Controle autonômico e hemodinâmico em pacientes com cirrose hepática: efeitos do exercício físico submáximo

Abstract

The present thesis was written based on the results from two original articles aiming to elucidate the autonomic and hemodynamic control in patients with hepatic cirrhosis and the effects of submaximal exercise on these variables. For the first study, we have identified extensive literature reporting that patients with cirrhosis present impaired baroreflex control of the heart rate. Furthermore, we also have found studies stating that patients with cirrhosis that presented decompensation triggered by portal hypertension exhibit poorer gain of this reflex mechanism in comparison with those with no decompensation. However, so far, no study have compared baroreflex latency between patients with cirrhosis with and without ascites. Then, we selected 10 patients with ascites and 11 without it, from both sexes. We estimated the gain and the latency of baroreflex control of heart rate. In this study, we observed that the gain of the aforementioned reflex are diminished in patients with ascites for both rising and falling blood pressures. Furthermore, we also shown that the latency is increased in patients with ascites. Thus, we concluded that patients with cirrhosis and ascites present a reduction in the gain and an augmentation in the latency of the baroreflex control of heart rate. In the second study, we have found few studies that addressed postexercise hypotension and the mechanisms underlying such effect in patients with cirrhosis. Only two articles reported results from this field of investigation. However, it was not delineated to investigate postexercise recovery specifically. Therewith, we investigated postexercise hypotension and autonomic and hemodynamic mechanisms related to this phenomenon in patients with hepatic cirrhosis. For this purpose, we selected 13 patients with cirrhosis (12 Child A and 1 Child B), from both sexes. They were submitted to two interventions: exercise and control. In the exercise day, we observed a small reduction in systolic arterial pressure after 30 minutes recovering from the exercise bout, but not after 60 minutes. This effect was due to systolic volume reduction as total peripheral vascular resistance was unaltered following exercise. On the other hand, in the control day, arterial pressure increased following intervention due to an augmentation in the total peripheral vascular resistance since stroke volume was reduced during this period. Furthermore, we observed an increase in the reactive hyperemia following aerobic exercise only. However, forearm blood low and forearm vascular resistance were unaltered during the recovery period. Similarly, it was observed no alteration in the cardiac autonomic modulation following both exercise and control interventions. In contrast, baroreflex control of the heart rate present some alterations during the recovery period. In the exercise day, it was observed reduction in the gain of the aforementioned reflex. This effect occurred for rising blood pressures mainly. In contrast, it was observed an increase in the gain of the arterial baroreflex following control intervention. Such effect occurred for downward changes of the arterial pressure mainly. On the other hand, the effectiveness of the arterial baroreflex function enhanced during postexercise recovery and remained unaltered post control intervention. In conclusion, patients with hepatic cirrhosis exhibit, during postexercise recovery, small reduction in the systolic arterial pressure due to stroke volume reduction; increase in the reactive hyperemia; forearm blood flow, forearm vascular resistance and heart rate variability unaltered; reduction in the gain of arterial baroreflex until 30 minutes postexercise, which was re-established at 60 minutes; and improvement of the effectivity of the arterial baroreflex.