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UT Arlington NURS 5315 - Patho-Study Guide 3

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Pathophysiology N5315 Study Guide for Test #3Cerebral; Dynamics1. What percent of ATP depletion leads to changes in neurologic cortical signs: speech, behavior, and memory. P. 1 - When ATP levels fall to around 55% of normali, we see difficulty with conduction. 2. At what temperature will brain cell death occur because of ATP depletion? P. 3This is not to say death can’toccur at lower temperatures but at 106 or higher it is deadly. -Hyperthermia results in a 10% increase in metabolic demand for every one degree elevation centigradein temperature over normal. At a temperature of 106 F, the brain rapidly advances to vegetation andbrain death due to rapid atp depletion3. In terms of a time frame, when does seizure activity become a medical emergency?. P. 2& 3- Seizure acitiy that is ongoing more than 20 to 30 minutes is a medical emergency due to rapid atp depletion4. Review the changes in blood flow during seizure activity (increased or decreased). P.2 & 4- The patient who can will attempt to increase cerebral blood flow as much as 250% to 300% in an attempt to meet the metabolic demands of seizure activity5. What is the primary energy source for brain function? P.1- The primary source of energy for the brain is glucose,which is converted to adenosine triphosphate (ATP). 6. Review cerebral blood flow. P. 5What effect would an increase or decrease in blood pressure have on the diameter of cerebral arteries? See page 6, pressure regulation.- The supply of glucose and oxygen, and therefore atp, is maintained by cerebral blood flow. Normally, the brain receives 750 ml of blood per minutes or 15% to 20% of the total resting cardiac output.- A decrease in blood pressure results in vasodilation protecting the brain from subflow states and subsequent infarction- When systemic arterial pressure or intracranial pressure increase, the arterioles vasoconstrict to safeguard the brain from a hyperemic flow state.7. Review the metabolic factors and pressure changes that affect the brain’s ability to auto-regulate (see Autoregulatory Failure). P. 7- Increased levels of PaCO2, carbon dioxide acts as a potent dilatory agent as the brain attempts to removethe products of cellular breakdown as efficiently as possible. In the rang of PaCO2 from 20 mm Hg to 80 mm Hg, CBF is halved if PaCO2 is halved, and doubled if PaCO2 is doubled- Decreased levels of PaO2, a PaO2 below 60 or an O2 saturation below 90 results in hyperemic flow state.- Head injuries, 90% of all moderately to severely head injured patients have ischemic brain tissure on post-mortem exam. Within ischemic tissue is contained massive quantities of waste the majority of which are vasodilatory agents. - Intracranial bleeds, Intracranial bleeds like subarachnoid hemorrhages can result in a loss of autoregulation. Blood contains many substances like calcium and free iron which are tolerated poorly in the ventricular system and the subarachnoid space of the brain.- when autoregulation is lost after SAH=stroke18. Know how to calculate MAP.p. 8 I typically use MAP = SBP – DBP/3 + DBP. In other words, subtract the DBP (diastolic blood pressure) from the SBP (systolic BP) and divide that number by 3. Then add to that number the DBP and that equals the MAP. For example, for a BP of 120/70, the difference would be 50 and 50/3 = 16.7. Then 16.7 + 70 = 86.7 for MAP. -MAP = SBP-DBP/3+ DBP- In normally normotensive patients a map <50 mm hg results in poorly perfused cerebral tissue with ischemic changes- In these same patient a MAP> 170 mm Hg causes a loss in the ability of the arterioles to constrict, whichcauses hyperemia and increased ICP9. Know that CPP = MAP – ICP. - The normal range for CPP is 50-150 mm Hg with an average of 80-100 mm Hg.- CPP of less than 50 result in ischemia and values of greater than 150 result in hyperemia- CPP < 50 mm Hg= ischemia- CPP >150 mm Hg-hyperemia- CPP < 30 is incompatible with life and results in neuronal hypoxia and cell death- When the MAP equals the ICP, the CPP is 0 and all CBF stops.10. What would classify an ischemic stroke as being embolic, thrombotic or sub-flow? P. 2-3 -Ischemic stroke is classified as embolic or thrombotic. Thrombotic strokes are more common than embolic strokes and occur in both small and large arteries. They result from an obstruction of blood flow in an artery due to a pathological process within that artery-Embolic strokes are caused when blood clots or atheromatous debris form outside the brain and becomelodged in the cerebral circulation. Emboli commonly originate in the heart or in the proximal arteries that supply the brain, the internal carotid or vertebral systems. -Hemorrhagic stroke accounts for the remaining twenty percent of strokes and occurs when a blood vessel supplying the brain ruptures. - When would t-PA be contraindicated in a patient with an ischemic stroke? See page 61. With reference to time frame, note the time frame has been extended from a maximum of 3 hours to 4.5 hours from onset of symptoms to latest time to receive tPA. recently revised to >4.5 for subset of patientsContraindicated when:- Symptoms minor or rapidly improving- Seizure at onset of stroke- Another stroke or previous head trauma within the past 3 months- Major surgery within 14 days- Known history of intracranial hemorrhage- Sustained systolic blood pressure > 185 mm Hg- Sustained diastolic blood pressure > 110 mm Hg- Aggressive treatment required to lower blood pressure- Symptoms suggestive of SAH- Gastrointestinal or urinary hemorrhage within 21 days- Arterial puncture at noncompressible site within 7 days- Received heparin within 48 hours and has elevated PTT- PT>15 sec or International Normalized Ratio (INR) >1.7- Platelet count <100,000 uL2- Serum glucose <50 or >400 mg/dl11. What is the usual cause of a subarachnoid hemorrhage? See page 6. How would a patient typically describe the headache associated with subarachnoid hemorrhage? - The usual cause is a rupture of a cerebral aneurysm. When an aneurysm ruptures blood enters the subarachnoid space encircling the brain. The result can be an increase in intracranial pressure. Furthermore, the blood can act as an irritant to the brain generating vasospasm.- Headache is many times the defining feature of SAH, occurring 85% of affected patients. Headache is usually characterized by the patient as sudden, intense, of no distinctive location or quality, and differentthan previous headaches. SAH should always be suspected if the patient


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