LP 11 Hypertension

Term
1 / 108
What is hypertension?
Click the card to flip 👆
Terms in this set (108)
What is hypertension?
Persistent levels of increased BP -
systolic greater than 140
diastolic greater than 90
What is considered hypertension in elderly?
Persistent levels of increased BP -
Systolic greater than 160
Diastolic greater than 90
What are the modifiable risk factors for hypertension?
Smoking, excessive caffeine consumption, excessive alcohol consumption, increased cholesterol/triglycerides, sedentary lifestyle, sodium intake, hypokalemia, diabetes (hyperglycemia causes hyperosmolar situation and increases vascular pressure), stress, oral contraceptives, diet pills, cold capsules, antihistamines, NSAIDs (constrict the renal arterioles and cause hypertension)
What are ways you can decrease hypertension?
Omega 2 fatty acids and fish oils can reduce BP and triglycerides, exercise can decrease renin levels and decrease BP, salt causes water retention which increases tension in vascular space so pt should follow DASH diet, low K+/Ca++/vitamin D is also associated with hypertension, young black men have higher BP and lower K+ in general so they need to be cautious
What are non-modifiable risk factors for hypertension?
Genetics, race, sex, age. Black pts has an increase in BP starting in pre-teen years, their BP stays higher at night rather than dropping (as usually happens for other races). With end-stage renal disease, the medication is better to give within the first 12 hours and is often given at night to help preserve kidney function. Men are more likely to get hypertension until menopause and then it equals out.
What are other risk factors for hypertension besides the general modifiable and non-modifiable?
atherosclerosis, arteriosclerosis, reduced baroreceptor sensitivity (baroreceptors are in blood vessel walls and are sensitive to pressure), decline in renal function, insomnia.
What is the MAP?
MAP is Mean Arterial Pressure and is comprised of cardiac output X total peripheral resistance.
MAP = CO x TPR
What determines cardiac output?
Hear rate times stroke volume
What affects cardiac output?
CNS outflow and preload
What medications affect CNS outflow to affect cardiac output?
The medications work on the hypothalamus.
The classification of the medication is alpha-2 receptor agonists.
Examples - Aldomet & Catapress
What medications directly affect cardiac output?The medications will act on the beta-1 receptors which are located on the heart and affect heart rate and stroke volume. The class of medication is beta-blockers Examples - "olols"What medications affect preload which affect cardiac output?The medications affect aldosterone secretion. The classifications are diuretics and ACE-inhibitors.What are alpha-1 antagonists?They alpha-1 receptors work on the blood vessels and cause vasodilation. Example - HytrinWhat are ARBs?They work on the angiotensin 2 receptor blockers; they block renin and cause vasodilation. Examples - Losartan, ValsartanWhat are calcium channel blockers?Calcium channel blockers block calcium channels and cause vasodilation. Calcium is needed for the muscle to contract so if you block the channel, there is no contraction and dilation occurs.What is the mechanism of hypertension that causes increased cardiac output?Sympathetic nervous system activation increases catecholamine and renin release. This can be combated with beta blockersWhat is the mechanism of hypertension that causes increased preload and vessel distension?Increased intravascular volume. This can be combated with diureticsHow does sodium affect vascular volume?Increased sodium intake brings increased fluid into the vessel. Decreased sodium means less fluid in the vessel.What type of medication affects the RAAS and therefore hypertension?ACE-inhibitorsHow does the RAAS work?Stimulation of the CNS causes the preganglionic fibers to release acetylcholine then affects the postganglionic fibers in the blood vessels. These then release norepinephrine causing a constriction of the blood vessels and an increased peripheral vascular resistance. This will effect the adrenal gland. The medulla of the adrenal gland secretes epinephrine and the cortex secretes cortisol and steroids which then causes additional vasoconstriction and decreases blood flow to the kidneys. Then renin is secreted, and gets converted to angiotensin I then angiotensin II, which causes aldosterone to be released. The aldosterone causes Na+ and H20 retention and then increase the intravascular volume.What are potential systemic damages from hypertension?Damage to intima (innermost coating of a blood vessel), fibrin accumulation in small blood vessels, localized edema, increased clotting, decreased tissue perfusionWhat are potential heart issues r/t hypertension?angina/MI, left ventricular failure, left heart failureWhat are potential kidney issues r/t hypertensiondamaged nephrons get replaced with scar tissue, azotemia (excessive nitrogen waste in the blood which elevates the BUN/Cr), elevated BUN/Cr, renal insufficiencyWhat are potential brain issues r/t hypertension?TIA/stroke, hemiplegia/alteration in vision, subarachnoid hemorrhage.What are potential retinal issues r/t hypertension?hemorrhage, exudate (fluid accumulation), narrowed arterioles, visual changes/blindnessWhat are the diagnostics for hypertension?Retinal exam, EKG (may show left ventricular hypertrophy), urinary analysis (may show protein in urine), electrolyte analysis (Na/K), fasting blood sugar, Bun/creat, IV pyelogram, renal arteriogram, serum cholesterol, lipid profileWhat are the guidelines for how to treat BP?See in blackboardwhat is normal BP and recommended follow up?<130/85 Normal follow up - recheck in 2 years High normal follow up - recheck in 1 yearWhat is stage I hypertension and recommended follow up?130-139/85-89 Stage I follow up - confirm within 2 monthsWhat is stage II hypertension?140-159/90-99 Stage II follow up - evaluate or refer for additional care within 1 monthWhat is stage III hypertension?180-209/110-119 Stage III follow up - evaluate or refer for additional care immediately or within 1 week.What are non-pharmacologic treatments for hypertension?weight reduction, DASH diet, sodium restriction, exercise, smoking cessationWhat is the DASH diet?Dietary Approaches to Stop Hypertension Focus is on low saturated fat, low total fat, low cholesterol, rich in fruits/vegetables, low in dairy products, rich in Mg, Ca, K+, protein, and fiber and should restrict sodium to 2400 mg per day (about 1 teaspoon). Pt should restrict caffeine, make occupational/lifestyle changes, biofeedback and relaxation techniques, and restrict alcoholWhat are examples of foods high in magnesium?spinach and other greens, wheat bran, broccoli, squash, popcorn, sunflower seeds, nuts, "hard" tap water, shrimp, pork, kidney beans, figs, peaches, avocados, bananas, berries.What are foods high in potassium?apples, bananas, cantaloupe, oranges, prunes, asparagus, broccoli, carrots, and potatoesWhere are common areas for atherosclerosis and potential treatments?Common area is the superficial femoral artery or anterior tibial artery. Pt may get treated with a femoral popliteal bypass graft around the occluded femoral artery or around the superficial femoral, popliteal nad proximal tibial arteries.What are major risk factors for peripheral artery disease?Age 40 or older, cigarette smoking (most powerful modifiable risk factor), diabetes mellitus, hyperlipidemia, hypertension, hyperchromocysteinemia.What is arterial disease?Stenosis of the artery; plaque builds up, there is a loss of vessel elasticity, the symptoms are dependent on collateral circulation, and claudication. May be acute or chronic. Progression may lead to chronic pain, ulcers, gangrene, and bluish gray mottling.What is claudication?Pain from walking, the lower extremities will get decreased blood flow when walking and is r/t sclerosis that causes a build up of lactic acid which causes the pain.What are site-dependent symptoms of claudication?Aortic - back Iliac - hips Femoral - lower thigh/calk Popliteal - lower calf Tibial - foot Peroneal - footWhat is acute arterial disease VS chronic arterial disease?Acute can be from emboli that got thrown from left side of heart that occludes the arteries Chronic will happen over time and you will see mottling.How is arterial disease diagnosed?Vascular history is taken, physical exam, ankle-brachial index (ABI) measurement, noninvasive lab tests, invasive lab tests such asan arteriogram which is when they inject dye to see where the occlusion isWhat type of subjective data is taken for a patient with arterial disease?Do you develop any cramping or fatigue in the muscles of either leg that occurs when you walk? Do symptoms only start when you walk? Do symptoms resolve once you stop walking? Do the symptoms occur in one or both legs? Do you have any pain in legs while resting? Do you have any non-healing foot wounds (typically the ulcerations are dry because there is a lack of oxygen)what physical assessment data is considered with arterial disease?Bilateral color/motion/temperature/sensation (CMTS), skin assessment (skin may be shiny/pale), hair growth (sparse or none at all), toenails (thickened), capillary refill (decreased), blood pressure (check in both arms), and ankle arm indexWhat is the peripheral pulse assessment scale?0 - no detectable pulse 1 - pulse thready, weak, difficult to detect 2 - difficult to palpate 3 - easily palpable 4 - strong/bounding If can't feel pedal or post tibial pulse the Doppler will be used but it will not get documented with this scale because it is not a detectable palpationWhat is the ankle-brachial index (ABI)?You take the BP and use the systolic number in the right ankle, then you use either the pedal or post tibial areas to get the systolic pressure of that area. Then you take the brachial pressure and divide the two numbers. With healthy arteries, the pressure in the ankle and brachial area will be the same and so the ABI will be 1. If the pulse cannot be found, use the BP cuff and the Doppler to find the systolic pressure.What are the the interpretations of the ankle-brachial index?0.91-1.0 is normal 0.41-0.91 is mild to moderate peripheral vascular disease 0.00-0.40 is severe peripheral vascular disease The severity of PAD is closely associated with the risk of MI, stroke and death from vascular causes. The lower the ankle-brachial index, the greater the risk of cardiovascular events. Pts who have the lowest ABI have an annual mortality rate of 25%What is the goal of treatment for hyperlipidemia?Serum LDL less than 100 Serum triglycerides less than 150 Statin agent will be initial therapy Niacin-lowers LDL levels nd triglycerides Dietary management/teaching low cholesterol ExerciseWhat are the goals of treatment for a patient with diabetes who has arterial disease?Intensive control of blood glucose prevents the microvascular complications. Monitor A1C - goal is <7% Dietary teachingWhat are some ways hypertension can be treated?DASH diet Beta blockers ACE Inhibitors - very beneficial with diabetic pt Angiotensin 2 receptor antagonists Goal of BP <120/80What are smoking cessation teachings?Hypnosis/support groups/nicorette may all help. There is a 25% rate of cessation with Wellbutrin and nicorette ptaches *50% risk of reduction for peripheral vasular disease*Why are high homocysteine levels associated with hypertension?They facilitate the oxidation of LDL cholesterol. Promote endothelial dysfunction Leads to acceleration of atherosclerosisWhat causes high homocysteine levels?Genetic defects Alterations in vitamin B12 metabolism Dietary folate deficiencyWhat are the treatments for high homocysteine levels?A level less than 12 is considered optimal. Eat a diet high in vitamin B and folic acidsWhat are antiplatelet drugs that are used for pts with peripheral vascular disease?aspirin ticlopidine (Ticlid) clopidogreal (Plavix)How does exercise affect hypertension?May improve arterial blood flow to the extremity through the buildup of collateral circulation. Should be individualized for each client Client with severe rest pain, venous ulcers or gangrene should not participate. Initiate gradually and slowly increase Walking is excellent Supervised walking based programs may be needed. Pt may be instructed to walk to the point of claudication, stop and rest, and then walk a little further.What is the action of diuretics?Volume depletion Sodium excretion Vasodilate the peripheral arteriolesWhat are the types of diuretics?Thiazide Loop Potassium sparingWhat are thiazide diuretics?Used in pts with normal renal function; increases excretion of Na and H20 by inhibiting reabsorption in the distal tubule of the nephron. If taken with NSAIDs, the effect is negated since the NSAIDs restrict the renal artery and conserve water. Examples: chlorothiazide and hydrochlorothiazideWhat are loop diuretics?Inhibits reabsorption of sodium and water in the Loop of Henle and the distal renal tubule. Increased excretion of sodium, water, chloride, phosphate, and bicarbonate. Examples: furosemide (Lasix) and bumetanide (Bumex)What are potassium sparing diuretics?Acts on the distal renal tubule to retain potassium and hydrogen and excretes sodium bicarbonate and calcium. It is a weak diuretic and hypotensive but it can be used with other diuretics. Examples: spironolactone (Aldactone) and amiloride (Midamor)What are advantages to thiazides?African Americans respond better than caucasians. They help manage concomitant heart failure. Elderly females and thiazides mean increased calcium reabsorption. Loop diuretics are effective in patients with severe renal insufficiency or CHF. Inexpensive. Protects against strokes. Reduction in morbidity and mortality demonstrated.What are the disadvantages of diuretics?They are at risk for fluid volume deficit. Orthostatic hyptension is possible so it is important to teach the pt to rise slowly and to monitor the BP while laying/sitting/standing to see how much the drop is. Hyperglycemia, hypokalemia (arrhythmias and dig toxicity) and increased uric acid levels are potential complications for pts taking thiazide and loop diuretics. Hyperkalemia is side effect of potassium sparing. Hearing loss is potential with loop IV rapid infusion. Hyponatremia. Decreased HDL /increased LDL (thiazide). Hirsutism/deep voice/menstrual irregularities from potassium sparing.What are the drug interactions with diuretics?NSAIDs - affect diuretic negated by renal artery vasoconstriction and resulting Na and H20 retention caused by NSAIDs. ACE inhibitors - inhibition of aldosterone by ACE results in risk of hyperkalemia and hypermagnesemia, blunting effects on lytes by diuretics (thiazide/loop). ACE inhibitors and potassium sparing diuretics increase risk for hyperkalemia.What are beta-blockers?Acts by pluggin beta receptors; so beta receptor stimulants (epinephrine/norepinephrine) can't make contact with the receptor, preventing beta stimulation.Where are beta 1 and beta 2 receptors located?Beta 1 receptors are located on SA node and myocardial cells Beta 2 receptors are located on bronchial smooth muscles; large arteries of arms/legs/cranium; hepatocytes for glucose production and skeletal muscle cells.What do beta blockers reduce?heart rate cardiac output (HRxSV) Renin release from kidneys Peripheral vascular resistanceWhat are the two types of beta blockers?noncardioselective and cardioselectiveWhat are examples of noncardioselective beta blockers?pindolol (Visken) nadolol (Corgard) propranolol (Inderal) timolol (Timoptic) labetalol (Normodyne, Trandate)What are noncardioselective beta blockers?They have an equal affinity for blocking beta 1 receptors (heart) and beta 2 receptors (bronchoconstriction, vasoconstriction of large arteries of the legs, blocks glycogenolysis, vasoconstriction of the large arteries of the cranium)What are the contraindications for beta blockers?Pts with respiratory conditions aggravated by bronchoconstriction (asthma/COPD); use with caution in pts with PVD and diabeticsWhat are cardioselective beta blockers?They affect only the beta 1 receptors of the heartWhat are examples of cardioselective beta blockersatenolol (Tenormin) *drug of choice for diabets* esmolol (Brevibloc) metoprolol (Lopressor) acebutolol (Sectral)What are the advantages of beta blockers?Reduction in morbidity/mortality demonstrated Minimal postural or exercise hypotension Modest cost Decreased mortality after MI Decreased incidence/progression CADWhat are clinical uses for beta blockers?Angina Arrhythmias MI Migraine Glaucoma Silent ischemia CHF GI bleeding (portal vein hypertension)What are the disadvantages/side effects of beta blockers?Not as effective for black people Bronchospasm (noncardioselective); use cautiously with asthma/emphysema May mask signs/symptoms of hypoglycemia in diabetes Bradycardia Do not D/C abruptly, especially with angina CHF- use cautiously Decrease quality of life Impotence May decrease HDLs and increase triglycerides Vasoconstriction large arteries legs/cranium/baldness/cold feet Exercise intolerance r/t decreased heart rateHow do calcium channel blockers work?Inhibit movement calcium ions across the cell membrane.What do calcium ions do?Helps with normal contraction of cardiac muscle (Stroke Volume) Constriction of vascular smooth muscle (vasoconstriction/increased BP)What ways do calcium channel blockers affect the body?Decrease arrhythmias Depression of impulse formation in specialized cardiac cells Relaxation of smooth muscle of blood vessels (vasodilation/reduced BP)What are 3 categories of calcium channel blockers?Dihydropyridines "pines" Diphenylalkylamines Benzothiazepine (Diltiazem)What are dihydropyridines?"Pines" - calcium channel blockers that increase the affinity for peripheral vascular calcium channels than myocardial calcium channelsWhat are diphenylalkylamines?Calcium channel blocker with both vascular and cardiac effectsWhat are benzothiazepines (Diltiazem)?1/5 as effective on cardiac muscle cells as peripheral vascular calcium channelsWhat are examples of calcium channel blockers?nifedipine (Procardia) nisoldipine (Sular) felodipine (Plendil) amilodipine (Norvasc) diltiazem (Cardizem) verapamin (Calan, Isoptin) - PVD and heart nicardipine (Cardene) isradipine (DynaCirc)What are the uses of calcium channel blockers?More effective in pts with higher pretreatment BP 1st or 2nd line prescription in pts with hypertension and co-existing angina Alternative to beta blockers Effective in African American/elderly hypertensionWhat are the advantages for calcium channel blockers?side effects decreased with slow release formulations No adverse effects on glucose No effects on quality of life May prevent progression of atherosclerosis Effective in CADWhat are the side effects of the calcium channel blockers?"pines" - vasodilating effects: reflex tachy; peripheral edema; headache Negative inotropic effects (means they can decrease the contractility of the heart) especially verapamil block Ca channels involved gut motility Infertility - problem with sperm penetration.What is the action of ACE inhibitors?Block enzyme known as ACE. ACE converts angiotensin I to angiotensin II in RAASWhat is the pathophysiology of hypotension/hypovolemia?If the kideny is not being perfused well, renin is like the "tattle-tale" who goes to the liver and causes it to secrete angiotensin I which causes the angiotensin converting enzyme in the lungs to convert angiotensin I to angiotensin II. Angiotensin II causes an increase in growth factors, it "tenses" your angios (vasoconstriction), and causes secretion of aldosterone from the adrenal cortex creating an increase in sodium and water retention which means an increased vascular volume and increased potassium secretion.What are other functions of angiotensin II?Increases inflammation in the arteries Prothrombotic (triggers clotting) Increases tissue resistance to insulinWhat are the functions of ACE inhibitors?Vasodilation/diuresis increased renal blood flow; preserve cardiac output Hyperkalemia - aldosterone production inhibited Decreased growth factors anti-inflammatory anti-thrombotic hypoglycemic decreased growth of tissue "remodeling"What are examples of ACE inhibitors?The "pril" family captopril (Capoten) enalapril (Vasotec) benazepril (Lotensin) lisinopril (Prinivil, Zestril) quinapril (Accupril)What are the clinical indications for ACE inhibitors?Hypertension CHF prevents/slows progression of diabetic nephropathy Post MI Reduces size of left ventricleWhat are the side effects of ACE inhibitors?Non-productive, irritating cough (ACE responsible for catabolism bradykinin which is a potent bronchospastic agent) more side effects for women than men Hypotension Hyperkalemia - pts with underlying renal insufficiency/high normal level potassium with normal renal function Don't want a pt on ACE inhibitor to use salt replacement because they will already have hyperkalemia r/t the medication Angioedema (life threatening, usually occurs after the first dose and more frequently seen in African Americans. This is when you see swelling of the tongue and airway). Use caution in pts with hay fever/eczema/asthma (edema may occur after 1st dose) HypoglycemiaWhat is the relationship between ACE inhibitors and NSAIDs?NSAIDs may reduce or negate the antihypertensive effects and risk the increase in renal failure. NSAIDs inhibit prostaglandin production that mormally maintains renovascular vasodilation which means vasoconstriction of afferent arteriole and decrease GFR. ACE inhibitors vasodilate the efferent arterioles. The combo of these decrease the pressure gradient for glomerular filtration. *clinoril is safest NSAID to use with ACE inhibitors* *Celcoxib/Rofecoxib - don't vasocontrict renal artery*Who are second line antihypertensive agents considered for first line therapy?Pts with diabetes and hypertension Post MI hypertension Dementia pt (improves cerebral blood flow) Type II db - elevated potassium occurs as a side effect decreases insulin release in pancreasWhat are positive side effects of ACE inhibitors?no sexual dysfunction, no CNS effects, no peripheral edema or constipation.ACE inhibitors are less effective in which people?Afro-American's and elderlyHow do ACE inhibitors slow diabetic neuropathy?Uncontrolled hyperglycemia results in increased angiotensin 2 which acts as growth hormone in glomerular tissue and constricts efferent arteriole. ACE inhibitors vasodilate efferent arterioles/blocks angiotensin 2 which causes efferent arteriole vasodilationWhat are the advantages of ACE inhibitors?Lacks CNS depression side effects Lack sexual dysfunction side effects Also effective in Rx heart failure. Decreases preload and after load Used to slow progression of diabetic neuropathy Renal function gets preserved Lack of aggravated asthmaWhat are some disadvantages/side effects of ACE inhibitors?nausea/fatigue/headache/diarrhea/expensive/cough/angioedema/neutropenia/agranulocytosis/orthostatic hypotension/nephrotoxicity (really watch electrolytes and BUN adn creatinine levels)/hyperkalemiaWhat are examples of ARBs?"The Sartans" losartan (Cozaar) valsartan (Diovan) irbesartan (Avapro) candesartan (Atacand)How to ARBs work?Bind to angiotensin II receptor sites, blocking the potent constrictor from binding to receptor sites in vascular smooth muscle/adrenal glandsWhat are the advantages of ARBs?No effect on renal function, prostaglandin levels, triglycerides, cholesterol or blood glucose No cough as with ACE inhibitors Orthostatic hypotension Dyspepsia, cramps, diarrhea, hyperkalemiaWhat is an example of an aldosterone receptor agonist?eplerenone (Inspra)What is the action of aldosterone receptor agonists?Lowers BP by blocking aldosterone binding at the mineralcorticoid receptor sites in the brain, kidney, heart and blood vessels.What are the disadvantages/side effects of aldosterone receptor agonists?Orthostatic hypotension Hyponatremia hyperkalemiaWhat are direct renin inhibitors?They bind with renin, causing a reduction of angiotensin I, angiotensin II, and aldosterone levels. It is used as monotherapy or in combo with other anti-hypertensive meds. Hyperkalemia is uncommon with monotherapy. Example - aliskiren (Tekturna)