Hemorrhagic Shock: Pathophysiological Aspects and Hemodynamic Management

Abstract

Hemorrhagic shock is characterized by a decrease in circulating blood volume that leads to a decrease in the venous return. Three stages occur during the hemorrhagic shock including an initial central sympathetic activation due to acute hypovolemia aiming to redistribute blood to vital organs, followed by a central sympathetic inhibition that occurs beyond 50% blood loss characterized by bradycardia called “paradoxical” aiming to optimize the passive ventricular filling and finally a reperfusion phase. In sacrificed areas (splanchnic, muscular and kidney vasculature beds), impaired microcirculation leads to systemic inflammatory response that is responsible for an inappropriate vasoplegia. The alteration of microcirculation also promotes coagulopathy. Recent studies show frequent adrenal insufficiency associated with increased need for vasopressors. As long as the bleeding is uncontrolled, the physician should maintain oxygen delivery to limit tissue hypoxia, inflammation and organs dysfunction. This strategy is called “damage control resuscitation”. It combines “permissive hypotension” and low-volume resuscitation. Our main objectives are to prevent overfilling and secondary haemodilution and too early use of vasopressors. Hemodynamic goals (excluding severe head injury) are to avoid exceeding a systolic blood pressure of 90 mmHg and a mean arterial pressure of 60 mmHg until hemostasis is achieved. Fluid resuscitation should favor crystalloids with an increasing role for balanced solutes. Norepinephrine is now recommended and management of catecholamine and fluid resuscitation should be associated with cardiac output monitoring.