Hydrocortisone effects on cardiovascular variability in septic shock: A spectral analysis approach*

Septic shock still places a bur-den on the healthcare system(1). The mechanisms of cardio-vascular dysfunction in sepsis may involve excessive release of vasodila-tors such as cytokines, platelet activating factor, prostacyclin, and nitric oxide. Si-multaneously, the response of vasocon-strictor systems such as the renin-angiotensin or the sympathetic nervous systems may be inhibited (2). Assessment of the variability of cardiovascular signals provides information on the control of vascular tone and heart by the autonomic nervous system (3). Then, studies on spectral analysis of heart rate and blood pressure signals suggested that a de-creased sympathetic modulation of the cardiovascular system could precede shock in endotoxin-challenged animals (4) and in patients with severe sepsis (5). These data together with recent post mortem findings of neuronal apoptosis in the cardiovascular autonomic centers ar-gued for a role of the dysfunction of the autonomic nervous system in the onset of shock in sepsis (6). Similarly, impaired hypothalamic pituitary adrenal axis is a common complication of severe sepsis (7–9), and exogenous administration of hydrocortisone restores the cardiovascu-lar homeostasis (10, 11). However, the exact mechanisms underlying the hemo-dynamic effects of hydrocortisone remain uncertain. Glucocorticoids inhibit the in-ducible form of the nitrite oxide synthase and the cyclooxygenase II via genomic interactions (12), and likely enhance the autonomic outflow and the coupling of the alpha receptor to its agonists (13). We hypothesized that, in sepsis, the early vascular effects of hydrocortisone could result, at least partly, from an im-provement in the autonomic nervous control of cardiovascular variability