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748

SECTION 7 Problems of Oxygenation: Perfusion

TABLE 33-8

DRUG THERAPY

Hypertension
MECHANISM
DRUG
OF ACTION
Diuretics
Thiazide and Related Diuretics

SIDE EFFECTS AND ADVERSE


EFFECTS

bendroflumethiazide (Naturetin)
benzthiazide (Aquatag, Exna)
chlorothiazide (Diuril)
chlorthalidone (Hygroton)
hydrochlorothiazide (Microzide,
Esidrix, HydroDIURIL, Oretic)
methyclothiazide (Enduron)
metolazone (Zaroxolyn)
trichlormethiazide (Metahydrin,
Naqua)

Inhibit NaCl reabsorption


in the distal convoluted
tubule; increase excretion of Na+ and Cl.
Initial decrease in ECF;
sustained decrease
in SVR.
Lower BP moderately
in 2-4 wk.

Fluid and electrolyte imbalances: volume


depletion, hypokalemia, hyponatremia,
hypochloremia, hypomagnesemia,
hypercalcemia, hyperuricemia, metabolic alkalosis; CNS effects: vertigo,
headache, weakness.
GI effects: anorexia, nausea, vomiting,
diarrhea, constipation, pancreatitis.
Sexual problems: erectile dysfunction,
decreased libido.
Dermatologic effects: photosensitivity,
skin rash.
Blood dyscrasias; decreased glucose
tolerance.

Monitor for orthostatic hypotension,


hypokalemia, and alkalosis. Thiazides
may potentiate cardiotoxicity of digoxin
by producing hypokalemia. Dietary
sodium restriction reduces the risk of
hypokalemia. NSAIDs can decrease
diuretic and antihypertensive effect
of thiazide diuretics. Advise patient to
supplement with potassium-rich foods.
Current doses are lower than previously
recommended.

Inhibit NaCl reabsorption


in the thick ascending
limb of the loop of
Henle. Increase excretion of Na+ and Cl.
More potent diuretic
effect than thiazides,
but shorter duration of
action. Less effective
for hypertension.

Fluid and electrolyte imbalances as with


thiazides, except no hypercalcemia.
Ototoxicity: hearing impairment, deafness, vertigo, that are usually reversible.
Metabolic effects: hyperuricemia, hyperglycemia, increased LDL cholesterol
and triglycerides, decreased HDL
cholesterol.

Monitor for orthostatic hypotension and


electrolyte abnormalities.
Loop diuretics remain effective despite
renal insufficiency. Diuretic effect of
drug increases at higher doses.

Reduce K+ and Na+


exchange in the distal
and collecting tubules.
Reduce excretion of K+,
H+, Ca+, and Mg+.

Hyperkalemia, nausea, vomiting, diarrhea,


headache, leg cramps, dizziness.

Monitor for orthostatic hypotension and


hyperkalemia.
Contraindicated in patients with renal
failure. Use with caution in patients on
ACE inhibitors or angiotensin II blockers.
Avoid potassium supplements.

Same as amiloride and triamterene.


May cause gynecomastia, erectile
dysfunction, decreased libido,
menstrual irregularities.

Monitor for orthostatic hypotension


and hyperkalemia. Do not combine
with potassium-sparing diuretics or
potassium supplements. Use with
caution in patients on ACE inhibitors
or angiotensin II blockers. These drugs
are also classified as potassium-sparing
diuretics.

NURSING CONSIDERATIONS

Loop Diuretics
bumetanide (Bumex)
ethacrynic acid (Edecrin)
furosemide (Lasix)
torsemide (Demadex)

Potassium-Sparing Diuretics
amiloride (Midamor)
triamterene (Dyrenium)

Aldosterone Receptor Blockers


spironolactone (Aldactone)
eplerenone (Inspra)

Inhibit the Na+-retaining


and K+-excreting effects
of aldosterone in the
distal and collecting
tubules.

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.

Dry mouth, sedation, erectile dysfunction,


nausea, dizziness, sleep disturbance,
nightmares, restlessness, depression.
Symptomatic bradycardia in patients with
conduction disorder.
Patch may cause pruritus, redness, or
darkening of skin.

Sudden discontinuation may cause


withdrawal syndrome including rebound
hypertension, tachycardia, headache,
tremors, apprehension, and sweating.
Chewing gum or hard candy may relieve
dry mouth. Alcohol and sedatives
increase sedation.
Transdermal patch may be related
to fewer side effects and better
compliance.

guanabenz (Wytensin)

Same as clonidine.

Same as clonidine.

Same as clonidine, but not available in


transdermal formulation.

guanfacine (Tenex)

Same as clonidine.

Same as clonidine.

Same as clonidine, but not available in


transdermal formulation.

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

SIDE EFFECTS AND ADVERSE


EFFECTS

methyldopa (Aldomet)

Sedation, fatigue, orthostatic


hypotension, decreased libido, erectile
dysfunction, dry mouth, hemolytic
anemia, hepatotoxicity, sodium and
water retention, depression.

Instruct patient about daytime sedation


and avoidance of hazardous activities.
Administration of a single daily dose at
bedtime minimizes sedative effect.

Same as clonidine.

NURSING CONSIDERATIONS

Peripheral-Acting -Adrenergic Antagonists


guanethidine (Ismelin)

Prevents peripheral
release of norepinephrine, resulting in
vasodilation.
Lowers CO and reduces
SBP more than DBP.

Marked orthostatic hypotension, diarrhea,


cramps, bradycardia, retrograde or
delayed ejaculation, sodium and water
retention.

May cause severe orthostatic hypotension; not recommended for use in


patients with cerebrovascular or coronary insufficiency or in older adults.
Advise patient to rise slowly and wear
support stockings.
Hypotensive effect is delayed for 2-3 days
and lasts 7-10 days after withdrawal.

guanadrel sulfate (Hylorel)


reserpine (Serpasil)

Same as guanethidine.
Depletes central and
peripheral stores of
norepinephrine.
Results in peripheral
vasodilation (decreases
SVR and BP).

Similar to guanethidine. Sedation and


inability to concentrate, depression,
nasal stuffiness.

Must be given twice daily.


Contraindicated in patients with history of
depression. Monitor mood and mental
status regularly. Advise patient to avoid
barbiturates, alcohol, and opioids.

doxazosin (Cardura)
prazosin (Minipress)
terazosin (Hytrin)

Block 1-adrenergic
effects, producing
peripheral vasodilation
(decreases SVR
and BP).
Beneficial effects on lipid
profile.

Variable amount of orthostatic hypotension depending on the plasma


volume. May see profound orthostatic
hypotension with syncope within
90 min after initial dose.
Retention of salt and water.

Reduced resistance to the outflow of


urine in benign prostatic hyperplasia.
Taking drug at bedtime reduces risks
associated with orthostatic hypotension.

phentolamine (Regitine)

Blocks 1-adrenergic
receptors, resulting in
peripheral vasodilation
(decreases SVR and
BP).

Acute, prolonged hypotension, cardiac


dysrhythmias, tachycardia, weakness,
flushing.
Abdominal pain, nausea, and exacerbation
of peptic ulcer.

Used in short-term management


of pheochromocytoma. Also used
locally to prevent necrosis of skin and
subcutaneous tissue after extravasation
of adrenergic drug. No oral formulation.

acebutolol (Sectral)
atenolol (Tenormin)
betaxolol (Kerlone)
bisoprolol (Zebeta)
carteolol (Cartrol)
metoprolol (Lopressor)
nadolol (Corgard)
nebivolol (Bystolic)
penbutolol (Levatol)
pindolol (Visken)
propranolol (Inderal)
timolol (Blocadren)

Reduce BP by antagonizing -adrenergic effects.


Cardioselective agents
block 1-adrenergic
receptors.
Nonselective agents
block 1- and 2adrenergic receptors.
Decrease CO and reduce
sympathetic vasoconstrictor tone.
Decrease renin secretion
by kidneys.

Hypotension, bronchospasm, atrioventricular conduction block, impaired


peripheral circulation.
Nightmares, depression, erectile dysfunction, weakness, reduced exercise
capacity.
May induce or exacerbate heart failure in
susceptible patients.
Sudden withdrawal of -adrenergic
blockers may cause rebound
hypertension and exacerbate
symptoms of ischemic heart disease.

-Adrenergic blockers vary in lipid


solubility, selectivity, and presence
of partial sympathomimetic effect,
which explains different therapeutic and
side effect profiles of specific agents.
Monitor pulse and BP regularly.
Use with caution in patients with diabetes
mellitus because drug may depress
the tachycardia associated with
hypoglycemia.
Nonselective agents may cause bronchospasm, especially in patients with a
history of asthma.

esmolol (Brevibloc)

Reduces BP by antagonizing 1-adrenergic


effects.

carvedilol (Coreg)
labetalol (Normodyne, Trandate)

1-, 1-, and 2-adrenergic


blocking properties producing peripheral vasodilation and decreased
heart rate.
Reduces CO, SVR, and
BP.

1-Adrenergic Blockers

-Adrenergic Blockers

IV administration; rapid onset and very


short duration of action.
Hypotension, bradycardia, orthostatic
hypotension, dizziness, fatigue, nausea,
vomiting, dyspepsia, paresthesia, nasal
stuffiness, erectile dysfunction, edema.
Hepatic toxicity.

Same as -adrenergic blockers. IV form


available for hypertensive crisis in
hospitalized patients.
Patients must be kept supine during
IV administration.
Assess patient tolerance of upright position
(severe orthostatic hypotension) before
allowing upright activities (e.g., commode).
Continued

750

SECTION 7 Problems of Oxygenation: Perfusion

TABLE 33-8

DRUG THERAPYcontd

Hypertension
MECHANISM
OF ACTION

SIDE EFFECTS AND ADVERSE


EFFECTS

fenoldopam (Corlopam)

Activates dopamine
receptors, resulting
in systemic and renal
vasodilation.

Tachycardia, angina, headache, nausea,


flushing.

IV use only for hypertensive crisis in


hospitalized patients.
Use cautiously in patients with glaucoma.
Patient should remain supine for 1 hr after
administration.

hydralazine (Apresoline)

Reduces SVR and BP by


direct arterial vasodilation.

Headache, nausea, flushing, palpitation,


tachycardia, dizziness, and angina.
Hemolytic anemia, vasculitis, and rapidly
progressive glomerulonephritis.

IV use for hypertensive crisis in


hospitalized patients.
Twice-daily oral dosage.
Not used as monotherapy because of side
effects.
Contraindicated in patients with coronary
artery disease; use with caution in
patients >40 yr.

minoxidil (Loniten)

Reduces SVR and BP by


direct arterial vasodilation.

Reflex tachycardia, marked sodium


and fluid retention (may require loop
diuretics for control), and hirsutism.
May cause ECG changes (flattened
and inverted T waves) not related to
ischemia.

Reserved for treatment of severe


hypertension associated with renal
failure and resistant to other therapy.
Once- or twice-daily dosage.

nitroglycerin (Tridil)

Relaxes arterial and


venous smooth muscle,
reducing preload
and SVR.
At low dose, venous
dilation predominates;
at higher dose, arterial
dilation is present.

Hypotension, headache, vomiting,


flushing.

IV use for hypertensive crisis in


hospitalized patients with myocardial
ischemia.
Administered by continuous IV infusion
with pump or control device.

sodium nitroprusside (Nipride)

Direct arterial vasodilation


reduces SVR and BP.

Acute hypotension, nausea, vomiting,


muscle twitching.
Signs of thiocyanate toxicity include
anorexia, nausea, fatigue, disorientation.

IV use for hypertensive crisis in


hospitalized patients.
Administered by continuous IV infusion
with pump or control device.
Intraarterial monitoring of BP
recommended.
Wrap IV solutions with an opaque material
to protect from light; stable for 24 hr.
Metabolized to cyanide, then thiocyanate.
Monitor thiocyanate levels with
prolonged use (>3 days) or doses
(4 mcg/kg/min).

Interrupts adrenergic
control of arteries,
results in vasodilation,
and reduces SVR and
BP.

Visual disturbance, dilated pupils, dry


mouth, urinary hesitancy, subjective
chilliness.

IV use for initial control of BP in patient


with dissecting aortic aneurysm.
Administered by continuous IV infusion
with pump or control device.

Hypotension, dizziness, loss of taste,


cough, hyperkalemia, acute renal failure,
skin rash, angioedema.

Aspirin and NSAIDs may reduce drug


effectiveness.
Addition of diuretic enhances drug effect.
Should not be used with potassiumsparing diuretics.
Inhibit breakdown of bradykinin, which
may cause a dry, hacking cough.
Captopril may be given orally for
hypertensive crisis.

Same as oral forms.

Given IV over 5 min; monitor 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.

enalapril (Vasotec IV)

Inhibits ACE when oral


agents not appropriate.

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

SIDE EFFECTS AND ADVERSE


EFFECTS

candesartan (Atacand)
eprosartan (Teveten)
irbesartan (Avapro)
losartan (Cozaar)
olmesartan (Benicar)
tasosartan (Verdia)
telmisartan (Micardis)
valsartan (Diovan)

Prevent action of A-II and


produce vasodilation
and increased salt and
water excretion.

Hyperkalemia, decreased renal function.

Full effect on BP may not be seen for


3-6 wk.
Do not affect bradykinin levels. Therefore
acceptable alternative to ACE inhibitors
in people who develop dry cough.

Directly inhibits renin,


thus conversion of
angiotensinogen to
angiotensin I.

Rash, diarrhea, increased creatine kinase


level, cough, hypotension, torsades de
pointes, acute renal failure, angioedema.

May cause angioedema of the face,


extremities, lips, tongue, glottis, and/
or larynx.
Not to be used in pregnancy.

Block movement of extracellular calcium into


cells, causing vasodilation and decreased
heart rate, contractility,
and SVR.

Bradycardia, first-degree AV block,


nausea, headache, dizziness, peripheral
edema, flushing, rash, gingival hyperplasia, constipation (with verapamil).

Use with caution in patients with heart


failure. Contraindicated in patients with
second- or third-degree heart block.
Avoid grapefruit when on nifedipine.
Use of sublingual short-acting nifedipine in
hypertensive emergencies is unsafe and
not effective. Serious adverse events
(e.g., stroke, acute Ml) have been
reported.
IV nicardipine available for hypertensive
crisis in hospitalized patients. Change
peripheral IV infusion sites every 12 hr.
Clevidipine is for IV use only.

NURSING CONSIDERATIONS

Renin Inhibitors
aliskiren (Tekturna)

Calcium Channel Blockers


amlodipine (Norvasc)
clevidipine (Cleviprex)
diltiazem extended release
(Cardizem CD, Cardizem LA,
Dilacor XR, Tiazac)
felodipine (Plendil)
isradipine (DynaCirc CR)
nicardipine sustained release
(Cardene SR)
nifedipine long acting (Adalat CC,
Procardia XL)
verapamil intermediate release
(Isoptin, Calan)
nisoldipine (Sular)
verapamil long acting (Isoptin SR,
Covera-HS, Calan SR)
verapamil timed release (Verelan
PM)

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

prevent A-II from binding to its receptors in the blood vessel


walls.
Most patients who are hypertensive will require two or more
antihypertensive medications to achieve their goal BP. Addition
of a second drug from a different class is started when use of
a single drug in adequate doses fails to achieve the goal BP.
These can be separate prescriptions or combination therapy
(Table 33-9). If a drug is not tolerated or is contraindicated, then
one from another class is used.
Once antihypertensive therapy is started, most patients should
return for follow-up and adjustment of medications at approximately monthly intervals until the goal BP is reached. More
frequent visits will be necessary for patients with stage 2 hypertension or with complicating co-morbid conditions. After BP is
at goal and stable, follow-up visits can usually be at 3- to 6-month
intervals. Co-morbidities (e.g., heart failure), associated diseases
(e.g., diabetes mellitus), and the need for ongoing monitoring
(e.g., laboratory testing) influence the frequency of visits.
Patient and Caregiver Teaching Related to Drug Therapy. Side
effects of antihypertensive drugs are common and may be so
severe or undesirable that the patient does not comply with
therapy. (Table 33-8 describes the major side effects of antihypertensive drugs.) Patient and caregiver teaching related to

752

SECTION 7 Problems of Oxygenation: Perfusion

TABLE 33-9

DRUG THERAPY

Combination Drug Therapy for Hypertension


COMBINATIONS
TRADE NAMES
Angiotensin-Converting Enzyme Inhibitors and Diuretics
benazepril/hydrochlorothiazide
captopril/hydrochlorothiazide
enalapril/hydrochlorothiazide
fosinopril/hydrochlorothiazide
lisinopril/hydrochlorothiazide
moexipril/hydrochlorothiazide
quinapril/hydrochlorothiazide

Lotensin HCT
Capozide
Vaseretic
Monopril-HCT
Prinzide, Zestoretic
Uniretic
Accuretic

Angiotensin II Receptor Blockers and Diuretics


candesartan/hydrochlorothiazide
eprosartan/hydrochlorothiazide
irbesartan/hydrochlorothiazide
losartan/hydrochlorothiazide
olmesartan medoxomil/
hydrochlorothiazide
telmisartan/hydrochlorothiazide
valsartan/hydrochlorothiazide

Atacand HCT
Teveten HCT
Avalide
Hyzaar
Benicar HCT
Micardis HCT
Diovan HCT

Tenoretic
Ziac
Lopressor HCT
Corzide
Inderide
Timolide

Centrally Acting Drugs and Diuretics


methyldopa/hydrochlorothiazide
reserpine/chlorthalidone
reserpine/hydrochlorothiazide
prazosin/polythiazide
guanethidine/hydrochlorothiazide
clonidine/chlorthalidone

Aldoril
Demi-Regroton
Hydropres
Minizide
Esimil
Combipres

Angiotensin-Converting Enzyme Inhibitors


and Calcium Channel Blockers
amlodipine/benazepril
enalapril/felodipine
enalapril/diltiazem
trandolapril/verapamil

Lotrel
Lexxel
Teczem
Tarka

Angiotensin II Receptor Blockers and Calcium


Channel Blockers
valsartan/amlodipine
olmesartan/amlodipine

Exforge
Azor

Diuretics and Diuretics


amiloride/hydrochlorothiazide
spironolactone/
hydrochlorothiazide
triamterene/hydrochlorothiazide

Clinical Question
For patients with hypertension (P), what factors (I) lead to nonadherence
with antihypertensive therapy (O)?

Best Available Evidence


Clinical practice guidelines based on systematic review and metaanalysis of randomized controlled trials (RCTs)

Critical Appraisal and Synthesis of Evidence


Nonadherence rates to prescribed medications are estimated at 50%;
slightly higher in elderly patients.
Nonadherence reasons are misunderstanding treatment, adverse
effects and/or concerns about these effects, complex dosing regimens, financial constraints, forgetfulness, and depression.

Conclusion
Many factors lead to nonadherence. Assess patient self-management
strategies to select specific interventions that promote adherence.

Implications for Nursing Practice

-Adrenergic Blockers and Diuretics


atenolol/chlorthalidone
bisoprolol/hydrochlorothiazide
metoprolol/hydrochlorothiazide
nadolol/bendroflumethiazide
propranolol/hydrochlorothiazide
timolol/hydrochlorothiazide

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

Teach and stress importance of medications as part of treatment


plan.
Offer positive reinforcement for patient efforts to manage medications.
Suggest patient adherence aids such as labeled pillboxes, audible
signals, and cueing medications to daily events (meals, bedtime).
Suggest patient consult with health care provider about long-acting
drugs or combination medications to simplify regimen, or less
expensive medications to decrease cost.

Reference for Evidence


Institute for Clinical Systems Improvement (ICSI): Hypertension diagnosis and treatment, Bloomington, Minn, 2008, Institute for Clinical
Systems Improvement (ICSI).
P, Patient population of interest; I, intervention or area of interest; O, outcome(s)
of interest (see p. 6).

of the autonomic nervous systems mechanisms for regulating


BP, which are required for position changes. Consequently,
the patient may feel dizzy, weak, and faint when assuming an
upright position after sitting or lying down. Table 33-14 (found
later in this chapter) presents specific measures to control or
decrease orthostatic hypotension.
DRUG ALERTDoxazosin (Cardura)

Use caution with administration of initial dose.


Syncope (sudden loss of consciousness) occasionally occurs 30 to
90 minutes following initial dose, a too-rapid increase in dose, or addition of another antihypertensive agent to therapy.

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

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