Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model

Irving Shen, Fiona H. Levy, Arnold M. Benak, Christine L. Rothnie, P. Pearl O'Rourke, Brian W. Duncan, Edward D. Verrier

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Background. Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support. Methods. We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic. Results. Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p <0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p <0.01) at 4 and 6 hours when compared with baseline. Conclusions. Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.

Original languageEnglish (US)
Pages (from-to)868-871
Number of pages4
JournalAnnals of Thoracic Surgery
Volume71
Issue number3
DOIs
StatePublished - 2001
Externally publishedYes

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Extracorporeal Membrane Oxygenation
Left Ventricular Dysfunction
Swine
Left Ventricular Function
Heart Ventricles
Stroke
Oxygen
Blood Pressure
Coronary Circulation
Atrial Pressure
Partial Pressure
Ventricular Pressure
Cardiac Output
Ventilation
Myocardium
Thorax
Animal Models
Perfusion
Pressure

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Shen, I., Levy, F. H., Benak, A. M., Rothnie, C. L., O'Rourke, P. P., Duncan, B. W., & Verrier, E. D. (2001). Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model. Annals of Thoracic Surgery, 71(3), 868-871. https://doi.org/10.1016/S0003-4975(00)02281-5

Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model. / Shen, Irving; Levy, Fiona H.; Benak, Arnold M.; Rothnie, Christine L.; O'Rourke, P. Pearl; Duncan, Brian W.; Verrier, Edward D.

In: Annals of Thoracic Surgery, Vol. 71, No. 3, 2001, p. 868-871.

Research output: Contribution to journalArticle

Shen, Irving ; Levy, Fiona H. ; Benak, Arnold M. ; Rothnie, Christine L. ; O'Rourke, P. Pearl ; Duncan, Brian W. ; Verrier, Edward D. / Left ventricular dysfunction during extracorporeal membrane oxygenation in a hypoxemic swine model. In: Annals of Thoracic Surgery. 2001 ; Vol. 71, No. 3. pp. 868-871.
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abstract = "Background. Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support. Methods. We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic. Results. Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p <0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p <0.01) at 4 and 6 hours when compared with baseline. Conclusions. Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.",
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AU - Shen, Irving

AU - Levy, Fiona H.

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AU - Rothnie, Christine L.

AU - O'Rourke, P. Pearl

AU - Duncan, Brian W.

AU - Verrier, Edward D.

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N2 - Background. Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support. Methods. We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic. Results. Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p <0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p <0.01) at 4 and 6 hours when compared with baseline. Conclusions. Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.

AB - Background. Perfusion of the coronary circulation with hypoxemic blood from the left ventricle has been postulated to cause myocardial dysfunction during venoarterial extracorporeal membrane oxygenation for respiratory support. Methods. We investigated this hypothesis in 10 anesthetized open-chest piglets (7 to 9 kg) undergoing venoarterial extracorporeal membrane oxygenation after placement of minor-axis sonomicrometry crystals and left ventricular micromanometer. The left atrial partial pressure of oxygen was made hypoxemic (25 to 40 mm Hg) after initiation of extracorporeal membrane oxygenation by ventilation with a hypoxic gas mixture. Left ventricular contractile function, including peak LV pressure, shortening fraction, maximum rate of increase of left ventricular pressure, velocity of circumferential fiber shortening, end-systolic pressure-minor axis dimension relationship, and preload recruitable dimensional stroke work, was measured or calculated on extracorporeal membrane oxygenation before (baseline) and at 4 and 6 hours after rendering the left atrial blood hypoxemic. Results. Left ventricular shortening fraction and velocity of circumferential fiber shortening were significantly lower (p <0.05) at 4 and 6 hours when compared with baseline. The slope of the end-systolic pressure-minor axis dimension relationship decreased but was not significantly different at 4 and 6 hours when compared with baseline owing to poor linear correlation (r = 0.30 to 0.93). The preload recruitable dimensional stroke work was more linear (r = 0.87 to 0.99), and the slope was significantly lower (p <0.01) at 4 and 6 hours when compared with baseline. Conclusions. Hypoxemic cardiac output from the left ventricle during venoarterial extracorporeal membrane oxygenation is associated with depression of left ventricular systolic function in this animal model. Current use of venoarterial extracorporeal membrane oxygenation for respiratory support may not provide adequate oxygen supply to the myocardium.

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