lewis HTN 33
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| What is blood pressure determined by | Systemic vascular resistance and cardiac output
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| What does abnormally high blood pressure lead to | excessive contraction of arteries, kidney disease, stroke, and heart attack
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| What is cardiac output controlled by | Renin-angiotensin-aldosterone system and Naturitic peptides
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| What is systemic vascular resistance controlled by | Vasocontrictors-Angiotensin, norepinephrine Vasodilators-prostaglandins
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| What is pulse pressure | difference between SBP and DBP
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| When is it increased | atherosclerosis
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| When is it decreased | CHF and Hypovolemia
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| What is Map and what does it measure | perfusion of organs must be above 60
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| What accounts for 90-95% of cases of HTN | Primary or essential
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| When is HTN classified as Pre-HTN | 120-139 or 80-89
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| When is HTN classified as Stage 1 | 140-159 or 90-99
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| When is HTN classified as Stage 2 | greater than 160 or greater than 100
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| What are risk factor for Primary HTN | Age,African American, high sodium intake
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| What does altered angiotensin mechanism cause | increased aldosterone and fluid retention
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| What does stress and SNS mechanism cause | increased vasoconstriction, HR, and Renin release
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| What does insulin resistance and hyperinsulinemia cause | stimulates SNS and vasodilator response
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| What is blood pressure determined by | Systemic vascular resistance and cardiac output
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| What does abnormally high blood pressure lead to | excessive contraction of arteries, kidney disease, stroke, and heart attack
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| What is cardiac output controlled by | Renin-angiotensin-aldosterone system and Naturitic peptides
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| What are urinalysis indications of renal disease | protein and hematuria
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| What is systemic vascular resistance controlled by | Vasocontrictors-Angiotensin, norepinephrine Vasodilators-prostaglandins
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| What serum or blood studies indicate HTN | serum electrolytes, glucose, creatnine, lipids,
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| What is pulse pressure | difference between SBP and DBP
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| What does ECG show in HTN | ischemic heart disease
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| When is it increased | atherosclerosis
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| What does echo show | LV hypertrophy
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| When is it decreased | CHF and Hypovolemia
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| What is Map and what does it measure | perfusion of organs must be above 60
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| What accounts for 90-95% of cases of HTN | Primary or essential
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| When is HTN classified as Pre-HTN | 120-139 or 80-89
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| When is HTN classified as Stage 1 | 140-159 or 90-99
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| When is HTN classified as Stage 2 | greater than 160 or greater than 100
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| What are risk factor for Primary HTN | Age,African American, high sodium intake
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| What does altered angiotensin mechanism cause | increased aldosterone and fluid retention
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| What does stress and SNS mechanism cause | increased vasoconstriction, HR, and Renin release
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| What does insulin resistance and hyperinsulinemia cause | stimulates SNS and vasodilator response
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| What are symptoms of HTN | Fatigue, reduced activity tolerance, palpitations, angina, dyspnea
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| What are complications of HTN | CAD, LVH, HF, kidney damage, PAD, and retinal damage
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| What are urinalysis indications of renal disease | protein and hematuria
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| What serum or blood studies indicate HTN | serum electrolytes, glucose, creatnine, lipids,
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| What does ECG show in HTN | ischemic heart disease
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| What does echo show | LV hypertrophy
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| What does eye exam show | retinal hemmorhage, AV nicking, and papilldoma
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| What eight loss is significant | 10-20 lbs show decrease in BP of 5-20 mmHg
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| What exercise level is recommended | 30 min aerobic 3 times per week
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| What is DASH diet plan | enphasizes fruits and vegetables, fat free milk products, whole grains, fish and poultry, beans,seeds and nuts
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| What is the most important role of the nurse in HTN diagnosis | TEACHING
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| Where do central adrenergic antagonist act | vasomotor Block SNS response
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| Where do peripheral adrenergic antagosist act | Sympathetic ganglion to vasomotor center Block SNS response
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| Where do Beta blockers act | Inhibit Renin release
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| Where do ACE inhibitors act | block production of angiotensin I
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| Where do angiotensin II blockers act | block angiotensin II from constriction blood vessels
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| Where do diuretics act | decrease sodium absorption
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| Where do calcium channel blockers, and direct arterial vasodilators act | block vasoconstriction
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| What med is used to counteract the baroreceptor | bet blocker
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| What med counteracts the concentrating effect of the kidneys | Ace inhibitor, ARB, or aldosterone inhibitor
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| What symptoms are often the reason for noncompliance with cardiac meds | Orthostatic hypotension, sexual dysfunction,dry mouth, and frequent urination
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| What is the result of diruetics | decrease blood volume, preload, cardiac output, and BP
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| What are 4 types of diuretics and where do they act | Loop-loop of henle Thiazide-proximal distal renal tubule Potassium sparing-distal renal tubule and collecting duct Osmotic-creates osmotic force in the lumen of the nephron (proximal convoluted tubule
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| Which diuretic is used for massive and quick diuresis and/or renal impairment | Loop Diuretics
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| Which diuretics are only PO | Thiazides
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| Which diuretics can increase glucose | Loop and Thiazides
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| Which diuretics cause skin reactions | thiazide and loop
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| Which diuretics can't be given with Sulfa allergy | Loops
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| Which diuretics are dosed daily | Thiazide and potassium sparing
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| Which diuretics are dosed twice daily | loop
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| What are dietary sources of potassium | bananas,orange or yellow fruits and vegetables, beans, potato
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| What teaching is needed with diuretics | hyperglycemia, NSAIDs reduce effectiveness and gout flares
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| What labs are monitored with diuretics | k+ and Mag
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| What are common diuretics | Lasix, HCTZ, spiolactone,diuril,mannitol
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| What are central acting adrenergic inhibitors | Catapres,aldomet,wytensin
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| What are peripheral acting adrenergic inhibitors | Reserpine,beDta blockers
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| How do beta blockers work | block catecholamine production which decreases HR and decreases renin
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| Why do you have to wean off BB | in diabetics it blunts hypoglcemia symptoms
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| What are common beta blockers | Tenormin, lopressor, toprol and olol's
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| What does hydralazine do | dilate arterioles, decrease afterload, and increase CO
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| What does Nitro do | dilates veins, decreases preload, CO,
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| What are adverse effects of vasodilators | postural hypotension, reflex tachycardia, and increased blood voulume
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| What is drug of choice in hypertensive crisis | Nipride-IV, immediate onset
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| What NI must be done when administering Nipride | BP every minute
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| What are adverse effects of Nipride | extreme hypotension, cyanide posioning, and thiocyanate toxicity
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| What is Angiotensin II | Neurohormone that promotes sodium and water retention, stimulates SNS, and promotes atherosclerosis
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| What do ACE inhibitors do | block the formation of angiotensin II
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| What are NI for Ace inhibitors or ARB | Monitor electrolytes, creatnine, fluid status, and blood pressure
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| What is a common side effect of ACE inhibitors or ARB | dry hacking cough
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| What teaching for ACE inhibitors or ARB | avoid alcohol and salt subtitutes
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| What are Angiotensin Receptor Blocker (ARB) | Block the receptor site of angiotensin II
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| What are ARB's | Benicar, coozar, Diovan
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| What are drug interactions for ACE inhibitors or ARB | potassium supplements, potassium sparing diuretics, and Lithium
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| What is the action of CCB | dilation of arterioles, decreased HR and afterload
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| What are S/E of CCB | Bradycardia, headache
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| What is a food interaction with CCB | grapefruit juice
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| What are some of the reasons for hypertension resistant HTN | Corticosteroids, licorice, erythropoetin, oral contraceptives, excessive alcohol intake
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| HTN in older persons | wide gap between korotkoff and subsequent beats white coat hypertension
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| What consistutes a Hypertensive crisis or malignant HTN | Severe increase in BP Evidence of acute target organ damage
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| How is malignant HTN treated | Direct Vasodilators-titrated to MAP monitor cardiac and renal function Neuro checks Bring BP down gradually investigate cause Teaching
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