Systemic oxygen delivery and consumption during acute lung injury in dogs

G. Richard Long; David P. Nelson; J. Lasha Sznajder; Lawrence D H Wood; Paul T. Schumacker

doi:10.1016/0883-9441(88)90109-8

Systemic oxygen delivery and consumption during acute lung injury in dogs

G. Richard Long, David P. Nelson, J. Lasha Sznajder, Lawrence D H Wood, Paul T. Schumacker^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

6 Scopus citations

Abstract

When oxygen delivery (QO₂ = Qt × CaO₂) is reduced in healthy animals, oxygen uptake by tissues (VO₂) is maintained by an increase in the O₂ extraction ratio ((CaO₂ - CvO₂)/CaO₂) until a critical level of delivery QO₂C is reached, below which VO₂ becomes dependent on QO₂. In patients with adult respiratory distress syndrome (ARDS), VO₂ becomes dependent on O₂ delivery even at high levels of QO₂ implying a systemic O₂ extraction defect. To determine whether lung injury, or its management with positive end-expiratory pressure (PEEP) and high inspired oxygen fractions (F1O₂), might disrupt O₂ extraction by peripheral tissues, we compared the critical O₂ delivery and extraction ratio in 30 anesthetized and paralyzed dogs in four groups. One group (n = 7) received oleic acid to produce an acute lung injury (F_lO₂ = 1.0) and a second group (n = 7) was maintained with PEEP (F_lO₂ = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (F_lO₂ = 1.0), and a fourth group received no oleic acid and was ventilated with room air. The critical O₂ delivery was determined in each animal as QO₂ was lowered in a stepwise manner by controlled blood removal. Neither the critical QO₂ nor critical O₂ extraction ratios were different (P > .05) among oleic acid, PEEP-treated, or hyperoxic control animals. Similarly, the critical QO₂ determined from the point at which arterial lactate began to increase showed no difference among groups. Thus, neither acute lung injury produced with oleic acid nor its treatment with PEEP was associated with a peripheral O₂ extraction defect. However, a linear regression across all groups demonstrated a positive correlation between the arterial PO₂ and corresponding critical O₂ delivery (r = < P < .05). These results suggest that high arterial O₂ tensions may contribute to an impairment of peripheral O₂ extraction.

Original language	English (US)
Pages (from-to)	249-255
Number of pages	7
Journal	Journal of Critical Care
Volume	3
Issue number	4
DOIs	https://doi.org/10.1016/0883-9441(88)90109-8
State	Published - Dec 1988

Funding

From the Section of Pulmonary cine, The University of Chicago. Supported by National Heart, Lung, and Blood Institute grants no. HL30835 and HL01682 and the Otho S.A. Sprague Memorial Fund. Address reprint requests to Paul T. Schumacker, PhD, Department of Medicine, Box 83. The University of Chicago, 5841 S Maryland Ave, Chicago, IL 60637. o 1988 by Grune & Stratton, Inc. 0883-9441/88/0304-0005$5.00/O

ASJC Scopus subject areas

Critical Care and Intensive Care Medicine

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10.1016/0883-9441(88)90109-8

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@article{6a6d05ba89be45c99c7188de44be0139,

title = "Systemic oxygen delivery and consumption during acute lung injury in dogs",

abstract = "When oxygen delivery (QO2 = Qt × CaO2) is reduced in healthy animals, oxygen uptake by tissues (VO2) is maintained by an increase in the O2 extraction ratio ((CaO2 - CvO2)/CaO2) until a critical level of delivery QO2C is reached, below which VO2 becomes dependent on QO2. In patients with adult respiratory distress syndrome (ARDS), VO2 becomes dependent on O2 delivery even at high levels of QO2 implying a systemic O2 extraction defect. To determine whether lung injury, or its management with positive end-expiratory pressure (PEEP) and high inspired oxygen fractions (F1O2), might disrupt O2 extraction by peripheral tissues, we compared the critical O2 delivery and extraction ratio in 30 anesthetized and paralyzed dogs in four groups. One group (n = 7) received oleic acid to produce an acute lung injury (FlO2 = 1.0) and a second group (n = 7) was maintained with PEEP (FlO2 = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (FlO2 = 1.0), and a fourth group received no oleic acid and was ventilated with room air. The critical O2 delivery was determined in each animal as QO2 was lowered in a stepwise manner by controlled blood removal. Neither the critical QO2 nor critical O2 extraction ratios were different (P > .05) among oleic acid, PEEP-treated, or hyperoxic control animals. Similarly, the critical QO2 determined from the point at which arterial lactate began to increase showed no difference among groups. Thus, neither acute lung injury produced with oleic acid nor its treatment with PEEP was associated with a peripheral O2 extraction defect. However, a linear regression across all groups demonstrated a positive correlation between the arterial PO2 and corresponding critical O2 delivery (r = < P < .05). These results suggest that high arterial O2 tensions may contribute to an impairment of peripheral O2 extraction.",

author = "Long, \{G. Richard\} and Nelson, \{David P.\} and Sznajder, \{J. Lasha\} and Wood, \{Lawrence D H\} and Schumacker, \{Paul T.\}",

note = "Funding Information: From the Section of Pulmonary cine, The University of Chicago. Supported by National Heart, Lung, and Blood Institute grants no. HL30835 and HL01682 and the Otho S.A. Sprague Memorial Fund. Address reprint requests to Paul T. Schumacker, PhD, Department of Medicine, Box 83. The University of Chicago, 5841 S Maryland Ave, Chicago, IL 60637. o 1988 by Grune \& Stratton, Inc. 0883-9441/88/0304-0005\$5.00/O",

year = "1988",

month = dec,

doi = "10.1016/0883-9441(88)90109-8",

language = "English (US)",

volume = "3",

pages = "249--255",

journal = "Journal of Critical Care",

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publisher = "W.B. Saunders",

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T1 - Systemic oxygen delivery and consumption during acute lung injury in dogs

AU - Long, G. Richard

AU - Nelson, David P.

AU - Sznajder, J. Lasha

AU - Wood, Lawrence D H

AU - Schumacker, Paul T.

N1 - Funding Information: From the Section of Pulmonary cine, The University of Chicago. Supported by National Heart, Lung, and Blood Institute grants no. HL30835 and HL01682 and the Otho S.A. Sprague Memorial Fund. Address reprint requests to Paul T. Schumacker, PhD, Department of Medicine, Box 83. The University of Chicago, 5841 S Maryland Ave, Chicago, IL 60637. o 1988 by Grune & Stratton, Inc. 0883-9441/88/0304-0005$5.00/O

PY - 1988/12

Y1 - 1988/12

N2 - When oxygen delivery (QO2 = Qt × CaO2) is reduced in healthy animals, oxygen uptake by tissues (VO2) is maintained by an increase in the O2 extraction ratio ((CaO2 - CvO2)/CaO2) until a critical level of delivery QO2C is reached, below which VO2 becomes dependent on QO2. In patients with adult respiratory distress syndrome (ARDS), VO2 becomes dependent on O2 delivery even at high levels of QO2 implying a systemic O2 extraction defect. To determine whether lung injury, or its management with positive end-expiratory pressure (PEEP) and high inspired oxygen fractions (F1O2), might disrupt O2 extraction by peripheral tissues, we compared the critical O2 delivery and extraction ratio in 30 anesthetized and paralyzed dogs in four groups. One group (n = 7) received oleic acid to produce an acute lung injury (FlO2 = 1.0) and a second group (n = 7) was maintained with PEEP (FlO2 = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (FlO2 = 1.0), and a fourth group received no oleic acid and was ventilated with room air. The critical O2 delivery was determined in each animal as QO2 was lowered in a stepwise manner by controlled blood removal. Neither the critical QO2 nor critical O2 extraction ratios were different (P > .05) among oleic acid, PEEP-treated, or hyperoxic control animals. Similarly, the critical QO2 determined from the point at which arterial lactate began to increase showed no difference among groups. Thus, neither acute lung injury produced with oleic acid nor its treatment with PEEP was associated with a peripheral O2 extraction defect. However, a linear regression across all groups demonstrated a positive correlation between the arterial PO2 and corresponding critical O2 delivery (r = < P < .05). These results suggest that high arterial O2 tensions may contribute to an impairment of peripheral O2 extraction.

AB - When oxygen delivery (QO2 = Qt × CaO2) is reduced in healthy animals, oxygen uptake by tissues (VO2) is maintained by an increase in the O2 extraction ratio ((CaO2 - CvO2)/CaO2) until a critical level of delivery QO2C is reached, below which VO2 becomes dependent on QO2. In patients with adult respiratory distress syndrome (ARDS), VO2 becomes dependent on O2 delivery even at high levels of QO2 implying a systemic O2 extraction defect. To determine whether lung injury, or its management with positive end-expiratory pressure (PEEP) and high inspired oxygen fractions (F1O2), might disrupt O2 extraction by peripheral tissues, we compared the critical O2 delivery and extraction ratio in 30 anesthetized and paralyzed dogs in four groups. One group (n = 7) received oleic acid to produce an acute lung injury (FlO2 = 1.0) and a second group (n = 7) was maintained with PEEP (FlO2 = 1.0) after receiving oleic acid. A third group (n = 8) received no oleic acid (FlO2 = 1.0), and a fourth group received no oleic acid and was ventilated with room air. The critical O2 delivery was determined in each animal as QO2 was lowered in a stepwise manner by controlled blood removal. Neither the critical QO2 nor critical O2 extraction ratios were different (P > .05) among oleic acid, PEEP-treated, or hyperoxic control animals. Similarly, the critical QO2 determined from the point at which arterial lactate began to increase showed no difference among groups. Thus, neither acute lung injury produced with oleic acid nor its treatment with PEEP was associated with a peripheral O2 extraction defect. However, a linear regression across all groups demonstrated a positive correlation between the arterial PO2 and corresponding critical O2 delivery (r = < P < .05). These results suggest that high arterial O2 tensions may contribute to an impairment of peripheral O2 extraction.

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Systemic oxygen delivery and consumption during acute lung injury in dogs

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