UNIT 4 Hypertension Flashcards
ThiaSystolic Blood Pressure
contraction phase; highest amount of pressure
Hypertension
increased pressure on arterial walls;
“silent killer”;
asymptomatic;
may lead to other complications: heart failure, cerebral hemorrhage - stroke, kidney failure, MI
Diastolic Pressure
relaxation phase; lowest amount of pressure
Normal Blood Pressure
Systolic: less than 120
Diastolic: less than 80
Two Types of Hypertension
Primary Hypertension/Essential Hypertension (most common)
Secondary Hypertension (a medical condition present)
Primary Hypertension/Essential Hypertension
most common;
cause is unknown;
risk factors: smoking, obesity, racial predisposition, family history, stress, sedentary lifestyle, high-fat diet
Seondary Hypertension
a medical condition present;
pregnancy, renal disease, drug-induces
Risk Factors for Hypertension
Stress, age: over 60, family history, gender: men and postmenopausal women, increased cholesterol, high sodium diet, sedentary lifestyles, smoking, diabetes
Baroreceptors
located in the internal walls of carotid arteries and the aortic arch and other vessels in the body sense the change in BP;
sensors that control BP
Blood Pressure Control
if BP decreases, baroreceptors sense the change; EPI and NE are released to constrict smooth muscle of the vessels; this increases BP
if BP increases, baroreceptors sense the change; vagus nerve is stimulated; HR, FOC, CO decrease; vasodilation occurs; this decreases BP
Renin-Angiotensin-Aldosterone System (RAAS)
maintains normal BP and blood volume
Angiotensin I is secreted by the kidney (is a vasoconstrictor; increases TPR and BP)
ACE is secreted by the liver
Angiotensin II is formed in the plasma; works on adrenal cortex and is a potent vasoconstrictor
Aldosterone is released by the adrenal cortex
Aldosterone works on the kidneys to conserve Na+ and H2O; this increases blood volume and BP
Angiotensin II stimulates the release of Antidiuretic hormone from the posterior lobe of the pituitary gland;
this stimulates the thirst center (higher fluid intake -> higher volume of blood)
this hormone also stimulates the kidney to pull water from the urine back into blood (higher blood volume); it is also a potent vasoconstrictor
Kidney
filter the blood, maintain water and electrolyte balance, maintains the acid-base balance, secretes urine, allows the blood to gain the necessary nutrients (water and electrolytes), is composed of nephrons
Nephron
a structure of the kidney;
consists of a glomerulus, a proximal collecting tubule, a loop of Henle, a distal convoluted tubule and a collecting duct
Rules with ions in kidneys
If Na+ goes out, so does H2O
If Na+ goes in, K+ comes out
If H+ goes in, Na+ goes out
If Cl- goes in, Na+ goes out
Urine Formation
Filtration - H2O, salts, sugars, acids, drugs, nitrogenous wastes leave the blood; large particles stay (proteins and blood cells)
Tubular Reabsorption - body retains H2O, salts, sugars
Tubular Secretion - substances from blood go back into the renal tubule (drugs, acids, nitrogenous wastes, salts and H2O) as wastes products to be excreted
Reabsorption
Glomerulus - filtration occurs
Tubular Reabsorption -
PCT & DCT - H+ is secreted; Na+ and H2O is reabsorbed
DCT - Aldosterone is secreted along with K+; Na+ and H2O are reabsorbed (increase in aldosterone may cause hyperkalemia)
Loop of Henle - CL- is reabsorbed along with Na+ and H2O
Collecting duct - ADH maintains the water balance, decrease in urine output, increase in blood volume
- No ADH: increase in urine output and decrease in blood volume
Tubular Secretion - occurs when ions from blood go into the tubules
Non-pharmacological Treatment of HTN
decrease sodium input, reduce fat intake, decrease stress, increase physical activity, rest, moderate alcohol intake, weight loss
Antihypertensive Pharmacological Treatment
Vasodilators, CCB, BB, diuretics, ACE inhibitors, ARB, renin inhibitors, combo therapy
Diuretics
USES: CHF, HTN, edema, anuria, renal disease
Types: Osmotic Diuretics, Thiazide/Thiazide-like Diuretics, Loop Diuretics (Organic Acid Diuretics)
Osmotic Diuretic
decreased ICP; pulls water from tissues (changes plasma osmolality)
mannitol (Osmitrol)
Thiazide/Thiazide-like Diuretics
do not spare K+;
block reabsorption of Na+, diuresis, Na+ and H2O loss
- sulfa derivative, if allergic to sulfonamides, these are contradicted
Thiazide Diuretic:
hydrochlorothiazide (HCTZ) (Hydrodiuril)
Thiazide-like Diuretic:
chlorthalidone (Hygroton)
indapamide (Lozol)
metolazone (Zaroxolyn)
Loop Diuretics (Organic Acid Diuretics)
do not spare K+ (secreted through urine)
USES: edema, HTN, pulmonary congestion, liver and kidney disease
MOA: inhibit Na+ and Cl- transport in Loop of Henle -> this increases Na+, Cl- and H2O secretion
DRUGS:
furosemide (Lasix)
torsemide (Demadex)
Potassium Sparing Diuretics (Aldosterone Receptor Antagonists)
control K+ depletion through urine
DRUGS:
amiloride (Midamor)
sprinolactane (Aldactone)
triamterene (Dyrenium)
(possible hyperkalemia and gynecomastia)
Diuretics (Common Side Effects)
Hypotension,
orthostatic hypotension,
reflex tachycardia,
thirsty/dry mouth,
nausea
Diuretics Patient Teaching
Take medication exactly as prescribed;
taking medication as prescribed helps control high BP and prevent complications;
syncope may be experienced (fainting may occur due to blood volume depletion, low BP, and low blood flow and O2 level)
Due to taking a diuretic, an increase in HR should be reported; a reflex tachycardia may occur due to lowering of BP);
if taking a diuretic and a cardiac glycoside, monitor pulse;
orthostatic hypotension may occur - be careful with changing positions;
patients should monitor and journal their daily weight; monitor for fluid gain;
monitor input and output for patients in hospitals
Thiazide Diuretics: Patient Teaching
Side Effects:
hypercalcemia, hyperglycemia, hyperlipidemia, hyperuricemia, hypokalemia ( may need to supplement with (dietary): bananas, papayas, mangos, lima beans, artichoke, cantaloupe, watermelon, apricots, nuts, oranges, dates and fish)
Symptoms Include: leg cramps, muscle weakness, less alert, lethargy, constipation, arrhythmias
Sympatholytics (lower HTN)
Beta Adrenergic Blockers, Peripheral Alpha-1 Blockers, Alpha-2 Central Agonists
Beta Adrenergic Blockers (Sympatholytics; lower HTN)
MOA: block beta-1 receptors - decrease BP and CO
block release of renin by kidneys - interferes with the RAAS
USES: HTN, CHF, angina, migraines, glaucoma, tachyarrhythmias
DRUGS: metoprolol (Lopressor)
propranolol (Inderal)
PATIENT TEACHING/SIDE EFFECTS: drowsiness, GI upset, bradycardia, CNS depression, monitor serum lipid levels, mental depression, monitor blood glucose levels in diabetics
Peripheral Alpha-1 Antagonists/Blockers (azosin)
USES: HTN, angina, BPH
MOA: block NE from binding to adrenergic alpha-1 receptors -> vasodilation
DRUGS: prazosin (Minipress)
doxazosin (Cardura)
terazosin (Hytrin)
PATIENT TEACHING/ SIDE EFFECTS: orthostatic hypotension - caution with changing positions, reflex tachycardia, GI upset, increased urination
Alpha-2 Central Agonists
USES: HTN, angina
MOA: inhibits CNS activity, lowers BP, acts on alpha-2 receptors -> vasodilation
DRUGS: clonidine (Catapres)
methyldopa (Aldomet)
PATIENT TEACHING/SIDE EFFECTS: hypotension, dry mouth, drowsiness
Vasodilators (lower HTN)
MOA: relaxes smooth muscle of the vessels
USES: HTN, CHF, CAD
DRUGS: hydralazine
minoxidil (Loniten, Rogaine)
nitroprusside (Nipride, Nitropress)
PATIENT TEACHING/SIDE EFFECTS: flushing, HA, hypotension, N/V, rapid heartbeat, cannot be used with ED meds
Hypotension (Symptoms)
dizziness, lightheadedness, syncope, nausea
Hypotension (Treatment)
rest - lay down, elevate legs, give O2, force fluids
Renin-Angiotensin II-Aldosterone System
Renin is secreted by the kidneys;
Angiotensin I is secreted by the liver (is a vasoconstrictor);
ACE is released by the lungs;
Angiotensin II is formed in the plasma;
Angiotensin II stimulates adrenal cortex to release aldosterone;
Angiotensin II stimulates posterior pituitary to release ADH,
Angiotensin II is a potent vasoconstrictor;
Angiotensin II stimulates the thirst center (more fluid intake, higher blood volume, higher BP)
Aldosterone works on the kidneys; they reabsorb Na+ and water back into blood (higher blood volume, higher BP)
AntiDiuretic Hormone works on the kidneys to take fluid from urine back into blood; is a vasoconstrictor
ACE Inhibitors (work against HTN)
Normal Process: ACE -> Angiotensin II
MOA: inhibits the ACE;
decrease of release of aldosterone; decreased reabsorption of Na+ and H2O; vasodilation
USES: HTN
DRUGS:
captoprin (Capoten)
enalapril (Vasotec)
lisinopril (Zesttril)
benazepril (Lotensin)
quinapril (Accupril)
ramipril (Altace)
PATIENT TEACHING/SIDE EFFECTS: Where does K+ go? -> K+ levels rise -> causing hyperkalemia, hypotension, angioedema, dizziness, HA, GI upset, rash, arrhythmias, coughing
Angiotensin II Receptor Blockers/Antagonists (ARBs) (work against HTN)
MOA: block effects of Angiotensin II; blocks the release of aldosterone, vasodilation
- No significant effects on K+, no angioedema
USES: HTN
DRUGS:
olmesartan (Belicar)
PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, HA, drowsiness, cough, N, monitor K+ levels
Renin Inhibitors (work against HTN)
MOA: inhibit actions of renin
USES: HTN
DRUGS: aliskiren (Tekturna)
PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, upset stomach, HA, cough, lightheadedness
Calcium Channel Blockers (CCBs) (work against HTN)
MOA: interfere with Ca2+ entry into the cardiac muscle cells and smooth muscle cells of the vessels; this results in a decrease of a venous return, decrease of BP, increase of blood flow in the coronary arteries, slower conduction; vasodilation
USES: HTN, tachyarrhythmias, angina
DRUGS:
nifedipine (Procardia), nisoldipine (Sular), amlodipine (Norvasc), verapamil (Calan), diltiazem (Cardizem)
PATIENT TEACHING/SIDE EFFECTS: hypotension, dizziness, HA, facial flushing, constipation, reflex tachycardia, xerostomia
BP Thresholds
1) Normal BP: less than 120/80 mm Hg
2) Elevated BP: 120-129/less than 80 mmHg
3) Stage 1 HTN: 130-139/80-89 mm Hg
4) Stage 2 HTN: equal or greater than 140/90 MM Hg
Normal BP recommendations
promote optimal lifestyle habits: healthy diet, weigh loss if needed, tobacco use cessation, alcohol moderation, physical activity;
reassess in a year
Elevated BP recommendations
Nonpharmacological treatment (Class I);
reassess in 3 to 6 months;
weight loss for overweight or obese patients;
healthy diet (DASH);
Sodium restriction;
potassium supplementation;
increased physical activity with structured exercise program;
limited alcohol: 1 per day (in women) and 2 per day (in men)
Stage 1 HTN
(ASCVD or estimated 10-y CVD risk greater than or equals to 10%)
BP: 130-139/80-89 mm Hg;
Nonpharmacological treatment and BP lowering medication (Class I);
reassess in 1 month (Class I);
if BP goal is met, reassess in 3 to 6 months (Class I);
if BP goal is not met, assess and optimize adherence to therapy (consider intensification of therapy)
Stage 1 HTN (130-139/80-89)
(no ASCVD or risk of CV of or greater than 10 %)
Nonpharmacologic therapy (Class I);
reassess in 3 to 6 months (Class I)
Stage 2 HTN
BP equals or is greater than 140/90;
nonpharmacologic treatment and BP lowering medication (Class I)
Stepped Care Approach to HTN
First-line options (single or in combination):
-ACE Inhibitors, ARBs, CCBs, and thiazide diuretics
-beta-blockers can be used in patients who have any of the following: CAD, dysrhythmia, post-myocardial infarction, and heart failure
(those older than 60 yrs old should not take beta blockers as initial agents; have not shown effective at preventing CV events
-for moderate HTN of >20 mm Hg:
take an ARBs or ACE Inhibitors with a diuretic or a dihydropyridine (DHP) calcium channel blocker (such as amlodipine, nifedipine, or felodipine) combination
-start with a low dose and titrate upwards
-if hypertension has not been controlled, the following may be added in the stepwise order:
*CCB or a thiazide diuretic (chlorthalidone is more potent than hydrochlorothiazide (HCTE); add whichever one has not been used); can use a combination low dose amiloride/HCTZ in appropriate patients;
-a vasodilating beta-blocker (such as carvedilol or nebivolol) and/or aldosterone blocker
-alpha-blockers, direct vasodilators; consider referral
Treatment Recommendations for Specific Patient Populations
-African-Americans should be prescribed CCB 1first
-those with chronic kidney disease, should be prescribe ACE Inhibitors or ARBs
-differences in ARBs agents and diuretics
*Losartan (Cozaar): weakest ARB; may require twice a day dosing;
*Valsartan (Diovan), telmisartan (Micardis), irbesartan (Avapro), candesartan (Attacand), olmesartan (Benicar) are all generic (except Edarbi) and can be used everyday
*more potent ARBs include olmesartan and azilsartan (which is the most potent)
*chlorthalidone is more potent than HCTZ
-for hypertension that is difficult to control:
*make sure that the patient is on sodium restricted diet of 1500-2000 mg per day and not taking OTC nonsteroidal or anti-inflammatory medication or drinking excess alcohol
*if a patient is on ACE Inhibitor/ARB with a thiazide diuretic and systolic pressure remains uncontrolled, change ACE inhibitor to ARBs, if a patient is on losartan, change to a more daily, once-daily ARB
*if the patient is on a beta-blocker for some other reason, the drug cab be changes to a vasodilating beta-blocker
*clinicians may use a dihydropyridine CCB; do not use nifedipine with LV systolic dysfunction
*may add an aldosterone blocker if BP remains unchanged
*clinicians may change HCTZ to chlorthalidone (more potent patient thiazide diuretic)
-for elevated isolated systolic pressure:
the Canadian guidelines recommend using an ARB, a thiazide diuretic, and/or dihydropyridine CCBs
