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/m(2); SI, 20 ± 3 mL/beat/m(2)) and returned to values similar to baseline after VR (CI, 4.25 ± 0.63 L/min/m(2); SI, 36 ± 6 mL/beat/m(2)). 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).
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/m(2); SI, 20 ± 3 mL/beat/m(2)) and returned to values similar to baseline after VR (CI, 4.25 ± 0.63 L/min/m(2); SI, 36 ± 6 mL/beat/m(2)). 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).