NURS 487 EXAM 2

NURS 487 EXAM 2 3 Essential Components of the cranial vault - ANSWER - brain, blood, CSF; Overall volume must remain constant; if not, increased ICP occurs Monro-Kellie hypothesis - ANSWER - theory that states that due to limited space for expansion within the skull, an increase in any one of the cranial contents—brain tissue, blood, or cerebrospinal fluid—causes the other 2 cranial conents to compensate by decreasing in volume Blood Brain Barrier - ANSWER - - Controls brain volume (mainly water found intracellularly) and contents by controlling permeability - Most drugs do not cross the BBB - Disruption results in increased brain volume - Permeable to: water, oxygen, lipid-soluble compounds, and carbon dioxide (slightly permeable to electrolytes) Cerebral Spinal Fluid - ANSWER - - Clear fluid that circulates in subarachnoid spaces and spinal cord and is reabsorbed into venous system - 8% of intracranial volume (150 mL) - Normal adult CSF pressure: 5-13 mmHg - Too much production leads to hydrocephalus (need drain) - Functions of CSF include acting as a cushion and support brain and spinal cord, maintaining stable chemical environment for CNS, and excreting toxic wastes (carbon dioxide, lactate, hydrogen ion) - Should not contain RBC or WBC and should not be cloudy - CSF usually obtained from doing a Lumbar Puncture (needle inserted b/w 3rd and 4th lumbar vertebrae, also done to measure pressure) Cerebral Perfusion: Arterial Circulation - ANSWER - - Delivers blood to the brain which contains oxygen, glucose, and substrates for energy - Arteries are thin, delicate (if HTN, increased risk for stroke or rupture bc of this) - High-pressure, high-resistance system - 2 major pairs: left and right internal carotids; left and right vertebral arteries - The laregest are the middle cerebral arteries and are the most frequent arteries involved in ischemic strokes - Circle of Willis: primary collateral pathway; protective mechanism when major cerebral vessels are occluded (if blood clot, ciricle of willis helps provide blood flow to infarcted area) Cerebral Perfusion: Venous Circulation - ANSWER - - Low pressure system - No valves so only drains by gravity (positioning very important) - Venous pressures reflects intracranial pressure (If there is an increase in CVP than there will be an increase in ICP) Cerebral Blood Flow: Autoregulation - ANSWER - - Compensatory mechanism - Cerebral arterioles alter blood flow to keep MAP within 60-130 - Keeps CBF constant to maintain adequate cerebral perfusion pressure (CPP) - Automatic constriction or dilation of cerebral blood vessels in response to changes in: systemic arterial pressure (systemic BP), blood levels of carbon dioxide, blood levels of O2 What affects cerebral blood volume? - ANSWER - - Systemic hypo-/hypertension - Body metabolic rate - Systemic acidosis/alkalosis - Cerebral vasodilation/constriction - Cardiac output Conditions resulting in decreased CBF - ANSWER - - Decrease in body metabolic rate (decrease CNS): sedation, paralysis, hypothermia, hypocapnia - Cerebral edema - Low cardiac output - Vasoconstriction - Alkalosis causes cerebral vasoconstriction to decrease CBF - Inadequate CBF can lead to cerebral hypoxia which leads to ischemia Conditions resulting in increased CBF - ANSWER - - Increased Metabolic Rate: high fever, pain, seizures, posturing - Acidosis (CO2 retention, Lactic Acidosis) causes cerebral vasodilation and increases CBF and ICP - Want to avoid this in pts with neurologcal injury and already increased ICP What happens with CBF when the brain does not get enough O2 and glucose? - ANSWER - Aerobic metabolism is not supported so the brain switches to anaerobic metabolism, lactate is produced and cannot cross the BBB, so it accumulates and leads to cerebral acidosis and cerebral vasodilation which upsets the state of equilibrium in cranial vault and increases CBF What if CBF is higher than metabolic needs? - ANSWER - A state of hyperemia exists, progressive vasodilation occurs, cerebral blood volume increases, and there is an eventual loss of autoregulation which leads to increased ICP and cerebral ischemia