Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation
Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex contro...
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| Veröffentlicht in: | American journal of physiology. Heart and circulatory physiology 2019-07, Vol.317 (1), p.H73-H86 |
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| container_title | American journal of physiology. Heart and circulatory physiology |
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| creator | Tsiklidis, Evan J Sinno, Talid Diamond, Scott L |
| description | Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex control was coupled to a local 24-level bifurcating vascular network that spanned diameters from the muscular artery scale (0.1-1.3 mm) to capillaries (5-10 μm) via conservation of momentum and conservation of mass boundary conditions. For defined injuries of severing all vessels at each
th-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows:
) the upstream vascular network rapidly depressurizes to reduce blood loss;
) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s
) to drive von Willebrand factor unfolding;
) full coagulopathy results in >2-liter blood loss in 2 h for severing all vessels of 0.13- to 0.005-mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to |
| doi_str_mv | 10.1152/ajpheart.00774.2018 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6692728</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2209597361</sourcerecordid><originalsourceid>FETCH-LOGICAL-c433t-839aa337d6d751d896ff64fc5785cc4a9d9c53e85199e54d6826fe4b26a815653</originalsourceid><addsrcrecordid>eNpdkUFrGzEQhUVoSRy3v6BQBL3ksq60s9JKl0IxTVoI9NKehSxpbRlptV2tCvn3leMktD1pxHzzmHkPoXeUbChl7Ud9nA5Oz8uGkL7vNi2h4gKtaqdtKAP5Cq0IcGg4BXaFrnM-EkJYz-ESXQGRvaDQrVDcJr0vIU16OTxgH6fgjV58GjMu2Y97rHEsYfHZ6OBwTNYFnAa8zLrEyhm8C87ZE1i_5nAuzJwarEeLo6-l8bMp4VH0DXo96JDd26d3jX7efvmx_drcf7_7tv1835gOYGkESK0Besttz6gVkg8D7wbDesGM6bS00jBwglEpHessFy0fXLdruRaUcQZr9OmsO5VddNa4sS4c1DT7qOcHlbRX_3ZGf1D79FtxLtu-FVXg5klgTr-Ky4uK1QIXgh5dKlm1LZFM9lDNXaMP_6HHVOaxnlcpVgEAcRKEM1UNyXl2w8sylKhTnOo5TvUYpzrFWafe_33Hy8xzfvAH7higLA</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2256133388</pqid></control><display><type>article</type><title>Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation</title><source>MEDLINE</source><source>American Physiological Society</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Tsiklidis, Evan J ; Sinno, Talid ; Diamond, Scott L</creator><creatorcontrib>Tsiklidis, Evan J ; Sinno, Talid ; Diamond, Scott L</creatorcontrib><description>Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex control was coupled to a local 24-level bifurcating vascular network that spanned diameters from the muscular artery scale (0.1-1.3 mm) to capillaries (5-10 μm) via conservation of momentum and conservation of mass boundary conditions. For defined injuries of severing all vessels at each
th-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows:
) the upstream vascular network rapidly depressurizes to reduce blood loss;
) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s
) to drive von Willebrand factor unfolding;
) full coagulopathy results in >2-liter blood loss in 2 h for severing all vessels of 0.13- to 0.005-mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to <100 ml within 2 min; and
) hemodilution from transcapillary refill increases blood loss and could be implicated in trauma-induced coagulopathy. A sensitivity analysis on length-to-diameter ratio and branching exponent demonstrated that bleeding was strongly dependent on these tissue-dependent network parameters. This is the first bleeding model that prescribes the geometry of the injury to calculate the rate of pressure-driven blood loss and local wall shear rate in the presence or absence of coagulopathic blood.
We developed a multiscale model that couples a lumped, global hemodynamic model of a patient to resolved, single-vessel wounds ranging from the small artery to capillary scale. The model is able to quantify wall shear rates, seal rates, and blood loss rates in the presence and absence of baroreflex control and hemodilution.</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00774.2018</identifier><identifier>PMID: 30978134</identifier><language>eng</language><publisher>United States: American Physiological Society</publisher><subject>Baroreceptors ; Baroreflex ; Bifurcations ; Bleeding ; Blood Coagulation ; Blood pressure ; Blood vessels ; Boundary conditions ; Capillaries ; Cardiovascular system ; Cardiovascular System - physiopathology ; Computer Simulation ; Conservation ; Growth rate ; Hemodynamics ; Hemorrhage - blood ; Hemorrhage - physiopathology ; Hemostasis ; Hemostatics ; Humans ; Injuries ; Microcirculation ; Microvasculature ; Models, Cardiovascular ; Pressure reduction ; Reflexes ; Sensitivity analysis ; Shear rate ; Trauma ; Von Willebrand factor ; Wall shear rate</subject><ispartof>American journal of physiology. Heart and circulatory physiology, 2019-07, Vol.317 (1), p.H73-H86</ispartof><rights>Copyright American Physiological Society Jul 2019</rights><rights>Copyright © 2019 the American Physiological Society 2019 American Physiological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-839aa337d6d751d896ff64fc5785cc4a9d9c53e85199e54d6826fe4b26a815653</citedby><cites>FETCH-LOGICAL-c433t-839aa337d6d751d896ff64fc5785cc4a9d9c53e85199e54d6826fe4b26a815653</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,3039,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30978134$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tsiklidis, Evan J</creatorcontrib><creatorcontrib>Sinno, Talid</creatorcontrib><creatorcontrib>Diamond, Scott L</creatorcontrib><title>Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation</title><title>American journal of physiology. Heart and circulatory physiology</title><addtitle>Am J Physiol Heart Circ Physiol</addtitle><description>Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex control was coupled to a local 24-level bifurcating vascular network that spanned diameters from the muscular artery scale (0.1-1.3 mm) to capillaries (5-10 μm) via conservation of momentum and conservation of mass boundary conditions. For defined injuries of severing all vessels at each
th-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows:
) the upstream vascular network rapidly depressurizes to reduce blood loss;
) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s
) to drive von Willebrand factor unfolding;
) full coagulopathy results in >2-liter blood loss in 2 h for severing all vessels of 0.13- to 0.005-mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to <100 ml within 2 min; and
) hemodilution from transcapillary refill increases blood loss and could be implicated in trauma-induced coagulopathy. A sensitivity analysis on length-to-diameter ratio and branching exponent demonstrated that bleeding was strongly dependent on these tissue-dependent network parameters. This is the first bleeding model that prescribes the geometry of the injury to calculate the rate of pressure-driven blood loss and local wall shear rate in the presence or absence of coagulopathic blood.
We developed a multiscale model that couples a lumped, global hemodynamic model of a patient to resolved, single-vessel wounds ranging from the small artery to capillary scale. The model is able to quantify wall shear rates, seal rates, and blood loss rates in the presence and absence of baroreflex control and hemodilution.</description><subject>Baroreceptors</subject><subject>Baroreflex</subject><subject>Bifurcations</subject><subject>Bleeding</subject><subject>Blood Coagulation</subject><subject>Blood pressure</subject><subject>Blood vessels</subject><subject>Boundary conditions</subject><subject>Capillaries</subject><subject>Cardiovascular system</subject><subject>Cardiovascular System - physiopathology</subject><subject>Computer Simulation</subject><subject>Conservation</subject><subject>Growth rate</subject><subject>Hemodynamics</subject><subject>Hemorrhage - blood</subject><subject>Hemorrhage - physiopathology</subject><subject>Hemostasis</subject><subject>Hemostatics</subject><subject>Humans</subject><subject>Injuries</subject><subject>Microcirculation</subject><subject>Microvasculature</subject><subject>Models, Cardiovascular</subject><subject>Pressure reduction</subject><subject>Reflexes</subject><subject>Sensitivity analysis</subject><subject>Shear rate</subject><subject>Trauma</subject><subject>Von Willebrand factor</subject><subject>Wall shear rate</subject><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFrGzEQhUVoSRy3v6BQBL3ksq60s9JKl0IxTVoI9NKehSxpbRlptV2tCvn3leMktD1pxHzzmHkPoXeUbChl7Ud9nA5Oz8uGkL7vNi2h4gKtaqdtKAP5Cq0IcGg4BXaFrnM-EkJYz-ESXQGRvaDQrVDcJr0vIU16OTxgH6fgjV58GjMu2Y97rHEsYfHZ6OBwTNYFnAa8zLrEyhm8C87ZE1i_5nAuzJwarEeLo6-l8bMp4VH0DXo96JDd26d3jX7efvmx_drcf7_7tv1835gOYGkESK0Besttz6gVkg8D7wbDesGM6bS00jBwglEpHessFy0fXLdruRaUcQZr9OmsO5VddNa4sS4c1DT7qOcHlbRX_3ZGf1D79FtxLtu-FVXg5klgTr-Ky4uK1QIXgh5dKlm1LZFM9lDNXaMP_6HHVOaxnlcpVgEAcRKEM1UNyXl2w8sylKhTnOo5TvUYpzrFWafe_33Hy8xzfvAH7higLA</recordid><startdate>20190701</startdate><enddate>20190701</enddate><creator>Tsiklidis, Evan J</creator><creator>Sinno, Talid</creator><creator>Diamond, Scott L</creator><general>American Physiological Society</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190701</creationdate><title>Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation</title><author>Tsiklidis, Evan J ; Sinno, Talid ; Diamond, Scott L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-839aa337d6d751d896ff64fc5785cc4a9d9c53e85199e54d6826fe4b26a815653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Baroreceptors</topic><topic>Baroreflex</topic><topic>Bifurcations</topic><topic>Bleeding</topic><topic>Blood Coagulation</topic><topic>Blood pressure</topic><topic>Blood vessels</topic><topic>Boundary conditions</topic><topic>Capillaries</topic><topic>Cardiovascular system</topic><topic>Cardiovascular System - physiopathology</topic><topic>Computer Simulation</topic><topic>Conservation</topic><topic>Growth rate</topic><topic>Hemodynamics</topic><topic>Hemorrhage - blood</topic><topic>Hemorrhage - physiopathology</topic><topic>Hemostasis</topic><topic>Hemostatics</topic><topic>Humans</topic><topic>Injuries</topic><topic>Microcirculation</topic><topic>Microvasculature</topic><topic>Models, Cardiovascular</topic><topic>Pressure reduction</topic><topic>Reflexes</topic><topic>Sensitivity analysis</topic><topic>Shear rate</topic><topic>Trauma</topic><topic>Von Willebrand factor</topic><topic>Wall shear rate</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tsiklidis, Evan J</creatorcontrib><creatorcontrib>Sinno, Talid</creatorcontrib><creatorcontrib>Diamond, Scott L</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tsiklidis, Evan J</au><au>Sinno, Talid</au><au>Diamond, Scott L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><addtitle>Am J Physiol Heart Circ Physiol</addtitle><date>2019-07-01</date><risdate>2019</risdate><volume>317</volume><issue>1</issue><spage>H73</spage><epage>H86</epage><pages>H73-H86</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Quantifying the relationship between vascular injury and the dynamic bleeding rate requires a multiscale model that accounts for changing and coupled hemodynamics between the global and microvascular levels. A lumped, global hemodynamic model of the human cardiovascular system with baroreflex control was coupled to a local 24-level bifurcating vascular network that spanned diameters from the muscular artery scale (0.1-1.3 mm) to capillaries (5-10 μm) via conservation of momentum and conservation of mass boundary conditions. For defined injuries of severing all vessels at each
th-level, the changing pressures and flowrates were calculated using prescribed shear-dependent hemostatic clot growth rates (normal or coagulopathic). Key results were as follows:
) the upstream vascular network rapidly depressurizes to reduce blood loss;
) wall shear rates at the hemorrhaging wound exit are sufficiently high (~10,000 s
) to drive von Willebrand factor unfolding;
) full coagulopathy results in >2-liter blood loss in 2 h for severing all vessels of 0.13- to 0.005-mm diameter within the bifurcating network, whereas full hemostasis limits blood loss to <100 ml within 2 min; and
) hemodilution from transcapillary refill increases blood loss and could be implicated in trauma-induced coagulopathy. A sensitivity analysis on length-to-diameter ratio and branching exponent demonstrated that bleeding was strongly dependent on these tissue-dependent network parameters. This is the first bleeding model that prescribes the geometry of the injury to calculate the rate of pressure-driven blood loss and local wall shear rate in the presence or absence of coagulopathic blood.
We developed a multiscale model that couples a lumped, global hemodynamic model of a patient to resolved, single-vessel wounds ranging from the small artery to capillary scale. The model is able to quantify wall shear rates, seal rates, and blood loss rates in the presence and absence of baroreflex control and hemodilution.</abstract><cop>United States</cop><pub>American Physiological Society</pub><pmid>30978134</pmid><doi>10.1152/ajpheart.00774.2018</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | American journal of physiology. Heart and circulatory physiology, 2019-07, Vol.317 (1), p.H73-H86 |
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| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Baroreceptors Baroreflex Bifurcations Bleeding Blood Coagulation Blood pressure Blood vessels Boundary conditions Capillaries Cardiovascular system Cardiovascular System - physiopathology Computer Simulation Conservation Growth rate Hemodynamics Hemorrhage - blood Hemorrhage - physiopathology Hemostasis Hemostatics Humans Injuries Microcirculation Microvasculature Models, Cardiovascular Pressure reduction Reflexes Sensitivity analysis Shear rate Trauma Von Willebrand factor Wall shear rate |
| title | Coagulopathy implications using a multiscale model of traumatic bleeding matching macro- and microcirculation |
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