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- Author or Editor: Natache A. Garofalo x
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Abstract
Objective—To compare hemodynamic effects in dogs anesthetized with remifentanilisoflurane and with isoflurane alone.
Animals—6 adult dogs.
Procedures—Mechanically ventilated, isoflurane-anesthetized dogs received increasing constant rate infusions (CRIs) of remifentanil (0.15, 0.30, 0.60, and 0.90 μg/kg/min) or physiologic saline (0.9% NaCl) solution (control treatment), with a 1-week washout interval between treatments. Each CRI of remifentanil or saline solution was maintained for 60 minutes with equipotent end-tidal isoflurane concentrations that corresponded to 1.3 times the minimum alveolar concentration. Hemodynamic measurements and plasma vasopressin concentrations were determined before and at the end of each CRI and 60 minutes after the end of the infusion regimen.
Results—Compared with the control treatment, remifentanil CRIs significantly decreased heart rate (HR) and cardiac index (CI) and significantly increased systemic vascular resistance index (SVRI) and plasma vasopressin concentration. Greatest differences in mean values between treatments were recorded for remifentanil at 0.60 μg/kg/min (HR and Cl were 55% and 47% lower, respectively, and SVRI was 91% higher than for the control treatment). Mean arterial pressure increased significantly during the highest remifentanil CRI (9% higher than for the control treatment). The increase in vascular resistance was positively correlated with increases in vasopressin concentrations (coefficient of determination, 0.65) during anesthesia with remifentanil-isoflurane.
Conclusions and Clinical Relevance—Anesthesia maintained with remifentanil-isoflurane may decrease tissue perfusion as a result of a decrease in Cl. However, hypotension may not develop because of systemic vasoconstriction. An increase in plasma vasopressin concentration was associated with the vasoconstriction observed in dogs anesthetized with remifentanil-isoflurane. (Am J Vet Res 2010;71:1133-1141)
Abstract
Objective—To evaluate the effects of remifentanil on isoflurane minimum alveolar concentration (ISOMAC) in dogs.
Animals—6 adult mixed-breed dogs.
Procedures—Dogs were anesthetized with isoflurane on 2 occasions. During the first set of experiments, ISOMAC was determined before remifentanil infusion (baseline), during constant rate infusion (CRI) of remifentanil (0.15, 0.30, 0.60, and 0.90 μg/kg/min), and 80 minutes after remifentanil infusion. After a 1-week washout period, dogs received a CRI of remifentanil (0.15 μg/kg/min) and ISOMAC was redetermined 2, 4, and 6 hours after commencing the infusion.
Results—Mean ± SD baseline ISOMAC was 1.24 ± 0.18%. Remifentanil infusion (0.15, 0.30, 0.60, and 0.90 μg/kg/min) decreased ISOMAC by 43 ± 10%, 59 ± 10%, 66 ± 9%, and 71 ± 9%, respectively. The ISOMAC values determined during the 0.30, 0.60, and 0.90 μg/kg/min infusion rates did not differ from each other, but these values were significantly lower, compared with the 0.15 μg/kg/min infusion rate. The ISOMAC recorded after remifentanil infusion (1.09 ± 0.18%) did not differ from baseline ISOMAC. There was no change in ISOMAC throughout the 6-hour period of a CRI of remifentanil.
Conclusions and Clinical Relevance—Remifentanil decreased ISOMAC in a dose-related fashion; the reduction in ISOMAC was stable over the course of a prolonged CRI (6 hours). A dose of 0.30 μg of remifentanil/kg/min resulted in nearly maximal isoflurane-sparing effect in dogs; a ceiling effect was observed at higher infusion rates.
Abstract
OBJECTIVE To compare changes in pulse pressure variation (PPV) and plethysmographic variability index (PVI) induced by hemorrhage followed by volume replacement (VR) in isoflurane-anesthetized dogs.
ANIMALS 7 healthy adult dogs.
PROCEDURE Each dog was anesthetized with isoflurane and mechanically ventilated. End-tidal isoflurane concentration was adjusted to maintain mean arterial pressure (MAP) at 60 to 70 mm Hg before hemorrhage. Controlled hemorrhage was initiated and continued until the MAP decreased to 40 to 50 mm Hg, then autologous blood removed during hemorrhage was retransfused during VR. Various physiologic variables including PPV and PVI were recorded immediately before (baseline) and after controlled hemorrhage and immediately after VR.
RESULTS Mean ± SD PPV and PVI were significantly increased from baseline after hemorrhage (PPV, 20 ± 6%; PVI, 18 ± 4%). After VR, the mean PPV (7 ± 3%) returned to a value similar to baseline, whereas the mean PVI (10 ± 3%) was significantly lower than that at baseline. Cardiac index (CI) and stroke index (SI) were significantly decreased from baseline after hemorrhage (CI, 2.07 ± 0.26 L/min/m2; SI, 20 ± 3 mL/beat/m2) and returned to values similar to baseline after VR (CI, 4.25 ± 0.63 L/min/m2; SI, 36 ± 6 mL/beat/m2). There was a significant positive correlation (r 2 = 0.77) between PPV and PVI after hemorrhage.
CONCLUSIONS AND CLINICAL RELEVANCE Results suggested that both PPV and PVI may be useful for identification of dogs that respond to VR with increases in SI and CI (ie, dogs in the preload-dependent limb of the Frank-Starling curve).
