Hypertension

Force exerted by blood against artery wall during ventricular contraction (systolic) and ventricular relaxation (diastolic) must be adequate to maintain tissue perfusion during activity and rest.

• Cardiac Output
• Systemic Vascular Resistance

• Sympathetic Nervous System (SNS)
• Cardiovascular System
• Renal and Endocrine System

• Sustained elevation of BP
• Systolic is > or = 140 mmHg and diastolic is > or = to 90 mmHg for extended periods of time
• Diagnosis based on 3 occasions of elevation within a several week period.

• High BP means the heart is working harder than normal, both heart and blood vessels are under strain
• Endothelial damage occurs

• MI
• CHF
• CVA
• Renal Failure
• PVD
• Retinal damage

• Often asymptomatic
• "SILENT KILLER!"

• Increased age
• African-Americans
• More prevalent in men than women
• Women after the age of 55
• Equal risk for men and women from 55-75 years of age and after 75 years of age more prevalent in women.

• Elevated BP without an underlying disease
• Accounts for 90-95% of all cases of Htn
• Caused by high sodium diets, obesity, sedentary lifestyles, etc

-Elevated BP with specific underlying cause—identify and correct underlying problem which usually corrects HTN as well

-Its the main cause of Htn in children (80%)

• Causes:
• -Hypokalemia
• -narrowing of the aorta
• -tachycardia
• -renal disease
• -Meds (NSAID’s)
• -Neurologic disorders (brain tumors)
• -endocrine disorders (Hyperaldosteronism)
• -Obstructive Sleep Apnea

May be asymptomatic, also known as “silent killer”, until it causes damage to target organs

• Secondary symptoms:
• -fatigue
• -decrease in activity
• -dizziness
• -palpitations
• -angina
• -dyspnea
• -H/A

• Htn is major risk factor
• exact mechanism unknown
• thought to be caused by a disruption of coronary artery endothelium due to high pressures

• Sustained high pressures increase cardiac workload
• Adaptive mechanism to increase CO by increasing contraction
• Heart failure occurs when the heart can no longer compensate for the increased pressures and demand to supply oxygen (enlarged heart on X-ray, SOB on exertion, fatigue, ECG changes-wide QRS, inverted T wave).

• Atherosclerosis is the most common cause of CVD
• Risk for stroke is 4 times higher in people with Htn
• If atherosclerotic plaques in carotid arteries can break off and cause TIA’s or a stroke
• Hypertensive encephalopathy may occur after prolonged Htn
• When blood pressure remains high, the cerebral blood vessels dilate producing edema and marked loss of consciousness and death may occur from brain damage

• Htn speeds up the process of atherosclerosis in the peripheral blood vessels
• Classic symptom: Intermittent claudication (ischemic muscle pain caused by activity, relieved with rest).

• Htn is the leading cause of end-stage renal disease!
• Direct result of ischemia caused by the narrowed lumen of intrarenal blood vessels
• Leads to atrophy of the tubules, destruction of the glomeruli, and eventual death of the nephron itself
• Lab tests to confirm are: BUN, creatinine, proteinuria, albuminuria, hematuria
• Nocturia is the earliest sign of renal dysfunction

• The retina is the only place in the body where blood vessels can be directly visualized
• Includes blurring of vision, retinal hemorrhages, loss of vision
• Damage to the retina gives an indication of cardiac vessel damage

• Normal: SBP < 120 DBP < 80 (encourage healthy lifestyle)
• Prehypertension: SBP 120-139 DBP 80-89 (strongly pursue lifestyle changes)
• Stage 1 HTN: SBP 140-159 or DBP 90-99 (initiate drug therapy, Thiazide = 1st line of treatment)
• Stage 2 HTN: SBP >160 or DBP > 100 (initiate two drug combination)

• Thiazides (#1)
• ACE
• ARB
• CCB

• -CHF
• -Angina
• -Post MI

-BBs can mask the signs of hypoglycemia and cause bronchospasm so monitor airway/breathing!

• -Dietary Changes
• -DASH diet
• -Limit alcohol consumption
• -Regular physical activity
• -Avoid tobacco use
• -Stress management

-Low Sodium (2g or less/day)

-Educate patient on how to read labels and about foods high in sodium (processed & canned foods, etc)

-Decreases preload

-Monitor fluids & Lytes

• -Decreases contractility & rate
• -Slightly decreases afterload

-Monitor for bradycardia, bronchospasm, and masked symptoms of hypoglycemia

• -Decreases contractility
• -Decreases afterload

-Monitor for headache, edema, CHF

• -Decreases afterload
• -Decreases preload

-Monitor renal fxn & potassium(same with ARBs) and for cough & angioedema

• Cost
• Side Effects (sexual dysfuntion, fatigue, frequent urination)
• Knowledge Deficit
• Lack of Symptoms
• Ask the Questions!!!

• -Severe abrupt elevation in BP
• -Diastolic > 140 mm Hg

• What is the etiology:
• -Abruptly stopping Beta Blockers or Clonidine
• -Non-compliance (of meds and new lifestyle modifications)
• -Street Drugs

Evidence of evolving organ damage to other organs besides the heart (target organ damage)

• Examples:
• -MI
• -Angina
• -TIA/CVA
• -Encephalopathy
• -Renal Failure
• -Aortic Dissection

Changes in capillary permeability causing cerebral edema

• Symptoms:
• -HA
• -N/V
• -seizures
• -confusion
• -coma

• Admit to ICU
• Continuous Monitoring (A-line, Tele, CVP monitor, etc)
• IV Nitroprusside via pump (potent vasodilator; decreases preload & afterload)
• titrate to BP
• Alternative= Cleviprex ( IV CCB)
• Gradually reduce MAP
• 25% in one hour (too rapid can cause CVA)
• 160/100-110 within 2-6 hours
• Monitor for signs of target organ damage (frequent neuro exams, EKG, cardiac enzymes, urine output, etc)
• Patient education when crisis resolved

Very high BP with no symptoms; BP is high enough to cause serious problems but isn't currently

• Treated inpatient, ED or outpatient:
• -monitor response to treatment
• -pt can go home if BP stabilizes
• -requires follow-up within 24 hours

Can be given oral drugs (Clonidine or Captopril)

• D - Daily weights
• I - I&O
• U - Urine output
• R - Response of BP
• E - Electrolytes
• T - Take pulses
• I - Ischemic episodes (TIA)
• C - Complications (4 C's: CAD, CRF, CVA, CHF)