Cardiac Power Output during Dobutamine Stress Test in Horses

Although echocardiography has greatly improved the diagnostic possibilities in equine medicine, determining the prognosis remains a difficult task. In humans, maximal cardiac power output (CPO) has been described as a powerful indicator of exercise capability and outcome in heart disease. The aim of the study is to describe the measurement of CPO by echocardiography and by thermodilution in healthy horses. Six healthy horses were studied. Cardiac output (CO) was measured by thermodilution and Doppler echocardiography at rest and during a pharmacologic stress test consisting of 35 μg/kg atropine followed by incremental steps 2, 4, 6, and 8 μg/kg/min of dobutamine infusion. Mean arterial pressure (MAP) was measured invasively by a catheter introduced into the transverse facial artery. CPO was calculated as the product of CO and MAP. Baseline CPO measured by thermodilution and by Doppler echocardiography was 10.7 ± 3.3 and 13.7 ± 4.5 watts, respectively. CPO increased significantly with pharmacologic stimulation and reached maximal CPO of 66.4 ± 3.6 and 60.4 ± 5.1 watts when measured by thermodilution and Doppler echocardiography, respectively. This study describes an estimation of CPO in horses. Further studies should demonstrate the usefulness of CPO as a predictive indicator in horses suffering from cardiac disease.     

Comparison of Fick and thermodilution cardiac output determinations in standing horses

The Fick and thermodilution (TD) methods are two currently popular techniques for determination of cardiac output (CO) in adult horses. To our knowledge, a comparison of these two techniques has not been reported. Six healthy, resting, fit, adult horses of either sex and weighing 516.5+/-33.2 kg (mean+/-SD) were instrumented to enable measurement of cardiac output. Resting CO was determined by the Fick method and by thermodilution while the horses stood quietly in the stocks. Fick and thermodilution CO measurements were repeated under conditions of increased cardiac output achieved with the use of a dobutamine infusion (5 microg kg(-1) min(-1), IV), and again under conditions of decreased CO induced by administration of xylazine (0.5 mg/kg, IV). Fick and thermodilution cardiac outputs were compared using Bland-Altman analysis for repeated measures. The mean of the differences+/-1.96SD (bias and precision) between the two techniques was 1.88+/-24.17 L/min. Variability between measurements with the two techniques was decreased to 3.41+/-46.78 mL kg(-1) min(-1) when CO was normalized for body size by calculation of cardiac index.     

Evaluation of Echocardiographic Parameters During Increasing Infusion Rates of Dobutamine in Isoflurane-Anesthetized Horses

The purpose of this study was to evaluate changes in echocardiographic parameters during increasing infusion rates of dobutamine in isoflurane-anesthetized horses and to compare our results with those of previous studies. Six Standardbred female healthy horses were included in this study. All animals were anesthetized and infused with dobutamine at different rates. mean arterial pressure (MAP), heart rate (HR), and some echocardiographic measurements were recorded. Statistical analysis was applied. Under basal conditions (time 0 [T0]), HR ranged between 32 and 42 beats per minute (bpm), and MAP was between 39 and 63 mm Hg. MAP increased significantly from T0 compared with values at T2, T2, and T3 in a dose-dependent manner, while HR increased significantly only at T3 if compared to the other measuring times. Left ventricular internal diameter during diastole (LVDs) decreased significantly in a dose-dependent manner, with increasing of the infusion rate of dobutamine. Interventricular septal dimension during diastole (IVSs) increased significantly, and end-systole left ventricular volumes (LVVols) decreased significantly at T2 and T3 compared to T1. Ejection fraction (%) increased significantly between T0 and T1, T2, and T3. Cardiac output increased significantly only at the higher dosage (T3 vs. others) of dobutamine, but cardiac power output was enhanced significantly at T2 versus that at T0 and T1 and at T3 versus all the previous measurements. Arrhythmias were diagnosed in 5 of 6 (83.3%). In this study, the increase of MAP was found to be dose-dependent, according with literature. The HR and MAP values registered at T0 were comparable to previous results obtained both in anesthetized and conscious horses, while at T1, T2, and T3, HR and MAP values were similar only too those reported in anesthetized horses. IVSs increased and LVDs decreased significantly with the increment of dobutamine infusion rate. These findings suggest that dobutamine, even at low infusion rates, induces an enhancement in cardiac systolic function. The dose-dependent increase of IVSs and decrease of LVDs measurements are in line with those reported for dobutamine administered in conscious horses but with lower values. The LVVols dose-dependent reduction obtained in this study is in line with that in other reports, but both LVold and LVVols values after dobutamine infusion at different dosages are lower if compared to previous studies. The low LVol values and the wide standard deviation have influenced consequently the derived indices values (stroke volume [SV], EF, cardiac output [CO]). In the present study, SV did not significantly increase during dobutamine infusion. These results disagree with those reported by others. The increment of CO might be due mainly to the enhanced HR rather than to the weak changes of SV. Cardiac power output increased significantly from the 5 mcg/kg/min dosage in a dose-dependent manner, as reported by others.