Evaluation of Hemodynamic Autonomic Control in an Animal Model of Acute Heart Failure Induced by High Dose of Halothane

Abstract

Acute animal models of cardiac failure are necessary to study new therapeutic options and should be thoroughly characterized from the hemodynamic point of view, including the response of the autonomic nervous system. Thus, the aim of this work was to characterize the pathophysiological adaptation of the autonomic nervous system to acute cardiac failure induced by high doses of halothane (4%). In six sheep, electrocardiogram, aortic pressure and flow were obtained and calculation of systemic vascular resistances was done. Variability analyses in the time and frequency domains were also performed. In the time domain, after heart failure induction using halothane 4%, a significant decrease of both aortic blood flow variability (from 0. 13 ± 0. 05 to 0. 09 ± 0. 02 L min -1, p < 0. 05) and the broad band spectra (from 1. 80 ± 0. 66 to 1. 25 ± 0. 57 L 2 min -2, p < 0. 005) was observed. Both mean RR (472 ± 44 to 567 ± 68 ms, p < 0. 01), and low frequency band of RR intervals (from 6. 2 ± 0. 9 to 7. 7 ± 1. 5 ms 2, p < 0. 05), showed a significant increase, and no change in systemic vascular resistance (from 54. 9 ± 29. 5 to 50. 3 ± 38. 4 mmHg min L -1), all of them after heart failure induction. We conclude that in this model of heart failure the autonomic nervous system activity is still functioning, the combination of increased mean and RR low frequency band, with no change in systemic vascular resistance suggest an increase in the sympathetic control (due to maintained SVR), in an attempt to compensate the depression in the cardiac activity and hemodynamic alterations after severe myocardial depression induced by halothane.