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Nitrous oxide reduces inspired oxygen fraction but does not compromise circulation and oxygenation during hemodilution in pigs
Author(s) -
SCHOU H.,
SÁ V. PEREZ DE,
ROSCHER R.,
LARSSON A.
Publication year - 1997
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1997.tb04810.x
Subject(s) - medicine , anesthesia , hematocrit , nitrous oxide , oxygenation , cardiac output , hemodynamics , oxygen , vascular resistance , chemistry , organic chemistry
Background: The use of nitrous oxide (N 2 O) during hemodilution has been questioned. Nitrous oxide reduces the inspired oxygen fraction (F 1 O 2 ), depresses myocardial function and may reduce cardiac output (CO) and systemic oxygen delivery (DO 2SY ). The aim of this study was to evaluate the importance of the effects of nitrous oxide on systemic and myocardial circulation and oxygenation during extreme, acute, normovolemic hemodilution. Methods: Ten midazolam‐fentanyl‐pancuronium anesthetized pigs were exposed to 65% N 2 O before and after extreme isovole‐mic hemodilution (hematocrit 33±1% and 10±1%, respectively). Systemic and myocardial hemodynamics, oxygen delivery and consumption and blood lactate were measured before (at FrO 2 1.0 and 0.35) and during N 2 O exposure. Results: Hemodilution caused an increase in CO from 137±43 to 229±32 ml kg ‐1 min ‐1 ( P < 0.01), a decrease in systemic vascular resistance (from 42±14 to 20±4 mmHg L ‐1 min ‐1 , P < 0.05), a decrease in mean arterial blood pressure (from 119±19 to 100±26 mmHg, P<0.05) and a decrease in DO 2SY from 21.1 ±6.9 to 13.7±2.1 ml kg ‐1 min ‐1 ( P < 0.01). Cardiac venous blood flow increased by 135% ( P < 0.01) and cardiac venous saturation from 25±6 to 41±5% ( P < 0.05). After hemodilution, changing F I O 2 from 1.0 to 0.35 reduced arterial blood oxygen content from 59.4±3.7 to 52.3±5.1 ml L ‐1 ( P < 0.01), mixed venous saturation (SvO 2 ) from 75±9 to 47±7% ( P < 0.05) and DO 2SY from 13.7±2.1 to 11.9+2.3 ml kg ‐1 ‐ min ‐1 ( P < 0.05). Dissolved oxygen at F 1 O 2 =1.0 and F 1 O 2 =0.35 constituted 25.4±3.1% and 10.1 ±1.5%, respectively, of systemic oxygen delivery after hemodilution, compared with 10.7±1.2% and 3.9±0.5% before hemodilution ( P < 0.01). Left ventricular oxygen delivery and consumption were unchanged. Exposure to N 2 O did not affect mean arterial blood pressure or systemic vascular resistance before or after hemodilution. After hemodilution during N 2 O‐exposure, CO and DO 2SY decreased by 9% ( P < 0.01 and P < 0.05, respectively), but no changes in SvO 2 , systemic oxygen uptake or arterial lactate were observed. The effect of N 2 O on myocardial oxygenation was similar before and after hemodilution; cardiac venous blood flow, left ventricular oxygen delivery and uptake decreased, but no animals showed left ventricular lactate production. Conclusion: Nitrous oxide did not compromise systemic and myocardial circulation and oxygenation during acute normovolemic hemodilution in pigs. Possible adverse effects from the use of nitrous oxide during hemodilution seem to be related to a reduced F I O 2 , reducing the safety margin for systemic oxygen delivery.