Use of chest circumference signal as an input to models of respiration–HRV interaction

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dc.contributor.authorYildiz M.
dc.contributor.authorIder Y.Z.
dc.date.accessioned2020-03-26T17:19:35Z
dc.date.available2020-03-26T17:19:35Z
dc.date.issued2007
dc.departmentSelçuk Üniversitesien_US
dc.descriptionAAPM;BMES;EFOMP;et al;IAEA;WHOen_US
dc.description10th World Congress on Medical Physics and Biomedical Engineering, WC 2006 -- 27 August 2006 through 1 September 2006 -- 163739en_US
dc.description.abstractContributions of respiration to the genesis of Heart Rate Variability are well known. Respiration not only generates the HF (High Frequency) component of the power spectrum of HRV, called respiratory sinus arrhythmia, but also contributes to the formation of the LF (Low Frequency) peak. Therefore it is necessary that respiration is also recorded during an HRV test so that LF/HF ratio, which is the most important parameter extracted from HRV for assessing sympathovagal balance, is more properly evaluated. LF components of lung volume (VL), intrathoracic pressure (PT), and abdominal pressure (PA), are more significant especially when respiration is slightly irregular, and may directly contribute to HRV LF power. Models developed to study these interactions need respiratory signal inputs. Measurements of VL, PT, and PA in a clinical setting are either not possible or induce stress in the patient and thus alter HRV. On the other hand chest and abdominal circumference signals (CT and CA respectively) are easier to acquire without inducing stress. It is shown that by appropriately scaling and offsetting CT and CA one obtains signals representative of PT and PA which then can be used as inputs to the models. VL can also be derived from PT through a linear empirical formula published elsewhere. CT, CA, and VL from 5 volunteers are recorded together with ECG. It is shown that CT is linearly related to VL, and hence to PT. The derived PT and PA signals are then applied to a Respiration-Cardiovascular System model and HRV is derived. It is observed that model derived and real HRVs are temporally well correlated. It is also shown that in the presence of increased LF power of the circumference signals HRV LF power also increases. © International Federation for Medical and Biological Engineering 2007.en_US
dc.identifier.endpage3448en_US
dc.identifier.issn1680-0737en_US
dc.identifier.issue1en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage3445en_US
dc.identifier.urihttps://hdl.handle.net/20.500.12395/21901
dc.identifier.volume14en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherSpringer Verlagen_US
dc.relation.ispartofIFMBE Proceedingsen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.selcuk20240510_oaigen_US
dc.subjectChest circumferenceen_US
dc.subjectHeart rate variabilityen_US
dc.subjectPhysiological modelingen_US
dc.subjectRespirationen_US
dc.subjectSimulationen_US
dc.titleUse of chest circumference signal as an input to models of respiration–HRV interactionen_US
dc.typeConference Objecten_US

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