Simulations of human hemodynamic responses to blood temperature and volume changes

An advanced version (AV) of special software based on modified quantitative models of mechanisms that provide the overall control of human circulation is proposed. AV essentially expands the range of tasks concerning the modeling of cardiovascular physiology, in particular, the range of mechanisms c...

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Автори: Grygoryan, R.D., Degoda, A.G., Lyudovyk, T.V., Yurchak, O.I.
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Problems in programming
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spelling pp_isofts_kiev_ua-article-5552023-10-23T11:18:38Z Simulations of human hemodynamic responses to blood temperature and volume changes Моделювання гемодинамічних реакцій людини на зміни температури та об’єму крові Grygoryan, R.D. Degoda, A.G. Lyudovyk, T.V. Yurchak, O.I. physiology; cardiovascular system; hemorrhage; acute and long-term control; model; simulator UDC 517.958:57 +519.711.3 + 612.51.001 фізіологія; серцево-судинна система; крововилив; гострий та віддалений контроль; модель УДК 517.958:57 +519.711.3 + 612.51.001 An advanced version (AV) of special software based on modified quantitative models of mechanisms that provide the overall control of human circulation is proposed. AV essentially expands the range of tasks concerning the modeling of cardiovascular physiology, in particular, the range of mechanisms controlling cardiac function, vascular hemodynamics, and total blood volume under unstable internal/ external physiochemical environments. The models are verified on data representing hemodynamic responses to certain physical tests. In the publication, two test scenarios, namely blood temperature and volume dynamic alterations, have been simulated and analyzed in detail. The user-friendly interface provides all stages of preparation and analysis of computer simulation. The PC-based simulator can also be used for educational purposes.Prombles in programming 2023; 1: 19-29  Запропоновано вдосконалену версію (ВВ) спеціального програмного забезпечення на основі модифікованих кількісних моделей механізмів контролю кровообігу людини. ВВ суттєво розширює коло завдань щодо моделювання фізіології серцево-судинної системи (ССС), зокрема механізмів, що контролюють роботу серця, судинну гемодинаміку та загальний об’єм крові в умовах нестабільного внутрішнього/зовнішнього фізико-хімічного середовища. Моделі перевірялися на даних, що представляють гемо- динамічні реакції на певні фізичні тести. У публікації було змодельовано та детально проаналізовано два тестових сценарія – динамічні зміни температури крові та її об’єму. ВВ надає фізіологам нову технологію дослідження, що істотно розширює та поглиблює фундаментальні знання про кровообіг людини. Результати моделювання містять більш повний спектр фізіологічної інформації, ніж традиційно надається в емпіричних дослідженнях. Це головна перевага нашої ВВ. Це також хороший сучасний інструмент на базі ПК для одночасної візуалізації динамічних характеристик ССС в залежності від обраних зі списку вхідних навантажень. Останній аспект сприятиме студентам-медикам краще розуміти неявну інтегративну фізіологію людини та спеціальні патології. ВВ також є гарною комп’ютерною програмою для використання в освітніх цілях для ілюстрації основних фізіологічних і деяких патологічних закономірностей. Ми плануємо розширити моделі та програмне забезпечення, щоби набагато реалістичніше симулювати сценарії як нормальної, так і патологічної фізіології людини. Програмне забезпечення, створене в рамках технології .NET, є автономним файлом .EXE для виконання на ПК.Prombles in programming 2023; 1: 19-29 PROBLEMS IN PROGRAMMING ПРОБЛЕМЫ ПРОГРАММИРОВАНИЯ ПРОБЛЕМИ ПРОГРАМУВАННЯ 2023-04-27 Article Article application/pdf https://pp.isofts.kiev.ua/index.php/ojs1/article/view/555 10.15407/pp2023.01.019 PROBLEMS IN PROGRAMMING; No 1 (2023); 19-29 ПРОБЛЕМЫ ПРОГРАММИРОВАНИЯ; No 1 (2023); 19-29 ПРОБЛЕМИ ПРОГРАМУВАННЯ; No 1 (2023); 19-29 1727-4907 10.15407/pp2023.01 en https://pp.isofts.kiev.ua/index.php/ojs1/article/view/555/607 Copyright (c) 2023 PROBLEMS IN PROGRAMMING
institution Problems in programming
baseUrl_str https://pp.isofts.kiev.ua/index.php/ojs1/oai
datestamp_date 2023-10-23T11:18:38Z
collection OJS
language English
topic physiology
cardiovascular system
hemorrhage
acute and long-term control
model
simulator
UDC 517.958:57 +519.711.3 + 612.51.001
spellingShingle physiology
cardiovascular system
hemorrhage
acute and long-term control
model
simulator
UDC 517.958:57 +519.711.3 + 612.51.001
Grygoryan, R.D.
Degoda, A.G.
Lyudovyk, T.V.
Yurchak, O.I.
Simulations of human hemodynamic responses to blood temperature and volume changes
topic_facet physiology
cardiovascular system
hemorrhage
acute and long-term control
model
simulator
UDC 517.958:57 +519.711.3 + 612.51.001
фізіологія
серцево-судинна система
крововилив
гострий та віддалений контроль
модель
УДК 517.958:57 +519.711.3 + 612.51.001
format Article
author Grygoryan, R.D.
Degoda, A.G.
Lyudovyk, T.V.
Yurchak, O.I.
author_facet Grygoryan, R.D.
Degoda, A.G.
Lyudovyk, T.V.
Yurchak, O.I.
author_sort Grygoryan, R.D.
title Simulations of human hemodynamic responses to blood temperature and volume changes
title_short Simulations of human hemodynamic responses to blood temperature and volume changes
title_full Simulations of human hemodynamic responses to blood temperature and volume changes
title_fullStr Simulations of human hemodynamic responses to blood temperature and volume changes
title_full_unstemmed Simulations of human hemodynamic responses to blood temperature and volume changes
title_sort simulations of human hemodynamic responses to blood temperature and volume changes
title_alt Моделювання гемодинамічних реакцій людини на зміни температури та об’єму крові
description An advanced version (AV) of special software based on modified quantitative models of mechanisms that provide the overall control of human circulation is proposed. AV essentially expands the range of tasks concerning the modeling of cardiovascular physiology, in particular, the range of mechanisms controlling cardiac function, vascular hemodynamics, and total blood volume under unstable internal/ external physiochemical environments. The models are verified on data representing hemodynamic responses to certain physical tests. In the publication, two test scenarios, namely blood temperature and volume dynamic alterations, have been simulated and analyzed in detail. The user-friendly interface provides all stages of preparation and analysis of computer simulation. The PC-based simulator can also be used for educational purposes.Prombles in programming 2023; 1: 19-29 
publisher PROBLEMS IN PROGRAMMING
publishDate 2023
url https://pp.isofts.kiev.ua/index.php/ojs1/article/view/555
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fulltext 19 Методи та засоби комп′ютерного моделювання УДК 517.958:57 +519.711.3 + 612.51.001 http://doi.org/10.15407/pp2023.01.019 R.D. Grygoryan, A.G. Degoda, T.V. Lyudovyk, O.I.Yurchak SIMULATIONS OF HUMAN HEMODYNAMIC RESPONSES TO BLOOD TEMPERATURE AND VOLUME CHANGES An advanced version (AV) of special software based on modified quantitative models of mechanisms that provide the overall control of human circulation is proposed. AV essentially expands the range of tasks concerning the modeling of cardiovascular physiology, in particular, the range of mechanisms controlling cardiac function, vascular hemodynamics, and total blood volume under unstable internal/ external physiochemical environments. The models are verified on data representing hemodynamic responses to certain physical tests. In the publication, two test scenarios, namely blood temperature and volume dynamic alterations, have been simulated and analyzed in detail. The user-friendly interface provides all stages of preparation and analysis of computer simulation. The PC-based simulator can also be used for educational purposes. Key words: physiology, cardiovascular system, hemorrhage, acute and long-term control, model, simulator Introduction Recently, we have proposed specialized software (SS) providing physiologists with ad- ditional research opportunities in the area of human cardiovascular system (CVS) [1,2]. De- spite SS being previously tested and tuned for a mean healthy person, additional tests revealed certain quantitative inaccuracies. This forced us to critically analyze certain mathematical formalisms. As a result, a new version of SS, namely SS1, is developed. This publication aims to illustrate both the correct models and their tests under certain simulation scenarios. A short description of the basic model SS is based on a complex quantitative mathematical model which presents the hu- man CVS as an open system interacting with a certain number of associated physiologi- cal systems (APS). Within the framework of traditional physiology some of these APS are known as circulation controllers. They could influence the total blood volume dynamics and current values of CVS’s parameters. The core model and models of certain APS are described in [1] while models of mod- ified APS are described in this paper. Structure of the complex model, necessary and sufficient for simulation of mechanisms controlling or modulating human hemodynamics under ex- ternal/internal influences, was presented in [1]. Modified models of CVS controllers Our models of cardiovascular control are based on concepts reflected in [3-6]. Sev- eral models are the advanced versions of the models proposed earlier [7-8]. Activities of efferent sympathetic ( )(tES ) and parasympathetic )(tEV nerves are under descending simulator ( )(tEbS ) or inhibi- tor ( )(tEbI ) influences of brain supra-bulbar neuronal structures. Simultaneously, ascending information originated in body different struc- tures (mechanoreceptors of CVS, muscles, pe- ripheral chemoreceptors) modulate )(tES and )(tEV . At last, a wide range of endogenous chemicals, penetrated into the brain through circulation, also modulate )(tES and )(tEV . In this version of the model, dynamics of effer- ent sympathetic ( )(tESh ) and parasympathetic ( )(tEVh ) heart nerves, as well as sympathetic vascular nerves ( )(tESv ) are described as: © R.D. Grygoryan, A.G. Degoda, T.V. Lyudovyk, O.I.Yurchak, 2023 ISSN 1727-4907. Проблеми програмування. 2023. №1 20 Методи та засоби комп′ютерного моделювання where µλχ ,, represent approximation constants, BNΣ is summary baroreceptor infor- mation, XNΣ is summary chemoreception. So, the complex model of the cardio- vascular control must include at least those mechanisms that modulate vascular tonus and parameters of HPF. Within the physiological interval maxmin )( FtFF ≤≤ , )(tF should be calculated as:            >+∆ ≤≤ ∆−∆+∆+ −>∆ = ∑ ∑∑ ∑ = + = − = + = − max 1 max maxmin 11 min 1 min )(, )( ),()()( )(, )( FFtFF FtFF tFtFTFF FFtFF tF a m i i n j i m i i o a a n j i Here aF is the heart rate under normal blood temperature ( oT ), biochemical characteris- tics of blood and biophysical characteristics of cells of sinus node, )( oTF∆ is elevation of aF with temperature increasing, )(tFi +∆ are ac- celerating effects of m mechanisms (including concentration of adrenalin), and )(tFj −∆ are re- tarding effects of n mechanisms. As the resistance depends on vascular volume, it is necessary to describe summary ( 1m ) nervous-humoral alterations of volumetric characteristics. ∑ ∑ = = ∆−= ∆+= 1 1 1 1 )(0)( ;)(0)( m i i m i i tDUtU tDDtD , where 0,0 UD represent the initial val- ues of )(tD and )(tU . Each mechanism forming its part of F∆ has its power and developmental inertia that have been taken into account by proper constants. Inotropic states of ventricles are un- der influences of local coronary flows )(tqc , adrenalin )(tAd , oT , )(tESh , and )(tEVh . A special version of the model includes effects of exogenous cardio-active agents )(tCa : The model describing hemodynamic effects of angiotensin II In our current model, central and local renin-angiotensin-aldosterone mechanisms, acting through angiotensin II, represent nega- tive feedbacks activated under lowered local blood flows in kidneys or other organs. Real CVS is not an isolated system as it is assumed in most models of hemodynam- ics. CVS interacts with multiple organs and anatomical-functional systems. In particular, total blood volume ( )(tVS ), that is the main modifier of both central venous pressure and mean arterial pressure (MAP), can be consid- ered to be constant only for very small values of the observation time τ . Modifiers of )(tVS are acting via changing the liquid intakes from the digestive system ( )(tqw ), by means of the diuresis ( )(tqd ), expirations in lungs and skin. So, these effectors obviously do not belong to CVS. (*) where qcf(t) are trans-capillary flows, qes(t) is the evaporation with sweat, )(tqee are expiratory fumes, Cbl(t) are blood salt concen- trations, )(tCbl are concentrations of blood lip- ids. The remained notations in (*) represent ap- proximation constants. The initial value of total blood volume )(tVS is assumed to be )0(V . The model and simulation algorithms provide dynamic bide- side alterations of )()0()( tVVtVS ∆±= . Vascular resistances )(trij , calculated as in [1,2], are changed via changes of ),(tVi in turn associated with regional ),(tUi ),(1 tU i ),(tDi and )(1 tD i . Usually, the local inflow mainly depends on input pressure. So, the model of central renin-angiotensin system de- 21 Методи та засоби комп′ютерного моделювання scribes the dynamics of blood renin concentra- tion Rnk(t) in association with the critical value of pressure in kidney arterioles Pkc(t) as: , where kη is sensitivity coefficient, RK is time constant characterizing the velocity of renin utilization. Assuming Rnh(t) is )(tRn associated with heart local renin-angiotensin system, dynamics of Rnh(t) is described depending on regional flow in coronary arteries ( )(tqc ) as: , Models of renin dynamics in brain Rnb(t), liver Rnl(t), and lungs RnL(t) are con- structed analogically. The total concentration of renin RnT(t) in blood is calculated as: The dynamics of blood concentrations of angiotensin II ( )(tAn ) is modeled as: Fig. 1. Simulation algorithm. 22 Методи та засоби комп′ютерного моделювання , where Ran is a time constant character- izing the velocity of angiotensin II utilization. Simulation algorithm A single simulation algorithm (SA) de- pends on: 1) actual configuration of physiolog- ical models (ACPM); and 2) actual group of input loads (AGIL). This can be illustrated by means of Fig.1 which represents the general view on SA. According to this algorithm, two in- dependent procedures have to be performed before the simulator is ready to execute cal- culations. As a result of the first procedure the user gets the actualized ACPM. The sec- ond procedure generates AIGL. Additionally, the user has to set the simulation duration. Changing at least one value in characteristics of ACPM and/or AGIL, the user can start the next simulation. Potentially, our simulator consists of 12 independently functioning physiologi- cal models and 10 models each representing one dynamic input load. So, the number of possible combinations of actualized ACPM and AGIL is too large. In fact, no empirical physiologist has ever observed hemodynam- ic effects of entire scenarios provided by our simulator. The user will be able to run and analyze the entire spectrum of simulations, he/she is provided by an effective user inter- face. Input loads Our models and the entire SS imitate dynamic physiological responses of a healthy person to dynamic input loads. Namely, a re- sponse depends on the absolute level and shape of the applied load. Theoretically, it is possible to create a simulator providing the construction of any arbitrary load profile. In this article, we consider only two input loads – alterations of blood temperature ( )(tT o ) and total blood vol- ume ( )(tVS ) Fig. 2. User interface in case of regulators standard configuration (intact organism). 23 Методи та засоби комп′ютерного моделювання Controlled linear alterations of total blood volume ( )(tVS ), namely ( V∆± ), are provided according to formulae: where Vab(t) is the abdominal vein vol- ume, VbT ∆ is the start time for the altering of total blood volume with the velocity val. Blood temperature ( )(tT o ) altera- tions ( oT∆± ) alter almost linearly the heart rate )(tF and regional vascular diameters. These effects have been modeled by us. In order to offer a user the access to these mechanisms, additional formulas describ- ing activation (deactivation) of these mech- anisms are needed. In our current SS, the incorporated formulas provide setting of numerical values of normal blood tempera- ture ( o NT ) and stable velocity of temperature elevation ( Tv+ ) until o NT reaches its maxi- mal level ( oTmax ): By analogy, under temperature lower- ing with stable velocity of ( Tv− ), and maxi- mal ( oTmax ) or minimal ( oTmin ) levels: Preparing computer experiments As it was already mentioned in [1,2], each simulation is an independent computer experiment with a configuration of previ- ously collected models. Opportunities for the forming of the actual model, experiment scenario, as well as for analyzing results in graph forms are presented in Fig. 2. This window is one of the main windows of the UI. The list of configurations is shown in the special pop-up window (see the middle-right part of Fig. 2). Operations needed to prepare every computer simulation and to provide its executing and results analysis, are listed in the window located on the left side of the UI. Information concerning details of every chosen string is indicated in the right side of the UI window. Model configuring is a multi-step op- eration aimed to create the desired combina- tion of activated regulator mechanisms, tests to be applied, and simulation duration. Addi- tional opportunities for models activation or deactivation are provided through the win- dows shown in the right sector of the main window. Some of these windows are pop-up windows. Simulation (when activated) will last until the exposure time (observation duration) is over. All simulation results are saved in the operative memory thus this parameter of PC is critical for determining the maximal simula- tion duration. Our simulator supports the creation of multiple biological model versions each of which is capable of providing hemodynamics under a single or several chosen input loads. In fact, these manipulations imitate empirical methods of certain control mechanisms deacti- vation (activation). Main simulation results and discussion The simulator described in the paper is autonomous software designed for IBM com- patible computers. The simulator was designed as an alternative method and specialized re- search tool for theorization of human physiol- ogy. Its physiological basis includes almost all local or organism-scale physiological mecha- nisms capable to modulate the cardiovascular physiology under external/internal challenges. In fact, for the first time, our simulator does provide fundamental investigations aimed to understand human integrative physiology by means of conceptual and methodological reno- vations. A part of these renovations has been published [3-8]. The key conceptual renovation concerns the creation of opportunities expand- ing the sector of theoretical computer-based research. Basic models include both acute and long-term responses of the human cardiovas- cular system to a wide range of input physical alterations. Each such alteration causes spe- cific physical (hemodynamic) alterations that 24 Методи та засоби комп′ютерного моделювання Fig. 3. Hemodynamic responses to hemorrhage of 1000 ml in human horizontal position. 25 Методи та засоби комп′ютерного моделювання Fig. 4. Hemodynamic responses to blood infusion of 1000 ml in human horizontal position. 26 Методи та засоби комп′ютерного моделювання Fig. 5. Hemodynamic responses to blood temperature elevation in 3oC in human horizontal position. 27 Методи та засоби комп′ютерного моделювання Fig. 6.Hemodynamic responses to blood temperature decrease in 3oC in human horizontal position. 28 Методи та засоби комп′ютерного моделювання in turn change the current mode of receptors associated with the nervous or humoral regu- lators. Their automatic response to these chal- lenges normally provide certain changes in the heart pump function, in rigidities and un- stressed volumes of vascular compartments, as well as in the total blood volume. In the frame of this publication, taking into account its limited volume, only alterations of two input variables are considered. The first one is total blood volume decrease (hemorrhage) or eleva- tion by 1000 ml (main results are presented in Fig. 3 and Fig. 4 respectively). Results for the second variable, namely, the blood temperature change (decrease or elevation by 3oC) are pre- sented in Fig. 5 and Fig. 6 respectively. Illustrations in Fig. 3 - Fig. 6 reflect only a part of the data provided by the simula- tor. We have here chosen and presented mainly those physiological characteristics that either are reflected in appropriate empirical research or cannot be invasively measured in humans because of ethics. Unfortunately, we have no space for demonstrating analogous empirical graphs but we have used them during the mod- els tuning [1, 6-8]. This statement concerns exclusively the case of alterations used for the total blood volume. The case of blood tempera- ture dose elevation or decrease is not provided by proper empiric data because these data are still absent. Therefore, the role and the merit of simulations are exclusive. It is necessary to note that our models do not include central mechanisms of thermoregulation. All we have formalized concerns biophysics of cardiac pacemaker cells, that alter their frequency al- most linearly with blood temperature changes. Another temperature target is smooth cells of arterioles. Their resistance is inversely related to local temperature. In case of further devel- opment, the central nervous control of activi- ties in both effectors have to be added. Conclusion For the first time, special software (SS) capable of simulating alterations of human he- modynamics via automatic or arbitrary activa- tions of main endogenous physiological mech- anisms, is developed. SS is based on quantita- tive mathematical models representing CVS as an open system interacting with multiple asso- ciated organs and systems. Models have been tested and validated on the knowledge basis concerning physiological norm. Additionally, main hypotheses of arterial hypertension etiol- ogy can be modeled. SS provides physiologists with a novel research technology essentially widening and deepening the fundamental knowledge con- cerning human circulation. Four simulation scenarios for the intact human model have been simulated. Two scenarios concern blood temperature dose both-side alterations, and two others concern total blood volume dose both- side alterations. Simulation results include the more comprehensive range of physiological information than conventionally provided in empirical studies. This is the main advantage of our SS. SS is also a good modern PC-based tool for simultaneously visualizing CVS’s dy- namic characteristics under the chosen list of input violations. The latter aspect will promote medical students to better understand non-ob- vious integrative human physiology and spe- cial pathologies. SS is also a good computer program to be used in educational purposes for illustrating main physiological and certain pathological regularities to medical students. We plan to expand the models and the software in order to simulate much more realistic sce- narios of both normal and pathological human physiology. References 1. Grygoryan R.D., Yurchak O.I., Degoda A.G., Lyudovyk T.V. Specialized software for simu- lating the multiple control and modulations of human hemodynamics. Problems in pro- gramming 2021; 2: 42-53. DOI: https://doi. org/10.15407/pp2021.02.042. 2. Grygoryan R.D. Modeling of mechanisms pro- viding the overall control of human circulation. Advances in Human Physiology Research,4,5- 21; https://doi.org/10.30564/ahpr.v4i1.4763. 3. Grygoryan RD. The optimal circulation: cells contribution to arterial pressure. N.Y.: Nova Science, 2017: 287p. ISBN 978-1-53612-295- 4. 4. Grygoryan RD. The Optimal Coexistence of Cells: How Could Human Cells Create The In- tegrative Physiology. Journal of Human Physi- ology.2019, 1 (01):8-28. DOI 10.30564/jhp. 29 Методи та засоби комп′ютерного моделювання v1i1.1386. 5. Grygoryan R.D., Sagach V.F. The concept of physiological super-systems: New stage of in- tegrative physiology. Int. J. Physiol. and Patho- physiology, 2018: 9,2,169-180. 6. Grygoryan R.D. Problem-oriented computer simulators for solving of theoretical and ap- plied tasks of human physiology. Problems of programming. 2017, №3, Р. 102-111. 7. Grygoryan R.D., Degoda A.G., Kharsun V.S., Dzhurinsky Y.A. A simulator of mechanisms of acute control of human hemodynamics. Prob- lems of programming, 2019;1:90-98.(Rus.) doi.org/10.15407/pp2019.01.090. 8. Grygoryan R.D., Degoda A.G., Dzhurinsky Y.A. A simulator of mechanisms of long-term control of human hemodynamics. Problems of programming, 2019;4:111-120.(Rus). doi. org/10.15407/pp2019.04.111. Received: 11.11.2022 About authors: Grygoryan Rafik Department chief, PhD, D-r in biology Publications number in Ukraine journals -150 Publications number in English journals -48. Hirsch index – 10 http://orcid.org/0000-0001-8762-733X. Degoda Anna, Senior scientist, PhD. Publications number in Ukraine journals – 15. Publications number in English journals -1. Hirsch index – 3. http://orcid.org/0000-0001-6364-5568. Lyudovyk Tetyana, Senior scientist, PhD. Publications number in Ukraine journals – 30. Publications number in English journals -17. Hirsch index – 5. https://orcid.org/0000-0003-0209-2001. Yurchak Oksana, Leading software engineer. Publications number in Ukraine journals – 14. Publications number in English journals - 0. Hirsch index –0. https://orcid.org/0000-0003-3941-1555. Affiliation: Institute of software systems of Ukraine National Academy of Sciences 03187, Кyїv, Acad. Glushkov avenue, 40, Phone.: 526 5169. Е-mail: rgrygoryan@gmail.com, anna@silverlinecrm.com, tetyana.lyudovyk@gmail.com, daravatan@gmail.com,