Aortic input impedance during nitroprusside infusion. A reconsideration of afterload reduction and beneficial action

Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input imp...

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Veröffentlicht in:The Journal of clinical investigation 1979-08, Vol.64 (2), p.643-654
Hauptverfasser: Pepine, C J, Nichols, W W, Curry, Jr, R C, Conti, C R
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container_title The Journal of clinical investigation
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creator Pepine, C J
Nichols, W W
Curry, Jr, R C
Conti, C R
description Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input impedance spectrum was examined in 12 patients with heart failure (cardiac index 20 mm Hg). This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P < 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P < 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. These data indicate that nitroprusside acutely alters both the mean and pulsatile components of vascular load to effect improvement in ventricular function in patients with heart failure. The evidence presented suggests that it may be possible to reduce vascular load and improve ventricular function independent of aortic pressure reduction.
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This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P &lt; 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P &lt; 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. These data indicate that nitroprusside acutely alters both the mean and pulsatile components of vascular load to effect improvement in ventricular function in patients with heart failure. 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A reconsideration of afterload reduction and beneficial action</title><title>The Journal of clinical investigation</title><addtitle>J Clin Invest</addtitle><description>Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input impedance spectrum was examined in 12 patients with heart failure (cardiac index &lt;2.0 liters/min per m(2) and left ventricular end diastolic pressure &gt;20 mm Hg). This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P &lt; 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P &lt; 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. These data indicate that nitroprusside acutely alters both the mean and pulsatile components of vascular load to effect improvement in ventricular function in patients with heart failure. The evidence presented suggests that it may be possible to reduce vascular load and improve ventricular function independent of aortic pressure reduction.</description><subject>Adult</subject><subject>Aorta - physiopathology</subject><subject>Blood Flow Velocity</subject><subject>Blood Pressure</subject><subject>Cardiac Output</subject><subject>Ferricyanides - administration &amp; dosage</subject><subject>Heart Failure - drug therapy</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Rate</subject><subject>Humans</subject><subject>Infusions, Parenteral</subject><subject>Middle Aged</subject><subject>Nitroprusside - administration &amp; dosage</subject><subject>Phenylephrine - administration &amp; dosage</subject><subject>Stroke Volume</subject><issn>0021-9738</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1979</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkDtPwzAUhT3wLgzsDJ7YUmzHiZOBoap4FFVigTm6sZ1ilNjBDyT-PaGtEExX-s4590gHoUtK5pQKdvO0XFFSF6Q4QKeEMJrVIq9O0FkI74RQzgt-jI54ISrBT1FcOB-NxMaOKWIzjFqBlRqr5I3dYGuid6NPIRilJ1OXgnF2jhfYa-nsD_UQJ4Rdh6GL2vcO1CSqJLcYrMKttroz0kCPYUvP0WEHfdAX-ztDr_d3L8vHbP38sFou1tnIijpmqiZUEsWqsmpbkILWhQIhqwoIzZkuC96WkmmhJLSC5jKv866qCOGcaCk45DN0u_s7pnbQSmobPfTN6M0A_qtxYJr_ijVvzcZ9NrlgtGRT_nqf9-4j6RCbwQSp-x6sdik0gpeMi1JMxqu_Rb8Nu5Xzb5sOf8o</recordid><startdate>19790801</startdate><enddate>19790801</enddate><creator>Pepine, C J</creator><creator>Nichols, W W</creator><creator>Curry, Jr, R C</creator><creator>Conti, C R</creator><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19790801</creationdate><title>Aortic input impedance during nitroprusside infusion. 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A reconsideration of afterload reduction and beneficial action</atitle><jtitle>The Journal of clinical investigation</jtitle><addtitle>J Clin Invest</addtitle><date>1979-08-01</date><risdate>1979</risdate><volume>64</volume><issue>2</issue><spage>643</spage><epage>654</epage><pages>643-654</pages><issn>0021-9738</issn><abstract>Beneficial effects of nitroprusside infusion in heart failure are purportedly a result of decreased afterload through "impedance" reduction. To study the effect of nitroprusside on vascular factors that determine the total load opposing left ventricular ejection, the total aortic input impedance spectrum was examined in 12 patients with heart failure (cardiac index &lt;2.0 liters/min per m(2) and left ventricular end diastolic pressure &gt;20 mm Hg). This input impedance spectrum expresses both mean flow (resistance) and pulsatile flow (compliance and wave reflections) components of vascular load. Aortic root blood flow velocity and pressure were recorded continuously with a catheter-tip electromagnetic velocity probe in addition to left ventricular pressure. Small doses of nitroprusside (9-19 mug/min) altered the total aortic input impedance spectrum as significant (P &lt; 0.05) reductions in both mean and pulsatile components were observed within 60-90 s. With these acute changes in vascular load, left ventricular end diastolic pressure declined (44%) and stroke volume increased (20%, both P &lt; 0.05). Larger nitroprusside doses (20-38 mug/min) caused additional alteration in the aortic input impedance spectrum with further reduction in left ventricular end diastolic pressure and increase in stroke volume but no additional changes in the impedance spectrum or stroke volume occurred with 39-77 mug/min. Improved ventricular function persisted when aortic pressure was restored to control values with simultaneous phenylephrine infusion in three patients. 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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection
subjects Adult
Aorta - physiopathology
Blood Flow Velocity
Blood Pressure
Cardiac Output
Ferricyanides - administration & dosage
Heart Failure - drug therapy
Heart Failure - physiopathology
Heart Rate
Humans
Infusions, Parenteral
Middle Aged
Nitroprusside - administration & dosage
Phenylephrine - administration & dosage
Stroke Volume
title Aortic input impedance during nitroprusside infusion. A reconsideration of afterload reduction and beneficial action
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