Cardiac output, left ventricular ejection rate, plasma volume, and heart rate changes in equine laminitis-hypertension.
Authors: Garner, Hahn, Salem, Coffman, Hutcheson, Johnson
Journal: American journal of veterinary research
Summary
# Editorial Summary Researchers induced acute laminitis through controlled carbohydrate overloading in eight horses, then tracked cardiovascular haemodynamics alongside clinical lameness progression (Obel grading) to understand the pathophysiology underlying this catastrophic condition. Within 16 hours of reaching Obel grade 3 lameness, cardiac output and left ventricular ejection rate had doubled (P<0.01), accompanied by significant increases in heart rate and arterial pressure, whilst peripheral resistance remained essentially unchanged and plasma volume decreased only after a 24-hour delay. This dissociation between markedly elevated cardiac output and stable peripheral resistance suggests a primary increase in myocardial contractility rather than compensatory mechanisms driven by volume loss or vasoconstriction—a distinction crucial for understanding laminitis as a systemic circulatory crisis rather than simply a local digit problem. The tight temporal relationship between these cardiovascular changes and the onset of clinical lameness suggests that the hypercontractile cardiac state may be mechanistically linked to the endotoxaemic and electrolyte disturbances known to occur during grain overload laminitis. For practitioners, this work underscores that laminitis involves profound systemic haemodynamic derangement occurring early in disease progression, informing both therapeutic targets and monitoring priorities during acute cases.
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Practical Takeaways
- •Early hemodynamic compensation (increased cardiac output and contractility) occurs within hours of acute laminitis onset, before plasma volume depletion becomes clinically apparent
- •Monitoring heart rate and blood pressure changes in the first 24 hours after suspected carbohydrate overload or early lameness signs may help identify horses developing acute laminitis before severe clinical signs manifest
- •The delayed plasma volume decrease suggests laminitis pathophysiology involves initial cardiovascular compensation followed by systemic decompensation, relevant to understanding critical intervention windows
Key Findings
- •Cardiac output and left ventricular ejection rate doubled within 16 hours of Obel grade 3 lameness onset
- •Heart rate and arterial pressure increased significantly (P < 0.01) with little or no change in peripheral resistance
- •Plasma volume decreased significantly 24 hours after Obel grade 3 lameness, suggesting increased myocardial contractility as a compensatory mechanism
- •Hemodynamic changes preceded and accompanied the clinical onset of acute laminitis, with time-dependent relationships to lameness severity