Coronary reserve: Concept and physiological variations
When myocardial oxygen consumption (MVO2 is constant, coronary blood flow is largely independent of coronary perfusion pressure within the limits of autoregulation. The relationship is described by a slightly rising plateau, the level of which depends on the value of MVO2. After maximum arteriolar v...
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Veröffentlicht in: | European heart journal 1995-08, Vol.16 (suppl-I), p.2-6 |
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description | When myocardial oxygen consumption (MVO2 is constant, coronary blood flow is largely independent of coronary perfusion pressure within the limits of autoregulation. The relationship is described by a slightly rising plateau, the level of which depends on the value of MVO2. After maximum arteriolar vasodilatation (hyperaemia) coronary blood flow is no longer autoregulated and varies linearly with perfusion pressure. The difference between the coronary blood flow corresponding to the autoregulation plateau under baseline conditions (Qbasal), and the coronary blood flow after maximum vasodilatation (Qmax) is the coronary flow reserve (CFR), which is generally expressed as the Qmax/Qbasal ratio, equal to 4 to 5 in normal subjects. A transient increase in the perfusion pressure within the autoregulation range, causes little or no change in the CFR, as basal flow and peak flow increase proportionally. The CFR decreases progressively with increasing heart rate. This decrease is partly due to an increase in basal flow, secondary to an increase in MVO2, whereas peak flow remains unchanged. An acute increase in left ventricular preload induces a decrease in CFR, due to an increase in basal flow secondary to increased wall stress and therefore increased MVO2, whereas peak flow remains unchanged. Experimentally, peak flow is not affected by an acute increase in contractility. |
doi_str_mv | 10.1093/eurheartj/16.suppl_I.2 |
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The relationship is described by a slightly rising plateau, the level of which depends on the value of MVO2. After maximum arteriolar vasodilatation (hyperaemia) coronary blood flow is no longer autoregulated and varies linearly with perfusion pressure. The difference between the coronary blood flow corresponding to the autoregulation plateau under baseline conditions (Qbasal), and the coronary blood flow after maximum vasodilatation (Qmax) is the coronary flow reserve (CFR), which is generally expressed as the Qmax/Qbasal ratio, equal to 4 to 5 in normal subjects. A transient increase in the perfusion pressure within the autoregulation range, causes little or no change in the CFR, as basal flow and peak flow increase proportionally. The CFR decreases progressively with increasing heart rate. This decrease is partly due to an increase in basal flow, secondary to an increase in MVO2, whereas peak flow remains unchanged. An acute increase in left ventricular preload induces a decrease in CFR, due to an increase in basal flow secondary to increased wall stress and therefore increased MVO2, whereas peak flow remains unchanged. Experimentally, peak flow is not affected by an acute increase in contractility.</description><identifier>ISSN: 0195-668X</identifier><identifier>EISSN: 1522-9645</identifier><identifier>DOI: 10.1093/eurheartj/16.suppl_I.2</identifier><identifier>PMID: 8829952</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Animals ; Blood Pressure ; contractility ; Coronary Circulation - physiology ; Coronary flow reserve ; coronary perfusion pressure ; Heart Rate ; Homeostasis ; Humans ; Myocardial Contraction ; Vasodilation ; Ventricular Function, Left ; ventricular preload</subject><ispartof>European heart journal, 1995-08, Vol.16 (suppl-I), p.2-6</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c342t-257c4240b65481a7dd91c305d50fa511febc05e595120d1c7686892c561489a83</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8829952$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bourdarias, J P</creatorcontrib><title>Coronary reserve: Concept and physiological variations</title><title>European heart journal</title><addtitle>Eur Heart J</addtitle><description>When myocardial oxygen consumption (MVO2 is constant, coronary blood flow is largely independent of coronary perfusion pressure within the limits of autoregulation. The relationship is described by a slightly rising plateau, the level of which depends on the value of MVO2. After maximum arteriolar vasodilatation (hyperaemia) coronary blood flow is no longer autoregulated and varies linearly with perfusion pressure. The difference between the coronary blood flow corresponding to the autoregulation plateau under baseline conditions (Qbasal), and the coronary blood flow after maximum vasodilatation (Qmax) is the coronary flow reserve (CFR), which is generally expressed as the Qmax/Qbasal ratio, equal to 4 to 5 in normal subjects. A transient increase in the perfusion pressure within the autoregulation range, causes little or no change in the CFR, as basal flow and peak flow increase proportionally. The CFR decreases progressively with increasing heart rate. This decrease is partly due to an increase in basal flow, secondary to an increase in MVO2, whereas peak flow remains unchanged. An acute increase in left ventricular preload induces a decrease in CFR, due to an increase in basal flow secondary to increased wall stress and therefore increased MVO2, whereas peak flow remains unchanged. Experimentally, peak flow is not affected by an acute increase in contractility.</description><subject>Animals</subject><subject>Blood Pressure</subject><subject>contractility</subject><subject>Coronary Circulation - physiology</subject><subject>Coronary flow reserve</subject><subject>coronary perfusion pressure</subject><subject>Heart Rate</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Myocardial Contraction</subject><subject>Vasodilation</subject><subject>Ventricular Function, Left</subject><subject>ventricular preload</subject><issn>0195-668X</issn><issn>1522-9645</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNo9kE1Lw0AQhhdRaq3-BCUnb2l3NtkvbxLUVgoiVChelu1mY1PTbNxNiv33Rlp6msPzvjPMg9Ad4DFgmUxs59dW-3YzATYOXdNUajYmZ2gIlJBYspSeoyEGSWPGxPISXYWwwRgLBmyABkIQKSkZIpY572rt95G3wfqdfYgyVxvbtJGu86hZ70PpKvdVGl1FO-1L3ZauDtfootBVsDfHOUIfz0-LbBrP315m2eM8NklK2phQblKS4hWjqQDN81yCSTDNKS40BSjsymBqqaRAcA6GM8GEJIYySIXUIhmh-8PexrufzoZWbctgbFXp2rouKM65wEDSPsgOQeNdCN4WqvHltv9LAVb_wtRJmAKmjsIU6Yu3xwvdamvzU-1oqOfxgZehtb8nrP23YjzhVE2Xn-p9MSXp8pUpnvwBEQR61g</recordid><startdate>19950801</startdate><enddate>19950801</enddate><creator>Bourdarias, J P</creator><general>Oxford University Press</general><scope>BSCLL</scope><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>7X8</scope></search><sort><creationdate>19950801</creationdate><title>Coronary reserve: Concept and physiological variations</title><author>Bourdarias, J P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c342t-257c4240b65481a7dd91c305d50fa511febc05e595120d1c7686892c561489a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Blood Pressure</topic><topic>contractility</topic><topic>Coronary Circulation - physiology</topic><topic>Coronary flow reserve</topic><topic>coronary perfusion pressure</topic><topic>Heart Rate</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Myocardial Contraction</topic><topic>Vasodilation</topic><topic>Ventricular Function, Left</topic><topic>ventricular preload</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bourdarias, J P</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European heart journal</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bourdarias, J P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Coronary reserve: Concept and physiological variations</atitle><jtitle>European heart journal</jtitle><addtitle>Eur Heart J</addtitle><date>1995-08-01</date><risdate>1995</risdate><volume>16</volume><issue>suppl-I</issue><spage>2</spage><epage>6</epage><pages>2-6</pages><issn>0195-668X</issn><eissn>1522-9645</eissn><abstract>When myocardial oxygen consumption (MVO2 is constant, coronary blood flow is largely independent of coronary perfusion pressure within the limits of autoregulation. The relationship is described by a slightly rising plateau, the level of which depends on the value of MVO2. After maximum arteriolar vasodilatation (hyperaemia) coronary blood flow is no longer autoregulated and varies linearly with perfusion pressure. The difference between the coronary blood flow corresponding to the autoregulation plateau under baseline conditions (Qbasal), and the coronary blood flow after maximum vasodilatation (Qmax) is the coronary flow reserve (CFR), which is generally expressed as the Qmax/Qbasal ratio, equal to 4 to 5 in normal subjects. A transient increase in the perfusion pressure within the autoregulation range, causes little or no change in the CFR, as basal flow and peak flow increase proportionally. The CFR decreases progressively with increasing heart rate. This decrease is partly due to an increase in basal flow, secondary to an increase in MVO2, whereas peak flow remains unchanged. An acute increase in left ventricular preload induces a decrease in CFR, due to an increase in basal flow secondary to increased wall stress and therefore increased MVO2, whereas peak flow remains unchanged. Experimentally, peak flow is not affected by an acute increase in contractility.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>8829952</pmid><doi>10.1093/eurheartj/16.suppl_I.2</doi><tpages>5</tpages></addata></record> |
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subjects | Animals Blood Pressure contractility Coronary Circulation - physiology Coronary flow reserve coronary perfusion pressure Heart Rate Homeostasis Humans Myocardial Contraction Vasodilation Ventricular Function, Left ventricular preload |
title | Coronary reserve: Concept and physiological variations |
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