Abstract
The aim of this study was to evaluate the hemodynamic and acid-base status of dogs subjected to acute normovolemic anemia. The dogs (n = 10) were evaluated 15 minutes and 24 hours after induction of anemia (hematocrit below 18%) with blood withdrawal and simultaneously replacement of same volume of Ringer's lactate solution and hydroxyethyl starch-based solution in a 2 : 1 ratio. The cardiac output was measured by Doppler echocardiography and blood pressure by oscillometric device, and posteriorly hemodynamic parameters were calculated. The anemic groups had increase in cardiac index (P < .05) (3.82 ± 1.05 to 5.86 ± 1.49 and 5.81 ± 1.63 L/min × m2) and decreases (P < .05) in the indices of total peripheral resistance (6797.81 ± 3060.22 to 3220.14 ± 1275.02 and 3887.74 ± 1394.89 dina·seg/cm5 × m2) and oxygen delivery (7942.84 ± 3344.00 to 4021.68 ± 1627.00 and 4430.82 ± 1402.61 mL/min × m2), respectively. There were no significant changes in pH, but PaO2 and SaO2 values were increased, and PaCO2 reduced in anemic dogs (P < .05). Therefore, acute normovolemic anemia can create significant hemodynamic changes and despite some hemogasometric changes, there were no changes in the acid-base status in dogs.
Highlights
Acute normovolemic anemia results from the withdrawal of blood and simultaneous replacement with an appropriate volume of colloid and crystalloid fluids to maintain normovolemia [1]
The cardiac output obtained by Doppler echocardiography was divided by body surface area to obtain the cardiac index
No animal showed signs of congestive heart failure or collapse, similar to the findings reported in an experimental model of acute normovolemic anemia [4]
Summary
Acute normovolemic anemia results from the withdrawal of blood and simultaneous replacement with an appropriate volume of colloid and crystalloid fluids to maintain normovolemia [1] This procedure has been used as a model of anemia in dogs [2,3,4,5]. Critical hemoglobin values occur when oxygen delivery (DO2) decreases below a critical level and the compensatory mechanisms become insufficient, resulting in decreased oxygen consumption (VO2) and increased lactate levels [1] In this setting, in addition to hemodynamic changes, there may be acid-base disturbances related to hemoglobin reduction, since hemoglobin accounts for more than 80% of the nonbicarbonate buffering capacity of whole blood [9]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
