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TABLE 33-8
DRUG THERAPY
Hypertension
MECHANISM
DRUG
OF ACTION
Diuretics
Thiazide and Related Diuretics
bendroflumethiazide (Naturetin)
benzthiazide (Aquatag, Exna)
chlorothiazide (Diuril)
chlorthalidone (Hygroton)
hydrochlorothiazide (Microzide,
Esidrix, HydroDIURIL, Oretic)
methyclothiazide (Enduron)
metolazone (Zaroxolyn)
trichlormethiazide (Metahydrin,
Naqua)
NURSING CONSIDERATIONS
Loop Diuretics
bumetanide (Bumex)
ethacrynic acid (Edecrin)
furosemide (Lasix)
torsemide (Demadex)
Potassium-Sparing Diuretics
amiloride (Midamor)
triamterene (Dyrenium)
Adrenergic Inhibitors
Central-Acting -Adrenergic Antagonists
clonidine (Catapres)
clonidine patch (Catapres-TTS)
Reduces sympathetic
outflow from CNS.
Reduces peripheral sympathetic tone, produces
vasodilation, decreases
SVR and BP.
guanabenz (Wytensin)
Same as clonidine.
Same as clonidine.
guanfacine (Tenex)
Same as clonidine.
Same as clonidine.
ACE, Angiotensin-converting enzyme; AV, atrioventricular; BP, blood pressure; CNS, central nervous system; CO, cardiac output; DBP, diastolic blood pressure; ECF, extracellular
fluid; ECG, electrocardiogram; GI, gastrointestinal; HDL, high-density lipoprotein; IV, intravenous; LDL, low-density lipoprotein; MI, myocardial infarction; NSAIDs, nonsteroidal
antiinflammatory drugs; SBP, systolic blood pressure; SVR, systemic vascular resistance.
749
CHAPTER 33 Hypertension
TABLE 33-8
DRUG THERAPYcontd
Hypertension
MECHANISM
DRUG
OF ACTION
Adrenergic Inhibitorscontd
Central-Acting -Adrenergic Antagonistscontd
methyldopa (Aldomet)
Same as clonidine.
NURSING CONSIDERATIONS
Prevents peripheral
release of norepinephrine, resulting in
vasodilation.
Lowers CO and reduces
SBP more than DBP.
Same as guanethidine.
Depletes central and
peripheral stores of
norepinephrine.
Results in peripheral
vasodilation (decreases
SVR and BP).
doxazosin (Cardura)
prazosin (Minipress)
terazosin (Hytrin)
Block 1-adrenergic
effects, producing
peripheral vasodilation
(decreases SVR
and BP).
Beneficial effects on lipid
profile.
phentolamine (Regitine)
Blocks 1-adrenergic
receptors, resulting in
peripheral vasodilation
(decreases SVR and
BP).
acebutolol (Sectral)
atenolol (Tenormin)
betaxolol (Kerlone)
bisoprolol (Zebeta)
carteolol (Cartrol)
metoprolol (Lopressor)
nadolol (Corgard)
nebivolol (Bystolic)
penbutolol (Levatol)
pindolol (Visken)
propranolol (Inderal)
timolol (Blocadren)
esmolol (Brevibloc)
carvedilol (Coreg)
labetalol (Normodyne, Trandate)
1-Adrenergic Blockers
-Adrenergic Blockers
750
TABLE 33-8
DRUG THERAPYcontd
Hypertension
MECHANISM
OF ACTION
fenoldopam (Corlopam)
Activates dopamine
receptors, resulting
in systemic and renal
vasodilation.
hydralazine (Apresoline)
minoxidil (Loniten)
nitroglycerin (Tridil)
Interrupts adrenergic
control of arteries,
results in vasodilation,
and reduces SVR and
BP.
DRUG
Direct Vasodilators
NURSING CONSIDERATIONS
Ganglionic Blockers
trimethaphan (Arfonad)
Angiotensin Inhibitors
Angiotensin-Converting Enzyme Inhibitors
benazepril (Lotensin)
Inhibit ACE, conversion
captopril (Capoten)
enalapril (Vasotec)
fosinopril (Monopril)
lisinopril (Prinivil, Zestril)
moexipril (Univasc)
perindopril (Aceon)
quinapril (Accupril)
ramipril (Altace)
trandolapril (Mavik)
of angiotensin I to
angiotensin II (A-II).
Inhibits A-IImediated
vasoconstriction.
ACE, Angiotensin-converting enzyme; BP, blood pressure; ECG, electrocardiogram; IV, intravenous; MI, myocardial infarction; NSAIDs, nonsteroidal antiinflammatory drugs; SVR,
systemic vascular resistance.
CHAPTER 33 Hypertension
TABLE 33-8
751
DRUG THERAPYcontd
Hypertension
MECHANISM
DRUG
OF ACTION
Angiotensin Inhibitorscontd
Angiotensin II Receptor Blockers
candesartan (Atacand)
eprosartan (Teveten)
irbesartan (Avapro)
losartan (Cozaar)
olmesartan (Benicar)
tasosartan (Verdia)
telmisartan (Micardis)
valsartan (Diovan)
NURSING CONSIDERATIONS
Renin Inhibitors
aliskiren (Tekturna)
Controversy exists as to the optimal choice of antihypertensive medications in the management of hypertension, particularly in regards to the preferred drugs for initial, single therapy
(monotherapy). Performance measures for health care providers who treat adult patients at risk for CVD require that BP be
below goal, or that at least two medications are prescribed.14
Although the precise action of diuretics in the reduction
of BP is unclear, it is known that they promote sodium and
water excretion, reduce plasma volume, and reduce the vascular response to catecholamines. Adrenergic-inhibiting agents
act by diminishing the SNS effects that increase BP. Adrenergic inhibitors include drugs that act centrally on the vasomotor center and peripherally to inhibit NE release or to block
the adrenergic receptors on blood vessels. Direct vasodilators
decrease the BP by relaxing vascular smooth muscle and reducing SVR. Calcium channel blockers increase sodium excretion
and cause vasodilation by preventing the movement of extracellular calcium into cells.
There are two types of angiotensin inhibitors. The first type
is angiotensin-converting enzyme (ACE) inhibitors. These prevent the conversion of angiotensin I to A-II and thus reduce
A-IImediated vasoconstriction and sodium and water retention. The second type is A-II receptor blockers (ARBs). These
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TABLE 33-9
DRUG THERAPY
Lotensin HCT
Capozide
Vaseretic
Monopril-HCT
Prinzide, Zestoretic
Uniretic
Accuretic
Atacand HCT
Teveten HCT
Avalide
Hyzaar
Benicar HCT
Micardis HCT
Diovan HCT
Tenoretic
Ziac
Lopressor HCT
Corzide
Inderide
Timolide
Aldoril
Demi-Regroton
Hydropres
Minizide
Esimil
Combipres
Lotrel
Lexxel
Teczem
Tarka
Exforge
Azor
Clinical Question
For patients with hypertension (P), what factors (I) lead to nonadherence
with antihypertensive therapy (O)?
Conclusion
Many factors lead to nonadherence. Assess patient self-management
strategies to select specific interventions that promote adherence.
EVIDENCE-BASED PRACTICE
Why Patients Do Not Adhere to Antihypertensive
Therapy
Moduretic
Aldactazide
Dyazide, Maxzide
drug therapy identifies and minimizes side effects and may help
the patient comply with therapy. Side effects may be an initial
response to a drug and may decrease over time. Informing
the patient about side effects that may decrease with time may
enable the individual to continue taking the drug. The number
or severity of side effects may relate to the dosage. It may be
necessary to change the drug or decrease the dosage. Advise the
patient to report all side effects to the health care provider who
prescribes the medication.
A common side effect of several of these drugs is orthostatic hypotension. This condition results from an alteration
Sexual dysfunction may occur with many of the antihypertensive drugs and can be a major reason that a patient does not comply with the treatment plan. Problems can range from decreased
libido to erectile dysfunction. Rather than discussing a sexual
problem with a health care provider, the patient may decide to
stop taking the drug. Approach the patient on this sensitive subject and encourage discussion of any sexual dysfunction that may
be experienced. The sexual problems may be easier for the patient
to discuss once you explain that the drug may be the source of
the problem. Changing to another antihypertensive drug can
decrease or eliminate these side effects. Encourage the patient to
discuss side effects with the health care provider who prescribes
the medication. If the patient is reluctant to do so, offer to alert