HYPERTENSION

Hesty Utami,M.Clin Pharm.,PhD.,Apt

 REFERENCE

The Seventh Report of The Joint National Committee on

Prevention, Detection, Evaluation and Treatment of High
Blood Pressure. JAMA 2003;289:2560-21.
2014 Evidence-Based Guidelines for the Management of
High Blood Pressure in Adults. Report from the Panel
Members Appointed to the Eighth Joint National
Committee (JNC 8).JAMA 2014;311:507-20.
Dipiro JT, R L Talbort, GC Yee, GR Matzke et
al,2008,Pharmacotheraphy:A Pathophysiologic
Approach.7th edition.
National Heart Foundation of Australia (National Blood
Pressure and Vascular Disease Advisory Committee).
Guide to management of Hypertension for Doctors 2008
Koda-Kimble and Young, 2006, Applied Therapeutics,
The clinical approach. 8th edition.
Our plan for today :
• Demography
• Etiology and Pathophysiology
• Clinical Presentation
• Diagnostic Considerations and Clinical Evaluation
• Classification of Hypertension
• Treatment Targets
• Management of Hypertension
• Case study
Demography

According to WHO, the number of patients with

hypertension approx 972 million people (26.4%)
worldwide in 2000. This number is expected to increase
to 29.2% in 2025.
Around 34.2% hypertensive patients come from
developed countries, while more than 60% live in
developing countries.
The prevalence of hypertension increases with
advancing age where more than half of elderly are
hypertensive patients,
Etiology

Blood Pressure (BP) is generated by the interplay

between blood flow and the resistance to blood flow

BP = cardiac output x peripheral vascular resistance

Systolic Pressure Diastolic pressure

 Peripheral
Cardiac
Vascular
output resistance

Arterial
Stroke Heart Venous Arterial Blood
Wall
volume rate capacitance contractility viscosity
elasticity
Pathophysiology

Increased sympathetic nervous system (α and β

receptor)
Increased renin angiotensin aldosterone (RAA) activity)
→ regulate systemic and renal blood flow
Deficiencies in release and/or activity of vasodilators i.e
nitric oxide, prostacyclin and natriuretic peptides
 • The majority of hypertensive
patients have primary/essential
hypertension with no
identifiable cause for their
disease
• Secondary hypertension has
Hypertension specific identified causes for
elevated BP, namely:
chronic kidney disease
coarctation of the aorta
Cushing’s syndrome
sleep apnea
phaechromocytoma
Primary Secondary primary aldosteronism
Hypertension Hypertension drug-induced
Throid/parathyroid
 Drugs Associated with Hypertension
• Adrenal steroids (prednisone, triamcinolone)
• Calcineurin inhibitors (cyclosporine, tacrolimus)
• Erythropoiesis stimulating agents (erythropoietin, darbepoietin)
• NSAIDs (ibuprofen, indomethacin, meloxicam), Cox-2 inhibitors
(celecoxib)
• Decongestants (phenylpropanolamin, pseudoephedrine)
• Amphetamines
• Estrogens (oral contraceptives)
• Natural products: cocaine, ephedra alkaloids, ergot-containing
herbal products, St John’s wort
• Food substance: sodium, licorice, ethanol, tyramine-containing
food if taking a monoamine oxidase inhibitor (e.g fermented food,
chocolate, soy sauce, aged cheese, shrim paste,smoked fish,
avocado.
 Clinical Presentation
 Generally, the patient may appear very healthy and asymptomatic,
or may have the presence of additional cardiovascular (CV) risk
factors:
 Age (>55 years for men, >65 years for women)
 Diabetes mellitus
 Dyslipidemia (LDL, total cholesterol, triglycerides, HDL)
 Microalbuminuria
 Obesity (BMI ≥30 kg/m2)
 Physical inactivity
 Tobacco use
 Diagnostic Considerations
• Hypertension is termed “silent killer” because most patients do not
have any symptoms ⇨ the primary finding is elevated BP.
• The diagnosis cannot be made based on one elevated BP
measurements ⇨ the average 2-two or more measurements taken
during two or more clinical encounters should be used.
• Routine laboratory tests recommended before initiating therapy
include:
ECG, urinalysis, blood glucose, hematocrit
Serum potassium, creatinine/eGFR, calcium
Lipid profile (LDL, triglycerides, HDL, total cholesterol)
• Optional tests include measurement of urinary albumin excretion or
albumin/creatinine ratio (except for those with diabetes or kidney
disease where annual measurement should be made)
• More extensive testing for identifiable causes is not generally
indicated unless BP control is not achieved or the clinical and lab
evaluation strongly suggests an identifiable secondary cause.
Screening Test for Secondary Hypertension
 Clinical Evaluation
• Patient evaluation is made through medical history,
physical examination, routine laboratory tests and other
diagnostic procedures.
• Evaluation of hypertensive patients has three objectives:

1. To assess lifestyle and identify other CV risk factors or

comorbidities that may affect prognosis and guide
treatment
2. To reveal identifiable causes of secondary hypertension
3. To assess the presence or absence of target-organ
damage and CV diseases.
Table 1. Classification of BP for adults according to JNC 7

BP Classification Systolic BP Diastolic BP

Normal <120 And <80

Prehypertension 120-139 Or 80-89

Stage 1 140-159 Or 90-99

hypertension
Stage 2 ≥160 Or ≥100
hypertension
Isolated systolic ≥140 And <90
hypertension
 Table 3. Target Organ
Damage
Heart: Left ventricular
hypertrophy, heart failure
Kidney: Microalbuminuria,
Chronic kidney disease
Vascular disease
(atherosclerotic plaque,
hypertensive retinopathy,
peripheral arterial disease)
Brain: Stroke, transient
ischaemic attack
Table 4. Associated
Clinical Condition
Family history of
premature cardiovascular
disease
Family history of
hypercholesterolaemia
Hypercholesterolaemia
Diabetes
Chronic heart failure
Cerebrovascular disease
Coronary heart disease
Table 2. Recommendation for follow up based on initial BP
for adults without acute target organ damage or associated
clinical conditions
Initial BP Follow up Recommendation

Normal Recheck in 2 years

Prehypertension Recheck in 1 year

Stage 1 hypertension Recheck within 2 months

Stage 2 hypertension Reassess or refer within 1 month.

Treat immediately for those with
SBP ≥180 and or DBP ≥110
 Table 5. Treatment Targets in Adults (JNC 7 vs JNC 8)
Patient group JNC 7 Target (mmHg) JNC 8 Target (mmHg)

People with <125/75 <140/90

proteinuria >1g/day
(with or without
diabetes)
People with target <130/80 <140/90
organ damage (table
3) or associated
clinical condition (table
4)
People without any <140/90 or lower if <140/90
target organ damage tolerated
or associated clinical
condition
Elderly (>60) <140/90 <150/90
 Hypertension
Management

Non-pharmacological Pharmacological

Ultimate goal :
Lowering hypertension-related
Morbidity and mortality
Non-pharmacological management: life style modification
to prevent and manage hypertension
 Pharmacological Management: drug therapy

• The decision to initiate pharmacological treatment

requires consideration of several factors:
The degree of elevation of blood pressure
The presence of target organ damage
The presence of cardiovascular disease or other risk
factors

The overall goal of treating hypertension : reduce

hypertension-associated morbidity and mortality
 Beta
blockers

Thiazide ACE
Diuretics inhibitors
FIRST
LINE

Calcium
Angiotension Channel
Receptor Blockers
Blockers
 First line anti-hypertensive agents
1. Low dose thiazide diuretics
 Initially, they induce natriuresis→decrease plasma volume then
after long-term use, BP lowering effects are maintained due to
sustained decrease in peripheral vascular resistance
 Effective especially in elderly and afro-american patients
 Dose-related side effects i.e hypokalemia, hyponatremia,
hyperuricemia, hyperglycemia, hypercholesterolemia can occur
particularly with high dose.
 Thiazide diuretics are recommended unless there are
contraindications or compelling indications for other agents

Drug Dose range in mg/day Daily frequency

Hydrochlorothiazide 12.5-50 1
Chlorthalidone 12.5-25 1
Indapamide 1.25-2.5 1
Metolazone 2.5-5 1
2. Beta blockers
 Mechanism : ↓cardiac contractility and cardiac output
↓heart rate
↓renin release
inhibit norepinephrine release
 Two pharmacodynamic properties that differentiate this class:
cardioselectivity & Intrinsic sympathomimetic activity/ISA.
 B1 and B2 adrenoceptors are distributed throughout the body but
thay are concentrated differenly in certain organs/tissues like B1
mainly in the heart and kidney, B2 mainly in the lungs, liver,
pancreas and arterial smooth muscle.
 Side effect : altered lipids and increased glucose, bradycardia, heart
block, exacerbate asthma and COAD especially with non-selectve
beta blockers
 For patients with hypertension without compelling indications, other
first line antihypertensives should be used as the initial first line
agents before beta blockers.
 Meta analysis data suggest beta blocker may not reduce CV events
as well as other first line agents when used as the initial
antihypertensives.
 Drug Receptor ISA Usual dose Usual daily
antagonised range in frequency
mg/day
Atenolol β1 - 25-100 1

Bisoprolol β1 - 2.5-10 1

Carvedilol α1,Β1, β2 - 25-50 1

Labetalol α1, β1, β2 - 200-400 2

Metoprolol β1 - 50-100 1-2

Oxprenolol β1, β2 + 80-160 2

Pindolol β1, β2 ++ 5-10 2-3

Propanolol β1,β2 - 40-160 2

3. ACE inhibitors
• Inhibit angiotensin converting enzyme → reduced angiotensin II-
mediated vasocontriction and aldosteron secretion → lower BP
• Contraindication: angioedema, renal artery stenosis
• Side effects : hypotension, dry cough, hyperkalemia, headache

Drug Dose Range (mg/day) Daily Frequency

Captopril 25-100 2

Enalapril 5-40 1-2

Fosinopril 10-40 1

Lisinopril 10-40 1

Perindopril 4-8 1

Ramipril 2.5-20 1
4. Angiotensin II receptor antagonist/ Angiotensin Receptor
Blockers
 Block angiotensin II receptor site → inhibit
vasocontriction and aldosteron release
 Contraindication: angioedema, renal artery stenosis
 Adverse effects : hyperkalemia, headache
Drug Dose Range (mg/day) Daily Frequency

Candesartan 8-32 2

Irbesartan 150-300 1

Losartan 25-100 1-2

Telmisartan 20-80 1

Valsartan 80-320 1-2

5. Calcium channel blockers (CCBs)
• Most dihydropiridine, except amlodipine, are formulated
as sustained release product
• Immediate release dihydropyridine (i.e nifedipine) has
been associated with severe hypotension, cerebral
ischaemia, acute MI
• Dihydropyridine can cause reflex tachycardia, peripheral
edema, headache, flushing
• Non-dihydropiridine (Verapamil and diltiazem) produces
negative inotropic & chronotropic effects ⇨ can cause
bradycardia and heart block so they are contraindicated
for systolic heart failure.
• Diltiazem is better tolerated than verapamil regarding
potential constipation.
Table 5. Pharmacologic action of calcium channel blockers
(CCBs)

Dihydropiridine Verapamil Diltiazem

Peripheral ↑↑ ↑ ↑
vasodilation
Heart rate ↑ ↓↓ ↓

Cardiac 0/↓ ↓↓ ↓
contractility
Coronary ↑↑ ↑ ↑
blood flow
SA/AV nodus 0 ↓ ↓
conduction
 Drugs Dose Range Daily Frequency
(mg/day)
Amlodipine 2.5-10 1

Nifedipine long acting 30-60 1

Nicardipine SR 60-120 2

Verapamil long acting 120-480 1-2

Diltiazem XR 120-540 1
 Other anti-hypertensive agents
6. Alpha-1 blockers (prazosin, terazosin)
 Inhibit catecholamine uptake in smooth muscle and cause
vasodilation
 Indicated in hypertension with benign prostat hyperplasia
 Side effects : postural hypotension

7. Central α2 agonists (clonidine, methyldopa)

 Stimulate inhibitory neurons and decrease sympathetic outflow
from CNS →↓CO and PVR
 Side effects : dizziness, sedation, dry mouth, possibly sexual
dysfunction
8. Adrenergic antagonists (reserpin, guanetidine)
 Not frequently used
 Deplete catecholamine from storage granules to
decrease BP
 Side effect: fluid retention

9. Arterial vasodilators (hydralazine, minoxidil)

o Reserved for resistant hypertension
o Side effect : reflex tachycardia, fluid retention
10. Aldosterone antagonists (spironolactone, eplerenone)
 Block aldosterone release →inhibit sodium and water
retention and inhibit vasoconstriction
 Side effect : hyperkalemia, gynecomastia (not with
eplerenone)

11. Aliskiren
 The first oral antihypertensive agents that directly inhibits renin ⇒
blocks the RAAS at its point of activation ⇒ reduced plasma renin
activity and BP lowering
 Due to lack of long-term studies evaluating CV event reduction and
significant drug cost ⇒ should be used as an alternative drug.
 Many adverse effects seen in ACEIs and ARBs apply to direct renin
inhibitor (e.g hyperkalemia, increased serum creatinine)
 Teratogenic effects ⇒ should never be used in pregnancy
JNC 7 Algorithm for Treatment of Hypertension
 JNC 8 Algorithm for Treatment of Hypertension

• hypertension\hypertension guideline
2014.pdf
 Compelling Indications
Hypertension may exist in association with comorbid conditions in
which there are compelling indications for use of a particular
treatment based on clinical trial data demonstrating long-term
benefits.
Compelling indications for specific therapy involve high-risk
condition that can be direct sequelae of hypertension (heart
failure/HF, ischaemic heart disease/IHD, chronic kidney
disease/CKD, recurrent stroke) or commonly associated with
hypertension (diabetes, high coronary disease risk).
Therapeutic decisions in such individuals should be directed at both
the compelling indication and BP lowering.
The absence of a positive indication can signify a lack of information
for a particular drug class. For example, in recurrent stroke ⇒ there
is no study employing CCBs.
Compelling Indication: Ischaemic Heart Disease (IHD)
Hypertensive patients are at increased risk for myocardial infarct
(MI) or other major coronary events.
Myocardial oxygen supply in hypertensive patients may be limited
by coronary artery disease (CAD), while myocardial oxygen demand
is often greater due to decreased left ventricular ejection or left
ventricular hypertropy (LVH).
Lowering BP reduces ischaemia and prevents cardiovascular
disease (CVD) events in patients with CAD, in part by reducing
myocardial oxygen demand.
Therapy is directed toward preventing MI, death and reducing
symptoms and the occurrence of ischaemia.
Unless contraindicated, drug therapy should be initiated with a BB
⇒reduced inotropy & heart rate decrease myocardial oxygen
demand.
If angina and BP are not controlled by BB alone or if BBs are
contraindicated (eg. Severe reactive airway disease, high degree
AV block, peripheral arterial disease) ⇨ long acting CCB.
However, combination of BB and non-dihydropyridine CCB ⇨
severe bradycardia and high degree of heart block
 Compelling Indication-Post MI
BB (those without intrinsic sympathomimetic activity/ISA eg:
atenolol, metoprolol, propanolol, bisoprolol, carvedilol ) and ACEI
are recommended.
These two drug classes, with BB first, are considered the first drugs
of choice for patients who have experienced a MI.
BB s decrease cardiac adrenergic stimulation and reduce the the
risk of subsequent MI or sudden cardiac death.
ACEIS improve cardiac remodelling, cardiac function and reduce CV
events post MI.
ARBs are considered alternatives to ACEIs for those not not
tolerating ACEIs
Eplerenone reduces CV morbidity & mortality in patients soon after
acute MI (within 3-14 days) → its use should only be used in
selected patients following a MI with very dilligent monitoring of
potassium level.
 Compelling Indication: Heart Failure
Hypertension precedes the development of HF in 90% of patients &
increases risk for HF by threefold.
ACEI with diuretic therapy is recommended as the first-line regimen.
ACEIs can reduce CV morbidity & mortality, whilst diuretics can
provide symptomatic relief of edema by inducing diuresis. Loop
diuretics are often needed especially in patients with more advanced
disease.
BB is appropriate to further modify disease and a component of
standard therapy (ACEI+diuretic+BB) for HF patients. BB must be
started in very low doses (much lower than that used to treat
hypertension) & titrate slowly to higher doses based on tolerability.
Bisoprolol, carvedilol and metoprolol are the only BB to be beneficial
in HF.
ARBs are acceptable as an alternative therapy for patients who
cannot tolerate ACEIs and possibly as add-on therapy to those
already on a standard three-drug regimen.
 Compelling Indication: Heart Failure
The addition of aldosterone antagonists can reduce CV morbidfity
and mortality in left ventricular dysfunction (LVD).
Spironolactone has been studied in severe LVD has shown benefit
in addition to standard therapy.
Eplerenone has been studied in patients with symptomatic LVD
within 3 to 14 days after an acute MI in addition to standard therapy.
An aldosterone antagonist may be considered in addition to a
diuretic, ACEI or ARB and BB.
It is currently not recommended to use BOTH an aldosterone
antagonist and and ARB as add-on therapy to a standard therapy
due to the increased risk of severe hyperkalemia.
 Compelling Indication: Diabetes
All patients with diabetes and hypertension should be treated with
either an ACEI or ARB. Pharmacologically, both of these agents
should provide nephroprotection as a result of vasodilation in the
efferent arteriole of the kidney,
A thiazide-type diuretic is recommended as the second agent to
lower BP and provide additional CV risk reduction.
CCBs are useful add-on agents for BP control in patients with
diabetes.
BBs reduce CV risk → these agents should be used when needed
as add-on therapy with other standard agents or treat another
compelling indications (eg. Post MI)
BBs (especially non-selective agents i.e propanolol, pindolol,
oxprenolol, labetalol, carvedilol) may mask the signs and symptoms
of hypoglycaemia in patients with tightly controlled diabetes because
most of the signs &symptoms of hypoglycaemia (i.e tremor,
palpitation, tachycardia) are mediated through sympathetic nervous
system.
Compelling Indication: Chronic Kidney Disease (CKD)
Patients with hypertension may develop damage to either the renal
tissue (parenchyma) or the renal arteries. CKD initially presents as
microalbuminuria (≥ 30 mg albumin in 24-hour urine collection) that
can progress to overt kidney failure.
The rate of kidney function deterioration is accelerated when both
hypertension and diabetes are present. Once patients have an
estimated GFR <60 ml/min/1.73 m2 or albuminuria → significant
CKD.
In addition to lowering BP, ACEIs and ARBs reduce intraglomerular
pressure can reduce the decline in kidney function. Both agents
have been shown to reduce progression of CKD in patients
with/without diabetes → firstline therapy to control BP & preserve
kidney function in CKD.
Patients may rarely experience acute kidney failure when given
ACEI/ARB → problematics particularly in patients with bilateral renal
artery stenosis or a solicitary functioning kidney with stenosis →
evaluating kidney function shortly after starting the drug can
minimise the risk
 Compelling Indication: Recurrent Stroke Prevention
Ischaemic stroke is considered target organ damage caused by
hypertension. Attaining goal BP in patients who have experienced a
stroke or transient ischaemic attack is considered primary modality
to reduce risk of a second stroke → BP <130/80 mmHg.
One clinical trial PROGRESS (Perindopril Protection Against
Recurrent Stroke Study) showed that the incidence of recurrent
stroke in patients with history of ischaemic stroke can be reduced
when thiazide diuretic is used in combination with an ACEI.
Reductions in risk of recurrent stroke have also been seen with
ARB.
Thus, both ACEI+diuretic or ARB-based therapy are evidence-
based antihypertensive regimens for patients with a history of
cerebrovascular disease, especially ischaemic stroke or transient
ischaemic attack, to prevent recurrent stroke.
These recommendations DO NOT APPLY to patients with a history
of haemmorhagic stroke.
 Special Population: Hypertension in Elderly
• Hypertension often presents as isolated systolic hypertension in the
elderly. Epidemiologic data indicate that CV morbidity and mortality
are more closely related to SBP than to DBP in patients ages 50
years and older ⇨ this population is at high risk for hypertension-
related target organ damage.
• The guidelines reveal that the BP target are independent of age ⇨
age-adjusted goals are inappropriate. Treatment of hypertension in
older patients should follow the same principles that are outlined for
general care of hypertension.
• However, initial drug doses may be lower and dosage titrations
should occur over a longer period of time to minimise the risk of
hypotension.
• An interim goal of a SBP of below 160 mmHg may be necessary for
those with very high initial SBP ⇨ but the ultimate goal should
depend on CV risk and comorbid conditions of the patient.
 Special Population: Hypertension in Pregnancy
• Hypertension during pregnancy is a major cause of maternal and
neonatal morbidity and mortality.

Hypertension
during
pregnancy

Superimposition
preeclampsia Eclampsia Gestational of preeclampsia
on chronic
pregnancy
 Special Population: Hypertension in Pregnancy
• Preeclampsia is defined as elevated BP ≥140/90 mmHg that
appears after 20 weeks gestation accompanied by new onset
proteinuria (≥ 300 mg/24 hrs), can lead to life-threatening
complications for both mother and fetus.
• Eclampsia ⇨the onset of convulsion in preeclampsia ⇨
medical emergency.
• Gestational hypertension ⇨ new-onset hypertension arising
after midpregnancy in the absence of proteinuria.
• Chronic hypertension ⇨ elevated BP that is noted before
pregnancy began. Women with chronic hypertension prior to
pregnancy are at increased risk of a number of complications
including preterm delivery, HF, acute renal failure, fetal
growth restriction and superimposed preeclampsia.
• Metildopa is still drug of choice vary safe based on longterm
followup data. BBs, labetalol and CCBs are also reasonable
alternative.
• ACEIs and ARBs are absolutely contraindicated. Aliskiren
should not be used.
 Hypertensive Urgencies and Emergencies
• Both hypertensive urgencies and emergencies are characterised by
the presence of very elevated BP >180/120 mmHg.
• The need for urgent or emergent antihypertensive therapy should be
determined based on the presence of acute or immediately
progressing target organ injury, but not elevated BP alone.
• Examples of acute target organ injury: encephalopathy, intracranial
haemorrhage, unstable angina, eclampsia during pregnancy, acute
left ventricular failure.
• Hypertensive urgency is not associated with acute or immediately
progressing target-organ injury, whilst hypertensive emergency is.
• Hypertensive urgencies are ideally managed by adjusting
maintenance therapy by adding a new antihypertensive and/or
increasing the dose of a present medication ⇨preferred approach
due to more gradual reduction in BP.
• Hypertensive urgency requires BP reduction with oral
anihypertensive agents to stage 1 value over a period of several
hours to several days ⇨ re-evaluation within 7 days.
 Hypertensive Emergency
• Hypertensive emergencies are those rare situations that require
immediate BP reduction to limit new or progressing target-organ
damage.
• This situation requires parenteral therapy, at least initially.
• The goal is not to lower BP to < 140/90 mmHg, rather a BP
reduction of up to 25% within minutes to hours is the initial target. If
then stable, BP can be reduced to 160/100-110 mmHg within the
next 2-6 hours.
• Precipitous drops in BP may lead to end-organ ischaemia or
infarction. If patients tolerate this reduction ⇨ additional gradual
reductions toward goal BP values can be attempted after 24-48
hours.
• The exception to this guideline is for patients with an acute
ischaemic stroke where maintaining elevated BP is needed for a
much longer period of time.
Parenteral Antihypertensive Agents for Hypertensive Emergency
 Resistant Hypertension
• Resistant hypertension is the failure to achieve goal BP in patients
who are adhering to full doses of an appropriate three-drug regimen
that includes a diuretic.
• Patients with newly diagnosed hypertension or who are not
receiving drug therapy should not be considered to have resistant
hypertension.
• Volume overload is the common cause ⇨ highlighting the
importance of diuretic therapy.
• In patients with severe CKD ⇨ a loop diuretic might be considered
over a thiazide.
 Clinical Monitoring

Disease
progression

Clinical
Monitoring

Efficacy Toxicity
 Clinical Monitoring: Disease Progression
 Patients should be monitored for signs and symptoms of target
organ disease.
 A careful history for chest pain, palpitations, dizziness, dyspnea,
sudden change in vision, one-sided weakness, slurred speech and
loss of balance should be taken to assess the presence of
hypertensive complications.
 Other clinical monitoring parameters that may be used include
funduscopic changes on eye examination, left ventricular
hypertrophy on electrocardiogram, proteinuria and changes in
kidney function.
 These parameters should be monitored periodically because any
sign of deterioration requires immediate assessment and followup.
 Clinical Monitoring: Efficacy and Toxicity

 BP response should be evaluated 2 to 4 weeks after initiating or

making changes in therapy.
 Once goal BP values are attained (assuming no sign
signs/symptoms of acute target organ disease) ⇒BP monitoring can
be done every 3-6 months.
 More frequent evaluations are required in patients with a history of
poor control, non-adherence, progressive target-organ damage or
symptoms of adverse drug events.
 The occurrence of an adverse drug event may require dosage
reduction or substitution with an alternative antihypertensive agent.
 Specifically, patients treated with an aldosterone antagonist
(eplerenone, spironolactone) should have potassium concentration
and kidney function assessed within 3 days and again at 1 week
after initiation to detect potential hyperkalemia.
Select Monitoring for Antihypertensive Agents
 Role of Pharmacists

• Collaborate with other healthcare professionals to

ensure the rational use of medicines in hypertensive
patients.
• Monitor the outcome of the treatment, the emergence of
side effects and the progression of the disease
• Patient education and counselling
 Case Study
1.R.C is a 57-year old man (wt 80 kg ht 160 cm) with type 2
diabetes first diagnosed 2 years ago. Other medical
problems include obesity and gout. He presents now
for routine mecical check up and is noted to have a
blood pressure of 168/100. Two weeks ago his blood
pressure was 160/100. Lab evaluation reveals serum
creatinine of 150 μmol/L (normal: 60-120), random
serum glucose of 9.8 mmol/L (Normal <7.8), normal
electrolytes. A 24-hr urine collection reveals a urinary
albumin excretion rate of 250 mg/day (Normal
<30mg/24 hrs).
a. Does this patient have target organ damage?
b. Should his blood pressure be treated?
c. What treatment strategy should be used for his
hypertension?
2. Mr DC is a 67-year old afro-american man (wt 108 kg, ht
175 cm) who complains of a headache in the morning for
the past week. He was diagnosed with hypertension 6
years ago and was initially treated with life style
modifications and then with HCT 25 mg/day. He took his
medication for 2 years and then discontinued it since he
thought that he didn’t need it. He smokes 1 pack of
cigarettes/day for 35 years.
Physical examination : BP 150/86, HR 82 BPM
ECG and Echocardiogram : severe left ventricle
hypertrophy with ejection fraction <20% (diagnosed with
heart failure)
Lab test:
K 4 mmol/L (3.5-5)
Creatinine 160 μmol/L (60-120)
Fasting glucose 5.6 mmol/L (<6.1)
Total cholesterol 8 mmol/L (<5)
a. What are the abnormality from his lab test?
b. Are there any target organ damage?
c. If any, what life style modifications would you
recommend on him?
d. How would you manage his hypertension?