Simulation of pulmonary ventilation and its control by negative feedback
The equivalent electronic circuit developed to simulate pulmonary ventilation is upgraded to incorporate homeostasis, i.e. a negative feedback loop. The latter can be made either inactive or active. In the former condition, only the immediate consequence of a disturbance shows up. In the latter cond...
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description | The equivalent electronic circuit developed to simulate pulmonary ventilation is upgraded to incorporate homeostasis, i.e. a negative feedback loop. The latter can be made either inactive or active. In the former condition, only the immediate consequence of a disturbance shows up. In the latter condition, however, full homeostatic—sometimes very complex—response can be studied.
The effects of three types of disturbances are studied in both conditions (i.e. open loop, closed loop): increased CO
2 production, temporary apnoea, and of bronchoconstriction (in the whole lung or only in part of the lung). The effect of increased CO
2 production is increase in pulmonary ventilation and increase in pCO
2. The latter strongly depends on the feedback response. Temporary apnoea results in a transient increase in pCO
2. However, if the time constant of the feedback loop is large enough, this type of disturbance results in a maintained periodic, Cheyne–Stokes-type breathing.
Bronchoconstriction in 100% of the lung results in a decrease in tidal volume. If homeostasis is active this decrease is compensated by an increase in the inspiratory effort. However, if bronchoconstriction occurs only in 50% of the lung, inspiratory effort is greatly changed through inter-alveolar elastic interactions, giving rise to the so-called pendelluft. |
doi_str_mv | 10.1016/j.compbiomed.2004.02.002 |
format | Article |
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The effects of three types of disturbances are studied in both conditions (i.e. open loop, closed loop): increased CO
2 production, temporary apnoea, and of bronchoconstriction (in the whole lung or only in part of the lung). The effect of increased CO
2 production is increase in pulmonary ventilation and increase in pCO
2. The latter strongly depends on the feedback response. Temporary apnoea results in a transient increase in pCO
2. However, if the time constant of the feedback loop is large enough, this type of disturbance results in a maintained periodic, Cheyne–Stokes-type breathing.
Bronchoconstriction in 100% of the lung results in a decrease in tidal volume. If homeostasis is active this decrease is compensated by an increase in the inspiratory effort. However, if bronchoconstriction occurs only in 50% of the lung, inspiratory effort is greatly changed through inter-alveolar elastic interactions, giving rise to the so-called pendelluft.</description><identifier>ISSN: 0010-4825</identifier><identifier>EISSN: 1879-0534</identifier><identifier>DOI: 10.1016/j.compbiomed.2004.02.002</identifier><identifier>PMID: 15582629</identifier><identifier>CODEN: CBMDAW</identifier><language>eng</language><publisher>United States: Elsevier Ltd</publisher><subject>Anatomy & physiology ; Colleges & universities ; Computer applications ; Computer Simulation ; Electric Conductivity ; Expert systems ; Feedback ; Health care ; Homeostasis ; Humans ; Lungs ; Mathematical models ; Medicine ; Models, Biological ; Pulmonary physiology ; Pulmonary Ventilation ; Simulation ; Ventilation</subject><ispartof>Computers in biology and medicine, 2005-03, Vol.35 (3), p.217-228</ispartof><rights>2004 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c460t-6f213fb42fb30872f17fef3a0081936cc69d8c56978a8ed2ebc8aa0ab81e991f3</citedby><cites>FETCH-LOGICAL-c460t-6f213fb42fb30872f17fef3a0081936cc69d8c56978a8ed2ebc8aa0ab81e991f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0010482504000265$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15582629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dolenšek, J.</creatorcontrib><creatorcontrib>Runovc, F.</creatorcontrib><creatorcontrib>Kordaš, M.</creatorcontrib><title>Simulation of pulmonary ventilation and its control by negative feedback</title><title>Computers in biology and medicine</title><addtitle>Comput Biol Med</addtitle><description>The equivalent electronic circuit developed to simulate pulmonary ventilation is upgraded to incorporate homeostasis, i.e. a negative feedback loop. The latter can be made either inactive or active. In the former condition, only the immediate consequence of a disturbance shows up. In the latter condition, however, full homeostatic—sometimes very complex—response can be studied.
The effects of three types of disturbances are studied in both conditions (i.e. open loop, closed loop): increased CO
2 production, temporary apnoea, and of bronchoconstriction (in the whole lung or only in part of the lung). The effect of increased CO
2 production is increase in pulmonary ventilation and increase in pCO
2. The latter strongly depends on the feedback response. Temporary apnoea results in a transient increase in pCO
2. However, if the time constant of the feedback loop is large enough, this type of disturbance results in a maintained periodic, Cheyne–Stokes-type breathing.
Bronchoconstriction in 100% of the lung results in a decrease in tidal volume. If homeostasis is active this decrease is compensated by an increase in the inspiratory effort. 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M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Simulation of pulmonary ventilation and its control by negative feedback</atitle><jtitle>Computers in biology and medicine</jtitle><addtitle>Comput Biol Med</addtitle><date>2005-03-01</date><risdate>2005</risdate><volume>35</volume><issue>3</issue><spage>217</spage><epage>228</epage><pages>217-228</pages><issn>0010-4825</issn><eissn>1879-0534</eissn><coden>CBMDAW</coden><abstract>The equivalent electronic circuit developed to simulate pulmonary ventilation is upgraded to incorporate homeostasis, i.e. a negative feedback loop. The latter can be made either inactive or active. In the former condition, only the immediate consequence of a disturbance shows up. In the latter condition, however, full homeostatic—sometimes very complex—response can be studied.
The effects of three types of disturbances are studied in both conditions (i.e. open loop, closed loop): increased CO
2 production, temporary apnoea, and of bronchoconstriction (in the whole lung or only in part of the lung). The effect of increased CO
2 production is increase in pulmonary ventilation and increase in pCO
2. The latter strongly depends on the feedback response. Temporary apnoea results in a transient increase in pCO
2. However, if the time constant of the feedback loop is large enough, this type of disturbance results in a maintained periodic, Cheyne–Stokes-type breathing.
Bronchoconstriction in 100% of the lung results in a decrease in tidal volume. If homeostasis is active this decrease is compensated by an increase in the inspiratory effort. However, if bronchoconstriction occurs only in 50% of the lung, inspiratory effort is greatly changed through inter-alveolar elastic interactions, giving rise to the so-called pendelluft.</abstract><cop>United States</cop><pub>Elsevier Ltd</pub><pmid>15582629</pmid><doi>10.1016/j.compbiomed.2004.02.002</doi><tpages>12</tpages></addata></record> |
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subjects | Anatomy & physiology Colleges & universities Computer applications Computer Simulation Electric Conductivity Expert systems Feedback Health care Homeostasis Humans Lungs Mathematical models Medicine Models, Biological Pulmonary physiology Pulmonary Ventilation Simulation Ventilation |
title | Simulation of pulmonary ventilation and its control by negative feedback |
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