Alterations of Important Regulators of Macro- and Microcirculation in the Critically III

Abstract

Profound (peripheral) circulatory defect is the predominant cause of progressive organ failure, and ultimately, death in the critically ill [1]. Regulation of sufficient nutritive tissue blood flow is likely to be due to a balance between systemic and local regulators of blood flow. Maintenance of adequate circulation and fluid homeostasis is controlled through complex mechanisms, which include antidiuretic hormone (ADH), the renin-aldosterone-angiotensin system, and the autonomic nervous system. The principal actions of these systems are to restore water or intravascular volume deficit and to guarantee sufficient organ perfusion. Altered activity of these regulating systems is known to occur in stress situations, e.g., trauma, surgery, and critical illness (Table 1) [2,3]. Several studies have shown a high incidence of postoperative complications in surgical patients as well as increased morbidity and mortality in intensive care patients with abnormal hormonal responses [5,6]. Loss of (microregional) vascular control will result in some capillary regions being overperfused while others will be underperfused relative to oxygen needs [6]. In recent years, vasoactive substances released by the heart (atrial natriuretic peptide [ANP]) and produced by the endothelium (e.g. nitric oxide [NO], endothelin) have offered a new dimension when looking at regulators of the circulation [8, 9, 10]. It has been shown that endothelial-derived vasoactive factors are intimately involved in the pathophysiology of circulatory abnormalities and inadequate tissue perfusion [11].