Cardiovascular Physiology - Science topic

According to Pathania (2021) in his research entitled "Alternatives for erroneous finger probe pulse oximetry in systemic sclerosis patients during COVID-19 pandemic", the other alternative in using pulse oximetry for patients in shock or COVID-19 patients who have diffuse involvement of all their fingers--an ear lobe, forehead and oesophageal oximetry might be used to monitor the oxygen saturation of the patients or individuals.

Debanjan Borthakur

1- Let's read these papers more carefully. Laborde et al. has mentioned in the introduction that "we refer to parasympathetic activity as vagal tone" that means that they are mixing all types of PNS activities together and call it vagal tone. So when reading this review keep this in mind. Also, they have mentioned that ""in this paper we refer to cardiac vagal tone as assessed by HRV measurement" well we cannot define a concept by a surrogate measure and use it as a method of validation. We need to always look at the gold standards; neural blockade studies and pharmacological blockade studies.

2- Grossman et al indeed have mentioned that "RSA has been shown to often provide a reasonable reflection of cardiac vagal tone when the above-mentioned complexities are considered", but also have listed 6 issues above of this that "can lead to misinterpretation of cardiovascular autonomic mechanisms" and one is respiratory parameters, please also see others. These are mostly overlooked by many researchers in psychophysiology.

3- HF, LF, or SDNN or RMSSD interpretation as a measure of cardiac vagal modulation requires paying attention to the issues raised by Grossman et al. When respiratory frequency changes from HF to LF, HF no longer represents the respiratory modulation of cardiac vagal activity, but LF does, as was shown by pharmacological blockade study. This doesn't mean that under resting state and with respiratory frequency being in HF band, LF still can represent vagal activity, this also has been shown by pharmacological blockade studies.

4- To interpret HRV, you need to first look at the physiology of HR modulation by ANS at the level of the heart and at cell level, as well as interaction between SNS and PNS at central and peripheral levels. As mentioned by Laborde et al "ease of access [and of measuring HR] should not obscure the difficulty of interpretation of HRV findings that can be easily misconstrued". We have too many studies using HRV to measure ANS activity but too little studies on the validity of such measures.

Finally, that many researchers repeatedly mentioned something does not mean that is correct. This is the problem with HRV interpretation in psychophysiology literature, unfortunately, and we continue repeating that without asking ourselves based on what evidence and based on what valid or gold-standard measure? If you look at cardiovascular physiology literature you usually don't see such misinterpretations. Same with 'resonant breathing', nice phrase but no strong evidence.

Please have a look at the following RG link.

Yes, you can estimate LV compliance from single P-V loop at steady state. The limitation Is it’s accuracy Issue.

dear Ali

you can find some suggestions of SAP-HP phase and gain analysis in A. Porta et al, Am. J. Physiol. 300, R378-R386, 2011 and J.C. Milan-Mattos et al, J. Appl. Physiol. 124, 791-804, 2018.

All the best, Alberto

Hi, for you to increase survival rate , there should reduced time of ligation and the positioning of the tie along the LAD.

Dear All,

I think, your data was collected from participants that breathed 6 times/min (6P breathing) first time.

We used 6P breathing (HRV biofeedback) for treatment asthma, depression, and fibromyalgia. Our patients (n > 100) received 10 sessions during 10 weeks. The session included four 5-minute tasks. We taught them to find individual breathing rate and trained to breathe not so deeply. Treatment effect was received after 4 procedure when patients caught the right skill of the breathing. Each patient found individual breathing frequency in range (0.076- 0.107 Hz) and individual tidal volume. After 4 sessions amplitude RRI oscillation was stable for 5 minute and usually HR decreased. Sometime HR increased if in base lane it was low (50-60 BPM).

Evgeny

Dear Md.abdul Awal,

Maybe you already know the following article and data-link on the subject:

Kavakiotis I, Tsave O, Salifoglou A, Maglaveras N, Vlahavas I, Chouvarda I. Machine Learning and Data Mining Methods in Diabetes Research. Comput Struct Biotechnol J 2017;15:104-116. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5257026/pdf/main.pdf

Selected Trend Table from Health, United States, 2011. Diabetes prevalence and glycemic control among adults 20 years of age and over, by sex, age, and race and Hispanic origin: United States, selected years 1988 - 1994 through 2003 – 2006: https://catalog.data.gov/dataset/selected-trend-table-from-health-united-states-2011-diabetes-prevalence-and-glycemic-contr-63c3a

All the best for your research,

Martin

Check this link

regards

After MI, Fb are activated throughout the LV, presumably through TGF-β1 in response to increased wall stress and/or inflammation. Additional regional specific signaling leads to interstitial fibrosis via collagen cross-linking in MIadjacent. Local LOX activity could be stimulated by higher mechanical load imposed by tethering to the infarct or signals could diffuse from the scar. Identifying specific signaling cues to maintain the mature state of MyoFb phenotype in the scar tissue may open new perspectives in targeting the MyoFb reversibility in interstitial fibrosis without damaging existing scar tissue.

Hi Terun Desai,

Increase or decrease in the stroke volume has some influence in the diastolic blood pressure (DBP). But It is directly proportional the total peripheral resistance (TPR) offered by blood vessels, whereas systolic blood pressure (SBP) is directly proportional to the stroke volume.

If there is increase in the peripheral resistance there will be increase in the DBP as seen in atherosclerosis in which condition there is decrease in the diameter of the blood vessel, will offer more resistance to blood flow. In order to pump adequate amount of blood to the tissues in this condition, there will be increase in the heart rate and stroke volume, therefore increase in the SBP. Hence there will be increase both SBP and DPB (Increase in BP).

Exercise causes increase in the SBP and a slight increase in the DBP. During exercise there will be increased production of metabolic waste product which will dilate the blood vessels. Therefore there will be decreased TPR, which will not allow to increase in the DPB much. At the same time, increase in the sympathetic during activity during exercise will increase the heart rate and stroke volume increases the SBP. Though sympathetic activity has vaso-constriction effect on blood vessels, where increase in TPR is expected, overwhelming activity by metabolic waste product eventually increase the diameter of the blood vessels causes decrease in DBP.

Therefore SBP is directly proportional to stroke volume and DBP is directly proportional to the TPR.

To answer the question asked by Sergey Kozhukhov in the last para, you need to understand the regulatory mechanism of BP. Whenever there is decrease in the heart rate (mostly happens if there is decrease in the sympathetic activity or increase in parasympathetic (vagal) activity), cause decrease in stroke volume (amount of blood pumped out per ventricle per beat(stroke) ~ 70 ml/beat), and cardiac output (amount of blood pumped out in one minute ~ 5L/min), therefore decreases in the SBP. Since there is no vaso-constrictor effect by sympathetic fibers, will cause dilatation/ relaxation of blood vessels. Hence decrease in the DBP. An overall decrease in the BP (SBP & DBP), cause a decrease in the activity of the baro-receptor (a pressure receptor that sense changes in the blood pressure). This will decrease inhibitory effect baro-receptors on the on the vasomotor center (which regulates sympathetic activity) in the brain. This will increase the sympathetic activity eventually will increase the SBP by increasing the hear rate & stroke volume and increase in the DBP by vaso-constrictor effect.

Hope you doubt is cleared. If not, mail me for more explanation

Best

Ramesh

The outcome of coronary artery occlusions is age-, species, severity of occlusion, duration, coronary collateral blood flow during ischemia (compared to baseline), operator and drugs used to support and stabilize hemodynamic.

In experimental models, regional ischemia is complicated by the above-mentioned factors and contributes to lack of reproducibility in the same laboratory and in literature.

It is seldom to see authors report complications, arrhythmia, fibrillation and mortality that why young investigators waste time and resources by following prior publications that do not report pitfalls of their studies. Swine model lacks coronary collateral, that is why pigs die with small risk areas (occlusion close to the apex) from arrhythmia and cardiac arrest not from infarction. Investigators treat all groups with lidocaine to attenuate arrhythmia and ventricular fibrillation, yet some more lidocaine and other inotropic drugs are used to minimize mortality.

Unlike regional ischemia, global ischemia and measuring load-independent indices of cardiac performance and correlating that to myocardial bioenergetics, marker enzymes of ischemia and infarction and the end-point of infarct size.

To obtain reproducible studies and results you must design experiments that have clinical relevance and try to minimize variations within same group and amongst other groups and time. GOOD LUCK

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.

Laboratory Analysis of Relative Plasmatic Fractional Protein level could be suggestive (Total Protein, Albumin & Globulin..... 

Generally speaking the measurement principles mentioned in previous posts do not estimate heart rate.

For example when using ECG to measure heart rate the peak electrical activity across cardiac tissue is measured against time. In the case of pulse oximeter (PPG) the peak volume of blood in a certain part of the body (usually finger) is measured against time. In short, heart rate is usually measured and rarely, to the best of my knowledge, estimated. 

In terms of event orientated, the heart reacts to certain neurotransmitters and biochemical markers that are released into the body and brain en masse when we register a change in our environment. This is how the body regulates the supply of blood to the different organs (i.e. Brain) in our body. 

For example when we are presented with a life threatening event our body is flooded with adrenalin while our brain is flooded with nano-adrenalin. In turn these neurotransmitters and biochemical markers cause the heart to beat quicker, transporting more blood, oxygen and nutrients around the body to the organs (i.e. muscles) that need it. 

A similar process occurs when were resting, sleeping, digesting etc. Although the neurotransmitters and biochemical markers will vary depending on the desired action, the heart (amongst other organs) reacts to the event the body encounters. 

So in short when our environment changes so to do the neurotransmitters and biochemical markers that regulate how the heart and our organs react. Some of these events have titles such as the flight or flight, rest and digest. They are phases that the body passes through during which the heart and other organs perform a certian task and can be viewed as event driven. 

Exceptions to this result in the body not functioning in a correct manner. One such exception, Orthostatic Hypotension occurs in people who've suffered damage to the autonomic nervous system or are consuming certian medications (i.e. L-DOPA). When people move from the supine position to upright, blood pools in lower limbs, blood pressure drops, heart rate fails to increase forcing vasovagal syncope (Fainting). In this case, the heart fails to responding correctly to the change in environment causing a change in homeostasis. Measuring heart rate during this phase would show a failure of the heart rate to adapt to an event the body encountered. 

If your signal is not a perfect sinusoid it will have harmonics. Simple like that. Study Fourier analysis.

You are most welcome 

Dear Laurent,

since 2008 I am working in a Cardiac Rehabilitation Unit linked to the University Hospital of Padua, Italy. Our Unit is located in the Alps (Cortina d'Ampezzo), at an altitude of 1315 m a.s.l.. Such an altitude is generally considered as "low altitude".

We usually receive patients with a combination of risk factors: middle age and elderly persons, with coronary heart disease or recent major clinical events (myocardial infarction, cardiac surgery), that are exposed to exercise-based rehabilitation during a two weeks (average) period. Among more than 2000 patients submitted to residential cardiac rehabilitation in the past few years, no major side-effects have been registered during the daily sessions of structured exercises. It must be said that exercise intensity was based on careful evaluation of patient's status and "monitored" with Borg scale. In patients with recent episodes of heart failure, a preliminari cardiopulmonary exercise test was performed, and exercise intensity was maintained at or around anaerobic threshold.

In this way, we believe that exercise-based cardiac rehabilitation is feasible and safe in this kind of patients also in a mountain resort.

No significant modifications have been observed also of blood pressure, heart rate or other clinical parameters with the rapid ascent from the University Hospital at Padua (12 m a.s.l.) to the level of 1315 m a.s.l. of the Rehabilitation Centre.[i] These results are somehow similar to what is knownin literature for patients with metabolic syndrome, that travelled from Innsbruck (576 m a.s.l) to Obertauern (1700 m a.s.l.), resided there during 3 weeks and went also hiking, taking care that physical effort did not exceed 55-65% of individual maximal heart rate, without major adverse effects.[ii] Furthermore, in literature can be found a paper reporting that patients with stable heart failure have been accompanied to an altitude of 3454 m a.s.l., where they were able to perform moderately vigorous effort, without serious events, demonstrating only a reduced performance that was approximately 22% less than their performance at lower altitudes.[iii]

Thus, we believe that it is possible to perform exercise-based rehabilitation at least at low mountain altitudes, provided that physical effort is maintained approximately below or around individual anaerobic threshold.

Hoping to having been somehow useful, I present my best regards.

Merry Christmas and Happy New Year.

Leonida Compostella, MD

[i] Carraro Umberto. [Effects of ascension to mountain in heart disease patients in subacute phase: an observational study]. Thesis for Graduation in Medicine, University of Padua, AA 2009-2010

[ii] Mair J, Hammerer-Lercher A, Mittermayr M et al. 3-week hiking holidays at moderate altitude do not impair cardiac function in individuals with metabolic syndrome. Int J Cardiol 2008; 123(2):186-188

[iii] Schmid JP, Nobel D, Brugger N et al. Short-term high altitude exposure at 3454 m is well tolerated in patients with stable heart failure. Eur J Heart Fail 2015; 17(2):182-186

Hello,

I would recommend a free antibody database available at labome.com. For antibodies to CKM for Western blotting you can check the following link: https://www.labome.com/review/gene/human/CKM-antibody.html. Santa Cruz Biotechnology provides goat polyclonal (N-13, sc-15161) ab suitable for WB on mouse or human samples. Also, Abcam has rabbit polyclonal ab83441 for WB (ref only for WB on human samples: Kitaoka et al., Mol Genet Metab. 2013). You can see the references and the description of the antibodies following the provided links.

I fully agree with the first answer. I would however like to suggest using two pneumotachographs, one in the inspiratory limb, one in the expiratory limb. The sum of flow rates of both gives you the total flow rate. This way, the pneumotachographs do not contribute to dead space. You may consider this principle also for filters etc.

Hopefully there's still someone following this question.. Do you know somehow recent article(s) supporting double product as an index of myocardial oxygen consumption?

HI,

I suggest using optical detection using a LED light source / photo detector such as the OSRAM 7050 ($0.75).  It can be digitally controlled using a TI AFE 4404 ($2.65), or driven using analog circuits.  The TI AFE 4044 may be driven using an I2C interface, for example from an Arduino for prototype.  Smaller systems may be developed using microcontrollers such as the NRF51822 from Nordic Semiconductor (or other similar microcontrollers that include BlueTooth LE) if you need the rat to be mobile.

Shave the rat.  Adhere the 7050 to the skin surface.  Set the Green LED to illuminate for about 100 uS every 1 ms.  You could use also the IR and the Red LED, but green seems to provide the best pulsatile information.   Read the output of the photodetector near the middle of the 100 us.  The little bumps are pulses.  Take the first derivative of the data and the bumps are larger & easier to detect.

This works on people with white and dark skin, not sure about rats.  

The TI AFE 4044 has an evaluation module that is $199.  

Alternately, you can build a basic ECG circuit using an instrumentation amplifier, or a "real" system using something like a TI ADS 1291.  As with the AFE 4044, there is an evaluation module available for $199.

We have had similar problem for several months. The main problem was probably in pH of Krebs-Henseleit solutions. Another big issue is temperature, which affects not only the heart itself (contractility), but also pH and amount of oxygen in solution.

You need good nerves to go through this. I wish you good luck!

Hi Simin

I employ SPSS but it has some limits...as in your instance.

IBM suggest: "IDI and NRI are not directly available in an SPSS Statistics procedure. An enhancement request has been filed with SPSS Development. An R package named survIDINRI ( see link) exists that provides these measures, so it may be possible to produce such measures using the R plugin (se 2nd link).

Good Luck and.....have a naice job

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

 Thanks a lot.....

Cardiac Tissue

At the cellular level, the main components of the postnatal heart are cardiomyocytes, cardiac fibroblasts, endothelial cells and vascular smooth muscle cells (Banerjee I, fusel JW, 2007). In a normal adult heart, cardiomyocytes occupy most of the tissue volume, but they are only 30% of the total number of cells. The remaining 70% consists of non-cardiomyocyte cell types, among which cardiac fibroblasts represent the vast majority (Jugdutt, 2003).

The heart is organized into a complex array of cellular and non-cellular components. Cardiomyocytes are diplayed in laminae (AA Young, IJ Legrice, 1998), which in turn are organized in layers of cardiomyocytes from two to five cells thick and surrounded by a network of endomysial collagen. In the other hand, the fibroblasts form a network of interconnected cells distributed among the endomysial collagen surrounding groups of cardiomyocytes (Borg TK, Ranson WF, 1981 - Camelliti P, Borg TK, 2005 - Goldsmith EC, Hoffman A, 2004 - Young AA, Legrice IJ, 1998). The distribution of endothelial cells and vascular smooth muscle is restricted to the vasculature. Based on this organization, it has been estimated that all cardiomyocytes would be connected directly to one to five cardiac fibroblasts (Kohl P, Camelliti P, 2005). Direct intercellular contacts of fibroblasts seem to be supported by at least two types of cell to cell connection molecules: connexins and cadherins. In rats, cardiac fibroblasts are connected by both cadherins and connexin-40, while connexin-45 serves as a connection between fibroblasts and cardiomyocytes. However, the distribution of different connexins may vary significantly between species (Banerjee I, K Yekkala, 2006 - Camelliti P, Green CR, 2004). Additionally, integrins mediate the connection between cardiac fibroblasts and the extracellular matrix.

Dear colleague recently completed an investigation in adults younger than 45 years with acute coronary syndrome. It basically I do not perform measurement of Framingham score, but its results could serve as a reference in some aspect of your research, you sent the links

 1- Valdés Martín A, Rivas Estany E, Martínez Benítez P, Chipi Rodríguez Y, Reyes Navia G, Echevarría Sifontes LA. Characterization of acute coronary syndrome in younger than 45 years old of one specialist institution in Havana, Cuba between 2013 and 2014. MÉD.UIS. 2015; 28(3):281-90.

 2-  Martínez Benítez P, Valdés Martín A, Chipi Rodríguez Y, Reyes Navia GC, Rodríguez Nandes L, Antuña Aguilar T. Clinical features and therapeutic strategies in young adults with acute coronary syndrome, 8-year study. Rev Cub Cardiol.2015; 21(3): 1-9.

 with pleasure

Alexander

I am not an arrhythmologist (I am a general cardiologist), but in my opinion, the EHRA score can be used for assessement AF related symptoms and to queality of life after ablation. therefore, maybe pre and post ablation EHRA score is useful for detection of effectiveness of the procedure. 

Lower body parts from iliac crest (waist), when enclosed inside a metallic chamber and subjected to negative pressure, causes a pulling of blood to the dependent parts of the body i.e. in the lower limbs.  It has been reported that -30 to -40 mm Hg of LBNP is equivalent to standing upright at +1Gz acceleratory force, which is nothing but standing on the earth. Upright posture pulls around 300-800 ml of blood to the lower limbs. However, the equivalence between +2Gz and +3Gz acceleratory forces with LBNP is difficult to establish and also not physiologically correct in the sense that G-force always involves the neurovestibular system, unlike LBNP where vestibular system involvement is virtually nil. Blood pulling to the lower limbs in LBNP causes deactivation of low pressure and high-pressure receptor resulting in sympathetic activation and parasympathetic augmentation. But, in G exposure, the dynamics of autonomic cardiovascular control of heart rate and blood pressure work differently with an involvement of neurovestibular system along with unloading followed by deactivation of baroreceptor resulting in sympathetic activation and parasympathetic enhancement. However, the intricate details of the physiological regulatory mechanisms in G exposure and LBNP exposure are very complex. For further details, you may follow any textbook on aerospace physiology/medicine.  

Regds

Dr (Prof) Biswajit Sinha

Scientist

Bangalore

IAM

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.

Hi Michael,

Our Dept. of Internal Medicine, AMC, Amsterdam has researched this topic extensively. The thesis of Dr Gisolf might be of help to you: http://www.descsite.nl/Publications/Thesis/Gisolf/Gisolf.htm

Good luck!

Lizzy Brewster 

Dear Zeynep. In my opinion for the studyorthostatic stress more interesting ratio thoracic and abdominal circles 

Thank you very much for suggesting the article, an interesting read with many promising paths to explore. 

The answer appears to be yes.  It is also complicated.  When patients appear in the emergency department out of breath, the question is whether to get a pulmonary or a heart consult.  The basic symptom is not definitive, but both organs could be involved.  However, there is an age dependence concordance between congestive heart failure (CHF), chronic kidney disease (CKD)(with a high incidence of DM), and cardiovascular disease.  The system blood flow depends on the ejection fraction from the lV to the aorta.  There can be backward failure or forward failure.  The expression of chest pain is a result of the vagus branch of the recurrent laryngeal nerve.  Only insufficient supply to the ventricle by the coronary artery branches can elicit vagal related pain, and it is accompanied by increase 3rd generation troponin I and T.  However, we now refer to type 1 and type 2 myocardial infarction.  Type 1 is by plaque rupture. 

Hallo Iqbal.  Thank you so much for your response. I am having a good time with literature review and what others are doing out there. With this Increase in ambient temperature,  especially in southern Africa,  i would really like to find out if there has been a correlate with the CVD related deaths. Will definitely keep you updated.  Again,  thank you 

alpha-, beta 1- and beta 2-adrenergic receptors in the kidney mediate vasoconstriction, renin secretion and vasodilatation, respectively. Blockade of beta-receptors may therefore be expected to influence renal blood flow and possibly glomerular filtration rate by intrarenal effects as well as by reducing cardiac output and blood pressure. Since the various beta-adrenergic blocking drugs available differ in the degree to which they block beta 2-receptors (cardioselectivity) and also in their intrinsic sympathomimetic activity, they would be expected to have different effects on renal function. The acute administration of beta-blockers usually results in a reduction in effective renal plasma flow and glomerular filtration rate, whether or not the drug is cardioselective or has intrinsic sympathomimetic activity, with the exceptions of nadolol, which has actually increased effective renal plasma flow in some studies and of tolamolol. With chronic oral administration, the non-cardioselective beta-blockers reduced glomerular filtration rate and effective renal plasma flow. The cardioselective drugs do not usually produce significant reductions in glomerular filtration rate or effective renal plasma flow, although small increases in serum urea during treatment do occur. Interestingly, in contrast to findings with intravenous administration, orally administered nadolol produced a slight reduction in glomerular filtration rate in 1 study, so the effect of this agent on renal function under clinical conditions remains uncertain. It seems likely that beta-blockers reduce renal function predominantly by blocking beta 2-receptors in the kidney. To keep area of discussion in perspective, it is important to realise that although there have been isolated reports of serious deterioration in renal function coinciding with beta-blocker treatment, the great majority of reports are of reduction in glomerular filtration rate which are not of clinical significance, even in patients with pre-existing impairment of renal function. The beta-blockers with low lipid solubility-i.e. atenolol, nadolol and sotalol-are not metabolised, and their dose must be reduced in renal failure. Propranolol has active metabolites and its dose must also be reduced slightly in uraemia.

Hi Alaa here I send  some papers  that could help you

Clin Exp Pharmacol Physiol. 1996 Sep;23 Suppl 3:S67-73. doi: 10.1111/j.1440-1681.1996.tb02816.x.

Human type-1 angiotensin II (AT1) receptor gene structure and function.

Nitric Oxide is another pathway involved in chronic exercise mediated cardio-protection. There was a paper from Dr. Calvert: 

Physiology (Bethesda). 2013 Jul;28(4):216-24. 

Role of β-adrenergic receptors and nitric oxide signaling in exercise-mediated cardioprotection.

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!

Atheroma site specificity correlates strongly with regions of disturbed shear stress, I.e. on the outer wall at a flow divider, e.g. bifurcation - where shear is low, or at regions of vessel curvature, e.g the aortic arch. Also, contrary to popular believe, shear is not uniform across the circulation. In fact, it is considerably higher in small arteries and especially arterioles. Also, between species there is an inverse relation between shear and body mass, e.g. shear is around 15 times higher in the abdominal aorta of a rat than the same region in a human. Coincidence that rats don't spontaneously develop atheroma?? Notably, shear is a powerful inducer and suppressor of the genes pertaining to vasodilation and vascular disease. 

Hope that helps,

Dave

Hi guys!! In all of the Balkan Peninsula countries we have the problems. For example in Slovenia there is only regulated profession as physical education teacher. Other field of sport sciences, such as kinesiologist or kinesiotherapist  are not currently regulated by the law. But currently there is a new proposal of the law in preparation, which will also include a work of kinesiologist in national health services. We are slowly establishing job positions for other sport sciences specialits, but we have still long path before us. Best regards, Tim.

The location and relative magnitude of the first and the second aortic pressure peak is a matter of interaction between forward and backward flow and pressure waves.

Although forward waves are less variable (at least when speaking of their shape in their first moments), the amplitude and timing of their reflections is very complicated. Taking into consideration a number of paper about wave trapping, re-reflection, etc., only reflections originated somehow close to the ascending aorta are able to impact in a considerable manner the ascending aortic waveform, thus determining the type of the shape. High reflection patterns create type A waveform, while low reflections result in a more type C aortic pressure wave. It is important to underline that type A and type C refer to aortic waveform, and have not meaning at radial artery, although surely aortic shape influences the radial one.

Considering these wave phenomena, it is unlikely that a lumped model can faithfully reproduce all these very characteristics details of a specific person. What you can obtain is a lumped representation of the heart load, which will derive from the choice of the parameters describing resistance, inertance and elastic properties. As you will not deal with any local properties which would results in a subject-specific reflection patter, I think that you will not be able to differentiate between type A and type C aortic waveforms.

Dear Mr. Mendiola,

Interesting question. I think depending of how high the calcium level is, it will mainly affect the cardiac muscle cells, if there is a balance of Ca, sufficient protein(kinases) and vitamin D to promote the Ca effect on the cells, it possibly works. But take into consideration, that only Ca supplemants have no positve effect, if the Ca transport  is not working properly (proteinkinases, phospholambam, cAMP). Please check the publications I have added below.

I work with Kubios Software. If you transfer your data in a .txt file it would be working.

I would very much like to see some of your tracings  I think there is something very interesting in your results

Hi, if you are working off-line on pre-recorded data, a simple way is to activate the piece of data of interest and choose spectrum view. Breathing data is usually clean enough to show one clear maximum in the spectrum, corresponding to true breathing frequency. No hassle with SD's. Of course, when you need the rate online, cyclic measurement is better.

Cheers,

-Esa

It is mandate to check bp while stress test because Hypertensive  bp response is an indication  to stop the tmt as it risks intracranial  hemorrhage  and seondly fall in bp upto 20 mmhg during  stress indicates  a  positive  outcome. 

The maximum achievable heart rate , HR max, of an individual is fixed and decreases with advancing age. When someone does intense exercise his/her HRmax can be achieved  earlier and that person who does the very intense exercises will work at close to this value for the period of intense exercise.

A person who is in a detrained state will also achieve heart rates close to HRmax on starting exercise programs (by doing relatively easy tasks) but as fitness increases the intensity of work required to achieve HR max increases.

In a nut shell HR MAX does not really increase at high work loads but a fit person is able to tolerate more work for longer periods at the HR max than an unfit person and also requires a higher volume and intensity of work to achieve this HRmax than an unfit person.

Aortic  regurgitation  should be also included  as a common  cause for lv non compaction. True  non compaction  is labeled  when we exclude all acquired  causes as mentioned. .

In my measurements accoustic frequency of S1 is 30-50Hz and S2 40-70 Hz with wide interpersonal variability and shifts secondary to technical equipment. Harmonic frequencies are also present  (to 500-700Hz).

Hi,

I believe you can find answers to your question here:   http://www.ncbi.nlm.nih.gov/pubmed/18561343 (Normal reference values of ratios of blood flow velocities in internal carotid artery to those in common carotid artery using Doppler sonography) or here: http://radiopaedia.org/articles/ultrasound-assessment-of-carotid-arterial-atherosclerotic-disease.

I hope it helps you.

Regards,

Francisco

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*

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.

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.

Main reasons of unsucessfull I/R protocols are: insufficient hypoxia, additional acidosis (which is per se protective), non physiologial external calcium, presence of serum in medium. My advice is to measure the actual oxygen partial pressure in the experimental medium et to evalutae the response to lack of oxygen via methylene blue test.

Of course it depends what you are looking for.  For a general evaluation and if you are not too confident with diagnosis of autonomic neuropathy I would strongly suggest the "modified" batterry of Ewing's cardiovascular autonomic tests : in essence . the measure of heart rate variability during a standardized valsalva manoeuvre, during a a standardized Lying to Standing and/or during a standardized "deep breathing".All about that you will find in a recent pubblication (which I coauthored) : Recomandations for the use of cardiovascular tests in diagnosis of autonomic neuropathy by Spallone V et al published in the january issue 2011 in Nutr.Metab. Cardiovascular Dis. (21:1).

I used power spewctral analysis since 1994 (you can see my publications in that field). but I am very sceptic about the use that now researchers do with this diagnostic tool as it is quite complex to be interpreted (in order of the mathematica model you use), has limitations in case of extrasistolics, it needs a long trial to understand what it gives in concret  it shows wide variabilty during the daytimes... it is a very refined method but, as I use to say: it is a "fFerrari" and not all people can drive it.. Sometimes it is better to drive a sure "Mondeo".

As far as baroreceptor sensitivity indexes, I belive that it will be probably the best methodology but, among so many differents methods proposed, which is the best? and they are  not so simple to perform and interpret as CV tests mentioned above.

Good luck

Federico Bellavere

We have been running experiments in psychophysiology with participants performing tasks sitting in front of a computer, so non-invasive methods are prefered.

Hi

Please see these links:

Hi Subhash,

1. that depends on the valve you're looking at.

120mmHg is the aortic pressure during end-systole. The aortic valve is open, thus there is no load on it (if wall shear stress or other are neglected). The main load on this valve is reached shortly after valve closure. Here is a picture were you can see some pressure gradients during the heart cycle: http://howmed.net/physiology/cardiac-cycle/  The max load on the aortic valve occurs after valve closure (pAorta - pLeftVentricle: ~100 mmHg).

Another question is if you are looking at healthy or diseased hearts.

2+3. You can find several publications on this topic I guess. Maybe start with the book 'Biomechanics - Mechanical Properties of Living Tissues' or '

Biomechanics: Motion, Flow, Stress, and Growth', both by Yuan-Cheng Fung

Okay, so we are talking about hIPS-cardiomyocytes.

This means that you can expect a heterogeneity regarding resting membrane potentials and AP configurations as you can see in the company’s flyer and in many publications which is typically attributed to the presence of ventricular-like, atrial-like and pacemaker-like CMs.

I do not have experience with commercial hIPS-CMs but with “custom made”. Depending on the quality of the preparation you will also find cells showing atypical APs which cannot classified into the above mentioned groups.

In general I would recommend to use intracellular/extracellular solutions from established/published protocols using this cell line (see links).

Are you sure about the 7 mM CaCl2 in your extracellular solution?

But before you start changing solutions – how do you check for seal quality? Do you work with ruptured or perforated patch? What is the geometry and resistance of your pipettes?

As you gathered from our comments seal quality is one possible problem. But you have to be able to check and estimate it.

Good point Alexandre. Based on %CO to different organ systems, one could determine the SVR for a specific organ system, this is where impedance measurements would come in handy. The total SVR is the sum or average of organ system SVR's, which would be based on the current oxygen demand of that organ system. During physical activity, SVR in the skeletal muscle decreases, due to high 02 demand, whilst gastrointestinal SVR increases, for example. The total SVR would not reflect this distribution then. In this light, I guess I would have to rephrase my question, in asking if there is an organ specific SVR maximum?

Hello Jordan,

If you are doing the occlusion by microfilament technique,  the idea is that it blocks complety the blood flow into the MCA. Howerver in our studies I have seen that there are some diferences in the vascularization, and in some animals this brain terretory can be perfused by other very small vessels. I think that one think you can do is meassure with doppler laser the blood flow drop during the surgery (or with other mothods if you have them available), and then make some anatomical studies to determine the size of your infarc and the size of the penunbra (the region that surrounding the ischemic core). In this mice that have additional vascularization you can note differences between the sizes and location of ischemic the core and penunbra. But you can be sure that the territory of the MCA will be completly occuded (and leds the tissue necrosis) if you perform the right technique and use the filament to do it (we use #22), and the other little ways (if there) are not significantly important.

You may want to contact my colleague here, Dr. Arkady Pertsov at

you can use labchart pro with ECG module. It finds times and voltages automaticly. I don't think that none of software can be use trustfully for diagnose any disorders from ECG.

Thank u Bojan i appreciate it! 

Try with FitLab App is not free but is really cheap. 

Chek it out: https://www.healthsportlab.com/ca/fitlab_getfitlab.php

Hi John, try this link to an article it may be of some use!

I am afraid that post-MI VSD closure remains technically difficult.

A few propositions:

1. if your patient is stable and does not need any mechanical assist: balloon pump or ECMO: wait for a few weeks to allow the tissues tos heal or scar and avoid further tearing of the VSD.

2. If the VSD is located mid-septal or apical, choose the jugular approach.

3. If you decide to make a arteriovenous loop (which is often necessary), try to avoid strenuous traction and never leave your guide wire uncovered.

4. choose a large sheath (14 F) (kink resistant) and try to keep a guide wire in position while you advance the device or advance your sheath a little bit further in the LV

Overall, there are not many ways you can control delivery of the sheath or device during the procedure in order to avoid tearing a fresh MI-VSD

Indeed it is best practice to minimize the dilution and deviation from the original starting volume. We target doses in the 10 uL range, with varying stock concentration to achieve the right physiological range, which is highly variable. There was one case, where the stock was not of sufficient concentration (solubility issues) and we had to lower the initial volume to achieve the correct final concentration. You need to be aware of final concentrations of your drugs while avoiding changing the concentrations/osmolarity of the buffer. Lastly, be aware that not all solvents are created equal in terms of physiology, for example ethanol can have profound physiological effects, but is often recommended as a solvent for certain drugs. Best of luck with your studies!

Swimming is an interesting measurement case, because you have

a) arm movement, which will ruin wrist-based optical measurement

b) need for internal memory if you can't get the data off straightaway 

c) chlorine or salt water bridging between your electrodes

and obviously

d) the water ruining your expensive devices

I have seen in action, but not used, waterproof Holter monitors. They will probably be a lot more expensive than sports monitors. Polar have water *resistant* monitors , and are supposed to be able to monitor while swimming... I'm not sure how popular they are, though. It is a bit of a tricky one.

Julian Koenig, who is on here, wrote a review on HRV monitoring concurrent to swimming training... from memory, I think at least the majority of these papers dealt with morning, pre-competition, etc. measurements over time. The article is here:

(Please note that above I am just dealing with HR... we are a few years away from an accurate portable low powered ambulatory blood pressure monitor!)

Seems to be the end-diastolic filling due to atrial contraction. 

Thanks for your input on this. What I was trying to say was if you increase your proportion of type I fibres by volume (not by proportion) then with the correct aerobic training as well - I thought it may be possible for increased oxidative capacity of the slow twitch fibres. With increased size of non oxidative fibres from standard hypertrophy training this could lead to a drop in oxidative capacity (oxygen has greater distances to diffuse in larger muscle fibres to reach mitochondria). It would be interesting to see if any difference existed between two groups who did HIT with one employing BFRRE as well?

The carotid sinus baroreceptors are innervated by the sinus nerve of Hering, which is a branch of cranial nerve IX (glossopharyngeal nerve)