Cerebrovascular accident, also known as stroke, cerebral infarction, brain attack, is any functional or structural abnormality of the brain caused by pathological condition of the cerebral vessels of the entire cerebrovascular system. It is the sudden impairment of cerebral circulation in one or more of the blood vessels supplying the brain. This pathology either causes hemorrhage from a tear in the vessel wall or impairs the cerebral circulation by a partial or complete occlusion of the vessel lumen with transient or permanent effects. The sooner the circulation returns to normal after a stroke, the better the chances are for complete recovery. However, about half of those who survived a stroke remain disabled permanently and experience the recurrence within weeks, months, or years.
Thrombosis, embolism, and hemorrhage are the primary causes for CVA, with thrombosis being the main cause of both CVAs and transient ischemic attacks (TIAs). The most common vessels involved are the carotid arteries and those of the vertebrobasilar system at the base of the brain.
A thrombotic CVA causes a slow evolution of symptoms, usually over several hours, and is “completed” when the condition stabilizes. An embolic CVA occurs when a clot is carried into cerebral circulation and causes a localized cerebral infarct. Hemorrhagic CVA is caused by other conditions such as a ruptured aneurysm, hypertension, arteriovenous (AV) malformations, or other bleeding disorders.
Nursing Care Plans
During the acute phase of CVA, efforts should focus on survival needs and prevention of further complications. Care revolves around efficient continuing neurologic assessment, support of respiration, continuous monitoring of vital signs, careful positioning to prevent aspiration and contractures, management of GI problems, and careful monitoring of electrolyte, and nutritional status. Nursing care should also include measures to prevent complications.
- Ineffective Cerebral Tissue Perfusion
- Impaired Physical Mobility
- Impaired Verbal Communication
- Disturbed Sensory Perception
- Ineffective Coping
- Self-Care Deficit
- Risk for Impaired Swallowing
- Activity Intolerance
- Risk for Unilateral Neglect
- Deficient Knowledge
- Other Nursing Diagnoses
- See Also and Further Reading
Ineffective Cerebral Tissue Perfusion
Ineffective Tissue Perfusion: Decreased in the oxygen resulting in the failure to nourish the tissues at the capillary level.
- 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
|Assess factors related to individual situation for decreased cerebral perfusion and potential for increased ICP.||Assessment will determine and influence the choice of interventions. Deterioration in neurological signs or failure to improve after initial insult may reflect decreased intracranial adaptive capacity requiring patient to be transferred to critical 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.|
|Closely assess and monitor 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 of damage. May also reveal presence of TIA, which may warn of impending thrombotic CVA.|
|Monitor vital signs:|
|changes in blood pressure, compare BP readings in both arms.||Fluctuations in pressure may occur because of cerebral 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.|
|Heart rate and rhythm, assess for murmurs.||Changes in rate, especially bradycardia, can occur because of the brain damage. Dysrhythmias and murmurs may reflect cardiac disease, which may have precipitated CVA (stroke after MI or from valve dysfunction).|
|Respirations, noting patterns and rhythm (periods of apnea after hyperventilation), Cheyne-Stokes respiration.||Irregularities can suggest location of cerebral insult or 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 brain stem is intact. Pupil size and equality is determined by balance between parasympathetic and sympathetic innervation. Response to light reflects combined function of the optic (II) and oculomotor (III) cranial nerves.|
|Document changes in vision: 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 and degree of cerebral involvement and may indicate deterioration or increased ICP.|
|Position with head slightly elevated and in neutral position.||Reduces arterial pressure by promoting venous drainage and may improve cerebral perfusion.|
|Maintain bedrest, provide quiet and relaxing environment, restrict visitors and activities. Cluster nursing interventions and provide rest periods between care activities. Limit duration of procedures.||Continuous stimulation or activity can increase intracranial pressure (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 or cerebral injury, requiring further evaluation and intervention.|
|Administer supplemental oxygen as indicated.||Reduces hypoxemia. Hypoxemia can cause cerebral vasodilation and increase pressure or edema formation.|
|Administer medications as indicated:|
|Alteplase (Activase), t-PA;||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.|
|Anticoagulants:warfarin sodium (Coumadin), low-molecular-weight heparin (Lovenox);||May be used to improve cerebral blood flow and prevent further clotting when embolism and/or thrombosis is the problem.|
|Antiplatelet agents: aspirin (ASA), dipyridamole (Persantine), ticlopidine (Ticlid);||Contraindicated in hypertensive patients because of increased risk of hemorrhage.|
|Antifibrinolytics: aminocaproic acid (Amicar);||Used with caution in hemorrhagic disorder to prevent lysis of formed clots and subsequent rebleeding.|
|Antihypertensives||Chronic hypertension requires cautious treatment because aggressive management increases the risk of extension of tissue damage.|
|Peripheral vasodilators: cyclandelate (Cyclospasmol), papaverine (Pavabid), isoxsuprine (Vasodilan).||Transient hypertension often occurs during acute stroke and resolves often without therapeutic intervention.Used to improve collateral circulation or decrease vasospasm.|
|Steroids: dexamethasone (Decadron).||Use is controversial in control of cerebral edema.|
|Neuroprotective agents: calcium channel blockers, excitatory amino acid inhibitors, gangliosides.||These agents are being researched as a means to protect the brain by interrupting the destructive cascade of biochemical events (influx of calcium into cells, release of excitatory neurotransmitters, buildup of lactic acid) to limit ischemic injury.|
|Phenytoin (Dilantin), phenobarbital.||May be used to control seizures and/or for sedative action. Note: Phenobarbital enhances action of antiepileptics.|
|Stool softeners.||Prevents straining during bowel movement and corresponding increase of ICP.|
|Prepare for surgery, as appropriate: endarterectomy, microvascular bypass, cerebral angioplasty.||May be necessary to resolve situation, reduce neurological symptoms of recurrent stroke.|
|Monitor laboratory studies as indicated: prothrombin time (PT) and/or activated partial thromboplastin time (aPTT) time, Dilantin level.||Provides information about drug effectiveness and/or therapeutic level.|