A SIMULATION STUDY OF MECHANISM OF POSTFLIGHT ORTHOSTATIC INTOLERANCE

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1 Proceedngs 3rd Annual Conference IEEE/EMBS Oct.5-8, 001, Istanbul, TURKEY A SIMULATION STUDY OF MECHANISM OF POSTFLIGHT ORTHOSTATIC INTOLERANCE W. Y HAO 1, J. BAI 1, W. Y. ZHANG, X. Y. WU 3 L. F. ZHANG 3 1 Department of Electrcal Engneerng, Tsnghua Unversty, Bejng 084, PR Chna Xjng hosptal and 3 Department of Aerospace Medcne, The Fourth Medcal Unversty, X an 73, PR Chna Abstract The am of ths study was to nvestgate the role played by the factors, such as altered vasoreactvty of resstance vessels n dfferent body regons, and depressed cardac contractlty n the geness of postflght cardovascular dysfuncton. The model we used s based on the model developed by Mechor et al. (1994) wth modfcaton by ncorporatng nto the model, some more detaled sub-models to descrbe blood redstrbuton, cardac contractlty, local vascular tone changes, and baroreflex control mechansm. The smulated cardovascular response to LBNP, HUT, and +Gz(low level) stresses have been shown to compare well wth the relevant expermental data. Further computer smulaton studes were performed to assess the contrbutons of each factor on cardovascular dysfuncton postflght. The smulaton demonstrated that both the hypovolema and depressed cardac contractlty elct obvous changes n cardovascular responses to orthostatc stress. Although an ncrease n vasoconstrctor responsveness of bran vessels does not elct sgnfcant changes for the man hemodynamc varables, the cerebral blood flow s decreased dramatcally. However, f the vasoreactvty of bran vessels kept unchanged, the decrease n vascular tone of vessels n lower body does not cause sgnfcant changes n cerebral blood flow. Key words Cardovascular system, computer smulaton, weghtlessness I. INTRODUCTION Othostatc ntolerance (OI) followng exposure to mcrogravty or head-down bed rest s frequently observed and s thought to be multfactoral orgn[1,]. Although hypovolema s consdered as the prmary cause of OI, the role played by other factors, such as the lowered vasoconstrctor responsveness (VCR) of resstance vessels, the enhanced vasoconstrcton response of cerebral vessels, and the depressed myocardal contractlty need to be elucdated[3,4]. It s dffcult to assess expermentally how each of these changes would affect orthostatc tolerance and how these factors nteract wth each other. An alternatve approach s to conduct smulaton studes by use of mathematcal models of cardovascular system (CVS) capable of smulatng the CVS response to orthostatc stress. Ths presentaton descrbes the constructon of the model used, and presents the prelmnary smulaton results llustratng the effects of varyng ndvdually the level of hypovolema, VCR of the resstance vessels n lower lmbs and abdomnal vscera, VCR of the bran vessels or myocardal contractlty on responses to orthostatc stress. The ultmate goal of our work was to ntegrate the new expermental fndngs and to smulate the complexty to get a thorough understandng of the mechansm of postflght cardovascular dysfuncton and orthostatc ntolerance. II. METHOD 1) Model Descrpton Based on the prevous work of Melchor et al[5], we have developed a mathematcal model by ncorporatng some more detaled sub-models to descrbe blood redstrbuton, cardac contractlty, perpheral crculaton, local vascular tone changes, and baroreflex control mechansm[6,7] (Fg. 1). Here we brefly revew the man ponts of the model. More detaled descrptons of the model have been gven n prevous work [6, 7] Because the arteres and capllares are much less complant than the vens, we assumed that blood volume redstrbuton durng LBNP takes place only n the venous beds. Venous blood volume s consdered to be stored n seven dfferent compartments representng the head and uplmbs (HUL), thoracc regon (THO), abdomen regon (ABD), pelvs and buttocks (PB), thgh (THI), calf (CAL) and foots (FT). We consdered the phenomena of collapse of venous vessels durng negatve transmural pressure and employed two tangent functons to descrbe the P-V relatons of each compartment. = m + m arctan[ C arctan[ C 0 0 P P trans m + trans m ] ( P trans >0) ] ( P trans <0) where = HUL, THO, ABD, PB, THI, CAL and FT; C 0 s /01$ IEEE

2 Report Documentaton Page Report Date 5 Oct 001 Report Type N/A Dates Covered (from... to) - Ttle and Subttle A Smulaton Study of Mechansm of Postflght Orthostatc Intolerance Contract Number Grant Number Program Element Number Author(s) Project Number Task Number Work Unt Number Performng Organzaton Name(s) and Address(es) Department of Electrcal Engneerng Tsnghua Unversty Bejng 084 PR Chna Sponsorng/Montorng Agency Name(s) and Address(es) US Army Research, Development & Standardzaton Group (UK) PSC 80 Box 15 FPO AE Performng Organzaton Report Number Sponsor/Montor s Acronym(s) Sponsor/Montor s Report Number(s) Dstrbuton/Avalablty Statement Approved for publc release, dstrbuton unlmted Supplementary Notes Papers from 3rd Annual Internatonal Conference of the IEEE Engneerng n Medcne and Bology Socety, October 5-8, 001, held n Istanbul, Turkey. See also ADM for entre conference on cd-rom., The orgnal document contans color mages. Abstract Subject Terms Report Classfcaton unclassfed Classfcaton of Abstract unclassfed Classfcaton of ths page unclassfed Lmtaton of Abstract UU Number of Pages 4

3 Proceedngs the complance 3rd for Annual the small Conference varatons IEEE/EMBS of P trans, Oct.5-8, m+ and 001, Istanbul, We used TURKEY the work of Melchor et al.[5] to correlated m- are the maxmal ncrement and decrement of each CVP and left ventrcular end-dastolc volume (VLVED) compartment. durng LBNP, then CVP= λ [exp( β V LVED ) exp( β V 0LVED where λ s a constant and β s left ventrcular elastc stffness. Fg1 Block dagram of the cardovascular model The heart rate and venous tone are modulated by the carotd baroreceptors, whereas the perpheral resstance s regulated by both carotd and cardopulmomary baroreceptors. The model was valdated for smulaton of the CVS response to exposure of LBNP, or HUT by the data obtaned from human experment and publshed data [6, 7]. ) Smulaton Procedure By use of the developed model, CVS responses to LBNP were smulated separately for each of the four knds of physologc changes that occurred n the smulated subject. The changes were: 1) decrease of blood volume; ) 1% decrease of blood volume plus decrease of VCR of resstance vessels n abdomnal vscera and lower lmbs; 3) 1% decrease of blood volume plus 30% decrease of VCR of resstance vessels n lower )] lmbs and abdomnal vscera plus enhanced vasoconstrcton of cerebral vessels; 4) 1% decrease of blood volume combned wth decrease of myocardal contractlty. The smulaton model was programmed wth MATLAB language and mplemented n an IBM compatble personal computer. III. RESULTS 1) Effects of blood volume decrease The more decrease of blood volume, the more changes wll be (fg ). If the amount of the decrease of blood volume s less than 5% of the total blood volume, HR and BP can be completely mantaned n ther physologcal range by the regulaton of baroreflex durng orthostatc stress exposure. If the amount of the decrease of blood volume s more than 15% of the total blood volume, the hemodynamc varables can be n normal range when the smulated subject s n supne and at rest. However, the BP falls steeply and CVS mght collapse wth orthostactc stress (even f the ntensty of the stress s relatvely low). Shock Index (SI, SI=HR/SBP) wll be greater than 1.0 (no shock occurs) durng LBNP stresses f the decrease of blood volume s more than 15% of the total blood volume. ) Effects of decrease of VCR of resstance vessels n lower body Smulaton results ndcated that the decrease of VCR of resstance vessels n lower body affected nsgnfcantly on HR and BP durng LBNP exposure. Fg Effects of hypovolema on HR, BP and Shock Index response to supne LBNP

4 Proceedngs 3rd Annual Conference IEEE/EMBS Oct.5-8, 001, Istanbul, TURKEY 3) Effects of enhanced vasoconstrctor of cerebral sharply wth the ncrement of LBNP exposure, and the vessels The smulaton results suggested that the enhanced system seemed to run nto collapse. Also CO s decreased vasoconstrcton response of cerebral vessels result n a sgnfcant decrease of cerebral blood flow veloctes, although t dd not elct obvous changes n HR and BP (fg 3). wth the decrement of myocarda contractlty and ncrement of LBNP. It s obvous that CO tends to a steady level when both the decreases of myocarda contractlty and LBNP are hgh. 4) Effects of depressed myocardal contractlty IV. DISCUSSION Sgnfcant ncrease of HR and decrease of BP can be seen when cardac contractlty s depressed (Tab 1). Table 1 Effect of depressed myocardal contractlty ( MC) on CVS response to LBNP (-50mmHg) Our smulaton results show that both the hypovolema and depressed myocardal contractlty mght elct obvous changes n cardovascular responses to orthostatc stress. Although an ncrease n vasoconstrctor responsveness of MC HR SBP DBP CO bran vessels does not elct sgnfcant changes for the man (%) (bpm) (mmhg) (mmhg) (L/mn) hemodynamc varables, the cerebral blood flow s decreased dramatcally. However, f the vasoreactvty of bran vessels kept unchanged, the decrease n vascular tone of vessels n lower body would not cause sgnfcant changes n cerebral As shown n Fg 4, the augment of HR s ncreased sgnfcantly as LBNP and myocarda contractlty s decreased. The decrement of SBP s reduced progressvely wth the decrement of myocarda contractlty. However, DBP s ncreased slghtly when myocarda contractlty s decreased slghtly wth low level LBNP. But f the decrement of myocarda contractlty s over 10%, DBP decreases blood flow. These results suggest that the role of changes of vasoreactvty n the OI need to be further elucdated. What we presented s a prelmnary result. Further mprovement of the present model s needed to ncorporate subsystems descrbng the adaptve changes, hemodynamcs, heart performance, and regonal crculaton durng mcrogravty base on new expermental fndngs. CBF(%) VCR cer = 10% VCR cer = 30% 70 SBP(mmHg) HR( bpm ) supne LBNP( mmhg ) Fg3 Effect of enhanced vasoconstrcton of cerebral vessels on CBF, BP and HR response to supne LBNP

5 Proceedngs 3rd Annual Conference IEEE/EMBS Oct.5-8, 001, Istanbul, TURKEY Fg4 Effect of depresson of myocardal contractlty on HR, SBP, DBP and CO response to supne LBNP REFERENCE: [1]. Watenpaugh DE and Hargens AR. The cardovascular system n mcrogravty. In: Fregly MJ and Blattes.CM eds. Handbook of Physology: Envronmental Physology. Ⅲ : The Gravtatonal Envronment,1: Mcrogravty. New York: Oxford Unversty Press, 1996: []. Blomqvst CG,and Stone HL. Cardovascular adjustment to gravtaton stress. In: Shepherd JT, Abboud FM, eds. Handbook of Physology. The Cardovascular System Perpheral crculaton and Organ Blood Flow. sect.,vol.Ⅲ,pt., Bethesda. MD: Am PhysolSoc, 1983: [3]. Zhang LF, Yu ZB, Ma J. Functonal alteratons n cardac muscle after medum- or long-term smulated weghtlessness and related cellular mechansms. J Gravt Physol, 1995; (1): 4-8 [4]. Zhang LF, J Ma,QW Mao, et al. Plastcty of arteral vasculature durng smlated weghtlessness and ts possble role n the geness of postflght orthostatc ntolerance. J Gravt Physol, 1997: 4(): 97- [5]. Melchor FM, Srnvasan RS, Thuller PH et al Smulaton of cardovascular response to lower body negatve pressure from 0 to -40 mmhg. J Appl Physol, 1994; 77: [6]. Hao WY, Wu XY, Zhang LF, et al. A computer smulaton of cardovascular response to lower body negatve pressure. Space Medcne & Medcal Engneerng, 1999; 1(4): 6-66 [7]. Hao WY, Zhang LF, Wu XY, et al. A smulaton of cardovascular response to head up tlt. Journal of Fourth Medcal Unversty, 000; 1(1): Address to correspondence: Weya Hao, Ph.D. Insttute of Bomedcal Engneerng Department of Electrcal Engneerng Tsnghua Unversty Bejng 084, Chna Emal: haowy@bme.tsnghua.edu.cn