Catecholamines and Vasopressin During Critical Illness

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Clinical pharmacology of catecholamines

The traditional subdivision of catecholamines into inotropes (ie, mainly acting on β receptors) and vasopressors (ie, mainly acting on α receptors) may be misleading because, to a substantial degree, most of them act on both receptor types. Exceptions are dopexamine and isoproterenol as pure β-adrenergic agonists and phenylephrine, which is the only pure α agonist.

Dobutamine has a weak affinity for α and β2 receptors and a stronger affinity for β1-adrenergic receptors. The rationale of using

Catecholamines and regional perfusion

The net effect of vasoactive drugs on peripheral organ perfusion, especially on the perfusion of the kidney and splanchnic organs, is strongly dependent on many variables, but a general consensus is established around the fact that adequate fluid resuscitation is a prerequisite for any successful vasoactive therapy [4], [5]. The specific impact of catecholamines and other vasoactive drugs on the perfusion of these organs is still not fully understood, mainly because observations in healthy

Metabolic effects of catecholamines

A re-established perfusion and oxygen delivery do not necessarily imply a functional recovery of the different tissues after a shock state. In fact, the metabolic changes induced by the underlying disease and by the therapeutic actions may potentially influence the outcome. During septic shock, a hypermetabolic condition associated with insulin resistance, hyperlactatemia, and increased oxygen demand may occur simultaneously with mitochondrial dysfunction and decreased organ perfusion [57], [58]

Catecholamines and immune modulation

An increasing body of evidence supports the role of adrenergic agents in the modulation of immune and inflammatory responses in critically ill patients and experimental models. Almost all inflammatory cells express α and β adrenoreceptors on their surface [66], [67], whereas D1 and D2 receptors are known to be present on lymphocytes and natural killer cells [68]. Although α2 adrenoreceptors may also induce the production of a variety of proinflammatory cytokines [69], the immunomodulatory

Vasopressin

Vasopressin is a natural hormone produced in magnocellular neurons of the hypothalamus and released from the posterior hypophysis. Its secretion is stimulated in response to increases in plasma osmolality and decreases in systemic blood pressure. Under physiologic conditions, vasopressin release is regulated only by changes in osmolality [84], whereas small reductions in arterial pressure have little or no effects. A significant loss in circulating fluid can increase vasopressin levels several

Effects of vasopressin on systemic hemodynamics during septic shock

According to almost all studies published on this topic, vasopressin [90], [94], [99], [100], [101], [102], [103], [104], [105], [106], [107] and its analogue terlipressin [108], [109], [110], [111] have been shown to be as efficient as norepinephrine for maintaining mean arterial pressure in septic shock. Simultaneously, cardiac output is decreased under vasopressin [99], [100], [101], [102], [104], [105], [106], [107]. A decreased cardiac output is also observed under terlipressin [108], [109]

Effects of vasopressin on regional hemodynamics during septic shock

The main rationale for using vasopressin and terlipressin to treat gastrointestinal bleeding is its supposed capacity to induce an intense and selective vasoconstriction in the splanchnic area. Obviously, such an effect may be deleterious in septic shock and has been addressed by different investigations. No definitive conclusions can be drawn with respect to the supposed vascular overconstriction and detrimental effects of vasopressin on splanchnic perfusion during septic shock. Among these

Summary

Catecholamines remain fundamental in the treatment of circulatory failure; however, clinicians must focus their attention not only on the hemodynamic effects but also on using a more rationale approach considering the metabolic, endocrinologic, and immunologic consequences of catecholamine administration. Looking at alternative strategies to catecholamines in the treatment of shock, evidence of their beneficial effects on hemodynamic endpoints of vasopressin during septic shock is accumulating.

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