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Antihypertensives
Week 6
| Question | Answer |
|---|---|
| Hypertension is a major risk factor for what conditions? | Coronary artery disease, CHF, stroke, renal failure, peripheral vascular disease |
| What are characteristics of primary (essential) hypertension? | Most common (92% of cases), no identifiable cause |
| What are characteristics of secondary hypertension? | 8% of hypertension cases, identifiable causes |
| What are the major changes from JNC 6 (1997) and JNC 7 (2003)? | Systolic BP for ages over 50 are more important than diastolic. 120-139/80-89 are prehypertensive. Thiazide diuretics are generally 1st choice of drug therapy. Many pts require 2 drugs |
| According to the JNC 7, what values are considered prehypertensive? | 120-139/80-89 |
| Which drug is generally 1st choice of therapy in treating hypertension? | Thiazide diuretics |
| What are normal values for blood pressure? | <120/<80 |
| What is stage 1 hypertension? | 140-159 systolic OR 90-99 diastolic |
| What drugs are used to treat stage 1 hypertension? | Thiazides, or ACEI, ARB, BB, CCB |
| What is stage 2 hypertension? | ≥160 systolic OR ≥100 diastolic |
| How is stage 2 hypertension treated? | With 2 drugs: thiazides, and ACEI, ARB, BB, CCB |
| What is the equation to find cardiac output? | CO = HR x SV Cardiac output equals heart rate times stroke volume |
| What is the equation to find blood pressure? | BP = CO x PVR Blood pressure equals cardiac output times peripheral vascular resistance |
| What are some mechanisms of blood pressure control? | SNS baroreceptor reflex. Renin-angiotensin-aldosterone system (RAAS). Renal regulation |
| What do alpha 1 receptors do in SNS? | Affect peripheral blood vessels; stimulates vasoconstriction |
| What do alpha 1 blockers do in SNS? | Cause vasodilation |
| What do alpha 2 receptors do in SNS, and where are they located? | Located in brain. Stimulation leads to vasodilation (opposite of alpha 1) |
| What do beta 1 receptors do in SNS, where are they located? | Primarily located in heart. Stimulation leads to increased HR and BP |
| What do beta 1 blockers do in SNS? | Causes decreased HR, BP and decreased contractility (may affect respirations) |
| What do beta 2 receptors do in SNS, where are the located? | Primarily respiratory/located in lungs. Stimulations leads to bronchodilation |
| How does the PNS (parasympathetic nervous system) affect BP? | Not as much as SNS |
| PNS is discussed more with ______ | Cardiac dysrhythmias |
| What does stimulation of the vagus nerve do? | Decreases HR. Causes bronchoconstriction |
| What triggers the RAAS system? | Low blood pressure/low blood volume |
| What does angiotensin II do? | Constricts renal and systemic blood vessels |
| What does aldosterone do? | Causes kidneys to retain sodium and water |
| What are some nonpharmacologic methods of managing hypertension? | Stress management, restriction of salt, exercise, weight loss, quitting smoking/tobacco, limiting alcohol, lower fats/triglycerides in the diet |
| What are 7 classes of medications used to treat hypertension? | Diuretics, sympatholytics, direct-acting vasodilators, calcium channel blockers, ACE inhibitors, angiotensin II receptor blockers, direct renin inhibitors |
| Which are the first-line medications? | Diuretics |
| Sympatholytics include what types of medications? | beta-adrenergic blockers, alpha 1 blockers, alpha/beta blockers, centrally acting alpha2 agonists, adrenergic neuron blockers |
| What is a prototype of thiazide diuretics? | Hydrochlorothiazide (Hydrodiuril) |
| What is a prototype of high-ceiling (loop) diuretics? | Furosemide (Lasix) |
| What is a prototype of a potassium-sparing diuretic (aldosterone antagonist)? | Spironolactone (Aldactone) |
| What is the MOA of beta-adrenergic blockers (beta-blockers)? | Impede action of catecholamines at heart receptors. Reduces HR, cardiac contractility, reduces impulses through AV node, reduces renin production in kidney |
| What receptors do non-selective beta-blockers act on? | Beta 1 and beta 2 |
| What receptors do selective beta-blockers act on? | More effect on beta 1 receptors |
| What is a prototype of a non-selective beta blocker? | Propranolol |
| What are characteristics of propranolol? | Can cause bronchospasm, impaired glucose mechanism, an be used in hyperthyroidism, tremors, migraines |
| What is a prototype of a selective beta blocker? | Metoprolol |
| What are characteristics of metoprolol? | less bronchospasm |
| What are adverse effects of beta blockers? | Bronchospasm. Masks SNS response to hypoglycemia. Can increase heart blocks. Can cause sexual dysfunction. Can intensify depression. Can cause fatigue. |
| What is the MOA of alpha1-blocking agents? | Block alpha 1 receptors in periphery, causing vasodilation of arteries and veins. Causes reduction of peripheral vascular resistance; reduces afterload of heart; reduces smooth muscle contractions in bladder neck and urethra |
| When should alpha1 blockers be taken? | At night due to hypotension |
| What is BPH? | Benign Prostatic Hypertrophy |
| Preload | End diastolic |
| Afterload | End-systolic wall stress |
| What are prototypes of Alpha 1 blocking agents? | Doxazosin (Cardura); terazosin (Hytrin) |
| What is doxazosin (Cardura) used for? | prevents sympathetic medicated vasoconstriction. May cause heart alterations including heart failure |
| What is terazosin (Hytrin) used for? | Used to reduce urinary frequency in men with BPH |
| What are alpha-beta blockers? | An unusual class of hypertensives that block both alpha1 and beta1 receptors |
| What are some prototypes of alpha-beta blockers? | Carvedilol (Coreg), Labetalol |
| What are some characteristics of alpha-beta blockers? | Also markedly affects BP; often used in CHF |
| What is the MOA of centrally acting alpha2 agonists? | Act centrally in the brain. Stimulation decreases SNS outflow. Reduces vasoconstriction. Reduces renin (which turns into angiotensin 1, then angiotensin 2, potent vasoconstrictor) |
| What is a prototype of an alpha 2 agonist? | Clonidine (Catapres) |
| What else can clonidine (Catapres) do (besides reduce vasoconstriction) | Reduces hot flashes in menopausal women |
| What 3 drugs are adrenergic neuron blockers? | guanethidine, guanadrel, reserpine |
| What is the MOA of adrenergic neuron blockers? | Decreases BP through actions in post-ganglionic sympathetic neurons. Either inhibit release of epinephrine (guanethidine, guanadrel), or decrease norepinephrine (reserpine) |
| What is the MOA of guanethidine and guanadrel? | Inhibit release of epinephrine |
| What is the MOA of reserpine? | Inhibit release of norepinephrine |
| What are the adverse reactions of guanethidine and guanadrel? | Severe orthostatic hypotension |
| What is the adverse reaction of reserpine? | Depression |
| What is the MOA of direct-acting vasodilators? | Act directly on smooth muscle to cause relaxation. Do NOT work on adrenergic receptors. Directly cause peripheral vasodilation. |
| What are direct-acting vasodilators indicated for? | Very quick acting and strong in their reduction of BP. Used in emergencies. Can be used alone or in combination. |
| What are SE/AE of direct-acting vasodilators? | Can have negative effects on brain, heart and eyes. Serious side effects. H/a, dizziness, orthostatic hypotension, dysrhythmias, sodium/water retention, n/v |
| What are contraindications of direct-acting vasodilators? | Known drug allergy, hypotension, cerebral edema, head injury, acute MI and CAD |
| Primary sign of toxicity/OD of direct-acting vasodilators? | hypotension |
| What are some important nursing care considerations with direct-acting vasodilators? | Careful monitoring of VS/EKG to quickly spot OD. Place pt in Trendelenberg position, check neuro status. Use care when administering to pt with CV history. |
| How is toxicity/OD of direct-acting vasodilators treated? | With SNS agonists (dopamine, epinephrine, norepinephrine), IV fluids |
| What is the Trendelenberg position? | Positioning the patient with head tilted down |
| What is a prototype of direct-acting vasodilators? | Hydralazine (Apresoline); first oral vasodilator, can be given IM |
| What is the direct-acting vasodilator that is used in life-threatening situations? | Sodium nitroprusside (Nitropress). Half-life of 2 minutes. Lowers BP quickly. |
| A/E of Nitropress? | Hypotension |
| Management of adverse effects of Nitropress? | Vasopressors |
| What role does calcium play in the body? | When calcium enters cell through calcium channels, action potential/muscular contraction is initiated |
| What is a calcium channel blocker? | Block calcium channels, inhibiting calcium from entering cell to initiate action potential |
| What is the action of calcium channel blockers? | Smooth muscle relaxation which lowers peripheral resistance and lowers BP. Variable potency |
| What are indications of calcium channel blockers? | Angina, dysrhythmias, high BP |
| Important nursing implications for calcium channel blockers? | Assess cardiac effects: EKG, BP, HR, VS |
| What are adverse effects of calcium channel blockers? | Reflex tachycardia (HR decreases due to rapid fall in BP); hypotension |
| What substance causes increased absorption of calcium-channel blockers? | Grapefruit juice. Increases effects of calcium-channel blockers |
| What is the MOA of calcium channel blockers? | Blocks calcium from entering the cell. Reduces cardiac contractility. Smooth muscle of vasculature is affected to to cause vasodilation. Heart rate is decreased |
| What effect do calcium channel blockers have on hypertension? | Vasodilation |
| What are the 2 groups of calcium channel blockers? | Dihydropyridines and nondihydropyridines |
| What is the prototype of a dihydropyridine calcium channel blocker? | Nifedipine (Procardia) |
| What does nifedipine (Procardia) do? | Major peripheral vasodilation. May increase CK (creatine kinase) and liver enzymes. |
| What is the prototype of nondihyrdopyridines? | Diltiazem (Cardiazem) |
| What does diltiazem (Cardiazem) do? | Less vasodilation then nifedipine (Procardia). Often used in atrial arrhythmia |
| What are some side effects of calcium channel blockers? | Hypotension, arrythmia, chest pain, peripheral edema, GI symptoms |
| What is to MOA of ACE inhibitors? | Blocks ACE produced in the lungs from converting angiotensin 1 to angiotensin 2. Blocks effects of angiotensin 2, which acts on the adrenal gland to release aldosterone (decreased BP and blood volume) |
| What do ACE inhibitors do in cases of kidney injury? | Slows progression of renal damage |
| What are ACE inhibitors indicated for? | Hypertension, heart failure, MI |
| What are some side effects of ACE inhibitors? | Usually minor. Cough, postural hypotension, hypersensitivity (swelling of skin, mucous membranes). Can develop laryngeal swelling that can be fatal, hyperkalemia from suppression of aldosterone release |
| What are some important nursing care considerations when administering ACE inhibitors? | Monitor first dose response, observe for hypersensitivity, hypotension. Look for: dry cough, change in neuro status, EKG, VS, fluid compartment changes, renal/liver damage |
| What are contraindications of ACE inhibitors? | Can cause serious fetal harm, esp. in 2nd and 3rd trimesters; contraindicated in pregnancy |
| What are prototypes of ACE inhibitors? | Captopril (Capoten); enalapril (Vasotec) |
| What are characteristics of captopril (Capoten)? | 1st developed, short half-life, requires 2 times or 3 times a day dosing What are characteristics of enalapril (Vasotec)? |
| What are angiotensin II receptor blockers? | Relatively new, blocks angiotensin II AFTER it is formed. Drop BP by affecting RAAS cycle. Block vasoconstriction and release of aldosterone. Effect is similar to ACE inhibitors, but w/ no dry cough. Often used in combo w other drugs |
| Where are angiotensin II receptors located? | Smooth muscle and adrenal gland. |
| Angiotensin II receptors blockers are also called ____ | ARBS. Angiotensin II receptor antagonists. |
| Compare angiotensin ii receptor blockers and ACE inhibitors | Both affect smooth muscles and adrenal gland. Equally effective in treating hypertension and both well tolerated. ARBs somewhat more effective after MI, but do not treat BP as effectively in CHF |
| Compared to ACE inhibitors, angiotensin II receptor blockers are more effective after ___ | MI. |
| Compared to ACE inhibitors, ARBs are not as effective in treating ___ in ___ | BP in CHF |
| What are ARBs indicated for? | Used widely, excellent in effects w/o adverse reactions |
| What are SE/AE of ARBs? | Upper respiratory infection, headache, dizziness, sleep, diarrhea, fatigue. Upper resp effects (dyspnea) most common AE. Long term effects not yet known |
| When should ARBs be used w/ caution? | Exercising, or in hot weather |
| Toxicity/OD of ARBs can cause hypotension, tachycardia. | |
| What is treatment of adverse reactions/OD of ARBs? | Symptomatic, includes meds and fluids to expand blood volume |
| What is a prototype of ARBs? | Losartan (Cozaar) |
| What are characteristics of losartan (Cozaar)? | Less problem with cough. Has potent effect. Not sure is as protective as ACE inhibitors (less research done) |
| What are some interactions of ARBs? | Can interact with cimetidine, phenobarbital, rifampin. Can cause hyperkalemia, so K+ monitoring is imp |
| What is MOA of direct renin inhibitors? | Suppress RAAS. Similar strength to ARBs, ACE inhibitors, CCBs |
| What is renin? | Produced by kidney, acts on angiotensinogen prod by liver |
| What are some side effects of direct renin inhibitors? | Diarrhea. Less problems w/ hyperkalemia, cough or angioedema than other antihypertensives |
| What is a prototype of renin inhibitors? | Aliskiren (Tekturna), ONLY drug in this category. AE not well known |
| What is the MOA for potassium-sparing aldosterone antagonists? | Promotes renal excretion of sodium and water without loss of potassium |
| What are some cautions when administering aldosterone antagonists? | Potassium is retained, which could lead to hyperkalemia |
| What is the prototype of potassium-sparing aldosterone antagonists? | Spironolactone (Aldactone) |
| What is the first priority in regards to hypertension? | Prevention is first priority. Stress management, diet, physical activity/exercise |
| What kinds of drug treatments are prescribed for hypertension? (what order) | Diuretics are usually prescribed first, then ACE inhibitors, ARBs. Beta-blockers are NOT as encouraged as next step after diuretics |
| How many antihypertensives should be used in treatment? | Relates to response of patient. Fewer meds, the better to reach normotensive BP. Drugs used from dif classes for best affect. Low doses initially, gradually increased |
| What are some important nursing actions when administering antihypertensives? | Check BP, HR. urine output, reduction of dependent edema, Na+, K+ Cl-, BUN levels, monitor for side effects, and for adherence |
| What is BUN? | Blood urea nitrogen |
| What are important aspects of giving antihypertensives? | Self-efficacy of patient (are they adhering to lifestyle modifications), try to to reduce meds/doses within first year, follow up w/ BP monitoring |
Created by:
kangaloo
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