Simple 7 – CVA (Brain attack/stroke)

1. Pathology – sudden loss of neurological Fn due to vascular injury (loss of bl. flow) to an area of
the brain.
~80% caused by cerebral infarction (blockage of carotid or intracerebral arteries by a clot or
atherosclerosis). (Called ‘ISCHEMIC’)
~20% ‘HEMORRHAGIC’  caused by bleeding into brain tissue…these have a higher incidence of
mortality (approx. 50%).
*During the evolution of an ischemic CVA, there is a core of dead/dying cells surrounded by an
ischemic band of minimally perfused cells called a penumbra, the survival of which depends on
timely return of circulation.

2. S/S – (1) sudden weakness or numbness of the face, arm or leg; (2) sudden loss of vision, double
vision, or dimming of vision in one or both eyes; (3) sudden difficulty speaking or understanding
speech; (4) sudden severe HA; (5) sudden falling, gait disturbance or dizziness.

3. Lab tests/radiologic studies – CT or MRI; (CT good for rapid I.D. of hemorrhage, but is not good
for I.D.ing ischemia or small infarcts. MRI good for I.D.ing ischemic lesions in all areas.
* Arteriography may be used to locate the site of the vascular abnormality.
- CBC (may suggest certain conditions, like anemia or infection, that may or may not be r/t CVA); Bl.
glucose (hyperglycemia causes worse outcomes; hypoglycemia  S/S may mimic a stroke); electrolytes
(imbalances may mimic a CVA); and coagulation studies (may indicate hemorrhagic CVA—abnormal
bleeding—or ischemic—abnormal clotting).

4. Meds – thrombolytics (for ischemic CVAs) like recombinant tissue plasminogen activator (rt-PA)
if recognized in first 90-180 min. & hemorrhage has been ruled out. Antiplatelets and
anticoagulants are the drugs used to mitigate the risk of recurrent stroke or to prevent stroke in
pts. w/risk factors. Some examples of antiplatelets include Aspirin, clopidogrel, dipyridamole
and ticlopidine, which work by inhibiting thromboxane production. (Thromboxane stimulates
platelet aggregation.) Anticoagulants like warfarin and heparin, on the other hand, slow clot
formation by competing with Vitamin K.

Aspirin
Indications – Prophylaxis/Tx for recurring CVAs

Side effects – most common are indigestion, epigastric distress, nausea

Therapeutic level – 10-20 mg/dL

Toxicity Signs – tinnitus, HA, hyperventilation, agitation, mental confusion, lethargy, diarrhea, sweating
Interactions – May ↑ the risk of bleeding with warfarin , heparin , heparin-like agents , thrombolytic
agents , dipyridamole , ticlopidine , clopidogrel , tirofiban , or eptifibatide , although these are frequently
used safely in combination & in sequence; may blunt therapeutic effects of diuretics & ACE inhibitors

Nsg Implications – monitor hepatic Fn before & during therapy; monitor serum salicylate levels to
ensure therapeutic levels; monitor for S/S of toxicity (above)

5. I. Ineffective Tissue Perfusion (Cerebral) r/t interruption of arterial blood flow & possible
increase in ICP secondary to CVA.
II. Impaired Physical Mobility & Self-Care Deficit r/t neuromuscular impairment or cognitive
impairment secondary to CVA.

6. For Dx I Assessment 1 - Assess for S/S of brain attack, esp. the following: F (Face – Are both
sides equal? Is the smile equal?); A (Arms – Can the pt. raise both arms equally?); S (Speech – is
speech slurred? Can the pt. make a sentence?); T (Time – Get help now. There is a small
window of opportunity.)

Intervention 1 – for pts. w/quickly-recognized ischemic stroke, thrombolytic therapy as ordered

Intervention 2 - lower HOB to 30 degrees or less; rationale is to inc. bl. flow to the ischemic
brain

7. For Dx II Intervention 1 – apply TEDS and SCDS or A/V boots as ordered to attenuate r/f DCT

Assessment 1/Intervention 2 – assess pt.’s ability to perform independent ADLs and collaborate
with rehabilitation therapists to make sure pt.’s assistance and teaching needs are provided for.

Intervention 3 – teach to perform active ROM exercises four times a day; or assist pt. w/passive
ROM exercises

8. still need to do