ASSESSMENT NURSING DIAGNOSIS

Subjective: madalas akomahilo, asverbalized by the patient. Objective: >lethargic >decreased cardiacoutput >decreased strokevolume >increased peripheral vascular resistance >VS taken asfollows: T: 37.2 PR: 83 RR: 18 BP: 180/ Decreased CardiacOutput r/t malignanthype rtension asmanifested bydecreased stroke volume.

PLANNING

INTERVENTION

RATIONALE

EVALUATION

STG:After 6 hrs of nursinginterv entions, theclient will have noelevation in blood pressure abovenormal limits andwill maintain blood pressure withinacceptabl e limits.LTG:After 5 days of nursinginterv entions, theclient will maintainadequa te cardiacoutput and cardiac index.

1.monitor BP every 1-2 hours, or every5 minutes duringactve t itration of vasoactive drugs. 2. monitor ECG for dysrrhythmias, conduction defectsand for heart rate.

3. suggest frequent position changes. 4.encourage patientto decrease intake of caffeine, cola and chocolates. 5. observe skincolor, temperature,capillary refill timeand diaphoresis. 6.auscultate hearttones. 7.administer medicin e as prescribed by the physician. 8. instruct client &family on fluid anddiet require mentsand restrictions of sodium.

1. changes in BPmay indicateschanges in patientstatus requiring prompt attention. 2. decrease incardiac output mayresult in changes incardiac perfusioncausingdy srhythmias. 3. it may decreases peripher alvenous pooling that may be potentiated byvasodilators and prolonged sitting or standing. 4. caffeine is acardiac stimulantand may adverselyaffect cardiacfunction. 5.peripheralvasoco nstrictionmay result in pale,cool, clammy skin,with prolongedcapillary refill time. due tocardiacdysfunctio n anddecreased cardiacoutput. 6.hypertensive pati ents often haveS4 gallops caused by atrialhypertrophy. 7. to promotewellness.8 . restrictions canassist with

STG:After 6 hrsof nursinginter ventions, theclient had noelevation in blood pressure abovenormal limits andwill maintain blood pressure withinacceptable limits.Goal was met.LTG:After 5 days of nursinginterven tions, theclient maintained anadequate cardiacoutput and cardiacindex.Goal was met

9. instruct client andfamily onmedications, sideeffects, contraindications and signs to report.

decreasein fluid retentionand hypertension,there by improvingcardiac output.9. promotesknowledg e andcompliance withdrug regimen

Pathophysiology
The clinical manifestations of hypertensive encephalopathy are due to increased cerebral perfusion from the loss of blood-brain barrier integrity, resulting in exudation of fluid into the brain. In normotensive individuals, an increase in systemic blood pressure over a certain range (ie, 60-125 mm Hg) induces cerebral arteriolar vasoconstriction, thereby preserving a constant cerebral blood flow and an intact blood-brain barrier. In chronically hypertensive individuals, the cerebral autoregulatory range gradually is shifted to higher pressures as an adaptation to chronic elevation of systemic blood pressure. This cerebral autoregulatory response is overwhelmed during a hypertensive emergency in which the acute rise in systemic blood pressure exceeds the individual's cerebral autoregulatory range, resulting in hydrostatic leakage across the capillaries within the central nervous system. With persistent elevation of the systemic blood pressure, arteriolar damage and necrosis occur. The progression of vascular pathology leads to generalized vasodilatation, cerebral edema, and papilledema, which clinically manifest as neurologic deficits and altered mentation in hypertensive encephalopathy.