ABSTRACT
OBJECTIVE: To determine if tissue oxygen saturation (StO2) correlates with oxygen delivery (DO2) and/or cardiac output (CO) in a canine hemorrhagic shock model. ANIMALS: 8 healthy purpose-bred dogs. METHODS: Dogs were anesthetized, and hemorrhagic shock was induced by withdrawing up to 60% of total blood volume, targeting a mean arterial pressure (MAP) of 40 mm Hg. The withdrawn blood was returned to the patient in 2 equal aliquots. Data was collected at 4 time points: 10 minutes after MAP was stabilized under anesthesia (time point [TP]-1), 10 minutes after up to 60% of blood volume was removed to target a MAP of 40 mm Hg (TP2), 10 minutes after the return of 50% of shed blood (TP3), and 10 minutes after the return of the remaining 50% of shed blood (TP4). Total blood volume withdrawn, StO2, CO, heart rate, and MAP were recorded, and DO2 was calculated at each TP. RESULTS: Mean StO2 significantly decreased between TP1 (77.8% [± 9.54]) and TP2 (44.8% [± 19.5]; P < .001 vs TP1). Mean StO2 increased to 63.1% (± 9.85) at TP3, but remained significantly lower compared to TP1 (P = .002). There was no difference between mean StO2 at TP4 (82.5% [± 12.6]) versus TP1 (P = .466). StO2 has a strong, positive correlation to both CO (r = 0.80; P < .001) and DO2 (r = 0.75; P < .001). CLINICAL RELEVANCE: A decrease in StO2 may be used in conjunction with physical examination findings and diagnostic parameters to support a diagnosis of shock. The return of shed blood was correlated with increases in StO2, DO2, and CO, suggesting that StO2 may be used as a marker of adequate resuscitation.
Subject(s)
Cardiac Output , Oxygen , Resuscitation , Shock, Hemorrhagic , Animals , Dogs , Shock, Hemorrhagic/veterinary , Shock, Hemorrhagic/therapy , Shock, Hemorrhagic/metabolism , Cardiac Output/physiology , Resuscitation/veterinary , Oxygen/metabolism , Oxygen/blood , Male , Dog Diseases/metabolism , Dog Diseases/physiopathology , Female , Oxygen Saturation/physiologyABSTRACT
OBJECTIVE: To determine whether shock index (SI) positively correlates with percentage blood loss and negatively correlates with cardiac output (CO) in a canine hemorrhagic shock model and whether SI and metabolic markers may be used as end point targets for resuscitation. ANIMALS: 8 healthy Beagles. PROCEDURES: Between September and December 2021, dogs underwent general anesthesia for experimental induction of hypotensive shock, with the total volume of blood removed, CO, heart rate, systolic blood pressure, base excess, blood pH, and concentrations of hemoglobin, lactate, ionized calcium recorded, and SI calculated at 4 time points (TPs): after anesthetic induction when the dog had been stable for 10 minutes (TP1), 10 minutes after the mean arterial pressure stabilized to a target of 40 mm Hg following jugular removal of up to 60% blood volume to induce hemorrhagic shock (TP2), 10 minutes after autotransfusion of 50% of the removed blood (TP3), and 10 minutes after autotransfusion of the remaining 50% of the removed blood (TP4). RESULTS: Mean SI increased between TP1 (1.08 ± 0.35) and TP2 (1.90 ± 0.73) and did not return to the prehemorrhage values for TP3 or TP4. SI correlated positively with percentage blood loss (r = 0.583) and negatively with CO (r = -0.543). CLINICAL RELEVANCE: An increase in SI may support diagnosis of hemorrhagic shock; however, SI cannot be used as the sole end point of resuscitation. Significant differences in blood pH, base excess, and lactate concentration suggested they may be useful markers of hemorrhagic shock and need for blood transfusion.