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Summary

Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 ± 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration. Results of this study indicated that induction of anesthesia with halothane and maintenance at an end-tidal halothane concentration of 1.13% induced significant changes in blood pressure, with minimal effects on cardiac output and pulmonary function, when administered to hypovolemic dogs.

Free access
in American Journal of Veterinary Research

Summary

Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered iv to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.

Free access
in American Journal of Veterinary Research

Summary

We investigated changes in hemostatic function after infusion of 6% dextran 70 (high molecular weight dextran) at 2 rates. Six healthy dogs underwent 3 regimens: 20 ml of dextran/kg of body weight administered in 1 hour (trial A), 20 ml of dextran/kg administered in 30 minutes (trial B) and 0.9% sodium chloride solution as a control administered over 1 hour to achieve hemodilution equivalent to that for 20 ml of dextran/kg (trial C). Before and at 2, 4, 8, and 24 hours after the start of trials A and B, we measured pcv, total solids (ts) concentration, amount of von Willebrand factor antigen (vWf:Ag), factor VIII coagulant activity (VIII:C), prothrombin time, activated partial thromboplastin time (aptt), platelet retention in a glass bead column, and buccal mucosa bleeding time (bmbt). Values were not obtained at 8 and 24 hours for trial C. Saline-induced changes in hemostasis were significant (P < 0.05) from baseline throughout the sample collection period. Significant differences (P < 0.05) between trial A and control were observed for vWf:Ag, VIII:C, bmbt, aptt, ts, and pcv values at 2 hours, and for VIII:C at 4 hours. Significant differences (P < 0.05) between trial B and control were observed for aptt, ts, and pcv values at 2 hours, and for vWf:Ag, VIII:C, bmbt, aptt, ts, and pcv values at 4 hours. During trials A and B, mean values of analytes infrequently deviated from reference intervals, and clinical signs of bleeding were not observed in any dog. Data for the dextran infusions paralleled each other and had a tendency to normalize, infrequently reaching baseline by 24 hours. Differences in overall hemostatic function were not detected between dextran infusions. Dextran 70 at a dosage of 20 ml/kg induces minimal hemostatic abnormalities when infused over 30 or 60 minutes to clinically normal dogs, but may precipitate bleeding in dogs with marginal hemostatic function.

Free access
in American Journal of Veterinary Research

SUMMARY

The cardiopulmonary effects of thiopental sodium were studied in hypovolemic dogs from completion of until 1 hour after administration of the drug. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 8 mg of thiopental/kg of body weight was administered iv to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to thiopental administration, heart rate and oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after thiopental administration, heart rate, mean arterial pressure, mean pulmonary arterial pressure, pulmonary vascular resistance, and mixed venous oxygen tension increased, whereas oxygen utilization ratio and arterial and mixed venous pH decreased from values measured prior to thiopental administration. Fifteen minutes after thiopental administration, heart rate was still increased; however by 60 minutes after thiopental administration, all measurements had returned to values similar to those obtained prior to thiopental administration.

Free access
in American Journal of Veterinary Research

SUMMARY

Conventional fluid resuscitation is unsatisfactory in a small percentage of equine emergency surgical cases because the large volumes of fluids required cannot be given rapidly enough to adequately stabilize the horse. In anesthetized horses, the volume expansion and cardiopulmonary effects of a small volume of highly concentrated hypertonic saline-dextran solution were evaluated as an alternative initial fluid choice. Seven halothane-anesthetized, laterally recumbent, spontaneously ventilating, normovolemic horses were treated with a 25% NaCl-24% dextran 70 solution (hsd) at a dosage of 1.0 ml/kg of body weight, iv, infused over 10 minutes, and the effects were measured for 120 minutes after infusion. Plasma volume expansion was rapid and significant (from 36.6 ± 4.6 ml/kg to 44.9 ± 4.8 ml/kg), and remained significantly expanded for the duration of the experiment. Packed cell volume, total blood hemoglobin, and plasma protein concentrations significantly decreased, confirming rapid and sustained volume expansion with hemodilution. Cardiac index and stroke index immediately increased and remained high for the entire study (from 69.6 ± 15.3 ml/min/kg to 106.6 ± 28.4 ml/min/kg, and from 1.88 ± 0.49 ml/beat/kg to 2.50 ± 0.72 ml/beat/kg, respectively). Systemic vascular resistance significantly decreased immediately after hsd infusion and remained decreased for the duration of the study (from 1.41 ± 0.45 mm of Hg/ml/min/kg to 0.88 ± 0.22 mm of Hg/ml/min/kg). Arterial and venous blood oxygen content decreased significantly because of hemodilution, but actual oxygen transport transiently increased at the 10-minute measurement before returning toward baseline. Plasma osmolality and sodium significantly increased and remained high for the entire 120 minutes (from 293 ± 2 osm/L to 326 ± 9 mosm/L, and from 142.8 ± 3.3 mM/L to 159.0 ± 6.2 mM/L, respectively). Urine output increased in 5 of 7 horses within minutes of hsd infusion, but the mean increase was not statistically significant.

Three horses developed transiently severe, clinically apparent intravascular hemolysis and hemoglobinuria. One horse developed multiple single premature ventricular contractions during the infusion with no persistent ecg changes after infusion. The potential benefit of using hsd as a rapid volume expander in anesthetized horses was documented because infusion of 1 ml of hsd/kg rapidly increased plasma volume by approximately 8 ml/kg. Substantial side effects developed in these normovolemic horses, however, and this solution requires further investigation before it can be recommended in hemodynamically unstable horses.

Free access
in American Journal of Veterinary Research