Nursing Diagnosis: Ineffective Cerebral Tissue Perfusion
May be related to
- Interruption of blood flow: occlusive disorder, hemorrhage; cerebral vasospasm, cerebral edema
Possibly evidenced by
- Altered level of consciousness; memory loss
- Changes in motor/sensory responses; restlessness
- Sensory, language, intellectual, and emotional deficits
- Changes in vital signs
- Maintain usual/improved level of consciousness, cognition, and motor/sensory function.
- Demonstrate stable vital signs and absence of signs of increased ICP.
- Display no further deterioration/recurrence of deficits
8 Cerebrovascular Accident (Stroke) Nursing Care Plans
- Ineffective Cerebral Tissue Perfusion — Stroke Nursing Care Plans
- Impaired Physical Mobility — Stroke Nursing Care Plans
- Impaired Verbal Communication — Stroke Nursing Care Plans
- Disturbed Sensory Perception — Stroke Nursing Care Plans
- Ineffective Coping — Stroke Nursing Care Plans
- Self-Care Deficit — Stroke Nursing Care Plans
- Risk for Impaired Swallowing — Stroke Nursing Care Plans
- Knowledge Deficit — Stroke Nursing Care Plans
Ineffective Cerebral Tissue Perfusion — Stroke (CVA) Nursing Care Plan (NCP)
|Determine factors related to individual situation/cause for coma/decreased cerebral perfusion and potential for increased ICP.||Influences choice of interventions. Deterioration in neurological signs/symptoms or failure to improve after initial insult may reflect decreased intracranial adaptive capacity requiring patient be transferred to critical care area for monitoring of ICP, other therapies. If the stroke is evolving, patient can deteriorate quickly and require repeated assessment and progressive treatment. If the stroke is “completed,” the neurological deficit is nonprogressive, and treatment is geared toward rehabilitation and preventing recurrence.|
|Monitor/document neurological status frequently and compare with baseline.||Assesses trends in level of consciousness (LOC) and potential for increased ICP and is useful in determining location, extent, and progression/resolution of CNS damage. May also reveal presence of TIA, which may warn of impending thrombotic CVA.|
|Monitor vital signs, i.e., note:Hypertension/hypotension, compare BP readings in both arms;Heart rate and rhythm; auscultate for murmurs;
Respirations, noting patterns and rhythm, e.g., periods of apnea after hyperventilation, Cheyne-Stokes respiration.
|Fluctuations in pressure may occur because of cerebral pressure/injury in vasomotor area of the brain. Hypertension or postural hypotension may have been a precipitating factor. Hypotension may occur because of shock (circulatory collapse). Increased ICP may occur because of tissue edema or clot formation. Subclavian artery blockage may be revealed by difference in pressure readings between arms.Changes in rate, especially bradycardia, can occur because of the brain damage. Dysrhythmias and murmurs may reflect cardiac disease, which may have precipitated CVA (e.g., stroke after MI or from valve dysfunction).Irregularities can suggest location of cerebral insult/increasing ICP and need for further intervention, including possible respiratory support.|
|Evaluate pupils, noting size, shape, equality, light reactivity.||Pupil reactions are regulated by the oculomotor (III) cranial nerve and are useful in determining whether the brainstem is intact. Pupil size/equality is determined by balance between parasympathetic and sympathetic enervation. Response to light reflects combined function of the optic (II) and oculomotor (III) cranial nerves.|
|Document changes in vision, e.g., reports of blurred vision, alterations in visual field/depth perception.||Specific visual alterations reflect area of brain involved, indicate safety concerns, and influence choice of interventions.|
|Assess higher functions, including speech, if patient is alert.||Changes in cognition and speech content are an indicator of location/degree of cerebral involvement and may indicate deterioration/increased ICP.|
|Position with head slightly elevated and in neutral position.||Reduces arterial pressure by promoting venous drainage and may improve cerebral circulation/perfusion.|
|Maintain bedrest; provide quiet environment; restrict visitors/activities as indicated. Provide rest periods between care activities, limit duration of procedures.||Continual stimulation/activity can increase ICP. Absolute rest and quiet may be needed to prevent rebleeding in the case of hemorrhage.|
|Prevent straining at stool, holding breath.||Valsalva maneuver increases ICP and potentiates risk of rebleeding.|
|Assess for nuchal rigidity, twitching, increased restlessness, irritability, onset of seizure activity.||Indicative of meningeal irritation, especially in hemorrhage disorders. Seizures may reflect increased ICP/cerebral injury, requiring further evaluation and intervention.|
|Administer supplemental oxygen as indicated.||Reduces hypoxemia, which can cause cerebral vasodilation and increase pressure/edema formation.|
|Administer medications as indicated:Alteplase (Activase), t-PA;
Anticoagulants, e.g., warfarin sodium (Coumadin), low-molecular-weight heparin (Lovenox); antiplatelet agents, e.g., aspirin (ASA), dipyridamole (Persantine), ticlopidine (Ticlid);
Antifibrolytics, e.g., aminocaproic acid (Amicar);
Peripheral vasodilators, e.g., cyclandelate (Cyclospasmol), papaverine (Pavabid), isoxsuprine (Vasodilan);
Steroids, e.g., dexamethasone (Decadron);
Neuroprotective agents, e.g., calcium channel blockers, excitatory amino acid inhibitors, gangliosides;
Phenytoin (Dilantin), phenobarbital;
|Thrombolytic agents are useful in dissolving clot when started within 3 hr of initial symptoms. Thirty percent are likely to recover with little or no disability. Treatment is based on trying to limit the size of the infarct, and use requires close monitoring for signs of intracranial hemorrhage. Note: These agents are contraindicated in cranial hemorrhage as diagnosed by CT scan.May be used to improve cerebral blood flow and prevent further clotting when embolus/thrombosis is the problem. Contraindicated in hypertensive patients because of increased risk of hemorrhage.Used with caution in hemorrhagic disorder to prevent lysis of formed clots and subsequent rebleeding.
Preexisting/chronic hypertension requires cautious treatment because aggressive management increases the risk of extension of tissue damage. Transient hypertension often occurs during acute stroke and resolves often without therapeutic intervention.
Used to improve collateral circulation or decrease vasospasm.
Use is controversial in control of cerebral edema.
These agents are being researched as a means to protect the brain by interrupting the destructive cascade of biochemical events (e.g., influx of calcium into cells, release of excitatory neurotransmitters, buildup of lactic acid) to limit ischemic injury.
May be used to control seizures and/or for sedative action. Note: Phenobarbital enhances action of antiepileptics.
Prevents straining during bowel movement and corresponding increase of ICP.
|Prepare for surgery, as appropriate, e.g., endarterectomy, microvascular bypass, cerebral angioplasty.||May be necessary to resolve situation, reduce neurological symptoms/risk of recurrent stroke.|
|Monitor laboratory studies as indicated, e.g., prothrombin time (PT)/activated partial thromboplastin time (aPTT) time, Dilantin level.||Provides information about drug effectiveness/therapeutic level.|
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