13-1

13 CASE SUMMARY

CHAPTER 13
A 64-year-old African American man with HTN, COPD, DM type
2, BPH, chronic kidney disease, and gout presents to his new fam-
HYPERTENSION ily medicine physician for evaluation and follow-up of his medical
problems. His BP is poorly controlled, despite treatment with dox-
Pass the Salt, Please  Level II azosin, hydrochlorothiazide/triamterene, and carvedilol. He states
Julia M. Koehler, PharmD, FCCP he is recovering from a cold, for which he has been taking guaife-
nesin and pseudoephedrine (Mucinex D), and it is possible that
James E. Tisdale, PharmD, BCPS, FCCP the use of this medication has contributed to his poorly controlled

INSTRUCTORS GUIDE TO
CHANGES IN THIS EDITION
CASEBOOK
Objectives
Revised slightly to reflect the fact that new JNC hypertension
guidelines are not yet available as of the time of writing of this
case, but will likely be released around the time that this book
is published.
Patient Presentation
Revisions to patient: 64-year-old (rather than 62 years old),
type 2 diabetes mellitus (DM) (rather than type 1 diabetes),
and new comorbid condition (gout). Patient is now also tak-
ing insulin lispro, carvedilol, fluticasone/salmeterol, naproxen,
and allopurinol.
Clinical Pearl
New clinical pearl added highlighting the fact that the majority
of patients with hypertension require two or more antihyper-
tensive medications to achieve blood pressure goal.
INSTRUCTORS GUIDE
Case Summary
Revised to include discussion of NSAIDs as possible contribu-
tor to lack of blood pressure control.
Problem Identification
Revised to include NSAIDs as a possible cause of poor BP
control.
Added discussion on use of -blockers for hypertension man-
agement in patients with COPD.
Therapeutic Alternatives
Added discussion of therapeutic alternatives for hypertension
in a patient with comorbid gout.
Optimal Plan
Added discussion about appropriateness of a nonselective
-blocker in a hypertensive patient with COPD and lack of
compelling indication for a -blocker in this case.
References
Revised and updated; two new references added.
Hypertension
HTN. In addition, the patient takes naproxen for relief of both
headaches and acute gout pain. Because NSAIDs may also exac-
erbate HTN, consideration of other options for HA and gout pain
relief should be explored. The patient admits a lack of adherence
to the low-sodium diet recommended by his former primary care
physician. Physical examination reveals signs and symptoms consis-
tent with target organ damage. Interventions for this patient should
include instruction on lifestyle modification, including appropriate
diet and exercise, and drug therapy. Selection of an antihypertensive
regimen should include consideration of the degree of this patients
HTN as well as patient-specific variables, such as ethnicity and
comorbid conditions. This case points out the need to treat each
patient as an individual and to consider all patient factors when
selecting drug therapy.
QUESTIONS
Problem Identification
1.a. Create a list of this patients drug-related problems, includ-
ing any medications that may be contributing to his uncon-
trolled HTN.
HTN inadequately treated with current lifestyle modifica-
tion recommendations and current pharmacotherapy; possi-
bly aggravated by current medication use for cold symptoms,
as well as NSAID use for headaches and episodes of acute
goutpain.
Mucinex D contains pseudoephedrine. Because pseu-
doephedrine has sympathomimetic activity, it has the
potential to increase BP or worsen BP control. A meta-
analysis analyzing the effects of pseudoephedrine on BP
illustrated that pseudoephedrine use contributed to a small
(~1 mm Hg) and statistically significant increase in both
systolic blood pressure (SBP) and heart rate. While the find-
ings of this meta-analysis suggest that the increases in BP
and heart rate observed with pseudoephedrine use may not
be clinically significant, the authors did note that shorter
duration of pseudoephedrine use, as well as higher doses
and immediate-release preparations, was associated with
greater increases in BP.1 In any case, consideration could be
given to discontinuation of Mucinex D if no longer indi-
cated in this patient, or possible switch to a preparation that
contains only guaifenesin.
Because of their potential to promote sodium retention,
NSAIDs, such as naproxen, may also precipitate increases in
blood pressure and may compromise the efficacy of blood
pressurelowering medications. Alternatives to NSAIDs for
headache relief and relief of pain secondary to acute gouty
attacks should be considered for this patient.

Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.

13-2
Possible doxazosin-induced orthostasis/dizziness.
Possible drugdisease contraindication between carvedilol (a
SECTION 2
nonselective -blocker) and COPD. In the absence of a clear
indication for carvedilol in this patient, either an alternative,
1-selective -blocker or another class of antihypertensive
agent should be substituted for carvedilol.
Nonadherence to lifestyle modification recommendations.
Chronic kidney disease with evidence of proteinuria.
1.b. How would you classify this patients hypertension, accord-
Cardiovascular Disorders
ing to current hypertension guidelines?
JNC 7 guidelines (current hypertension guidelines at the time
of writing of this casebook chapter) recommend the following
classification system for BP2:
Category Systolic BP (mm Hg) Diastolic BP (mm Hg)
Normal <120 <80
Prehypertension 120139 8089
Stage 1 HTN 140159 9099
Stage 2 HTN 160 100
Based on his BP readings of 162/90 and 164/92 mm Hg, this
patient can be classified as having Stage 2 HTN. (When systolic
and diastolic BPs fall into different categories, the higher of the
two numbers is used to classify the patients stage of HTN.)
In general, there is a strong correlation between BP and CV
morbidity and mortality. According to JNC 7 guidelines, a
patients risk for developing cardiovascular disease (CVD)
doubles with each increment of 20/10 mm Hg above a BP of
115/75 mm Hg. For this reason, JNC 7 guidelines recommend
that for patients whose BP falls in the category of Stage 2, more
than one BP-lowering medication will be necessary in order to
adequately lower BP and reduce the risk of CVD.
1.c. What are the patients known CV risk factors, and what is his
Framingham risk score?
According to JNC 7, the risk factors for CVD are HTN, smok-
ing, obesity (BMI >30 kg/m2), physical inactivity, dyslipidemia,
DM, microalbuminuria, kidney disease (estimated glomeru-
lar filtration rate <60 mL/min), age (men >55 years or women
>65 years), and family history of premature CVD (men
<55years or women <65 years).2 (Note: The American Society
of Hypertension [ASH] defines a family history of premature
CVD as age <50 in men, and age <60 in women. Additional
CV risk factors defined by ASH but not specifically defined
by JNC 7 include: high heart rate, central obesity [increased
abdominal circumference and/or waist-to-hip ratio], psycho-
social stressors, and elevated high-sensitivity C-reactive protein
[hs-CRP].)3
This patients CV risk factors, as defined by JNC 7, include:
HTN
Estimated glomerular filtration rate <60 mL/min
Proteinuria
DM
Age (male >55 years)
Physical inactivity
Family history cannot necessarily be included as a known CV
risk factor for this patient based on the information given.
The Framingham risk score is intended for patients who are
at risk for, but who do not yet have, coronary heart disease. In
Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.
addition, since DM and chronic kidney disease are considered
coronary heart disease risk equivalents, the Framingham risk
score is not intended for patients with DM and/or chronic kid-
ney disease; in patients with DM and/or chronic kidney disease,
the 10-year risk for heart disease is >20%. Therefore, it is not
necessary to calculate the Framingham risk score in this patient.
Given the patients comorbid diagnoses of DM and chronic
kidney disease (i.e., CHD risk equivalents), aggressive CV
risk reduction is warranted.
1.d. What evidence of target organ damage or clinical CVD does
this patient have?
Evidence of target organ damage or clinical CVD:
Eyes: arteriovenous nicking
Kidneys: (+) proteinuria, elevated serum creatinine (SCr)/
chronic kidney disease
Heart: LVH, EF 45%
Desired Outcome
2. List the goals of treatment for this patient (including his
goalBP).
The goal BP according to JNC 7 guidelines for a patient with
diabetes (or kidney disease) is <130/80 mm Hg. This is also
the recommended goal BP according to the National Kidney
Foundation and the American Diabetes Association and is con-
sistent with the recommendations for a patient with high coro-
nary artery disease risk, according tothe2007 American Heart
Association scientific statement onthe management of HTN in
patients at risk for or with known IHD.4
The general goal when treating HTN is to prevent or reduce
the likelihood of morbidity and/or mortality resulting from
uncontrolled high BP (e.g., retinal damage leading to blind-
ness, renal dysfunction or progression of existing kidney dis-
ease, stroke, heart failure, acute myocardial infarction). This
should be accomplished while attempting to maximize both
pharmacotherapeutic and pharmacoeconomic benefits, while
minimizing the risk for adverse drug events.
Additionally, other modifiable risk factors for coronary artery
disease should be treated when present.
Therapeutic Alternatives
3.a. What lifestyle modifications should be encouraged for this
patient to achieve and maintain adequate BP reduction?
In order for this patient to receive maximal benefit from the
drug therapy for his HTN, lifestyle modifications should be
again encouraged, instituted, and continued indefinitely.
Recommended lifestyle modifications should include the fol-
lowing:
Weight reduction: Maintain normal body weight (BMI
18.524.9 kg/m2). A 10-kg weight loss may result in an
approximate 520 mm Hg decrease in SBP.2
Sodium restriction: Not more than 2.4 g of sodium or 6 g of
sodium chloride (NaCl) per day. Adequate sodium restric-
tion may yield an estimated 28 mm Hg decrease in SBP.
Dietary Approaches to Stop Hypertension (DASH) diet: A
diet that is high in calcium, high in potassium, and low in
saturated fat.5 The DASH diet is rich in fruits, vegetables,
and low-fat dairy products. It has been demonstrated to be
particularly effective in producing BP lowering in African
American patients.6 The DASH diet may decrease BP by
814 mm Hg.

Moderation of alcohol intake: Not more than 1 oz or 30 mL
of ethanol per day (e.g., 24 oz of beer, 10 oz of wine, or 3 oz
of 80-proof whiskey in men; one drink per day in women
and lighter-weight persons).
Exercise: 30 minutes per day most days of the week.
Recommended exercise should include regular aerobic
activity, such as brisk walking.
Smoking cessation (or encouragement to continue avoiding
smoking in this patient case).
3.b. What reasonable pharmacotherapeutic options are available
for controlling this patients BP, and what comorbidities
and individual patient considerations should be taken into
account when selecting pharmacologic therapy for his HTN?
How might Mr Franks HTN medications potentially affect
his other medical problems?
There are several classes of antihypertensive agents that can be
considered in the treatment of HTN. Available classes of anti-
hypertensive agents include the following:
Thiazide and thiazidelike diuretics work by blocking sodium
reabsorption in the distal tubule. Thiazides have been dem-
onstrated to reduce morbidity and mortality in patients
with HTN and are considered the first-line drugs of choice
according to JNC 7 guidelines and the findings of the
Antihypertensive and Lipid-Lowering Treatment to Prevent
Heart Attack Trial (ALLHAT).7 Thiazide diuretics, as well
as calcium channel blockers, may have greater BP-lowering
effects in African-American patients compared to other
classes of antihypertensives.6
-Blockers lower BP by directly blocking adrenergic stimu-
lation of receptors. They are relatively contraindicated in
patients with known obstructive lung disease, because of
their potential to cause bronchospasm. If used in patients
with obstructive lung disease, 1-selective agents, such as
metoprolol, are preferred, and nonselective -blockers,
such as carvedilol or labetalol, should generally be avoided.
-Blockers may also mask the signs and symptoms of
hypoglycemia in patients with diabetes. In comparison to
ACE inhibitors, -blockers were demonstrated to be equally
effective in controlling BP and reducing the complications
of diabetes in the UKPDS trial.8 When used as mono-
therapy, -blockers may produce less BP-lowering effects in
African Americans compared to Caucasians.6
ACE inhibitors inhibit angiotensin-converting enzyme,
thereby blocking the conversion of angiotensin I to angio-
tensin II. ACE inhibitors have been shown to be especially
beneficial in lowering CHD risk in high-risk patients with
and without diabetes.9,10 According to JNC 7 guidelines,
ACE inhibitors are also considered first-line drugs of choice
in patients with diabetes, as they have been demonstrated
to reduce proteinuria and retard the progression of kidney
disease in such patients.2 As with -blockers, ACE inhibi-
tors, when used as monotherapy, may produce diminished
BP-lowering effects in African Americans compared to
Caucasians.6 The BP-lowering effects of ACE inhibitors may
be augmented, however, with concomitant diuretic use.
Compared to Caucasians, African Americans appear to be
at increased risk for experiencing ACE inhibitorinduced
angioedema and ACE inhibitorinduced cough.6
Angiotensin II receptor blockers (ARBs) directly antagonize
angiotensin II receptors. Although their mechanism is
similar to that of ACE inhibitors, ARBs differ in that they
spare angiotensin-converting enzyme and, therefore, allow
Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.
13-3
for the breakdown of bradykinin. (It is believed that accu-
mulation of bradykinin in the lungs is the etiology of ACE
CHAPTER 13
inhibitorassociated cough.) Similar to ACE inhibitors,
ARBs have also been demonstrated to reduce proteinuria
and delay the progression of kidney disease in patients with
diabetes. Typically, ARBs are reserved for patients who are
intolerant of ACE inhibitors due to cough.
Calcium channel blockers impair transport of calcium
through voltage-sensitive calcium channels in vascular
smooth muscle. Nondihydropyridine calcium channel
Hypertension
blockers, such as verapamil and diltiazem, work directly on
the myocardium, producing both negative inotropic and
negative chronotropic effects. Dihydropyridine calcium
channel blockers, such as amlodipine and nifedipine, yield
peripheral vasodilatory effects and may produce a second-
ary increase in heart rate, or reflex tachycardia. Although
the amount of existing data is small compared to that which
exists for ACE inhibitors, nondihydropyridine calcium
channel blockers may reduce coronary events, and data
from short-term studies illustrate that nondihydropyridines
reduce proteinuria in patients with diabetes.2,11 Although
calcium channel blockers may have greater BP-lowering
efficacy in African-American patients compared to other
classes of antihypertensives, they are typically not preferred
as first-line treatments either over thiazide diuretics in
patients without compelling comorbid indications or over
other treatments such as ACE inhibitors, in patients with
HTN, diabetes, and/or high CHD risk.2
1-Adrenergic blockers inhibit adrenergic stimulation of
peripheral 1 receptors, resulting in reduced peripheral
resistance and vasodilation. Although these agents are
effective in relieving the symptoms of BPH, they must be
used with caution in elderly patients due to the risk of diz-
ziness, orthostatic hypotension, and resultant potential for
syncope. When compared to chlorthalidone as a first-line
antihypertensive agent, doxazosin use was associated with
a higher incidence of congestive heart failure and combined
CVD outcomes in the ALLHAT study.7 The doxazosin arm
of the ALLHAT trial was discontinued early, and current
guidelines no longer recommend the use of 1-adrenergic
blockers as monotherapy in the treatment of HTN.2
Central-acting -agonists, such as clonidine, work by
directly simulating presynaptic 2-receptors in the brain-
stem, thereby reducing sympathetic outflow. This class of
antihypertensive agents is considered to be equally effective
in lowering BP in all ages and races. This class of medica-
tions carries an extensive side-effect profile, which includes
drowsiness, sedation, fatigue, depression, dry mouth,
orthostasis, bradycardia, and rebound HTN. As such, this
class of medications is poorly tolerated by many patients
and is not recommended by the JNC for first- or second-line
consideration in the management of HTN.2
Direct vasodilators, such as hydralazine and minoxidil, work
by directly relaxing arterial smooth muscle and reducing
peripheral vascular resistance. Because these drugs may
produce profound peripheral vasodilation, they often cause
significant side effects, such as peripheral edema and reflex
tachycardia, which warrant additional treatment (i.e., they
typically must be used in combination with a -blocker and
a loop diuretic). These agents are most commonly reserved
for refractory HTN despite modest doses of three or more
antihypertensive agents.
Peripheral adrenergic neuron antagonists, such as reser-
pine, deplete norepinephrine from peripheral neurons and
13-4
inhibit release of norepinephrine in response to sympathetic
stimulation. Much like central-acting 2-agonists, this class
SECTION 2
of drugs is associated with significant side effects, such
as orthostasis, GI disturbances, bradycardia, drowsiness,
depression, and nightmares, which limit the utility of these
agents for most patients.
The direct renin inhibitor aliskiren was approved by the
FDA in 2007. This newer class represents the first new type
of antihypertensive available for the treatment of HTN in
more than a decade. Aliskiren is indicated either alone or
Cardiovascular Disorders
in combination with other antihypertensives, such as thiaz-
ide diuretics or ARBs. It is administered once daily for the
treatment of HTN. Because of the cost of this agent and the
limited data available in treating patients with HTN and
other comorbidities, it is not currently recommended as a
first-line antihypertensive agent.
Comorbidities that must be specifically taken into account when
selecting pharmacologic antihypertensive therapy for this patient
include:
DM:
ACE inhibitors are typically the drugs of choice in patients
with diabetes, as they have been demonstrated to reduce
proteinuria and delay progression of kidney disease. ARBs
have also been demonstrated to have renal protective
effects, particularly in patients with type 2 diabetes and in
those with advanced kidney disease. There is no indication
in this patient to select an ARB over an ACE inhibitor at
this time, particularly since it is also important to note
the demonstrated benefit of CV risk reduction with ACE
inhibitors.
-Blockers have also been shown to control BP and reduce
the complications of diabetes.8 Caution should be used
when selecting a -blocker for a patient with diabetes, as
-blockers may mask signs and symptoms of hypoglycemia
and may contribute to glucose intolerance. This is not an
absolute contraindication, however.
Thiazides are recommended as first-line antihypertensives
in patients with or without diabetes for control of HTN
and reduction of morbidity and mortality.7 It is important
to note, however, that in high doses, thiazides may increase
blood glucose and cause other metabolic derangements.
Chronic obstructive pulmonary disease:
-Blockers are relatively contraindicated in patients with
moderate to severe obstructive lung disease. Consideration
must therefore be given to the severity of the disease,
risk versus potential benefit, and relative -receptor
selectivity.
ACE inhibitors are not contraindicated in patients with
obstructive lung disease. It is important to note, however,
that these drugs may cause cough in 1020% of patients,
and this is an important monitoring parameter in patients
with obstructive lung disease.
Benign prostatic hyperplasia:
1-Blockers are drugs of choice for symptomatic relief.
These agents should not be used as monotherapy in the
treatment of HTN, however, based on the findings of the
ALLHAT study.12
Chronic kidney disease:
Both ACE inhibitors and ARBs have been shown to reduce
the incidence and severity of proteinuria and delay the
progression of kidney disease in patients with diabetes.
Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.
ACE inhibitors have been shown to delay the progression of
kidney disease in nondiabetic nephropathy.13
Thiazide diuretics are considered to be ineffective when
CrCl is <30 mL/min. Although this patients estimated CrCl
is not below 30 mL/min currently, continuous monitoring
of the progression of this patients kidney disease is impor-
tant and could affect the potential efficacy of a thiazide
diuretic in the future.
Potassium-sparing diuretics should be used with caution in
patients with mild kidney disease and should be avoided in
patients with significant kidney disease.
Gout:
In high doses (e.g., 50 mg of hydrochlorothiazide), thiazide
diuretics may increase serum uric acid concentrations and
cause other metabolic derangements, such as alterations in
blood glucose and serum lipid concentrations.
Left ventricular hypertrophy:
ACE inhibitors have been shown to reduce LV mass, as have
most classes of antihypertensive agents, with the exception
of direct vasodilators.
African-American race (not a comorbidity but an important
consideration):
-Blockers and ACE inhibitors are generally thought to be
less effective when used as monotherapy for BP lowering in
this population of patients. The BP-lowering effect of ACE
inhibitors can be enhanced with the addition of a diuretic.
Diuretics and calcium channel blockers are considered to
have greater BP-lowering effects than most other antihyper-
tensive classes in African-American patients.
Optimal Plan
4.a. Recommend specific lifestyle modifications for this patient.
Nonpharmacologic therapy for this patient should include the
following:
Weight reduction. The patients current weight is 95 kg, and
his BMI is 27 kg/m2. The patients IBW = 82.2 kg. Weight
reduction by caloric restriction has been shown to reduce
BP, even if IBW is not achieved. A goal for the patient should
be to achieve and maintain a BMI of 18.524.9 kg/m2.
Sodium restriction. The patient has been nonadherent to his
prescribed low-sodium diet. Ideally, he should be restricted
to not more than 2.4 g of sodium (6 g NaCl) per day. The
patient should be instructed not to add salt to his food. He
should also be advised to seek out foods that are low in
sodium and/or consult with a dietician to assist with imple-
menting a low-sodium diet.
DASH diet. The patient should be given information about
and encouraged to try this diet, which is low in sodium, high
in calcium and potassium, and low in both saturated and
total fat. This diet has been shown to be particularly effec-
tive in African American hypertensives and may reduce BP
better than both weight loss and sodium restriction alone in
these patients.
Moderation of alcohol intake. The patient should be encour-
aged to limit his alcohol intake to not more than 1 oz of
ethanol, 24 oz of beer, 10 oz of wine, or 3 oz of 80-proof
whiskey per day.
Exercise. The patient should be encouraged to participate
in 3045 minutes of aerobic activity most days of the week.
Although this can help lower his BP and reduce his overall

CV risk, this level of activity may not be feasible for this
patient, as he may be limited by the severity of his COPD.
Continued smoking avoidance. This patient who was a long-
time smoker successfully quit smoking 3 years ago. The
patient should be congratulated for his successfully having
quit smoking, and he should be encouraged to continue
to refrain from smoking and to minimize his exposure to
second-hand smoke whenever possible. Smoking cessation
results in overall CV risk reduction and may continue to
positively affect the rate of decline in the patients FEV1
due to his COPD. If not currently enrolled in a pulmonary
rehabilitation program, the patient should receive a referral
and be given encouragement to participate in the program
in order to improve his functional capacity.
4.b. Outline a specific and appropriate pharmacotherapeutic reg-
imen for this patients uncontrolled HTN, including drug(s),
dose(s), dosage form(s), and schedule(s).
Drug therapy for HTN must be individualized based on the
patients age, race, known pathophysiologic variables, and
comorbid conditions. Treatment regimens should be designed
not only to achieve desired BP goals (<130/80 mm Hg for this
patient), but also to reduce morbidity and mortality associated
with HTN.
Consideration should be given to either discontinuing the
guaifenesin/pseudoephedrine preparation altogether (especially
if no longer needed for the treatment of specific cold symptoms
in this patient) or switching the product to a preparation that
contains guaifenesin without pseudoephedrine.
Because this patient has Stage 2 HTN and his current BP is
more than 20/10 mm Hg above his goal BP, and because he
has both DM and chronic kidney disease, a minimum of two
antihypertensive medications are indicated for adequate BP
lowering.2,14
Because this patient has diabetes, chronic kidney disease with
proteinuria, LVH, and is considered to be at high risk for
experiencing a CHD-related event, an ACE inhibitor should be
added to the patients current antihypertensive regimen. A long-
acting agent that can be given once daily, such as lisinopril
5mg po once daily or ramipril 2.5 mg po once daily, should
be initiated in this patient and titrated upwards as tolerated
in order to achieve the desired BP goal. While ACE inhibitors
can cause cough as an adverse effect, the fact that this patient
complains of a cough prior to the initiation of ACE inhibitor
therapy is not a reason to withhold ACE inhibitors. In addi-
tion, the fact that this patient has CKD with a SCr concentra-
tion of 2.2mg/dL is also not a reason to withhold therapy with
ACE inhibitors; ACE inhibitors have been shown to prevent
the progression of kidney disease in patients with SCr concen-
tration 1.53.0 mg/dL.13
Hydrochlorothiazide should be continued in this patient, because
it is considered an appropriate first-line antihypertensive
according to JNC 7 guidelines and, when given in combina-
tion with an ACE inhibitor, the two drugs may work synergisti-
cally to lower BP in this African-American patient. The dose of
hydrochlorothiazide should not be increased, due to the poten-
tial for higher doses to cause elevations in blood glucose and
other metabolic derangements, including possible elevations
in serum uric acid concentration, in this patient with diabetes
and gout.
Consideration should be given to changing the triam-
terene/hydrochlorothiazide combination that the patient
is currently taking to hydrochlorothiazide only, due to the
13-5
potential for hyperkalemia when combined with an ACE
inhibitor, particularly in view of the fact that the patient
CHAPTER 13
has CKD.
Doxazosin may be continued in this patient for control of his
symptoms of BPH. If continued, consideration should be given
to changing the dosing schedule to QHS dosing to reduce possible
doxazosin-induced orthostasis/dizziness. As an alternative, the
doxazosin could be changed to tamsulosin, but it should be
noted that this medication, which is specific for receptors in
the prostate, will not have an impact on BP lowering.
Hypertension
There is no reason to select or recommend an ARB over an
ACE inhibitor at this time. ARBs are more expensive than
ACE inhibitors and, although they have been shown to reduce
proteinuria and delay the progression of kidney disease, data
regarding their impact on CV risk reduction are lacking. Thus,
an ARB should only be prescribed if the patient develops intol-
erance to the ACE inhibitor, such as ACE inhibitorinduced
cough.
Carvedilol should be discontinued in this patient. Nonselective
-blockers should generally be avoided in this patient with
moderate obstructive lung disease, especially since there is no
compelling indication to select a -blocker for the patient at
this time. If a -blocker is chosen, preference should be given
to a 1-selective agent, such as metoprolol.
Outcome Evaluation
5. Based on your recommendations, what parameters should be
monitored after initiating this regimen and throughout the
treatment course? At what time intervals should these param-
eters be monitored?
Monitor adherence to and accomplishment of lifestyle modi-
fications, including dietary adjustments, exercise, and weight
reduction. Because of the close interrelationship of lifestyle
modifications with HTN and CV risk, these interventions
should be reinforced at each visit throughout the course of
treatment.
JNC 7 guidelines recommend that BP be monitored at least
monthly until it is controlled. More frequent monitoring
should be considered in patients with Stage 2 HTN. In this
patient, the BP should be rechecked in 24 weeks.2
General laboratory monitoring for this patient should include
chemistries (specifically serum sodium, potassium, creatinine,
and glucose), uric acid, and a fasting lipid profile. Recheck a
follow-up chemistry in 24 weeks, and if laboratory results are
normal, rechecking follow-up chemistry once every 6 months
is reasonable.
Monitor serum potassium and BUN/SCr closely (e.g.,
ideally, approximately 1 week after initiating ACE inhibi-
tor therapy). If SCr increases significantly (i.e., by >30%),
discontinue the ACE inhibitor and evaluate the patient for
renal artery stenosis.
Monitor for the occurrence of significant adverse effects of
drug therapy. If an ACE inhibitor and thiazide diuretic combi-
nation was chosen, these adverse effects would include, but not
be limited to, orthostasis, headache, dizziness, lightheadedness,
sexual dysfunction, glucose intolerance, potassium imbalance,
worsening kidney function, and dry cough. If the patient devel-
ops a bothersome dry cough, consider switching to an ARB.
After initiating an ACE inhibitor in this patient, also monitor
closely for the occurrence of angioedema, which occurs most
commonly in the African-American patient population (esti-
mated at 56% of patients). If angioedema occurs, discontinue
Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.
13-6
the ACE inhibitor immediately and consider whether or
not a switch to an ARB would be safe for this patient. (In a
SECTION 2
recent meta-analysis, the risk of developing any subsequent
angioedema with ARB use following ACE inhibitorinduced
angioedema was reported as 217%.15) As an alternative, a
nondihydropyridine calcium channel blocker, such as vera-
pamil or diltiazem, could be considered for renal protective
effect if the patient could not take either an ACE inhibitor or
an ARB. (Note: In light of this patients already reduced left
ventricular ejection fraction [45%], close monitoring for signs
Cardiovascular Disorders
of worsening cardiac function and possible development of
systolic heart failure is warranted. In the event that this patient
does eventually develop systolic dysfunction, a nondihydro-
pyridine calcium channel blocker would then be contraindi-
cated.) Amlodipine and felodipine are safe for use in patients
with heart failure, but there are few data regarding their effi-
cacy for renal protection.
Patient Education
6. Based on your recommendations, provide appropriate educa-
tion to this patient.
Antihypertensive agents in general:
These medicines do not cure high blood pressure. You will
probably need to continue taking these medications on a long-
term basis to keep your blood pressure controlled.
Take these medications exactly as prescribed, do not skip doses,
and if you do miss a dose, do not double up by taking two
doses at once.
Because these drugs lower your blood pressure, you may feel
dizzy or lightheaded when going from lying down or sitting
to a standing position. Use caution and rise slowly from these
positions until you know how your body reacts. As your body
gets accustomed to these new medicines and your lower blood
pressure, this effect may diminish.
If dizziness is extreme or continues beyond a few days, inform
your health care provider.
These medications can affect different body systems in addition
to lowering your blood pressure; they may affect your heart rate
and some of your blood tests. It is extremely important to keep
all scheduled appointments with your health care providers to
properly monitor your progress.
Thiazide diuretic (e.g., chlorthalidone or hydrochlorothi-
azide):
This medication is used to lower your blood pressure.
One of the ways this medicine lowers blood pressure is to cause
you to lose extra fluid through increased urination. Because of
this, you will want to take this medication early in the day, to
avoid having to get up at night to go to the bathroom.
You may take this medication with food, milk, or on an empty
stomach.
Thiazide diuretics can make you sensitive to sunlight. Be sure
to apply a sunscreen with a sun protection factor (SPF) of at
least 15 before any extended exposure to sunlight.
Thiazide diuretics may cause you to lose potassium. Your phy-
sician will monitor your potassium balance carefully. If you
experience cramping in your feet or lower extremities, this may
be a sign that your potassium has dropped. If this occurs, notify
your physician.
Copyright 2011 by The McGraw-Hill Companies, Inc. All rights reserved.
ACE inhibitor (e.g., lisinopril, ramipril):
This medicine lowers BP by relaxing your blood vessels.
This medication works together with your diuretic, allowing
you to use lower doses of both medications and decrease the
chance of side effects from either drug.
This type of medicine can sometimes cause a chronic dry
cough. If this occurs, please contact your heath care provider.
This is not dangerous, but it can be bothersome.
If you experience any swelling in your face, lips, or tongue, or
have breathing problems, immediately stop taking this medica-
tion and go to the emergency department for immediate medi-
cal attention.
If you experience a significant decrease in urinary frequency
while taking this medication, be sure to contact your provider.
Doxazosin:
This medicine treats the symptoms of BPH, or an enlarged
prostate. It may also treat your high blood pressure.
This medicine may make you dizzy or drowsy. Avoid driving,
using machines, or doing anything else that could be dangerous
if you are not alert.
Because you report symptoms of dizziness currently after tak-
ing this medicine in the morning, begin taking this medication
at night, before you go to bed. If you continue to experience
symptoms of dizziness or lightheadedness, or if you experience
fainting, notify your physician.
Notify your physician if you begin to experience pain on urina-
tion, changes in how much or how often you urinate, or red or
dark brown urine.
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13-7
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CHAPTER 13
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