Exam 2 topic 6 antihypertensive drugs Flashcards

1
Q

Adrenergic drugs

A

Large group of antihypertensive drugs. The alpha blockers and combined alpha/beta blockers.

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2
Q

Adrenergic drugs mechanism of action

A

Have central action (in the brain) or peripheral action (at the heart and blood vessels).
-Adrenergic neuron blockers (central and peripheral)
-Alpha 2 receptor agonists (central)
-Alpha 1 receptor blockers (peripheral)
-Beta receptor blockers (peripheral)
-Combination alpha 1 and beta receptor blockers (peripheral)
Action: stimulation of SNS leads to an increase in HR and force of contraction, constriction of blood vessels, & release of renin from kidneys, resulting in hypertension

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3
Q

What are the centrally acting adrenergic drugs and their mechanism of action

A

Clonidine and methyldopa stimulate the alpha 2-adrenergic receptors in the brain.

  • receptor stimulation reduces sympathetic outflow & results in lack of norepinephrine production, reducing BP
  • stimulation also affects the kidneys, reducing activity of renin
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4
Q

Define renin

A

The hormone and enzyme that converts the protein precursor of angiotensin II (AII), a potent vasoconstrictor that raises BP

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5
Q

Mechanism of action for alpha 1 blockers in the periphery

Drugs: Doxazosin (Cardura)

A

Work by blocking the alpha 1-adrenergic receptors
-when alpha 1-adrenergic receptors are stimulated by circulating norepinephrine, they produce increased BP, thus when they are blocked by these drugs BP decreased

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6
Q

The drug effects of the alpha 1 blockers (Doxazosin [Cardura]) are primarily related to?

A

Their ability to dilate arteries and veins, which reduces peripheral vascular resistance and subsequently decreases BP. This produces a marked decrease in the systemic and pulmonary venous pressures and an increase in cardiac output
-they also increase urinary flow rates and decrease outflow obstruction by preventing smooth muscle contractions in the bladder neck and urethra which can be beneficial in cases of benign prostatic hyperplasia (BPH)

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7
Q

Beta blockers mechanism of action

-Drugs: Metoprolol (Lopressor), Nebivolol (Bystolic)

A

Act in the periphery, their antihypertensive effects are related to their reduction of the HR through beta 1 receptor blockade.

  • Also cause reduction in secretion of renin which in turn reduces both AII-mediated vasoconstriction and aldosterone-mediated volume exspansion
  • long term use reduces peripheral vascular resistance
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8
Q

Adrenergic drugs indications

A

Tx of hypertension, either alone or in combination w/other hypertensive drugs

  • various forms of glaucoma may also respond to Tx
  • alpha 1 blockers (Doxazosin [Cardura]) used to relieve symptoms associated w/BPH. Also proved effective in management of severe heart failure when used with cardiac glycosides
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9
Q

Contraindications for adrenergic antihypertensive drugs

A
  • known drug allergy
  • acute heart failure
  • concurrent use of monoamine oxidase inhibitors
  • peptic ulcer
  • severe liver or kidney disease
  • Asthma contraindication for use of any noncardioselective beta blocker
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10
Q

Adverse effects for adrenergic antihypertensive drugs

A
  • bradycardia w/reflex tachycardia
  • postural and postexercise hypotension
  • dry mouth
  • drowsiness
  • dizziness
  • depression
  • edema
  • constipation
  • sexual dysfunction
  • HA
  • Sleep disturbances
  • nausea
  • rash
  • palpitations
  • Orthostatic hypotension w/those taking alpha blockers
  • abrupt discontinuation of centrally acting alpha 2 receptor agonists=rebound hypertension (sudden & very high elevation of BP)
  • nonselective blocking drugs associated w/bronchoconstriction & metabolic inhibition of glycogenolysis in liver
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11
Q

Any change in the dosing regimen for cardiovascular medications should be?

A

Undertaken gradually and with appropriate patient monitoring and follow-up

  • abrupt dosing changes of cardiovascular medications, either up or down, can be especially hazardous for the patient
  • some drugs can cause disruptions in blood count as well as serum electolyte levels and renal function
  • periodic monitoring of WBC count, serum potassium, sodium and creatinine levels is necessary
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12
Q

Antihypertensive Adrenergic drugs interactions

A

-Can cause additive CNS depression when taken w/alcohol, benzodiazepines, and opioids

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13
Q

Alpha 2-adrenergic receptor stimulators (agonists) Clonidine (Catapress)

A
  • Mostly used & is prototypical drug for this class
  • may be used as adjunct drugs in Tx of HTN after others failed, may be used in conjunction w/other antihypertensives such as diuretics
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14
Q

Clonidine (Catapress)

A
  • decrease BP
  • management of opioid withdrawal
  • better safety profile than other centrally acting adrenergics & advantage of being available in several dosage formulations, including topical and oral
  • when patch used, remove old patch before applying new one
  • DON’T discontinue abruptly, will lead to severe rebound hypertension
  • contraindicated in pt’s with shown hypersensitivity reactions to it
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15
Q

Alpha 1 blockers (Doxazosin (Cardura, Cardura XL)

A

Contraindicated in pt’s who have shown hypersensitivity to them.

  • pregnancy category C drugs
  • ONLY oral preparations
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16
Q

(Doxazosin (Cardura, Cardura XL)

A

Alpha 1 blocker

  • reduces peripheral vascular resistance & BP by dilating both arterial & venous blood vessels
  • available in immediate & extended release formulations
  • when drug released from extended-release form, matrix of capsule is expelled in stool (educate pt’s about this & reassure that active drug has been absorbed, because confusion could cause pt’s to take more than prescribed)
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17
Q

Beta receptor blocker (Nebivolol)

A

New, released in 2008

  • Beta 1-selective beta blocker approved for hypertension
  • also for Tx of heart failure
  • similar to other beta 1 selective blocker but in additon to blocking beta 1 receptors, also produces vasodilation, resulting in decrease SVR
  • causes less sexual dysfunction
  • do NOT stop abruptly, but tapered over 1-2 weeks
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18
Q

Nursing process for antihypertensive drugs as indicated by the National Institutes of Health

A

Switched from stepped approach to a guideline-based approach to the diagnosis and Tx of HTN

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19
Q

Nursing assessment for antihypertensive drugs

A
  • obtain thorough health history
  • head-to-toe
  • measure/document BP, pulse, respirations, pulse oximetry
  • ECG
  • Monitor lab tests (serum sodium, potassium, chloride, mg, C+, CBC/platelet count, renal function studies (BUN, serum, urinary creatinine levels; C-reactive protein (CRP) to measure systemic inflammation; cholesterol/lipid profiles; hepatic function studies (serum levels of ALT & AST)
  • if MI suspected, additional lab tests include arterial blood gases (ABG’s); erythrocyte sedimentation rate (ESR); specific cardiac biomarkers/enzymes (tropinins; usually elevated w/in 4-6 hrs after MI, reliable indicator up to 14 days); creatine phosphokinase-myocardial band (CPK-MB), LDH, myoglobin levels
  • noninvasive ophthalmoscopic examination of eye structures by advanced practice allows easy visualization of structures impacted by HTN (if present, narrowing of blood vessels in eyes, oozing of fluid, spots on retina, swelling of macula & optic nerve, bleeding of back of eye)
  • prevented by controlling BP/Tx of hypertension
  • use caution in older adults/chronic illnesses
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20
Q

Nursing assessment for alpha-adrenergic agonists

A
  • BP, pulse, weight before & during Tx (due to strong vasodilation properties & subsequent hypotensive AE)
  • these may be associated w/edema & fluid retention so assess heart/breath sounds & I&O, & dependent edema
  • alpha-adrenergic antagonists use cautiously due to potential for hypotension-induced dizziness & syncope
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21
Q

Nursing assessment for adrenergic drug Doxazosin

A

First-dose orthostatic hypotension may occur w/in 2-6 hours; therefore, carefully assess blood pressures (supine & standing) & measure corresponding pulse rates before first dose & 2-6 hours afterward subsequent increase in dosing

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22
Q

When any antihypertensive drug is used, the nurse should?

A

Measure BP & pulse rates (supine & standing), & assess for cautions, contraindications, drug interactions

  • with centrally acting alpha blockers, also assess WBC counts, serum potassium & sodium levels, & level of protein in urine (to identify proteinuria)
  • note route of administration specified in the drug order because of concerns associated w/diff routes (e.g clonidine transdermal patches, assess the skin for rashes,redness, drainage, or broken integrity prior to application)
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23
Q

Before administering beta blockers the nurse should?

A

Review their mechanism of action because of risk for complications in certain patient populations

  • if drug is nonselective beta blocker, it blocks both beta 1 & 2 receptors & will have both cardiac and respiratory effects, whereas if drug is beta 1-blocking drug, the cardiac system will be affected (pulse rate & BP decrease) but no affect on beta 2. This limits concern regarding respiratory problems (e.g. bronchoconstriction). Therefore if pt needs beta blocker but has restrictive airway problems, beta 1 recommended (to avoid bronchoconstriction). If no history of respiratory illness/concerns, the nonselective beta blockers may be effective
  • for those w/heart failure, beta blockers have a negative inotropic effect on the heart (decreased contractility); their use would lead to worsening of heart failure, which calls for a completely diff. class of antihypertensives
  • assess BP and apical pulse rate immediately before EACH dose. If systolic BP <90mmHg or pulse rate is <60 beats/min, notify prescriber because of risk of AE (hypotension, bradycardia). Drug would usually be withheld
  • assess breath/heart sounds BEFORE & DURING drug therapy
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24
Q

Patient centered care: cultural implications for antihypertensives drug therapy

A
  • Both thiazide-type diruetics & calcium channel blockers (CCBs) recommended first line therapy for management in BLACK patients
  • ASIAN pt’s receiving CCB report highest rates of control for HTN. ARBs & ACEIs have tolerability &/or adherance advantages
  • low diuretics use in ASIANS related to occurrance of serious AE (hypokalemia)
  • many ASIAN pt’s will require @least two antihypertensive medications to achieve BP control. Single pill combinations improve convenience & simplicity of regimens
  • Tx w/thiazide diuretic, CCB, or ARB for isolated systolic HTN recommended as first-line therapy in the Taiwanese
  • due to high rate of cardiac morbidity in Hispanic Americans, ACEIs & ARBs are useful in this population in protecting against end-organ damage secondary to HTN
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25
Q

Focus nursing goals for antihypertensive therapy on educating patient, family, and/or caregiver about the critical importance of adequate management to prevent end organ damage. Goals must include?

A
  • Making sure pt understands the nature of the disease, its symptoms & Tx
  • importance of adhering to Tx regimen
  • come to terms w/diagnosis as well as w/fact that there is no cure for the disease & Tx will be lifelong
  • emphasize influence of chronic illness & importance of nonpharmacologic therapy, stress reduction, follow-up care plan
  • plan for ongoing assessment of BP, weight, diet, exercise, smoking habits, alcohol intake, compliance w/therapy, & sexual function
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26
Q

Pressure mnemonic for antihypertensive drugs

A
Pressure (blood) monitor
Rise slowly to reduce orthostatic hypotension
Eating must be considered (diet)
Stay on medications
Skipping or stopping is a no-no
Undesirable responses
Remind to exercise, no alcohol
Eliminate smoking; educate
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27
Q

Antihypertensives are often associated w/multiple AE’s that may impact pt’s energy level, self-concept, and/or sexual integrity. These AE’s may lead patients to?

A

Abruptly stop taking the medication. Inform pt’s that any abrupt withdrawal is a serious concern because of risk for REBOUND HYPERTENSION (sudden & very high elevation of BP)
-this places pt at risk for a cerebrovascular accident or other cerebral or cardiac AE’s

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28
Q

With ALL hypertensives there is a risk for?

A

Rebound hypertension (with abrupt withdrawal), and prevention of this through patient education is critical to pt safety

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29
Q

Because of the potential for drug-related orthostatic hypotensive effects, patients taking alpha-adrenergic agonists will need to monitor?

A

Their BP & pulse rate at home or have these parameters measured by a family member (NOT ones in grocery stores)

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30
Q

Alpha-adrenergic antagonist drugs are associated with?

A

First-dose syncope, so, to avoid injury, advise patients to remain supine for the first dose of the drug

  • may take 4-6 weeks to take full effect. Educate about this delay
  • pt needs continuous monitoring for dizziness, syncope, edema & other AE’s (SOB, exacerbation)
  • Diuretics are adjunctive therapy to minimize AE’s of edema, may lead to more dizziness & electrolyte problems
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31
Q

Centrally acting alpha blockers require the same type of nursing interventions as other alpha blockers; however, as their name indicates, the mechanism of action of these drugs is?

A

Central, so AE’s are often more pronounced (e.g hypotension, sedation, bradycardia, edema)

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32
Q

The beta blockers are either nonselective (block both beta 1 and 2 receptors) or cardioselective (block mainly beta 1 receptors) with any beta blocker what should we educate the pt on?

A

Careful adherence to drug regimen is critical to pt safety.

  • pt’s taking beta blockers may experience an exacerbation of respiratory diseases such as asthma, bronchospasm, and COPD (because of increased bronchoconstriction due to beta 2 blocking) or an exacerbation of heart failure (because of drugs negative inotropic effects, i.e. decreased contractility due to beta 1 blocking)
  • provide clear and concise instructions about reporting AE’s & instructions for taking BP & pulse rates
  • if beta 1 blocker causes SOB, most likely due to edema and/or exacerbation of heart failure
  • any dizziness, postural hypotension, edema, constipation, or sexual dysfunction needs to be reported to the prescriber immediately
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33
Q

Always base nursing interventions on a thorough assessment and plan of care that also includes consideration of the patient’s cultural and ethnic group. This is particularly important with?

A

Antihypertensives, because research studies have documented differences in responses to antihypertensives among different racial & ethnic groups

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34
Q

Because patients with HTN are at a high risk for cardiovascular injury, it is critical for them to?

A

Adhere to both their pharmacologic and nonpharmacologic Tx regimens
-monitor for AE’s & toxic effects to identify potentially life-threatening complications

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35
Q

The most important aspect of the evaluation for antihypertensives is?

A

Collecting data and monitoring patients for evidence of controlled BP.

  • BP must maintained at values lower than parameters established by JNC or below the levels for prehypertension (120-139/80-89). If pt has diabetes mellitus or kidney disease, BP is lower
  • measure BP at periodic intervals
  • pt education about self-monitoring important
  • prescriber will measure fundus of the eye (changes in fundus are more reliable indicator of long-term effectiveness of Tx than blood pressure readings because changes in vasculature of the eye caused by high BP)
  • continually monitor pt for development of end-organ damage
  • Counsel and constantly monitor male pt’s for complaints of sexual dysfunction
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36
Q

What happens when patients abruptly stop taking antihypertensives

A

They are at a high risk for rebound hypertension & possible stroke or other complications

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37
Q

What are the therapeutic effects of antihypertensives

A

Improvement in BP & in the disease process

  • return to a normal baseline level of BP w/improved energy levels and decreased s/s of HTN (less edema, improved breath sounds, no abnormal heart sounds, capillary refill <5 seconds, less SOB)
  • monitor AE
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38
Q

Antihypertensives patient education (General)

A
  • take as ordered
  • adherence to regimen/diet
  • pt monitor stress levels & use biofeedback, imaginary massage
  • avoid smoking, excessive alcohol intake/exercise, hot climates, saunas, hot tubs, hot environment (heat precipitates vasodilation & leads to worsening hypotension)
  • frequent lab tests
  • keep out of reach of children (extreme toxicity). Transdermal patches check on, dont let fall off)
  • medical alert bracelet (house, car, etc.)
  • record BP/daily weights in journal. (Weights done morning before breakfast, at same time, same amount of clothing). Report an increase in weight by 2 lbs or more over a 24-hr period or 5lbs in a week
  • educate to inform all health care providers (dentists, surgeon) of taking antihypertensives
  • careful purposeful, & cautious changing of positions encouraged due to AE of postural hypotension and associated risk for dizziness, lightheadedness, and possible fainting and falls
  • keep adequate supply of medications on hand
  • schedule periodic eye exam (Q6 months)
  • w/successful therapy conditions will improve, but NEVER stop abruptly. Life-long therapy
  • saliva substitutes, use of sugar-free hard candy/gum and forcing fluids helps with dry mouth
  • forcing fluids and increasing dietary fiber may help w/preventing constipation
  • sexual dysfunction
  • may lead to depression and to report any change in emotional status to the prescriber
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39
Q

Alpha-Adrenergic agonists patient teaching

A
  • first-dose syncope, avoid conditions/situations/drugs that would exacerbate this
  • careful w/driving or anything involving alertness
  • report dizziness, palpitations, orthostatic hypotension
  • centrally acting alpha blockers affect sexual dysfunction inform pt of these AE’s, report if problematic
  • transdermal patches of clonidine are applied to non-hairy areas, rotate sites. Clean off residual w/lukewarm water & thoroughly dry area
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40
Q

Beta blockers patient teaching

A
  • move & change position slowly to avoid dizziness, fainting, and falls
  • report pulse rate lower than 60 beats/min, dizziness, or systolic BP of 90 or lower
  • prolonged sitting/standing & excessive physical exercise may lead to exacerbation of hypotensive effects, so counsel pt to avoid these activities or counteract them w/healthy practices such as pumping the feet up and down while sitting
  • heat may exacerbate hypotensive effects. Avoid saunaus, hot tubs, excessive heat, syncope (fainting) may result
41
Q

All antihypertensives in some way affect cardiac output. Cardiac output is the?

A

Amount of blood ejected from the left ventricle and is measured in liters/min

42
Q

The major groups of antihypertensives are?

A

Diuretics, alpha blockers, centrally acting alpha blockers, beta blockers, ACE inhibitors, vasodilators, CCBs, and ARBs

43
Q

Work by blocking a critical enzyme system responsible for the production of AII (angiotensin II; a potent vasoconstrictor). They prevent vasoconstriction caused by AII, prevent aldosterone secretion and therefore sodium and water resorption, and prevent the breakdown of bradykinin (potent vasodilator) by AII

A

ACE inhibitors

44
Q

Blocking the binding of angiotensin at the receptors; the end result is a decrease in BP

A

ARBs

45
Q

Calcium channels blockers may be used to treat

A

Angina, dysrhythmias, HTN to help reduce BP by causing smooth muscle relaxation and dilation of blood vessels. If calcium is not present, the smooth muscle of the blood vessels cannot contract

46
Q

A thorough nursing assessment for antihypertensives includes?

A

Determining whether the patient has any underlying causes of HTN such as renal or liver dysfunction, a stressful lifestyle, Cushing’s disease, Addison’s disease, renal artery stenosis, peripheral vascular disease, or pheochromocytoma

47
Q

Always assess for the presence of contraindications, cautions, and potential drug interactions BEFORE administering any of the antihypertensive drugs. Contraindications include a?

A

History of MI or chronic renal disease. Cautious use is recommended in pt’s with renal insufficiency or glaucoma. Drugs that interact with antihypertensives drugs include other antihypertensive drugs, anesthetics, and diuretics

48
Q

Hypertension is managed by both pharmacologic and nonpharmacologic measures. Patients need to?

A

Consume a diet low in fat, make any other necessary modifications in their diet (decrease intake of sodium and increase fiber intake), engage in regular supervised exercise, and reduce the amount of stress in lives

49
Q

Angiotensin-converting enzyme (ACE) Inhibitors

A
  • safe and efficacious & often used as first-line drugs in Tx of both heart failure and HTN
  • ALL ACE inhibitors have detrimental effects on the unborn fetus and neonate
  • classified as pregnancy category C in first trimester & pregnancy category D in 2nd or third trimester. Only used in pregnant if there are no safer alternatives
50
Q

Angiotensin-converting enzyme (ACE) Inhibitors:

Drug: Captopril (Capoten)

A
  • Shortest half life so dosed more frequently. This is a drawback for pt’s w/history of nonadherence
  • on the other hand it may be best to start with this drug in a pt who is critically ill, so if problems were to arise they will be short lived
  • Both Captopril and Enalapril can be dosed multiple times a day
  • Captorpil and Lisinopril are the ONLY two ACE inhibitors that are NOT prodrugs. This characteristic is important advantage in treating a pt w/liver dysfunction
  • minimizing or preventing left ventricular dilation and dysfunction (Ventricular remodeling) that can arise in acute period after an MI and thereby improve pt’s survival
  • also reduce risk for heart failure
51
Q

Define prodrug

A

Drug that is inactive in its administered form and must be metabolized to its active form in the body, generally by the liver, to be effective

52
Q

Angiotensin-converting enzyme (ACE) Inhibitors:

Drug: Enalapril (Vasotec)

A
  • Both Captorpil and Enalapril can be dosed mult. X/day
  • ONLY ACE inhibitor available in oral and parenteral forms
  • parenteral form: active drug, offers the hemodynamic benefit of inhibiting ACE activity in an acutely ill pt who can’t tolerate oral medications. Doesn’t require cardiac monitoring
  • oral form differs from captopril in that it is a prodrug, pt must have functioning liver
  • improve chance of survival after MI and reduces incidence of heart failure
53
Q

ACE Inhibitors mechanism of action

A

Inhibit angiotensin-converting enzyme (responsible for converting angiotensin I, formed through action of renin, to angiotensin 2). AII is a potent vasoconstrictor & induces aldosterone secretion by adrenal glands. Aldosterone stimulates sodium and water resorption, which raises BP. Together these processes are referred to as the renin-angiotensin-aldosterone system. By inhibiting this process, BP is lowered.

54
Q

The primary effects of ACE inhibitors are?

A

Cardiovascular and renal

  • Cardiovascular effects: due to their ability to reduce BP by decreasing systemic vascular resistance (SVR). Do this by preventing breakdown of vasodilating substance bradykinin and substance P, and preventing formation of AII. These combined effects decrease afterload, or the resistance against which the left ventricle must pump to eject volume of blood during contraction
  • beneficial in Tx of heart failure: prevent sodium and water resorption by inhibiting aldosterone secretion. This eases diuresis, which decreases blood volume and return to the heart. This in turn decreases preload, or the left ventricular end-diastolic volume, & work required of heart
55
Q

ACE Inhibitors indications

A

Antihypertensives and adjunctive drugs for Tx of heart failure

  • used alone or combination w/other drugs such as diuretics in Tx of HTN or heart failure
  • can stop progression of left ventricular hypertrophy (seen after MI), known as ventricular remodeling (cardioprotective effect)
  • decrease morbidity & mortality in pt’s w/heart failure
  • drugs of choice for hypertensive pt’s w/heart failure
  • have protective effect on the kidneys, they reduce glomerular filtration pressure. So good for diabetic pt’s
  • reduce proteinuria, standard therapy for diabetic pt’s to prevent the progression of diabetic nephropathy
56
Q

ACE Inhibitors contraindictions

A
  • known drug allergy, previous reaction to angioedema (larygeal swelling) to an ACE inhibitor
  • pt’s w/baseline potassium level of 5 mEq/L or higher may not be suitable candidates because they can promote hyperkalemia
  • lactating women, children, pt’s w/bilateral renal artery stenosis
57
Q

ACE Inhibitors adverse effects

A

Major CNS effects include: fatigue, dizziness, mood changes, HA

  • Dry nonproductive cough that is reversible with discontinuation of the therapy
  • first-dose hypotensive effect can cause significant decline in BP
  • loss of taste, hyperkalemia, angioedema, renal impairment
  • in pt’s w/severe heart failure whose renal function may depend on the activity of the renin-angiotensin-aldosterone system, Tx w/Ace inhibitors promote potassium resorption in the kidney, so serum potassium levels must be monitored regularly, especially w/concurrent therapy w/potassium-sparing diuretics
58
Q

ACE Inhibitors toxicity and management of overdose

A

Most pronounced symptom is HYPOTENSION

  • tx is symptomatic and supportive and includes administration of IV fluids to expand blood volume
  • hemodialysis is effective for the removal of captopril and lisinopril
59
Q

ACE Inhibitors interactions

A

NSAIDs such as ibuprofen can reduce the antihypertensive effect of ACE inhibitors

  • use of NSAIDs and ACE inhibitors may predispose pt to development of acute renal failure
  • concurrent use of ACE inhibitors and other antihypertensive or diuretics can have hypotensive effects
  • giving lithium and ACE inhibitors together can result in lithium toxicity
  • potassium supplements and potassium-sparing diuretics, when administered w/ACE inhibitors may result in hyperkalemia
  • monitor serum potassium levels
60
Q

Nursing assessment with ACE inhinibitors

A
  • Assess BP, apical pulse rate, and respiratory status (because AE of dry, hacking, chronic cough)
  • take BP readings immediately before initial and subsequent doses of drug so extreme fluctuations id’d early
  • assess serum potassium, sodium, chloride levels
  • tests of baseline cardiac functioning
  • due to potential AE’s of neutropenia, assess CBC BEFORE and DURING therapy
61
Q

Planning for antihypertensive drugs

A
  • Goals focused on education about importance of adequate management to prevent end-organ damage
  • Tx lifelong
  • Don’t abruptly stop taking medications>rebound hypertension
62
Q

Implementation for ACE inhibitors

A
  • take as prescribed
  • contact prescriber if angioedema occurs
  • wean off drug to avoid rebound HTN
  • monitor serum sodium/potassium levels during therapy
  • serum potassium levels increase as AE resulting in hyperkalemia
  • Impaired taste=AE can last 2-3months
  • takes several weeks to see therapeutic effects
  • DON’T take potassium supplements
63
Q

Contraindications for ARBs

A
  • known drug allergy
  • pregnancy
  • lactation
  • use w/caution in older adults and in patients w/renal dysfunction
  • BP & apical pulse rate assessed BEFORE & DURING drug therapy
64
Q

Adverse effects of ARBs

A

Chest pain, fatigue, hypoglycemia, diarrhea, UTI, anemia, weakness
-hyperkalemia & cough less likely to occur than with the ACE Inhibitors

65
Q

Toxicity and management of overdose with ARBs

A

Overdose may manifest as hypotension and tachycardia; bradycardia occurs less often
-Tx is symptomatic and supportive, includes administration of IV fluids to expand the blood volume

66
Q

ARBs interactions

A
  • NSAIDs
  • lithium
  • rifampin
  • potassium supplements and potassium-sparing diuretics
  • can promote hyperkalemia, especially when taken concurrently with potassium supplements (happens less frequently than with ACE)
  • monitoring of serum potassium level is necessary for all patients
67
Q

ARBs: Losartan (Cozaar)

A
  • Beneficial in patients w/HTN & heart failure
  • contraindicated in pt’s who are hypertensive to any component of this product
  • use w/caution in pt’s w/renal artery stenosis
  • breastfeeding women DON’T take because it can cause serious AEs on nursing infant
68
Q

As a class calcium channel blockers are used for?

A

Several indications and have many beneficial effects and relatively few AEs

  • primary use for tx of HTN and angina
  • effectiveness in Tx HTN related to ability to cause smooth muscle relaxation by blocking the binding of calcium to its receptors, thereby prevents contraction
  • due to their effectiveness/safety they are added to list of first-line drugs for HTN
  • also effective antidysrhythmics
  • sometimes used in Tx of Raynaud’s disease and migraine HA
  • used in combination w/other drugs
69
Q

Calcium-channel blockers: Amlodipine (Norvasc)

A

Most commonly used for HTN

70
Q

Diuretics are drugs that?

A

Accelerate the rate of urine formation via a variety of mechanisms. The result is the removal of sodium and water from the body.
-first-line drugs in Tx of HTN

71
Q

The hypotensive activity of diuretics is due to many different mechanisms.

A
  • Cause direct arteriolar dilation, which decreases peripheral vascular resistance
  • reduce extracellular fluid volume, plasma volume, & cardiac output, which accounts for decrease in BP
72
Q

Two advantages of diuretics

A

-relatively low coast and favorable safety profile

73
Q

Main problem with diuretic use

A

Metabolic adverse effects that can result from excessive fluid and electrolyte loss. Usually dose related & controllable with dosage titration (careful adjustment)

74
Q

All diuretics work primarily in the?

A

Kidney, they exert their effect in the nephron

75
Q

The most potent diuretics are the?

A

Loop diuretics, followed by mannitol, metolazone (a thiazide-like diuretic), the thiazides, and the potassium-sparing diuretics

76
Q

The potency of diuretics is a function of?

A

Where they work in the nephron to inhibit sodium and water resorption
-the more sodium and water they inhibit from resorption, the greater the amount of diuresis and therefore the greater the potency

77
Q

Diuretic: Carbonic anhydrase inhibitors (CAIs)

A

Chemical derivatives of sulfonamide antibiotics

  • Inhibit activity of the enzyme carbonic anhydrase, found in the kidneys, eyes, and other parts of the body
  • work at the location of the carbonic anhydrase enzyme system along the nephron, primarily proximal tubule
78
Q

Diuretic: Carbonic anhydrase inhibitors (CAIs) Mechanism of action

A

Carbonic anhydrase system in the kidney is located distal to glomerulus in the proximal tubules, where 2/3 of all sodium and water is resorbed into blood

  • in proximal tubules, there is an active transport system that exchanges sodium for hydrogen ions. For sodium and water to be resorbed back into blood, hydrogen must be exchanged, w/out hydrogen this can’t occur, & sodium/water will be eliminated w/urine
  • carbonic anhydrase makes hydrogen ions available for this exchange. When its actions are inhibited, little sodium and water can be resorbed into blood and they are eliminated w/urine
  • CAIs reduce formation of hydrogen and bicarbonate ions from carbon dioxide and water through noncompetitive, reversible inhibition of carbonic anhydrase activity
  • results in reduction in the availability of the ions, mainly hydrogen, for use by active transport systems
  • reduction in the formation of bicarbonate and hydrogen ions can have effects on other body parts
79
Q

Diuretics: CAIs can induce?

A

Respiratory and metabolic acidosis. Both respiratory and metabolic acidosis can increase oxygenation during hypoxia by increasing ventilation, cerebral blood flow, & dislocation of oxygen from oxyhemoglobin
-These actions beneficial to pt
-

80
Q

An undesirable effect of the diuretic CAIs is?

A

Elevation of blood glucose level and glycosuria in diabetic pt’s. May be due in part to CAI-enhanced potassium loss through urine

81
Q

Diuretic: Carbonic Anhydrase Inhibitors (CAIs) Indications

A
  • Tx of glaucoma, edema, high-altitude sickness
  • used as adjunct drugs in long-term management of open-angle glaucoma that CAN’T be controlled by topical miotic drugs or epinephrine derivatives alone
  • When CAIs given, an increase in outflow of aqueous humor results
  • also for short term in conjunction w/miotics to lower intraocular pressure in preparation for ocular surgery and as an adjunct in Tx of secondary glaucoma
82
Q

Diuretic Carbonic Anhydrase Inhibitors (CAIs) Drug: Acetazolamide (Diamox)

A
  • Manage edema secondary to heart failure that has become resistant to other diuretics
  • as a class, CAIs less potent diuretics than loop diuretics or thiazides, & because of metabolic acidosis they induce, their effectiveness diminishes in 2-4 days
  • effective in both the prevention and Tx of the symptoms of high-altitude sickness (HA, nausea, SOB, dizziness, drowsiness, and fatigue)
83
Q

Diuretic Carbonic Anhydrase Inhibitors (CAIs) Contraindications

A
  • known drug allergy
  • hyponatremia, hypokalemia
  • severe renal or hepatic dysfunction
  • adrenal gland insufficiency
  • cirrhosis
84
Q

Adverse effects of Diuretic Carbonic Anhydrase Inhibitors (CAIs)

A
  • Metabolic abnormalities such as acidosis and hypokalemia
  • drowsiness
  • anorexia
  • paresthesias
  • hematuria
  • urticaria
  • photosensitivity
  • melena (blood in stool)
85
Q

Interactions for Diuretic Carbonic Anhydrase Inhibitors (CAIs)

A

Since they can cause hypokalemia, an increase in digoxin toxicity may occur when combined w/digoxin

  • use w/corticosteroids may cause hypokalemia
  • effects of amphetamines, carbamazepine, cyclosporine, phenytoin, & quinidine may be increased when taken concurrently w/CAIs
86
Q

Diuretic CAI: The usual dose of acetazolamide is?

A

250-500 mg/day, may be given orally or IV

87
Q

Diuretic Carbonic Anhydrase Inhibitors (CAIs) Drug: Acetazolamide (Diamox)

A
  • Contraindicated in pt’s w/hypersensitivity to is as well as in those w/significant liver or kidney dysfunction, low serum potassium or sodium levels, acidosis, or adrenal gland failure
  • oral and parenteral forms
  • pregnancy category C
88
Q

Diuretics nursing assessement

A
  • Baseline breath/heart sounds, neurologic status, skin turgor (for edema), moisture levels of mucus membranes, capillary refill
  • vital signs, weights, I&O measurements (because fluid volume levels & electrolyte concentrations are affected by them)
  • assess postural BP (lying, standing, sitting) BEFORE & DURING drug therapy because of diuretic-induced fluid volume loss possibly precipitating postural or orthostatic hypotension
  • postural or orthostatic hypotension=drop in BP of 20 mm Hg or more upon standing
  • assess specific lab values associated w/renal and hepatic functioning (BUN, Creatinine level, ALP/AST, LDH for hepatic function)
  • Serum electrolyte levels BEFORE & DURING therapy
  • obtain/document serum potassium, sodium, chloride, Mg, Calcium, uric acid, creatinine levels
  • ABGs
89
Q

Nursing assessment for diuretics: Carbonic anhydrase inhibitors

A
  • Close assessment of sodium & potassium levels
  • DON’T give to pt’s w/history of renal or liver dysfunction
  • as w/any diuretic resulting in potassium loss (excluding potassium sparing diuretic), if these drugs are given concurrently w/digoxin, there is an increased risk for digoxin toxicity because of the hypokalemia
90
Q

Diuretic Implementation

A
  • Measure/record BP, pulse rate, I&O, daily weights during therapy
  • Changes from initial baseline assessment that alert you to possible problems w/drug therapy include: presence of dizziness, fainting, lightheadedness on standing or changing positions, weakness, fatigue, tremor, muscle cramping, changes in mental status, or cold, clammy skin
  • diuretic therapy may precipitate cardiac irregularities or palpitations; therefore monitor HR and rhythm
  • fluid loss from action of diuretic may lead to AE of constipation, so preventive measures needed, such as increased I&O of fluids and fiber and/or use of natural bulk-forming products
  • give as directed
  • dosing & timing of drugs important to enhance therapeutic effects & minimize AEs
  • if taken in late afternoon or evening may lead to nocturia & subsequent loss of sleep, usually scheduled for morning
  • safety concerns exist with nocturia because of possible confusion and dizziness
91
Q

The therapeutic effects of diuretics include

A

Resolution of or reduction in edema, fluid volume overload, heart failure, HTN, or return to normal intraocular pressures

92
Q

Evaluation for diuretics

A
  • Monitor pt for occurrence of AEs (hypotension, electrolyte imbalance, metabolic acidosis, drowsiness, hypokalemia, tachycardia, hyperkalemia
  • hypokalemia may manifest by anorexia, nausea, lethargy, muscle weakness, mental confusion, hypotension
93
Q

Patient education: Patients taking diuretics need to maintain proper?

A

Nutritional Intake and fluid volume and eat potassium-rich foods, except when contraindicated or when potassium-sparing diuretics are used.
-Foods high in potassium include bananas, oranges, apricots, dates, raisins, broccli, green beans, potatoes, tomatoes, meats, fish, wheat bread, legumes

94
Q

Diuretics Patient education: Potassium supplementation may be recommended by a prescriber depending on the?

A

Symptoms that patient presents and the serum levels. Normal serum potassium levels are 3.5-5 mEq/L

95
Q

Diuretic Patient education: Frequent lab tests may be indicated when?

A

At the beginning of and during therapy w/diuretics. These tests may include measurement of electrolytes, uric acid, blood gases

96
Q

Diuretic patient education: Encourage patients to change positions how?

A

Slowly and to rise slowly after sitting or lying to prevent dizziness and possible fainting (syncope)

97
Q

Diuretic patient education: Forcing fluids may be needed to prevent?

A

Dehydration and minimize constipation. Increased consumption of fiber may also help with constipation

98
Q

Diuretic patient education: any unusual adverse effects or problems, such as?

A

Excessive dizziness, syncope, weakness, or muscle aches, need to be reported immediately to the prescriber

99
Q

Adrenergic drugs: Alpha 2 Adrenergic receptor stimulant

Drug name: Clonidine (Catapress)

A
  • Alpha 2 receptor is located in the post ganglionic sympathetic nerve endings
  • when stimulated, it INHIBITS the release of norepineprine thus leading to a decrease in BP
  • Thus A2 Receptors LOWER BP