Nitrous Oxide Worsens Myocardial Ischemia in Isoflurane-anesthetized Dogs

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Abstract
Two equipotent anesthetic regimens, isoflurane 1.8% in 50% nitrogen/oxygen and isoflurane 1.4% in 50% nitrous oxide/oxygen, were compared to test if nitrous oxide, without changing the depth of anesthesia, can affect myocardial function, blood flow, and metabolism in an ischemic region of the heart. In 14 dogs, anesthesia was induced with sodium thiopental. Following tracheal intubation, they were ventilated with isoflurane in oxygen. The chest was opened, the LAD coronary artery cannulated, and flow to it controlled with an autoperfusion circuit. Systolic shortening in the LAD and circumflex regions was measured with a sonomicrometer via pairs of piezo-electric crystals placed in the subendocardium. Regional myocardial blood flow was measured with radioactive microspheres injected into the left atrium. Regional myocardial lactate metabolism was assessed by withdrawing blood from a catheter placed in the anterior cardiac vein. Measurements were made during the imposition of a stenosis on the perfusion circuit sufficient to decrease systolic shortening by 10-20%. The same stenosis was imposed three times in a randomized and balanced crossover design. Treatment with nitrous oxide was associated with small increases in heart rate and systolic blood pressure (5 and 8%, respectively), as well as 19% reduction in systolic shortening and a 30% fall in endo/epi blood flow ratio in the hypoperfused LAD region distal to the stenosis. Lactate extraction was low or negative during both anesthetics, but differences were not statistically significant. The data indicate that the substitution of 505 nitrous oxide for 0.4% isoflurane caused a reduction in mechanical function and a further maldistribution of blood flow in ischemic myocardium. The mechanism of this deleterious effect must be discovered in order to determine if it is safe to use nitrous oxide with isoflurane to anesthetize patients with ischemic heart disease.