Vasopressor Therapy and the Brain: Dark Side of the Moon

Abstract

Sepsis, a leading cause of morbidity and mortality, is caused by a deregulated host response to pathogens, and subsequent life-threatening organ dysfunctions. All major systems, including the cardiovascular, respiratory, renal, hepatic, hematological, and the neurological system may be affected by sepsis. Sepsis associated neurological dysfunction is triggered by multiple factors including neuro-inflammation, excitotoxicity, and ischemia. Ischemia results from reduced cerebral blood flow, caused by extreme variations of blood pressure, occlusion of cerebral vessels, or more subtle defects of the microcirculation. International guidelines comprehensively describe the initial hemodynamic management of sepsis, revolving around the normalization of systemic hemodynamics and of arterial lactate. By contrast, the management of sepsis patients suffering from brain dysfunction is poorly detailed, the only salient point being mentioned is that sedation and analgesia should be optimized. However, sepsis and the hemodynamic consequences thereof as well as vasopressors may have severe untoward neurological consequences. The current review describes the general neurological complications, as well as the consequences of vasopressor therapy on the brain and its circulation and addresses methods for cerebral monitoring during sepsis.

Impaired cerebral autoregulation detected in early prevasospasm period is associated with unfavorable outcome after spontaneous subarachnoid hemorrhage: an observational prospective pilot study

“…Some patients in our study received administration of vasopressors at individually adjusted dosages to regulate ABP. Although, applied pharmaceutical treatment by anesthetics (mainly propofol) and vasopressors can affect both CA and BRS test results by blocking the cardiovascular reflex response [ 40 ] or affecting cerebrovascular reactivity [ 41 , 42 ], however, recent study showed that propofol did not produce a significant alteration in the average heart rate, which serves as the basis for measuring baroreflex sensitivity [ 43 ].…”

The Impact of Inotropes and Vasopressors on Cerebral Oxygenation in Patients with Traumatic Brain Injury and Subarachnoid Hemorrhage: A Narrative Review

“…The BBB is known to contain MAO [22,23], which may limit or prevent the systemic vasoconstrictive effects of noradrenaline from affecting cerebral circulation. However, emerging studies indicate that high doses of noradrenaline or damage to the BBB can be associated with cerebral vasoconstriction [127,128]. For example, during DCI in SAH patients, hypertensive therapy with norepinephrine has been shown to deteriorate the neurological status progressively with dose escalation [129].…”

Noradrenaline‐induced changes in cerebral blood flow in health, traumatic brain injury and critical illness: a systematic review with meta‐analysis

“…The review did not perform a meta-analysis, meta-regression or explore the factors modulating the noradrenaline-induced CBF changes. Our knowledge gap is echoed by a recent review that called the relationship between vasopressor therapy and the brain ``the dark side of the moon´´ [6].…”