Hypertension
Introduction
1-Hypertension is defined as persistently elevated
arterial blood pressure (BP).
2-Isolated systolic hypertension is diastolic
blood pressure (DBP) <80 mm Hg and
systolic blood pressure (SBP) ≥130 mm Hg.
3-Hypertensive crisis (BP >180/120 mm Hg)
is categorized as hypertensive emergency
(extreme BP elevation with acute or
progressing end-organ damage) or
hypertensive urgency (extreme BP elevation
without acute or progressing end-organ
injury).
End-organ damage
Pathophysiology
1-Hypertension may result from an
unknown etiology (primary or essential
hypertension) or from a specific cause
(secondary hypertension).
2-Secondary hypertension (<10% of
cases) is usually caused by chronic kidney
disease (CKD) or renovascular disease.
3-Examples of drugs that may increase BP
include corticosteroids, estrogens, NSAIDs,
cyclosporine, erythropoietin, and venlafaxine.
4-Major causes of death include
cerebrovascular events, cardiovascular (CV)
events, and renal failure.
Probability of premature death correlates
with the severity of BP elevation.
Clinical presentation
1-Patients with uncomplicated primary
hypertension are usually asymptomatic
initially.
2-Patients with secondary hypertension
may have symptoms of the underlying
disorder.
Diagnosis
1-Elevated BP may be the only sign of primary
hypertension on physical examination.
2-Diagnosis should be based on the average
of two or more readings taken at each of two
or more clinical encounters.
3-Signs of end-organ damage occur primarily
in the eyes, brain, heart, kidneys, and
peripheral vasculature.
4-Laboratory tests: Blood urea nitrogen
(BUN), serum creatinine with estimated
glomerular filtration rate (eGFR), fasting
lipid panel, fasting blood glucose, serum
electrolytes, uric acid, hemoglobin and
hematocrit, and spot urine albumin-to-
creatinine ratio.
A 12-lead electrocardiogram (ECG) should
also be obtained.
Treatment
1-Goals of Treatment: The overall goal is
to reduce morbidity and mortality from
CV events.
The 2017 ACC/AHA guideline
recommends a goal BP of <130/80 mm
Hg for most patients.
2-For institutionalized older patients and
those with a high disease burden or
limited life expectancy, consider a
relaxed SBP goal of <150 mm Hg (or <140
mm Hg if tolerated).
Nonpharmacologic Therapy
A-Implement lifestyle modifications in all
patients with elevated BP or stage 1 or 2
hypertension.
B-These measures alone are appropriate initial
treatment for patients with elevated BP or
stage 1 hypertension who are at low risk of
ASCVD (ie, primary prevention with a 10-year
ASCVD risk <10%). Start drug therapy for these
patients when BP is ≥140/90 mm Hg.
https://clincalc.com/Cardiology/ASCVD/PooledCohort.aspx
C-For patients with stage 1 or 2
hypertension who already have ASCVD
(secondary prevention) or an elevated
10-year ASCVD risk ≥10%, the threshold
for starting drug therapy is ≥130/80 mm
Hg with a goal BP of <130/80 mm Hg.
D-Lifestyle modifications shown to lower BP
include:
(1) weight loss if overweight or obese, (2) the
Dietary Approaches to Stop Hypertension (DASH)
eating plan, (3) reduced salt intake, ideally to 1.5
g/day sodium (3.8 g/day sodium chloride), (4)
physical activity (90–150 min/week of aerobic or
dynamic resistance training), and (5) moderation of
alcohol intake (≤2 drinks/day in men and ≤1
drink/day in women). Although smoking cessation
does not control BP, it reduces CV disease risk and
should be encouraged.
Lifestyle Modifications
Approximate SBP
Modification Recommendation
Reduction (mm Hg)*
Weight loss Maintain normal body weight (body mass 5–20 per 10-kg
2
index 18.5–24.9 kg/m ) weight loss
DASH-type Consume a diet rich in fruits, vegetables, 8–14
dietary and low-fat dairy products with a reduced
patterns content of saturated and total fat
Reduced salt Reduce daily dietary sodium intake as much 2–8
intake as possible, ideally to 65 mmol/day (1.5
gm/day sodium, or 3.8 g/day sodium
chloride)
Physical Regular aerobic physical activity (at least 30 4–9
activity min/day, most days of the week)
Moderation of Limit consumption to 2 drinks/day in men 2–4
alcohol intake and 1 drink/day in women and lighter-weight
persons
DASH, Dietary Approaches to Stop Hypertension.
*Effects of implementing these modifications are time and dose dependent and could be greater for some patients.
Pharmacologic Therapy
General Approach to Treatment
1-Initial drug selection depends on the degree
of BP elevation and presence of compelling
indications for certain drugs.
2-Use a single first-line drug as initial therapy
in most patients with newly diagnosed stage 1
hypertension.
3-Start combination drug
therapy (preferably with two
first-line drugs) as the initial
regimen in patients with
newly diagnosed stage 2
hypertension.
4-The four first-line options
are angiotensin-converting
enzyme (ACE) inhibitors,
angiotensin II receptor
blockers (ARBs), calcium
channel blockers (CCBs), and
thiazide diuretics.
5-β-Blockers should be reserved to treat a
specific compelling indication or in
combination with a first-line antihypertensive
agent for patients without a compelling
indication.
6-Other antihypertensive drug classes (α1-
blockers, direct renin inhibitors, central α2-
agonists, and direct arterial vasodilators) may
be used for select patients after
implementing first-line agents.
Compelling Indications
Compelling indications are specific
comorbid conditions for which clinical
trial data support using specific
antihypertensive drug classes to treat
both hypertension and the compelling
indication.
A-Heart Failure with Reduced Ejection Fraction
(HFrEF)
1-Medical therapy consists of three to four drugs:
ACE inhibitor or ARB plus diuretic, followed by
addition of an evidence-based β-blocker and
possibly a mineralocorticoid receptor antagonist.
Ejection Fraction
2-After implementation of a standard
three-drug regimen (ACE inhibitor or
ARB, β-Blockers plus diuretic), other
agents may be added to further reduce
CV morbidity and mortality, and reduce
BP if needed.
A mineralocorticoid receptor antagonist
(spironolactone or eplerenone) may be
considered at this point
B-Heart Failure with Preserved Ejection Fraction
(HFpEF)
1-Unlike interventions in HFrEF that decrease
morbidity and mortality, trials using the same
medications in HFpEF have not shown similar
benefits.
2-Therefore, treatment should be targeted at signs
and symptoms (eg, dyspnea, fatigue, edema),
appropriate management of underlying coronary
artery disease, and attainment of goal BP to
prevent HF progression.
3-Patients should use a β-blocker or an
ACE inhibitor (or ARB) for treatment of
hypertension, and they should receive a
diuretic if signs and symptoms of edema
are present.
C-Stable Ischemic Heart Disease (SIHD)
1-β-Blockers (without ISA) are first-line
therapy in SIHD; they reduce BP and improve
angina symptoms by decreasing myocardial
oxygen consumption and demand.
2-β-Blockers should be used for
hypertension treatment in patients with
SIHD.
3-For acute coronary syndromes, first-line
therapy includes a β-blocker and ACE
inhibitor (or ARB).
D-Diabetes Mellitus
1-All four first-line antihypertensive classes (ACE
inhibitors, ARBs, CCBs, thiazides) reduce CV events
in patients with diabetes, with no evidence of
difference in all-cause mortality, CV mortality, HF, or
stroke.
2-The risk of kidney disease progression is low in
the absence of albuminuria (urine albumin-to-
creatinine ratio ≥30 mg/g [3.4 mg/mmol
creatinine]). Therefore, any first-line agent can be
used to control hypertension in patients with
diabetes in the absence of albuminuria.
3-Regardless of the initial agent selected, most
patients require combination therapy, which
typically includes an ACE inhibitor (or ARB) with a
CCB or thiazide.
4-After first-line agents, a β-blocker is a useful add-
on therapy for BP control in patients with diabetes.
However, they may mask symptoms of
hypoglycemia (tremor, tachycardia, and palpitations
but not sweating) in tightly controlled patients, and
delay recovery from hypoglycemia Despite these
potential problems, β-blockers can be used safely
in patients with diabetes.
E-Chronic Kidney Disease
1-In addition to lowering BP, ACE inhibitors
and ARBs reduce intraglomerular pressure,
which may further slow CKD progression.
2-Start with low doses and evaluate the
serum creatinine soon after starting therapy
to minimize the risk of rapid and profound BP
drops that could precipitate acute kidney
injury (AKI).
F-Secondary Stroke Prevention
1-A thiazide diuretic, either alone or
combined with an ACE inhibitor, is
recommended for patients with history of
stroke or transient ischemic attack.
2-The threshold for starting antihypertensive
drug therapy in patients with a history of
stroke is when BP is >140/90 mm Hg (goal of
<130/80 mm Hg).
Angiotensin-Converting Enzyme Inhibitors
(captopril, enalapril, fosinopril, imidapril, lisinopril,
perindopril, quinapril, ramipril, and trandolapril)
1-ACE inhibitors block conversion of angiotensin I to
angiotensin II, a potent vasoconstrictor and
stimulator of aldosterone secretion.
2-Starting doses should be low with slow dose
titration. Acute hypotension may occur at the onset
of therapy.
3-ACE inhibitors decrease aldosterone
and can increase serum potassium
concentrations.
Hyperkalemia occurs primarily in
patients with CKD or those also taking
potassium supplements, potassium-
sparing diuretics, mineralocorticoid
receptor antagonists, ARBs, or direct
renin inhibitors.
4-AKI is an uncommon but serious side
effect; preexisting kidney disease
increases risk. Bilateral renal artery
stenosis or unilateral stenosis renders
patients dependent on the
vasoconstrictive effect of angiotensin II
on efferent arterioles, making them
particularly susceptible to AKI.
5-Serum creatinine concentrations often
increase, but modest elevations (eg, absolute
increases <1 mg/dL) do not warrant
treatment changes. Discontinue therapy or
reduce dose if larger increases occur.
6-Angioedema occurs in <1% of patients.
Drug withdrawal is necessary, and some
patients may require drug treatment and/or
emergent intubation to support respiration.
Angioedema
7-An ARB can generally be used in patients
with a history of ACE inhibitor-induced
angioedema, with careful monitoring.
8-A persistent dry cough occurs in up to 20%
of patients and is thought to be due to
inhibition of bradykinin breakdown.
10-ACE inhibitors (as well as ARBs and direct
renin inhibitors) are contraindicated in
pregnancy.
Angiotensin II Receptor Blockers (candesartan,
eprosartan, irbesartan, losartan, olmesartan,
telmisartan, and valsartan)
1-The ARBs directly block the angiotensin II type 1
receptor that mediates the effects of angiotensin
II.
2-Unlike ACE inhibitors, ARBs do not block
bradykinin breakdown and this accounts for the
lack of cough as a side effect.
3-The combination of an ACE inhibitor and ARB
has no additional benefit but is associated with a
higher risk of side effects and should be avoided.
4-All ARBs have similar antihypertensive efficacy.
Addition of a CCB or thiazide diuretic significantly
increases antihypertensive efficacy.
5-ARBs have a low incidence of side effects. Like
ACE inhibitors, they may cause renal insufficiency,
hyperkalemia, and orthostatic hypotension.
Calcium Channel Blockers
1-Dihydropyridine and nondihydropyridine CCBs are
first-line antihypertensive therapies and are also
used in addition to or instead of other first-line
agents for the compelling indication of ischemic
heart disease.
2-Dihydropyridine CCBs may cause reflex
sympathetic activation, and all agents (except
amlodipine and felodipine) may have negative
inotropic effects.
3-Verapamil decreases heart rate, slows
atrioventricular (AV) nodal conduction, and
produces a negative inotropic effect that may
precipitate HF in patients with borderline cardiac
reserve. Diltiazem decreases AV conduction and
heart rate to a lesser extent than verapamil.
4-Diltiazem and verapamil can cause cardiac
conduction abnormalities such as bradycardia, AV
block, and HF. Both can cause peripheral edema
and hypotension. Verapamil causes constipation in
about 7% of patients.
5-Dihydropyridines cause a
baroreceptor-mediated reflex increase in
heart rate because of potent peripheral
vasodilating effects.
Dihydropyridines do not decrease AV
node conduction and are not effective
for treating supraventricular
tachyarrhythmias.
6-Short-acting nifedipine may rarely increase
frequency, intensity, and duration of angina in
association with acute hypotension. This
effect may be obviated by using sustained-
release formulations of nifedipine or other
dihydropyridines.
7-Other side effects of dihydropyridines are
dizziness, flushing, headache, gingival
hyperplasia, and peripheral edema.
Diuretics
1-Thiazides are the preferred type of diuretic
and are a first-line option for most patients
with hypertension. Chlorthalidone (thiazide-
like) is preferred over hydrochlorothiazide,
especially in resistant hypertension, because it
is more potent on a milligram-per-milligram
basis.
2-Loop diuretics (Furosemide, Bumetanide
and Torasemide) are more potent for
inducing diuresis but are not ideal
antihypertensives unless edema treatment is
also needed.
Loop diuretics are sometimes required over
thiazides in patients with severe CKD when
eGFR is <30 mL/min/1.73 m2, especially when
edema is present.
3-Potassium-sparing diuretics are weak
antihypertensives when used alone and
provide minimal additive effect when
combined with a thiazide or loop diuretic.
Their primary use is in combination with
another diuretic to counteract potassium-
wasting properties.
4-Mineralocorticoid receptor antagonists
(spironolactone and eplerenone) are also
potassium-sparing diuretics that are usually
used to treat resistant hypertension because
elevated aldosterone concentrations are
prevalent in this setting. They are also used
as add-on agents in patients with HFrEF with
or without concomitant hypertension.
5-Acutely, diuretics lower BP by causing diuresis.
With chronic therapy, reduced peripheral vascular
resistance is responsible for persistent hypotensive
effects.
6-Combining diuretics with other antihypertensive
agents usually results in an additive hypotensive
effect because of independent mechanisms of
action. Furthermore, many nondiuretic
antihypertensive agents induce sodium and water
retention, which is counteracted by concurrent
diuretic use.
7-Side effects of thiazides include hypokalemia,
hypomagnesemia, hypercalcemia, hyperuricemia,
hyperglycemia, dyslipidemia, and sexual
dysfunction.
8-Loop diuretics have less effect on serum lipids and
glucose, but hypokalemia is more pronounced, and
hypocalcemia may occur.
9-Hypokalemia and hypomagnesemia may cause
muscle fatigue or cramps, and severe electrolyte
abnormalities may result in serious cardiac
arrhythmias.
10-Potassium-sparing diuretics may cause
hyperkalemia, especially in patients with CKD or
diabetes and in patients receiving concurrent
treatment with a mineralocorticoid receptor
antagonist, ACE inhibitor, ARB, direct renin inhibitor,
or potassium supplement.
11-Spironolactone may cause gynecomastia in up
to 10% of patients; this effect occurs rarely with
eplerenone.
β-Blockers
1-Evidence suggests that β-blockers may not reduce
CV events as well as ACE inhibitors, ARBs, CCBs, or
thiazides when used as the initial drug in patients who
do not have a compelling indication for a β-blocker.
2-β-Blockers are appropriate first-line agents when
used to treat specific compelling indications or when
an ACE inhibitor, ARB, CCB, or thiazide cannot be used.
3-β-Blockers also have an important role as add-on
therapy to first-line agents in patients with
hypertension but no compelling indications.
4-Atenolol, betaxolol, bisoprolol, metoprolol,
and nebivolol are β1-cardioselective at low.
As a result, they are less likely to provoke
bronchospasm and vasoconstriction and are
safer than nonselective β-blockers in patients
with asthma or diabetes who have a
compelling indication for a β-blocker.
Cardioselectivity is a dose-dependent
phenomenon, and the effect is lost at higher
doses.
5-Acebutolol, carteolol, and pindolol possess
intrinsic sympathomimetic activity (ISA) or
partial β-receptor agonist activity.
Theoretically, these drugs may have
advantages in select patients with HF or sinus
bradycardia. Unfortunately, they do not
reduce CV events as well as other β-blockers
and may increase CV risk in patients with
SIHD. Thus, agents with ISA are rarely
needed and have no role in hypertension
management.
6-Atenolol and nadolol have relatively long
half-lives and are excreted renally; the
dosage may need to be reduced in patients
with renal insufficiency.
7-Even though the half-lives of other β-
blockers are shorter, once-daily
administration still may be effective.
8-Cardiac side effects include bradycardia, AV
conduction abnormalities, and acute HF.
Blocking β2-receptors in arteriolar smooth
muscle may cause cold extremities and
aggravate intermittent claudication or
Raynaud phenomenon because of decreased
peripheral blood flow.
9-Increases in serum lipids and glucose
appear to be transient and of little clinical
significance.
10-Abrupt cessation of β-blocker therapy can
produce cardiac ischemia (angina, chest
pain), a CV event, or even death in patients
with coronary artery disease. In patients
without heart disease, abrupt discontinuation
of β-blockers may be associated with
tachycardia, sweating, and generalized
malaise in addition to increased BP. For these
reasons, the dose should always be tapered
gradually over 1–2 weeks before
discontinuation.
α1-Receptor Blockers
1-Prazosin, terazosin, and doxazosin are selective α1-
receptor blockers that inhibit catecholamine uptake in
smooth muscle cells of peripheral vasculature, resulting
in vasodilation and BP lowering.
2-A first-dose phenomenon characterized by
orthostatic hypotension accompanied by transient
dizziness or faintness, palpitations, and even syncope
may occur within 1–3 hours of the first dose or after
later dosage increases.
3-The patient should take the first dose (and
subsequent first increased doses) at bedtime.
Occasionally, orthostatic hypotension and dizziness
persist with chronic administration.
4-Sodium and water retention can occur withα1-
Receptor Blockers; these agents are most effective
when given with a thiazide to maintain
antihypertensive efficacy and minimize edema.
5-These agents block postsynaptic α1-adrenergic
receptors on the prostate capsule, causing
relaxation and decreased resistance to urinary
outflow. Although they can provide symptomatic
benefit in men with benign prostatic hyperplasia,
they should be used to lower BP only in
combination with first-line antihypertensive
agents.
Direct Renin Inhibitor
Aliskiren blocks the RAAS at its point of
activation, resulting in reduced plasma renin
activity and BP. It is approved for
monotherapy or in combination therapy. Its
role in the management of hypertension is
limited.
Central α2-Agonists
1-Clonidine, guanfacine, and methyldopa
lower BP primarily by stimulating α2-
adrenergic receptors in the brain, which
reduces sympathetic outflow from the
vasomotor center.
2-Clonidine is often used in resistant
hypertension, and methyldopa is frequently
used for pregnancy-induced hypertension.
3-Chronic use results in sodium and fluid
retention. Other side effects include
depression, orthostatic hypotension,
dizziness, and anticholinergic effects (eg, dry
mouth, sedation).
Abrupt cessation may lead to rebound
hypertension
4-Methyldopa rarely causes hepatitis or hemolytic
anemia. A transient elevation in hepatic
transaminases occasionally occurs. Discontinue
therapy if persistent increases in liver function tests
occur, because this may herald onset of fulminant,
life-threatening hepatitis. Coombs-positive
hemolytic anemia occurs rarely, and 20% of
patients exhibit a positive direct Coombs test
without anemia. For these reasons, methyldopa
has limited usefulness except in pregnancy.
The direct Coombs test is used to test for
autoimmune hemolytic anemia
Direct Arterial Vasodilators
1-Hydralazine and minoxidil directly relax
arteriolar smooth muscle, resulting in
vasodilation and BP lowering. Compensatory
activation of baroreceptor reflexes increases
sympathetic outflow, thereby increasing heart
rate, cardiac output, and renin release.
Consequently, hypotensive effectiveness of
direct vasodilators diminishes over time
unless the patient is also taking a diuretic
and a β-blocker.
2-Direct vasodilators can precipitate angina in
patients with underlying SIHD unless the
baroreceptor reflex mechanism is blocked
with a β-blocker.
Nondihydropyridine CCBs can be used as an
alternative to β-blockers in patients with
contraindications to β-blockers.
3-Hydralazine may cause a dose-related,
reversible lupus-like syndrome, which is more
common in slow acetylators.
4-Minoxidil cause reversible
hypertrichosis on the face, arms, back,
and chest may be troublesome. Minoxidil
is reserved for resistant hypertension and
for patients requiring hydralazine who
experience drug-induced lupus.
Another types of hypertension
• Malignant hypertension
I. Occur in 1% of people with hypertension it is
common in younger adults ,african american
men and woman who have pregnancy
toxemia.
II.Diastolic blood pressure goes over 130
III.Sholud treated in hospital.
Resistant hypertension •
I. When the doctor prescribed three different
types of antihypertensive medications and
blood pressure is still too high.
II.Occur in 20-30 % of hypertensive patients.
III.May have genetic component and is more
common in people who are older
,obese,female african american or have
underlying illness such as diabetes or kidney
disease.
Special Populations
Older Persons
1-Older patients may present with either isolated
systolic hypertension or elevation in both SBP and
DBP. CV morbidity and mortality are more directly
correlated to SBP than to DBP in patients aged 50
and older.
2-First-line antihypertensives provide significant
benefits and can be used safely in older patients,
but smaller-than-usual initial doses must be used
for initial therapy.
Children and Adolescents
1-In children, hypertension is defined as SBP or DBP
that is >95th percentile for the same sex, age, and
height on at least three occasions. For adolescents,
BP values between the 90th and 95th percentile, or
>120/80 mm Hg, is considered elevated BP.
2-Because secondary hypertension is more
common in children and adolescents than in
adults, an appropriate workup is required if
elevated BP is identified.
3-Nonpharmacologic treatment for
hypertension in childern is the cornerstone
of therapy for primary hypertension.
4-ACE inhibitors, ARBs, β-blockers, CCBs, and
thiazide diuretics are all acceptable drug
therapy choices forhypertension in childern .
Pregnancy
1-Preeclampsia is defined as hypertension
(elevated BP ≥140/90 mm Hg on more than 2
occasions at least 4 hours apart after 20
weeks’ gestation or ≥160/110 mm Hg
confirmed within a short interval) in
association with thrombocytopenia, impaired
liver function, new-onset renal insufficiency,
pulmonary edema, or new-onset cerebral or
visual disturbances. It can lead to life-
threatening complications for both mother
and fetus.
2-Eclampsia is the onset of convulsions in
preeclampsia and is a medical emergency.
3-Definitive treatment of preeclampsia is
delivery, and labor induction is indicated if
eclampsia is imminent or present. Otherwise,
management consists of restricting activity,
bed rest, and close monitoring. Salt
restriction or other measures that contract
blood volume should be avoided.
4-Antihypertensives are used before induction of
labor if DBP is >105 mm Hg, with a target DBP of
95–105 mm Hg. Intravenous (IV) hydralazine is most
commonly used; IV labetalol is also effective.
5-Chronic hypertension is hypertension that
predates pregnancy. Labetalol, long-acting
nifedipine, or methyldopa is recommended as
first-line therapy due to favorable safety profiles. β-
Blockers (except atenolol) and CCBs are also
reasonable alternatives.
African Americans
1-Hypertension is more common and more difficult
to control in African Americans than in those of
other races; treatment usually requires two or
more antihypertensives to reach a BP goal of
<130/80 mm Hg.
2-CCBs and thiazides are most effective in African
Americans and should be first-line in the absence of
a compelling indication.
Pulmonary Disease and Peripheral Arterial
Disease (PAD)
1-Although β-blockers (especially nonselective
agents) have generally been avoided in
hypertensive patients with asthma and COPD
because of fear of inducing bronchospasm,
cardioselective β-blockers can be used safely.
2-β-Blockers can theoretically be problematic
in patients with PAD because of possible
decreased peripheral blood flow secondary to
unopposed stimulation of α1-receptors that
results in vasoconstriction. However, available
data indicate that β-blockers do not worsen
claudication symptoms or cause functional
impairment. Therefore, antihypertensive
treatment for patients with PAD should
follow the same general principles as
patients without PAD.
Hypertensive Urgencies and Emergencies
1-Acute administration of a short-acting oral
drug (captopril, clonidine, or labetalol)
followed by careful observation for several
hours to ensure a gradual BP reduction is an
option in Hypertensive Urgencies .
3-Hypertensive emergencies require
immediate BP reduction with a
parenteral agent to limit new or
progressing end-organ damage.
Nitroprusside is the agent of choice for
minute-to-minute control in most cases.
JNC 8 treatment algorithm
Canadian guidelines for treatment of
hypertension
Evaluation of therapeutic outcomes
1-Encourage patients to obtain a home BP
monitor, record the results, and bring them to
follow-up clinic visits.
2-Evaluate BP response in the clinic 4 weeks
after initiating or making changes in therapy
and compare the results to home BP readings.
3-Once goal BP is obtained, monitor BP
every 3–6 months, assuming no signs or
symptoms of acute end-organ damage.
4-Automated BP monitoring can be
useful to establish effective 24-hour
control and confirm white coat or
masked uncontrolled hypertension.
5-Monitor patients routinely for adverse drug
events, which may require dosage reduction or
substitution with an alternative antihypertensive
agent.
6-Monitor patients for signs and symptoms of
hypertension-associated complications.
(by heart, eye, and kidney examination).
7-Assess patient adherence with the regimen
regularly.
Thank You
