Acepromazine exacerbated hypotension, but CO did not change in dogs anesthetized with propofol and isoflurane. Dexmedetomidine reduced CO but prevented propofol-isoflurane-induced hypotension. In general, oxygen-carrying capacity and PCV were higher in dexmedetomidine-treated than in acepromazine-treated dogs anesthetized with propofol and isoflurane.

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OBJECTIVE To investigate the relationship between invasively measured stroke volume (SV) and (1) esophageal Doppler-derived indices such as stroke distance (StrokeD), flow time corrected (FTc), stroke distance variation (SDV), and peak velocity variation (PVV); and (2) arterial load (AL) variables during evaluation of fluid responsiveness (FR) in anesthetized dogs undergoing sudden hemodynamic shifts in blood volume. ANIMALS 6 healthy male dogs. PROCEDURES Dogs were anesthetized with isoflurane, ventilated mechanically, and instrumented to undergo sequential, nonrandomized experimental stages. The dogs transitioned from normovolemia (NORMO-BL) to hypovolemia (30% blood loss; HYPO-30), followed by autologous blood transfusion, and then to hypervolemia (colloid bolus). During each stage, SV was quantified using pulmonary artery thermodilution and its relationship with StrokeD, FTc, SDV, and PVV; and AL variables such as effective arterial elastance (Ea), dynamic arterial elastance (Eadyn), and total arterial compliance (Ca) were established. RESULTS As SV decreased significantly during HYPO-30 compared to NORMO-BL, there was a significant (P < .001) decrease in StrokeD, FTc, and Ca, with simultaneous increases in SDV, PVV, Ea, and Eadyn. Upon restoration of blood volume, these values stabilized closer to NORMO-BL. A significant (P < .001) correlation was observed between SV and StrokeD, FTc, Ea, Eadyn, and Ca. CLINICAL RELEVANCE Minimally invasive StrokeD, FTc, SDV, and PVV act as SV surrogates and help assess FR during different blood volume stages in healthy dogs. During hypovolemia-induced hypotension, Ea, Eadyn, and Ca may be able to guide therapeutic decisions favoring improvement in blood pressure and SV.

OBJECTIVE To evaluate the use of a modified passive leg-raising maneuver (PLRM) to predict fluid responsiveness during experimental induction and correction of hypovolemia in isoflurane-anesthetized pigs. ANIMALS 6 healthy male Landrace pigs. PROCEDURES Pigs were anesthetized with isoflurane, positioned in dorsal recumbency, and instrumented. Following induction of a neuromuscular blockade, pigs were mechanically ventilated throughout 5 sequential experimental stages during which the blood volume was manipulated so that subjects transitioned from normovolemia (baseline) to hypovolemia (blood volume depletion, 20% and 40%), back to normovolemia, and then to hypervolemia. During each stage, hemodynamic variables were measured before and 3 minutes after a PLRM and 1 minute after the pelvic limbs were returned to their original position. The PLRM consisted of raising the pelvic limbs and caudal portion of the abdomen to a 15° angle relative to the horizontal plane. RESULTS Hemodynamic variables did not vary in response to the PLRM when pigs were normovolemic or hypervolemic. When pigs were hypovolemic, the PLRM resulted in a significant increase in cardiac output and decrease in plethysomographic variability index and pulse pressure variation. When the pelvic limbs were returned to their original position, cardiac output and pulse pressure variation rapidly returned to their pre-PLRM values, but the plethysomographic variability index did not. CONCLUSIONS AND CLINICAL RELEVANCE Results suggested a modified PLRM might be useful for identification of hemodynamically unstable animals that are likely to respond to fluid therapy. Further research is necessary to validate the described PLRM for prediction of fluid responsiveness in clinically ill animals.

Objective To describe a case of successful return of spontaneous circulation in an anesthetized dog that developed spontaneous ventricular fibrillation during CPR that was refractory to multiple defibrillation attempts by utilizing pharmacological antiarrhythmic therapy. Case summary Cardiopulmonary arrest occurred during surgical preparation in a 1‐year‐old German Shepherd Dog under general anesthesia for fluoroscopic implantation of an Amplatz canine duct occluder for treatment of a patent ductus arteriosus. Pulseless electrical activity was initially diagnosed, and resuscitative efforts were immediately initiated, including basic cardiac life support, discontinuation of anesthesia with administration of reversal agents, and low‐dose epinephrine administration (0.01 mg/kg, IV). After 10 minutes of CPR, the patient developed ventricular fibrillation and single‐dose monophasic defibrillation attempts of escalating energy were performed. Despite these efforts, return of spontaneous circulation was unable to be achieved. However, administration of magnesium sulfate (20 mg/kg, IV) along with an additional single monophasic defibrillation attempt was successful in achieving return of spontaneous circulation. New or unique information provided Under current advanced cardiac life support guidelines, the best resuscitation strategy for refractory ventricular fibrillation, in which the arrhythmia persists despite multiple defibrillation attempts, remains unclear. This is especially true for veterinary patients, where refractory ventricular fibrillation is an uncommon cardiac arrest rhythm. Although guidelines for the use of antiarrhythmic therapy during cardiac arrest are well established in human medicine, evidence‐based guidelines to support best practices in companion animals do not exist due to sparse data gathered through experimental studies. Only a few case reports describe successful return of spontaneous circulation following prolonged ventricular fibrillation in clinical veterinary patients. Although the use of magnesium sulfate as an antiarrhythmic agent during refractory ventricular fibrillation has been previously reported in people, this is the first case to our knowledge of refractory ventricular fibrillation in a dog that responded to magnesium sulfate.