mod 2 hypertension Flashcards
(33 cards)
renin angiotensin aldosterone system (RAAS)
RAAS- regulates long term BP and extracellular volume
angiotensionogen- released by LIVER from LOW BP and change BLOOD VOLUME (SODIUM)
- stimulates kidney to release RENIN
RENIN- converts angiotensinogen to ANGIOTENSIN 1
- ANGIOTENSIN 1 travels to LUNG and converts to ANGIOTENSIN II by ACE (angiotensin converting enzyme)
- ANGIOTENSIN II acts ADRENAL GLANDS release ALDOSTERONE (fluid retention)
ANGIOTENSIN II- potent vasoconstrictor
- causes NEPRHON to retain fluid and BP INCREASES
RAAS activated when:
- Loss blood volume or drop BP
- decrease renal perfusion
- chronic stress
other mechanisms affect BP
arterial baroreceptors- receptors in carotid sinus, aorta, and l ventricle - ALTERS HR, vasodilation and vasoconstriction
vascular autoregulation- maintain tissue perfusion, regulates mean arterial pressure (MAP), resistance (diameter) arterioles
**helps consistent BP at tissues despite changes elsewhere
types hypertension- primary and secondary
categories
- normal - less 120, less 80
- elevated - 120-129, less 80
- high BP (hypertension) stage 1- 130-139, 80-89
- high BP stage 2- 140 higher, 90 higher
- hypertensive crisis (consult dr immediately)- inc 180, incr 120
primary hypertension
- essential hypertension, NO KNOWN CAUSES, idiopathic most common
Why?- interactions genetics and environment - SNS, RAAS, natriuretic peptides
risk factors
- smoking, excess sodium intake, sedentary lifestyles, hyper-lipidemia, stress, family history, obesity, age > 60, african americans, high alcohol consumption
secondary hypertension
KNOWN CAUSE associated
- treat underlying condition
- renal disorders, adrenocortical tumors, adrenomedullary tumors (pheochromocytoma), drugs
hypertension causes
primary- excess salt, abnormal arteries, incr blood volume, genetic disorders, stress
secondary- health conditions, meds, rec drugs, pregnancy, hormone therapy
S/S hypertension
silent killer must look at END-ORGAN damage - chest pain- heart - head ache- brain - visual changes- eyes - weakness/pain extremities- brain/stroke
long term outcomes hypertension
cardiac- inc l ventricle work
- hypertrophy, accelerated progress atherosclerosis, inc risk aortic aneurysm (weakened walls)
kidneys- primary cause end stage renal disease
brain- higher risk stroke, aneurysm, hemorrhage
eyes- retinopathy, blindness
lower extremities- gangrene, intermittent claudication
hypertensive crisis
systolic >180 and diastolic >120
- occurs with PRIMARY hypertension
hypertensive urgency vs emergency
urgency- no S/S end organ damage, BP > 180/120, Tx w oral agents and GRADUALLY decr BP
- causes: anxiety, pain, abrupt withdrawal
- emergency- lead to END ORGAN damage BP >180/120,
S/S organ damage- headache, blurred vision, stroke, brain hemorrhage, chest pain, acute coronary syndrome, heart dysfunction
**aggressively LOWER BP in mins to hrs (IV meds)
hypertensive meds - gen diuretics (water pills) - remove excess sodium and water
MOA- incr urinary output, decr circulating volume, decr arterial resistance
Lower BP by decr CARDIAC OUTPUT - block sodium and chloride reabsorption
- can enhance effect other hypertensives
- least expensive
usually first line defense
hypokalemia = low K
loop and thiazide diuretics can cause
normal- 3.5-5
mild- 3-3.4
moderate- 2.5-2.9
severe- <2.5
decr K = cardiac arrythmias
angiotensinogen
released by liver in response to low BP and low Na and blood volume
renin
released by kidney
stimulated by low fluid volume and low Na
- causes liver to convert angiotensinogen to angiotensin 1
angiotensin I
travels from liver to lungs
ACE - angiotensin converting enzyme
converts angiotensin I to angiotensin II
angiotensin II
acts on adrenal glands
releases aldosterone
angiotensin II potent VASOCONTRICTOR
increase BP
aldosterone
from adrenal glands
causes increase Na, fluid retention, BP, and decrease K
goal RAAS
to increase BP
meds to treat hypertension
diuretics sympathetic nervous system blockers beta blockers calcium channel blockers vasodilators
diuretics (water pills) - 3 classes
- potassium-sparing- mild
- thiazide- mild
- loop- moderate to profound
MOA
- increase urinary output
- decrease circulating volume
- decrease arterial resistance
Results
- lower BP by decreasing CARDIAC OUTPUT
- – block sodium and chloride reabsorption
- enhance effectiveness other hypertensives
- least expensive
- impacts stroke volume
- usually 1st line therapy
thiazide diuretics - 1st line management mild hypertension
Drugs
- hydrochlorothiazide (HCTZ) - HydroDiuril
- metolazone - Zaroxolyn
MOA
- distal convoluted tubule inhibit reabsorption Na, K, Cl = decr cardiac output= water loss
- relaxes arterioles = decre PVR
side effects
- electrolyte and metabolic disturbances
- HYPOKALEMIA (LOW K)
- orthostatic hypotension, worsen renal insufficiency, hyper uricemia
nursing actions
- monitor K levels, K supplements, K enriched foods
loop diuretics - also given in fluid overload
drugs
- furosemide - Lasix
- Bumetanide - Bumex
- torsemide - Demadex
MOA
- inhibit kidney reabsorb Na ** LOOP OF HENLE
- kidney put more Na in urine = incr urine
- decrease fluid in blood vessels = decr cardiac output
- *PROFOUND DIURESIS
side effects
- HYPOKALEMIA
- dehydration, hypotension, ototoxicity
nursing considerations
- monitor K levels, K supplements
- if not have incr urine output, contact HCP
potassium-sparing diuretics (aldosterone agonist)
drugs
- spironolactone - Aldactone
- triamterene - Dyerenium
MOA
- block action aldosterone (Na, H2O retention) = K retention and excretion Na and H2O
only provide small amount diuresis, given with combo hypertensives/diuretics to get lower chance of hypokalemia
side effects
HYPERKALEMIA
- deepened voice, impotence, irreg menstual cycles, gynecomastia, hirsutism
sympatholytics 3 classes
Alpha-adrenergic blockers
centrally-acting alpha 2 agonists
beta adrenergic blockers
goal - SNS blockers cause PARASYMPATETIC response
- decreases vasoconstriction, decreases blood pressure by decreasing PVR - peripheral vascular resistance
