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66 Cards in this Set
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- Back
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Pathophysiology of stroke |
Blood supplied to brain by 2 major pairs of arteries: Carotid arteries (anterior circulation) vertebral arteries (posterior circulation) carotid: middle cerebral arteries and anterior cerebral arteries Vertebral: join to form basiliar artery Anterior and posterior circulation connected at the circle of willis |
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Brain blood flow rate |
Must be maintained at 750-100 mL/min or 20% CO for optimal brain functioning Brain is well protected from changes in mean systemic arterial BP over a range of 50-150 mmhg by cerebral autoregulation |
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When cerebral ischemia occurs cerebral autoregulation may be impaired AND is often dependent on changes in BP |
CO2 is a potent cerebral vasodilator - changes in arterial CO2 increase cerebral blood flow Very low arterial oxygen pressures (PaO2 <50 or increases in H+ concentration) also increase cerebral BF Decreased CO2 levels decrease cerebral BF |
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Factors that affect cerebral BF |
Systemic BP CO Blood viscosity Changes in CO, vasomotor tone, and distribution of BF normally maintain adequate BF to the brain CO has to be reduced by 1/2 before cerebral BF is reduced Changes in cerebral blood viscosity affect BF with decreased viscosity increasing flow - Collateral circulation may develop over time to compensate for decreased BF in the brain -Increased ICP causes brain compression and reduced cerebral BF |
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Non modifiable RFs for Stroke |
Age- increases w/ OA and doubles each decade after 55 Gender: stroke more common in men, women more likely to die from it Ethnicity/ race: African Americans have higher incidence of stroke and higher death rate Genetics- Pt w/ family hx of stroke has an increased risk of having a stroke |
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Modifiable RFs |
Hypertension * Most important DM Heart disease- A-fib*, MI, cardiomyopathy, valve abnormalities, congential degects Smoking excessive alcohol intake - w: 1+ drinks , M: 2+ drinks/day Abdominal Obesity Sleep apnea Metabolic syndrome (^ cholesterol) Lack of physcial exercise Poor diet Drug abuse- Cocaine Migraine headaches Inflammatory conditions Hyperhomocysteinemia SCD Birth control w/ high levels of progestin and estrogen |
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TIA (another risk factor for stroke) |
TIA is a transient episode of neuro dysfunction caused by focal brain, spinal cord, or retinal ischemia, but without acute infarction of the brain Clinical symptoms last less than 1 hr PT still need to seek tx if experiencing a TIA TIAs may be due to microemboli that temporarily block the BF TIA is warning sign of progressive cerebrovascular disease Still tx as a medical emergency |
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S/S of TIA involving carotid system |
Temp loss of vision in one eye (amaurosis fugax) Transient hemiparesis Numbness/ loss of sensation Sudden inability to speak |
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S/S TIA involving vertebrobasilar system: |
Tinnitus Vertigo Dark/blurred vision Diplopia Ptosis Dysarthria Dysphagia Ataxia unilateral/ bilat numbness or weakness |
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Strokes |
Result in infarction and cell death Classified as ischemic or hemorrhagic based on cause and underlying patho |
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Ischemic Stroke : 1) 2) |
Results from inadequate BF to the brain from partial or complete occlusion of the artery TIA is precursor to ischemic stroke Further divided into: Thrombotic and embolic strokes Most pt w/ ischemic stroke do not have a decreased LOC in first 24 hr Ischemic stroke symptoms may progress in the first 72 hours as infarction and cerebral edema increase |
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Thrombotic stroke |
Occurs from injury to a blood vessel wall and formation of a blood clot Lumen of BV becomes narrowed and if it becomes occluded, infarction occurs Thrombosis occurs where atherosclerotic plaques have already narrowed blood vessels MC of stroke , highly associated with HTN , DM Preceded by TIA in 30-50% |
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Embolic stroke |
Occurs when embolus lodges in and occludes a cerebral artery, resulting in infarction and edema of the area supplied by the involved vessel Most emboli originate in endocardial layer of the heart w/ plaque breaking off from the endocardium and entering the circulation Embolus travels up the cerebral circulation and lodges where vessel narrows or bifurcates |
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Heart conditions associated w/ emboli |
Atrial fibrillation MI Infective endocarditis Rheumatic heart disease -young-middle age Valvular prostheses Atrial septal defects Atherosclerosis- OA less common: Air and fat from long bone (femur fx) |
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Pt w/ embolic stroke |
Commonly has several clinical symptoms that occur suddenly Warning signs are less common Occurs rapidly with little time to accomodate by developing CC Pt usu remains conscious, may have headache Prognosis r/t the amount of brain tissue that is deprived of blood supply Effects of emboli are initally characterized by severe neuro deficits, can be temp if clot breaks and allows blood to flow Smaller emboli can continue and obstruct smaller vessels, involve smaller portions of the brain w/ fewer deficits noted Recurrence of embolic stroke is common unless underlying cause is aggressively tx |
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Hemorrhagic stroke |
Result from bleeding into the brain tissue itself (intracerebral or intraparenchymal hemorrhage) or into subarachnoid space or ventricles (subarachnoid or intraventricular hemorrhage) |
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Intracerebral hemorrhage |
Bleeding w/n the brain caused by a rupture of a vessel POOR PROGNOSIS w/ 30 day mortality rate of 40-80% and 50% of deaths within the first 48 hr HTN is MC cause others: Vascular malformations Coag disorders ANticoagulant and antithrombolytic drugs Brain tumors Ruptured aneurysms |
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CHARACTERISTICS OF INTRACEREBRAL HEMORRHAGE |
COMMONLY OCCURS DURING PD OF ACTIVITY Sudden onset of symptoms w/ progression over minutes to hours b/c of ongoing bleeding |
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Manifestations |
Neuro deficits Headache Nausea Vomiting Decreased LOC (in 50%) HTN Extent of s/s depends on amount, location, duration of the bleeding A clot w/n the closed skull can result in a mass that causes pressure on brain tissue, decreases cerebral BF., displaces brain tissue, and leads to ischemia and infarction |
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Putaminal and internal capsule bleeding |
Weakness on one side (face, arm, leg) Slurred speech Deviation of eyes Progression of a severe heomorrhage: hemiplegia Fixed and dilated pupils Abnormal body posturing Coma |
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Thalamic hemorrhage |
results in hemiplegia w/ more sensory than motor loss |
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Subthalamic bleeding |
Leads to problems of vision and eye mvmt |
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Cerebellar hemorrhages |
Characterized by severe headaches Vomiting loss of ability to walk Dysphagia Dysarthria Eye mvmt disturbances |
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Hemorrhage in pons |
MOST SERIOUS BAsic life functions (Breathing) are rapidly affected Characterized by: hemiplegia leading to complete paralysis, coma, severe headache, vomiting, loss of ability to walk, dysphagia, dysarthria, eye mvmt disturbances |
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Subarachnoid hemorrhage |
Occurs when there is intracranial hemorrhage into the cerebrospinal fluid filled space btw the arachnoid and pia mater mb on the surface ot the brain MCC is ruptured cerebral aneurysm others: Trauma Cocaine Pt die during first episode or from subsequent bleeding Incidence increases w/ age and is higher in men than women |
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S/S in subarachnoid hemorrhage |
Pt may have warning symptoms if the ballooning artery applied pressure to brain tissue, or minor warning symptoms may result from leaking of an aneurysm b4 major rupture Cerebral aneurysms are viewed as silent killer since typically no warning signs of an aneurysm until rupture has occurred Loss of consciousness may or may not occur (can range from alert to comtatose depending on bleed) Focal neuro deficits Cranial nerve deficts N/V Seizures Stiff neck |
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classic symptom of ruptured aneurysm |
Sudden onset of a severe headache that is different from a previous headache "worst headache of my life" |
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Complications of aneurysmal SAH |
Death, may pt w/ SAH die Survivors left w/ significant morbidity and cognitive difficulties Rebleeding before surgery or other therapy is initiatied Cerebral vasospasm, can lead to cerebral infarction Peak vasospasm is 6-10 days after inital bleed Cerebral vasospasm due to interaction of metabolites in blood and vascular SM During lysis of subarachnoid blood clots, metabolites released Metabolites can cause endothelial damage and vasoconstriction Release of endothelin (a vasoC) can induce cerebral vasospasm after SAH PT kept in ICU 14 days until the threat if vasospasm is reduced |
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Motor function |
Impairment of Mobility Respiratory function Swallowing/ speech Gag reflex Self care abilities Characteristics motor deficits include a loss of skilled voluntary mvmt (akinesia) -Impairment in integration of mvmts, alteration in muscle tone, alterations in reflexes Inital hyporeflexia progresses to hyperreflexia for most patients Motor deficits after stroke follow certain specific patterns, lesion on one side of the brain affects motor function on the opposite side of the body (contralateral) The arms and legs of the affected side may be weakened or paralyzed to different degrees depending on which part and what extent cerebral circulation was compromised |
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Stroke affecting middle cerebral artery lead to: |
greater weakness in the upper extremity than the lower extremity -Affected shoulder rotates internally, hip rotates externally -Affected foot is plantar flexed and inverted -Inital pd of flaccidity may last from days to several weeks and is r/t nerve damage -Spacicity of muscles, follows flaccid stage is r/t interruption of upper motor neuron influence Dominant side: Aphasia Motor & sensory deficit Hemianopsia Nondominant side: Neglect Motor & sensory deficit Hemianopsia |
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Anterior cerebral |
Motor and/or sensory deficit (contralateral) Sucking or rooting reflex Rigidity Gait problems Loss of proprioception and fine touch |
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Posterior cerebral |
Hemianopsia Visual hallucination Spontaneous pain Motor deficit |
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Vertebral |
Cranial nerve deficits Diplopia Dizziness N/V Dysarthria Dysphagia Coma |
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Communication |
Left hemi dominant for language Pt may experience aphasia -receptive aphasia- loss of comprehension -expressive aphasia- inability to produce languag -global aphasia- total inability to communciate Dysphasia-impaired ability to communicate |
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Nonfluent aphasia - minimal speech activity w/ slow speech that requires obvious effort Fluent aphasia- speech is present but contains little meaningful communication |
Dysarthria doesnt affect the meaning of communication or the comprehension of language, but it does affect the mechanics of speech Some pt experience a combo of aphasia and dysarthria |
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Affect |
Pt who have had stroke have trouble controlling their emotions -exaggerated or unpredictable emotion responses -depression w/ changes in body image, loss of function, frustrated by mobility and communication probs As RN, help pt and family understand that frustration and depression are common in first yr after a stroke |
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Intellectual function |
BOth memory & judgement may be impaired as a result of stroke -Impairments can occur with strokes affecting either side of the brain -Left sided stroke is more likely to result in memory problems r/t language -LS stroke more cautious in making judgements -RS stroke are more impulsive and move quickly |
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Spatial perceptual alterations |
RS stroke more likely to have problems in spatial perceptual orientation 1) result of damage to parietal lobe and causes pt to have incorrect perception of self and illness 2) Pt neglects all input from the affected side (erroneous perception of self in space) may be worsened by homonymous hemianopsia where blindness occurs in the same half of the visual fields on both eyes & pt has difficulty judging distances 3) agnosia - inability to recognize object by sight, touch, hearing 4) apraxia - inability to carry out learned sequential mvmts on command |
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Elimination |
Most probs w/ urinary & bowel elimination occur initially and temporarily Stroke affects 1 hemisphere of the brain , prognosis for normal bladder funct' is excellent At least partial sensation to bladder filling remains and voluntary elimination is present PT may experience urgency, frequency, incont atleast initally Motor control of bowel is not usually a problem, but pt are frequently constipated (immobility) Urinary and bowel probs may be r/t inability to express needs and manage clothing |
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Dg studies for stroke |
Tests done to ; 1) confirm int is a stroke and not another brain lesion 2) ID the likely cause of the stroke CT scan &MRI can rapidly distinguish btw ischemic and hemorrhagic stroke and help det the size and location of stroke Serial CT scans to assess effectiveness of tx and evaluate recovery Time is brain function, so rapidly asses and dg pt |
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CT angiography |
Provides visualization of cerebral blood vessels Can be performed at same time of after the noncontrast CT scan Can provide estimate of the perfusion and detect filling defects in cerebral arteries |
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MRA Magnetic resonance angiography |
Can detect vascular lesions and blockages CT/ MRI perfusion and diffusion imaging may also be done |
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Other tests: |
Cardiac imaging also recco b/c many strokes are caused by blood clots from the heart Angiography to ID cervical and cerebrovascular occlusion, atherosclerotic plaques, malformation of vessels Cerebral angiography is definitive study to ID source of SAH |
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Intraarterial digital subtraction angiography |
reduces dose of contrast material Uses smaller catheters Shortens length of procedure compared to conventional antgiography DSA involves the injection of contrast to visualize BVs in neck and large vessels of the circle of willis Considered safer than cerebra angiography b/c less vascular manip required |
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Transcranial doppler ultrasonography |
Noninvasive study that measures velocity of BF thru the major cerebral arteries Effective in detecting microemboli and vasopasm and is ideal for pt suspected of having SAH |
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LP |
May be done to look for evidence of RBCs in CSF is SAH is suspected but the CT does not show hemorrhage Avoided if pt suspected of obstruction in foramen magnum or other signs of increased ICP because of the danger of herniation of brain downward, leading to pressure on cardiac and resp centers in brainstem and potential death |
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Preventative therapy for Stroke |
Health diet Weigh control Regular exercise No smoking Limitation of alcohol consumptiom Routine health assessments Close management in pt w/ RFs such as DM, HTN, obesity, high serum lipids, cardiac dysfunction |
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Preventive drug therapy |
Measures to prevent the development of thrombus or embolus used in pt w/ TIAs since at high risk for a stroke Antiplatelet drugs are usu chosen tx to prevent stroke in pt w/ TIA -Asprin 81-325 mg/day -Ticlopidine -CLopidogrel -Dipyridamole -Statins effective for prevention of stroke pt who have had TIA in the past -A-fib: oral anticoagulation w/ warfarin, rivaroxaban, padaxa |
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Surgical therapy for TIA and stroke prevention |
TIAs due to corotid disease: carotid endarectomy, transluminal angioplasty, stenting, extracrainal intracranial bypass - anastomosing a branch of extracranial artery to an intracranial artery, usu reserved for pt who do not respond to other methods of therapy |
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Acute care for ischemic stroke |
Most important piece during assessment is the TIME OF ONSET OF SYMPTOMS Manage ABCs -O2 admin, intubation, oral airway, mechanical ventilation Baseline neurologic function assessment, pt monitored for increasing neuro deficit (can worsen in first 24-48hr) |
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Elevated BP is common immediatley after stroke and may be protective response to maintain cerebral perfusion However it can be detrimental |
Immediately after ischemic stroke in pt who do not get fibrinolytic therapy, use of drugs to reduce BP is used only if SBP> 220 or DBP > 120 Pt going to have fibrinolyitc therapy: BP needs to be less than 180/105 and then maintained at below 180-105 for atleast 24 hr after fibrinolytic therapy In acute stroke, IV labetalol and nicardipine are preferred |
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Low BP us uncomon immediately after stroke, but if it happens hypotension and hypovolemia should be corrected |
Keep pt hydrated to promote perfusion and decrease further brain injury -Overhydration = cerebral edema and further damage -Monitor I&O to ensure pt is not dehydrated and maintain balance btw over and underhydration |
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IF ADH secretion occurs in response of stroke |
UO decreases, fluid is retained Low sodium serum (hyponatremia) may occur *IV solutions w/ glucose and water are avoided because they are hypotonic and may futher increase cerebral edema and ICP hyperglycemia may ne asssociated with furhter brain damage and should be treated |
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Increased ICP |
More likely to occur in hemorrhagic strokes, but can occur in ischemic ICP from cerebral edema usu peaks in 72 hr and may cause brain herniation Tx: Elevated HOB maintaining neck & head alignment Avoid hip flexion Management of hyperthermia 96.8 -98.6 goal Drug therapy to reduce seizures pain management avoidance of hypovolemia Management of constipation CSF drainage may be done to reduce ICP in some pt |
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Rehabilitation care |
After stroke pt has stabilized for 12-24 hr, collabo care shifts from preserving life to lessening disability and attaining optimal function |
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Assessment Description of current illness w/ attention to intial symptoms, symptom onset and duration, nature, changes Hx of similar symptoms previously experienced Current meds Hx of RFs and other illnesses such as HTN Family hx of Stroke or CDV diseases |
Secondary assessment LOC using NHI stroke scale Cognition Motor abilities Cranial nerve function sensation Prioprioception Cerebellar function DTRs |
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Uncontrolled or undiagnosed HTN is the primary cause of stroke |
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Stroke pt is at increased risk for aspiration pneumonia PT mech vented, provide oral care q2h to prevent VAP |
Impaired LOC, dysphagia Airway obstruction from probs w/ chewing, swallowing, food pocketing, tongue falling back Pt may require ET and mechanical ventilation initally Enteral tube feedings also place pt at risk for aspiration pneumonia Pt should be screened for ability to swallow and placed on NPO until dysphagia ruled out Oropharyngeal airway used in comatose pt to prevent tongue falling ack and obst airway, assists with suctioning Nasopharyngeal airway used to provide airway protection and access Tracheostomy for LT use |
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Care of ICP in pt that has unclipped or uncoiled aneurysm |
Pt may experience rebleeding w/ possibility of increasing ICP further with coughing or suctioning Reduce these interventions while maintaining a proper airway |
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NIH Stroke Scale |
Primary clinical assessment tool to evaluate and doc neuro status in acute stroke pt Measures stroke severity Predictor of short and long term outcomes of stroke patients |
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Additional neuro assessment |
Mental status Pupillary responses Extremity movement & strength VS: decreasing LOC may indicate increasing ICP Monitor ICP and CPP |
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Cardiovascular system hypertension is sometimes seen after stroke as body attempts to increase cerebral BF |
Goals aimed at maintaining homeostasis Many pt w/ stroke have decreased cardiac reserves secondary to cardiac disease Monitor VS Cardiac rhythms Calculate I&Os - noting imbalances Regulate IV infusions Adjusting fluids to individual pt needs Monitoring lung sounds for crackles and rhonchi = pulmonary congestuon Monitor heart sounds for murmurs and S3, S4 |
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After stroke, VTE risk is real so VTE prevention is key |
(weak and paralyzed extremities) VTE r/t immobility, loss of venous tone, decreased muscle pumping in leg Keep pt moving is most effective prevention Active or passive ROM exercises depending on voluntary mvmt passive for hemiplegia Positioning to minimize dependent edema Use of SCDs and ted hose VTE prophylaxis: w/ LWMH (enoxaparin) Assessment: measure the calf and thigh daily, observe for swelling in lower ext, unusal warmth in leg, and ask pt about pain in calf |
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MUSCULOSKELETAL |
Goal: maintain optimal function by preventing joint contractures and muscular atrophy ROM exercises and positioning in acute pahse Passive ROM started on first day of hospital Exercise prevents muscular atrophy |
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Positioning Position each joint higher than the proximal to it to prevent dependent edema Careful positioning and mvmt of affected arm may prevent development of painful shoulder Do not immobilize the affected upper ext --> painful hand shoulder syndrome |
Nursing interventions to optimize musk function 1) trochanter roll at the hip to prevent external rotation 2) Hand cones to prevent hand contractures 3) Arm supports w/ slings and lap boards to prevent shoulder displacement 4) Avoid puling pt by arm to prevent shoulder displacement 5) Posterior leg splints, footboards, high top tennis shoes 6) hand splints for reducing spasticity |
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Integumentary system: high risk for skin breakdown immobility, decreased circulation, loss of sensation, advanced age, incont, poor nutrition, dehydration |
Pressure relief by position changes special mattress / wheelchair cushions Good skin hygiene Emollients applied to skin Early mobility Max 2 hr limit on any position, Position pt on paralyzed/ weak side for only 30 min Area of redness develops and doesnt return to normal color w/n 15 min, epidermis and dermis are damaged DONT MASSAGE DAMAGED AREA |
