Assessment of Critical Thresholds for Cerebral Perfusion
Assessment of Critical Thresholds for Cerebral Perfusion
An intractable increase in intracranial pressure (ICP) leading to a progressive decrease in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) is the dominating cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF) and significantly contributes to death. In addition, the injured brain is sensitive to raised CPP due to an increased permeability of the blood–brain barrier (BBB) to crystalloids and an impaired pressure autoregulation of the CBF. Given these circumstances, an increase in CPP will cause a net transport of water across the BBB and a further elevation in ICP. Accordingly, the assessment of the lower critical threshold for CPP is important for neurological intensive care. This level varies among different patients and different areas of the brain. In fact, the penumbral zones surrounding focal brain lesions appear to be the most sensitive. In the individual patient, preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.
An intractable increase in ICP leading to a progressive decrease in CPP and CBF is the dominant cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF), and hemorrhagic shock is a common complicating factor that significantly contributes to death. In addition, hypotensive episodes unrelated to hemorrhagic hypovolemia have been reported to be relatively frequent and associated with an unfavorable patient outcome. Furthermore, CBF is often variable in severe brain trauma, and regional CBF is frequently very low in pericontusional areas. Based on these experiences, it might seem logical both to restore circulating blood volume and to use vasopressors liberally to achieve a further increase in CPP. This idea has gained additional support from the (previously) generally accepted hypothesis that a pharmacologically induced increase in MABP effectively decreases ICP. In one study, Rosner, et al., asserted that the minimal level of CPP should be greater than 70 mm Hg and that certain patients might require a level of 100 mm Hg or more. Nonetheless, if the traumatized brain always benefits from increasing the CPP, what then is the point of assessing a minimal acceptable level? Perhaps an increased blood pressure is harmful to the injured brain, which implies that many patients might benefit from a pharmacological reduction in CPP. In an effort to respond to these issues, I will first briefly review the regulation of brain volume under physiological and pathophysiological conditions.
An intractable increase in intracranial pressure (ICP) leading to a progressive decrease in cerebral perfusion pressure (CPP) and cerebral blood flow (CBF) is the dominating cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF) and significantly contributes to death. In addition, the injured brain is sensitive to raised CPP due to an increased permeability of the blood–brain barrier (BBB) to crystalloids and an impaired pressure autoregulation of the CBF. Given these circumstances, an increase in CPP will cause a net transport of water across the BBB and a further elevation in ICP. Accordingly, the assessment of the lower critical threshold for CPP is important for neurological intensive care. This level varies among different patients and different areas of the brain. In fact, the penumbral zones surrounding focal brain lesions appear to be the most sensitive. In the individual patient, preservation of normal cerebral energy metabolism within areas at risk during a decrease in CPP can be guaranteed by performing intracerebral microdialysis and bedside biochemical analyses.
An intractable increase in ICP leading to a progressive decrease in CPP and CBF is the dominant cause of death in patients with severe brain trauma. Arterial hypotension may further compromise CPP (and CBF), and hemorrhagic shock is a common complicating factor that significantly contributes to death. In addition, hypotensive episodes unrelated to hemorrhagic hypovolemia have been reported to be relatively frequent and associated with an unfavorable patient outcome. Furthermore, CBF is often variable in severe brain trauma, and regional CBF is frequently very low in pericontusional areas. Based on these experiences, it might seem logical both to restore circulating blood volume and to use vasopressors liberally to achieve a further increase in CPP. This idea has gained additional support from the (previously) generally accepted hypothesis that a pharmacologically induced increase in MABP effectively decreases ICP. In one study, Rosner, et al., asserted that the minimal level of CPP should be greater than 70 mm Hg and that certain patients might require a level of 100 mm Hg or more. Nonetheless, if the traumatized brain always benefits from increasing the CPP, what then is the point of assessing a minimal acceptable level? Perhaps an increased blood pressure is harmful to the injured brain, which implies that many patients might benefit from a pharmacological reduction in CPP. In an effort to respond to these issues, I will first briefly review the regulation of brain volume under physiological and pathophysiological conditions.
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