Management of Refractory Vasodilatory Shock

Refractory shock is a lethal manifestation of cardiovascular failure defined by an inadequate hemodynamic response to high doses of vasopressor medications. Approximately 7% of critically ill patients will develop refractory shock, with short-term mortality exceeding 50%. Refractory vasodilatory shock develops from uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms. Standard approaches to the initial management of shock include fluid resuscitation and initiation of norepinephrine. When these measures are inadequate to restore BP, vasopressin or epinephrine can be added. Few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to this standard approach. Adjunctive therapies, such as hydrocortisone, thiamine, and ascorbic acid, may increase BP in severe shock and should be considered when combination vasopressor therapy is needed. Novel vasopressor agents, such as synthetic human angiotensin II, can increase BP and reduce the need for high doses of catecholamine vasopressors in severe or refractory vasodilatory shock. Few effective rescue therapies exist for established refractory shock, which emphasizes the importance of aggressive intervention before refractory shock develops, including the earlier initiation of rational combination vasopressor therapy. The present review discusses the diagnosis and management of refractory shock to offer guidance for management of this important clinical problem and to provide a framework for future research. Refractory shock is a lethal manifestation of cardiovascular failure defined by an inadequate hemodynamic response to high doses of vasopressor medications. Approximately 7% of critically ill patients will develop refractory shock, with short-term mortality exceeding 50%. Refractory vasodilatory shock develops from uncontrolled vasodilation and vascular hyporesponsiveness to endogenous vasoconstrictors, causing failure of physiologic vasoregulatory mechanisms. Standard approaches to the initial management of shock include fluid resuscitation and initiation of norepinephrine. When these measures are inadequate to restore BP, vasopressin or epinephrine can be added. Few randomized studies exist to guide clinical management and hemodynamic stabilization in patients who do not respond to this standard approach. Adjunctive therapies, such as hydrocortisone, thiamine, and ascorbic acid, may increase BP in severe shock and should be considered when combination vasopressor therapy is needed. Novel vasopressor agents, such as synthetic human angiotensin II, can increase BP and reduce the need for high doses of catecholamine vasopressors in severe or refractory vasodilatory shock. Few effective rescue therapies exist for established refractory shock, which emphasizes the importance of aggressive intervention before refractory shock develops, including the earlier initiation of rational combination vasopressor therapy. The present review discusses the diagnosis and management of refractory shock to offer guidance for management of this important clinical problem and to provide a framework for future research. Serum Calcium Values and Refractory Vasodilatory ShockCHESTVol. 155Issue 1PreviewWe read with interest the recent review in CHEST (August 2018) by Jentzer et al1 on the management of refractory vasodilatory shock. We were also delighted to find reference to the possible etiologic role of hypocalcemia. However, it is only partially clear from the text how reduced calcium levels could determine vasodilatory shock. Indeed, as pointed out by the authors, the finding of reduced serum calcium values should be viewed as an epiphenomenon, casting doubts on its role as a pathogenetic mechanism. Full-Text PDF ResponseCHESTVol. 155Issue 1PreviewWe appreciate the insightful comments and considerations elucidated by Minisola and colleagues in their letter regarding our recent review article on refractory shock.1 The issue of optimal treatment of ionized hypocalcemia in patients with vasodilatory shock or myocardial dysfunction remains a complex and controversial one with a dearth of high-quality evidence. Reportedly, low serum levels of ionized calcium have been associated repeatedly with hypotension and adverse outcomes among critically ill patients, although a cause-and-effect relationship or specific benefit of calcium repletion has not been shown. Full-Text PDF