Alterações fisiológicas, cardiovasculares, neuroendócrinas e suas correlações com as variações da pressão arterial, durante a hemodiálise, em pacientes com insuficiência renal crônica

• Ano de defesa: 2010
• Autor(a) principal: Gutiérrez Adriánzen, Oswaldo Augusto
• Tipo de documento: Tese
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Hipertensão; Fenômenos Fisiológicos Cardiovasculares; Sistema Nervoso Autônomo
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/3741

The pathophysiologic mechanisms of arterial hypertension (AH) during hemodialysis (HD) in patients with end-stage renal disease (ESRD) are still poor understood. In its pathogeny, multifactorial, we can emphasize: hypervolemia, increase in the activity of renin-angiotensin-aldosterone system, increase in the activity of sympatic nervous system (SNS), endothelial dysfunction. Objective. To investigate physiologic, cardiovascular and neuroendocrine abnormalities in patients with ESRD and its correlations with changes in blood pressure (BP) during HD session. Methods and Cases. Observational study, in patients with ESRD in chronic hemodialysis treatment (CH), in the period from March to July 2008. It were excluded 21 patients, selected through blood pressure monitoring, during HD session: patients who presented increase in BP were included in group A (study) and patients who presented decrease in BP during HD session in group B (control). Five echocardiograms were performed during each individual HD session, with 1 hour intervals, to evaluate cardiac output (CO) and systemic vascular resistance (SVR). The activity of SNS was evaluated through spectral analysis of cardiac frequency variability (CFV). Before and after HD session brain natriuretic peptide (BNP), catecholamines, endothelin-1 (ET-1), nitric oxide (NO), electrolytes, hematocrit (Ht), albumin (Alb) and nitrogenous substances were dosed. Data were stored through the program SPSS. Results. The mean age of the patients was 43±4.9 years, and 45.4% were male. SVR significantly increased in patients from group A, when compared with patients from group B (p <0.001). The variability of cardiac frequency (VCF) in frequency domain, through low frequency/high frequency ratio (LF/HF), revealed that SNS activity, in patients from group A, was not higher than in patients from group B. (Group:p=0.445);Time:p=0.348); Group.Time:p=0.486. The mean value of ET-1, pre HD, was 10.8±0.74 pg/mL in patients from group A and 11.1±0.46 pg/mL in group B (p=0.788). The mean value of ET-1 post HD, was 25.9± 0.89 pg/mL in patients from group A and 13.3±0.54 pg/mL, in group B. (p=<0.001). The mean value of NO (nitrate+nitrite), pre HD, was 84.63±5.42 µM in patients from group A and 86.3±6.01 µM in group B (p=0.621). The mean value of NO (nitrate+nitrite) post HD, was 90.3±8.82 µM in group A and 79.9±4.39 µM in group B (p=0.692). The mean value of BNP, pre HD, was 1643±851 pg/mL in patients from group A and 1720±583 pg/mL, in group B (p=0.231). The mean value of BNP, post HD, was 1574±815 pg/mL in group A and 1382±495 pg/mL in group B (p=0.573). The mean value of adrenalin, pre HD was 208.4±63.86 pg/mL in patients from goup A and 153±69.28 pg/ml in group B (p=0.622). The mean value of adrenalin, post HD, was 80.4±11.60 pg/mL in group A and 212.1±94,91 pg/mL in group B (p=0.084). The mean value of noradrenalin, pre HD, was 337±76.79 pg/mL in patients from group A and 487.8±153.26 pg/mL in group B (p=0.672). The mean value of noradrenalin, post HD, was 194±32.68 pg/mL in patients from group A and 318.5±84.35 pg/mL in group B (p=0.481). The mean value of dopamin, pre HD, was 75.5±5.17 pg/mL in patients from group A, and 71.2±6.67 pg/mL in group B (p=0.549). The mean value of dopamin, post HD, was 74.1±8.32 pg/mL in group A and 79.5±9.41 pg/mL in group B (p=0.672). Conclusion. Patients with ESRD presented different hemodynamic patterns during HD session, with significantly increase in blood pressure in patients from group A, due to elevation in SVR secondary to endothelial dysfunction, evidenced by a significantly increase in serum levels of ET-1.