treatment; but I would ask if you are aware about the most precise and accurate method for doing that.
I read in a handbook of psychophysiology (by J. Blascovich et al.) that ECG in combination with phonocardiography can be used (as an alternative to impedance cardiography) in order to measure stroke volume and pre-ejection period. I wonder whether any of you has ever used this approach and might present its pros and cons. Thank you!
The papers I know only show a slow down of the oscillations. It does not stop oscillations. Why?
Please let me know if there is any standard reference for
1. Max and Min load acting on a heart valve (artificial/real).
Are the max and Min values acting on the valve disc 120 and 80 mm Hg?
2. Types and orientation of loads/pressure acting on a valve during opening and closing operation (eg: aortic valve)
In addition to the disc and wall supports, will there be any additional forces.....
3. Bio-mechanics of heart valve (free body diagram, external loads, internal reactions etc)
I try to patch cardiomyocytes but I only have “bad” signal.
I think the medium is OK.
The problem is the quality of the seal or an error of configuration of the software. I work with pClamp 9 and 10.
Could someone, who knows this software, help me to verify the configuration?
We can calculate a heart rate maximum for humans using the equation 220-years of age. However, is there a systemic vascular resistance maximum for humans in either absolute or percentage?
When performed experimentally for stroke/ischemia/reperfusion models, does MCAO completely prevent blood flow to the occluded side or just significantly reduce it by cutting off the main source? Or to rephrase, are there redundant mechanisms/vessel pathways in the rodent brain that supply at least some blood flow to the occluded side during MCAO?
Does anyone have info on the shear modulus of healthy and fibrotic heart? I need values in Shear modulus, not Youngs modulus.
I want to do complete analysis from ecg signal,like any disorders are present in the signal pattern etc.
So is there any open source library available to do the analysis in matlab or c.
In my experience we've found interesting data, especially in soccer players. We are trying to identify HRV changes as a biomarker in the control of weekly training load impact before soccer games.
Currently I´m interested on how entropy could help endurance athletes to determine degree of training load, recovering, etc. I have data to work with, but I would like to compare it with some simulated HRV data.
My group is trying to develop digital phantoms that will ultimately be useful when quantitatively characterizing scar tissue after cardiac ablation. I have found several papers on scar tissue in the cornea following refractive eye surgery et al, but nothing for cardiac tissue.
Alternatively, does anyone know the general composition of cardiac scar tissue (e.g., proportion of different types of collagen, muscle, etc.)? Many thanks in advance!
There are still many limitations in a transcatheter closure of post-MI septal defect including the rigid delivery sheath that could tear the borders of VSD or dislocation of sheath into the right ventricle after wire removal. Also, currently available occluders are suboptimal.
We have Isolated tissue bath, we work on it, herbal, drug blocker....etc
If our krebs solution in organ is 10 ml, I read paper it said you can not adding more than 0.5 ml , is eqaul to 10.5 ml
If more than 0.5 all results become ERROR
Can any one help me ?
A common problem encountered while performing water immersion research, is that water is not friendly to monitoring equipment such as EKG, heart rate, blood pressure, Sp02% etc. What methods of measurement have other researchers used that have recorded accurate physiological data, without interference/interruption, whilst being immersed in water? Does simply using Tegaderm or another waterproof covering help?
Could it be because of O2 and nutrient changing into CO2 and body waste?
Do not change the molecules causes the volume change?
As the findings of this study also found hypertrophy of the type I fibers - do you think BFRRE could be used to substantially increase the ratio of type I to type II fibers and when accompanied with endurance training substantially increase the oxidative capacity of the muscle fibers? I.E. Larger type I fibers may increase mitochondrial content when endurance training is employed also. Also out of interest what rep range was used for the study?
Conference Paper Hypertrophic signaling is restored after a ten-day break bet...
Baroreceptors in the carotid sinus are stretch receptors in the arterial wall. How these receptors are stimulated by external pressure as with carotid massage?