Key result
Large fluid bolus raises cardiac output ~75% driven solely by tachycardia as stroke volume falls.
Why the study?
A fluid challenge is judged by a rise in stroke volume or cardiac output based on assumptions that they reflect the same physiological effect and circulatory benefit, which needed testing.
Does intravenous fluid loading with 0.9% saline increase stroke volume and cardiac output concordantly in conscious sheep?
Does intravenous fluid loading with 0.9% saline increase stroke volume and cardiac output concordantly in conscious sheep?
p-value: p=0.22
In conscious sheep, fluid loading increases cardiac output via tachycardia while stroke volume falls, indicating that stroke volume is not a reliable surrogate for systemic flow or oxygen delivery.
Questions SV as fluid responsiveness surrogate in conscious models; challenges consensus assumption and leaves open human translation.
Background. A fluid challenge is judged by a rise in stroke volume or cardiac output, on the twin assumptions that the two report the same physiological effect and that either reflects circulatory benefit. We tested these assumptions across a fourfold crystalloid load in conscious sheep with intact autonomic reflexes. Methods. We performed a secondary analysis of 26 intravenous infusions of 0.9% saline (25, 50 or 100 mL·kg−1 over 20 min) in 13 conscious splenectomized sheep, a within-animal crossover. Cardiac output, arterial and central venous pressures and blood hemoglobin were recorded and mean systemic filling pressure was estimated by the Parkin analogue. Results. Stroke volume and cardiac output dissociated with dose. At 100 mL·kg −1 cardiac output rose +75% carried entirely by heart rate (+143%) while stroke volume fell −25%; across the crossover cardiac output and heart rate scaled with dose, whereas stroke volume showed a non-significant monotonic decline (Friedman p = 0.22). Arterial pressure was the most defended variable, held to a ~16% ceiling by a load-scaled vasodilation (resistance −35% at the highest load). The flow gains barely raised oxygen delivery, which fell 8–14% below baseline by 180 min as hemoglobin was diluted. Filling pressure rose about threefold more than blood volume at every dose. Conclusions. In the conscious animal a fluid-induced rise in cardiac output can be carried entirely by an autonomic, Bainbridge-type tachycardia while stroke volume falls, and need not improve oxygen delivery or arterial pressure. A favorable stroke-volume reading is not a surrogate for systemic flow, and flow for oxygen delivery.
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O'Brien et al. (2026) studied conscious splenectomized sheep (n=13). 0.9% saline vs. within-animal crossover was evaluated on Stroke volume and cardiac output (p=0.22). In conscious sheep, a 100 mL/kg fluid load increased cardiac output by 75% entirely due to a 143% rise in heart rate, while stroke volume fell by 25%.
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