Vasoplegia as
catecholamine resistent
hypotension occurs in severe hemorrhagic or
septic shock and post
cardiopulmonary bypass. The entire rational behind this phenomenon is still unclear. An
ATP-shortage in the vascular musculature, disregulation of
vasopressin release, and the activation of
ATP-dependent
potassium-channels are discussed. In the last years, attention is drawn towards the activation of
ATP-dependent
potassium-channels and the possible therapeutic inhibition by glibenclamid. However, inhibition of
potassium-channels does not normalize blood pressure under all circumstances. In particular in
septic shock other mechanisms have to be involved. Overall, the sometimes desperate clinical situation has led to a large number of case reports und uncontrolled series of retrospectively analysed cases, where
vasopressin or methylenblue were discribed as successfully reversing
catecholamine resistent
hypotension. Nevertheless, in hemorrhagic and
septic shock scientific evidence of the clinical effects and the right dose as well as placebo controlled studies comparing the agents and possible combinations of agents are desirable but hardly available yet. In the case of severe
hypotension following surgery under
cardiopulmonary bypass results of the first randomized and placebo controlled studies describe successful restoration of blood pressure and even a decrease in perioperative mortality. Concerning the side effects,
vasopressin and methylenblue, like most vasopressors, can cause gastrointestinal
ischemia, but with the small number of patients enrolled so far, further major side effects can not be ruled out. Accordingly, the identification of risk factors for the development of
vasoplegia and the prediction of the extent of the response or the rate of non-responders to these treatments are widely unknown. However, although the administration of
vasopressin and methylenblue can not be recommended as a standard treatment it provides an additional option in individual cases of life threatening
vasoplegia.