Hypertension

Abate W, Clinical Pharmacist

Debre Berhan University
Asrat Woldeyes Health Sciences
Campus
Pharmacy Dept 1
 Objectives
At the end of this session, students able to
know:
1. Definition of HTN
2. Classification of HTN
3. Major complications of HTN
4. DX of HTN
5. Non-pharmacological and
pharmacological RX of HTN
6. Monitoring and evaluation parameter of
2
HTN
 Clinical Evaluation
 Patient Presentation
 Case 1
G.R. is a 44-year-old black man who presents to his primary
care provider concerned about high BP. His BP was 144/84
and 146/86 mm Hg last year during an employee health
screening at work. G.R.’s father had HTN and died of an MI at
age 54. His mother had DM and HTN and died of a stroke at
age 68. G.R. smokes one pack per day of cigarettes and thinks
his BP is high because of job-related stress. He does not
believe that he really has HTN. G.R. does not engage in any
regular exercise and does not restrict his diet in any way,
although he knows he should lose weight.
• Physical examination shows he is 175 cm tall, weighs 108 kg
(body mass index [BMI] 35.2 kg/m2),

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• BP is 148/88 mm Hg (left arm) and 146/86 mm Hg (right
arm) while sitting, and heart rate is 80 beats/minute. Six
months ago, his BP values were 152/88 mm Hg and
150/84 mm Hg when he was seen by his primary care
provider for allergic rhinitis.
• Funduscopic examination reveals mild arterial narrowing
and arteriovenous nicking, with no exudates or
hemorrhages. The other physical examination findings
are essentially normal.
 G.R.’s fasting laboratory serum values are as follows:
• Blood urea nitrogen (BUN), 24 mg/dL
• Creatinine, 1.0 mg/dL
• Glucose, 105 mg/dL
• Potassium, 4.4 mEq/L
• Uric acid, 6.5 mg/dL
• Total cholesterol, 196 mg/dL 4
• Low-density lipoprotein cholesterol (LDL-C), 141 mg/dL
• High-density lipoprotein cholesterol (HDL-C), 32 mg/dL
• Triglycerides, 170 mg/dL
• An electrocardiogram (ECG) is normal except for left
ventricular hypertrophy (LVH).
• G.R. has HTN. He has had elevated BP values and
meets the diagnostic criteria for HTN because two or
more of his BP measurements are elevated on separate
days.

 What is the proper assessment of G.R. ’s BP?

 Why does G.R. have HTN?

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1. Should G.R. start antihypertensive drug therapy, or are
lifestyle modifications alone sufficient?
Ans; lifestyle modifications can partially achieve BP goal and has
early evidence of hypertension-associated comlication.
1.1 Which antihypertensive agents are appropriate first-line
treatments for G.R.?
Ans; G.R. is black and does not have CKD, thiazide diuretics or
CCBs as first-choice antihypertensive therapy
2. Should monotherapy or two-drug therapy be started in G.R. as
his initial regimen?
Ans; A monotherapy approach is an option for him. Monotherapy
with a CCB, or thiazide diuretic will likely reduce his BP to less
than 140/90 mm Hg.
3. How should G.R.’s race influence the selection of an
antihypertensive regimen?
4. Which lifestyle modifications can G.R. implement to lower his6
BP?
 Hypertension(HTN )

Defn ─ Hypertension is defined as an elevated SBP, DBP, or

both.
……..(A sustended rise arterial BP).
• A clinical diagnosis of HTN is based on the mean of two or
more properly measured seated BP measurements taken on
two or more occasions.
• It is a "silent killer―.

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 HTN Conti…
 Blood Pressure
 During systole, the left ventricle contracts, ejecting blood
systemically into the arteries causing a sharp rise in arterial BP.
This is the systolic BP.
 The left ventricle then relaxes during diastole, and arterial BP
decreases to a trough value as blood returns to the heart from the
venous system. This is the diastolic BP.
 When recording BP (e.g., 120/76 mm Hg), the numerator is the
SBP and the denominator is the DBP.
 Mean arterial pressure (MAP) is sometimes used to
represent BP, especially in patients with hypertensive
emergency. MAP collectively reflects both SBP and DBP

 BP = CO × TPR (CO is the major determinant of SBP, whereas total

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peripheral resistance (TPR) largely determines DBP.
 Epidemiology
• Approximately 80 million Americans have HTN.
• About 77% of those are using antihypertensive medication, but
only 54% of those are controlled (defined as both systolic BP
[SBP] <140 mm Hg and diastolic BP [DBP] <90 mm Hg).
• WHO reported that Non-communicable diseases (NCDs)
accounted for 30% of deaths in Ethiopia in 2014.
 The four major NCDs, namely cardiovascular diseases,
cancers, diabetes and chronic respiratory diseases were
responsible for more than 80% of NCD-related deaths.

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1. Primary(Essential) HTN (over 90%):
• Most individuals with high BP have essential or primary
hypertension.
• Results from unknown pathophysiologic etiology
• This form of hypertension cannot be cured, but it can be
controlled.
2. Secondary HTN (up to 10%):
• Either a comorbid disease or a drug (or other product) is
responsible for elevating BP.
• Much less common than primary hypertension.
• When a secondary cause is identified, removing the
offending agent (when feasible) or treating/correcting the
underlying comorbid condition should be the first step in10
management.
11
• 90 – 95% have essential HTN
 Env’tal Factors –
. weight gain
. Diet - ↑ Nacl ,↓K
. Cigarette
. Excess alcohol

 Genetic
Angiotensinogen & ACE polymorphism – HTN & Salt
Alpha Adducin gene - ↑ renal tubular absorption of Na
Others- AT1 receptor,aldostrone synthase,B2
adrenoreceptors

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 Various neural and humoral factors are known to
influence and regulate BP.
1) Neural Mechanism
• Central and autonomic nervous systems are intricately
involved in the regulation of arterial BP.
• Pathologic disturbances in any of the four major
components (autonomic nerve fibers, adrenergic
receptors, baroreceptors, or central nervous system)
could conceivably lead to chronically elevated BP.

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2)Renal Mechanism
Defect in the kidney’s ability to excrete
excess Na load→plasma vol
expansion→autoregulation by ↑systemic
Vascular resistance

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3) HORMONAL MECHANISM (R-A-A)

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4)VASCULAR MECHANISM
• Resistance to blood flow.
• Endothelial cell dysfunction
- endothelial dependent vasodil.. Impaired in HTN b/c of
production of reactive oxygen spp that ↓ NO.
 Vascular remodelling
Due to – endoth dysfn , Neurohorm ,↑ BP
Eutrophic – in small arteries
.↑syst. Vascular resistance
.Hallmark of diastolic HTN
Hypertrophic – in large arteries
.Hallmark of ISH

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21
Clinical Presentation of Primary (Essential) Hypertension

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 Goals of initial evaluation
o Measurement & staging of BP
o Ass’t of overall cardiac status
o Detection of 2nd ry causes
• Hypertension is called the silent killer because most patients
do not have symptoms.
• The primary physical finding is persistently elevated BP.
• The diagnosis of hypertension cannot be made based on one
elevated BP measurement.
• The average of two or more BP measurements taken during
two or more clinical encounters is required to diagnose
hypertension.

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BP CLASSIFICATION
SBP DBP
• Normal • <120 & < 80
• Pre-HTN • 120 – 139 or 80 –89
• Stage 1 • 140 – 159 or 90 – 99
• Stage 2 • ≥ 160 or ≥ 100
• Isolated Systolic HTN • ≥ 140 & < 90
• Isolated Diastolic HTN • <140 & > 90

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• The relationship between BP and risk of CVD
events is continuous, consistent, and
independent of other risk factors
• DBP is a more potent cardiovascular risk factor
than SBP until age 50; thereafter, SBP is more
important

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Risk factors for CV disease
.age>45 male,55 female
.smoking
.dyslipedemia
.DM
.FHx of premature CVD
.Abd. Obesity
Emerging risk factors. – Lipoprotien a
Homocysteine
prothrombotic factors
proinflammatory factors

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 Pathologic Consequences of Hypertension
 Heart: Hypertensive heart disease(HHD) is the result of structural
and functional adaptations leading to left ventricular hypertrophy,
CHF, atherosclerotic coronary artery disease and microvascular
disease, and cardiac arrhythmias, including atrial fibrillation.
─ Abnormalities of diastolic function that range from asymptomatic
heart disease to overt heart failure are common in hypertensive
patients.
 Brain; Elevated blood pressure is the strongest risk factor for stroke.
Approximately 85% of strokes are due to infarction, and the
remainder are due to either intracerebral or subarachnoid
hemorrhage.
 Kidney; the kidney is both a target and a cause of hypertension.
Primary renal disease is the most common etiology of secondary
hypertension. Mechanisms of kidney-related hypertension include a
diminished capacity to excrete sodium, excessive renin secretion in
relation to volume status, and sympathetic nervous system
overactivity. Conversely, hypertension is a risk factor for renal injury
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and ESRD.
 Pathologic Consequences…

 Clinically, macroalbuminuria (a random urine albumin/creatinine

ratio >300 mg/g) or microalbuminuria (a random urine
albumin/creatinine ratio 30–300 mg/g) are early markers of renal
injury.
 Peripheral Arteries ;blood vessels are a target organ for
atherosclerotic disease secondary to longstanding elevated blood
pressure. In hypertensive patients, vascular disease is a major
contributor to stroke, heart disease, and renal failure.
─ The ankle-brachial index is a useful approach for evaluating PAD
and is defined as the ratio of noninvasively assessed ankle to brachial
(arm) systolic blood pressure. An anklebrachial index <0.90 is
considered diagnostic of PAD and is associated with >50% stenosis in
at least one major lower limb vessel. An ankle-brachial index <0.80 is
associated with elevated blood pressure, particularly systolic blood
pressure.
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29
 Treatment
HTN is treated with both lifestyle modifications
and pharmacotherapy.
Desired Outcomes
Hypertension management is useful in reducing
the risk of heart attack, heart failure, stroke, and
kidney disease morbidity and mortality.

The goal of blood pressure management is to

reduce the risk of cardiovascular disease and
target organ damage. 30
• Benefits of Rx
 from the extent of BP reduction rather than how
it is reduced
o ↓es incidence of Stroke by 35-40%
MI by 20-25%
HF by >50%

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 Goals of HTN Rx
- The 2017 ACC/AHA guideline goal BP of <130/80 mm Hg for most
HTNsive patients
- The American Diabetes Association recommends a goal of <140/90
mm Hg for most patients with DM, with a lower goal of <130/80 for
those at high risk of ASCVD
- The Kidney Disease Improving Global Outcomes (KDIGO)
guidelines a BP goal of ≤140/90 for patients with HTN and CKD
(nondialysis), with a lower BP goal of ≤130/80 only for those patients
who have persistent albuminuria (≥30 mg urine albumin excretion
per 24 hr. (JNC-8 guidelines)...

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• Indicated for BP ≥ 140/90 in office and home despite
non-pharmacolgic Rx.
• Selection of antihypertensive agents and combinations
of agents should be individualized, taking into account
age, severity of hypertension, other cardiovascular
disease risk factors, comorbid conditions, and practical
considerations related to cost, side effects, and
frequency of dosing.

 First line ant-HTN – Thiazides

ACE-I/ARBs
Calcium channel blockers
Beta Blockers

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 There is considerable variation in individual responses to
different classes of antihypertensive agents.
 Monotherpy based on age & race – based on short term
efficacy trials – AB/CD rule(with only HTN)
. Old & black – CCB/Diuretics
.Young & white – ACE-I/ARB/BB
 Patients with Compelling Indications
• Compelling indications represent specific comorbid
conditions where evidence from clinical trials supports
using specific antihypertensive classes to treat both the
compelling indication and hypertension.

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36
Management of compelling indications

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 Resistant Hypertension
• Resistant hypertension is defined as failure to achieve goal
BP with the use of three or more antihypertensive drugs
with complementary mechanisms of action (ideally using
optimal doses, one of which is a diuretic) or when four or
more antihypertensive drugs are needed to achieve BP
control.
• Difficult-to-control hypertension is persistently elevated BP
despite treatment with two or three drugs, which fails to
meet the criteria for resistant hypertension.
• Volume overload is a common cause and Drug-induced or
other causes. Nonadherence and Inadequate doses.
• The management of resistant hypertension: (a) assuring
adequate diuretic therapy, (b) appropriate use of
combination therapy, and (c) using alternative
antihypertensive agents when needed.
• Rx; Thiazide(chlorthalidone best) and MRA(spironolactone38
 First-Line Antihypertensive Agents
 Diuretics
o There are four subclasses of diuretics: thiazides, loops,
potassium-sparing agents, and mineralocorticoid
receptor antagonists.
o A thiazide is the preferred diuretic for hypertension and
is considered a first-line therapy option in most patients.
• loop diuretics are sometimes required over a thiazide for
hypertension in patients with severe CKD when
estimated GFR is <30 mL/min/1.73 m2, especially when
edema is present.
• Potassium-sparing diuretics are very weak
antihypertensive agents when used alone,their use in
hypertension is in combination with another diuretic to
counteract the potassium-wasting properties of the other
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diuretic agent.
• Diuretics should be dosed in the morning when given
once daily and in the morning and late afternoon when
dosed twice daily to minimize nocturnal diuresis.
• chlorthalidone is 1.5 to 2 times more potent than
hydrochlorothiazide.This is likely attributed to a longer
half-life (45- 60 hours vs 8-15 hours) and longer duration
of effect (48-72 hours vs 16-24 hours) with
chlorthalidone.
• Side effects of a thiazide include hypokalemia,
hypomagnesemia, hypercalcemia, hyperuricemia,
hyperglycemia, dyslipidemia, and sexual dysfunction.
• Current guidelines recommend dosing
hydrochlorothiazide up to 50 mg/day or chlorthalidone up
to 25 mg/day, which markedly reduces the risk for most
metabolic side effects.
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 Beta Blockers
• For patients with hypertension but without compelling
indications, a β-blocker should not be used as the initial
first-line agent.
• A β-blocker is only an appropriate first-line agent in
hypertension when used to treat specific compelling
indications (eg, ischemic heart disease, HFrEF).
• studies have shown that bisoprolol, carvedilol, and
metoprolol succinate reduce mortality in patients with
HFrEF who are treated with a diuretic and ACEi.
• There are important pharmacodynamic and
pharmacokinetic differences among β-blockers, but all
agents provide a similar degree of BP lowering.
• There are three pharmacodynamic properties of β-
blocker therapy that differentiate this class:
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cardioselectivity, ISA, and membrane-stabilizing effects.
• Cardioselective β-blockers (eg, bisoprolol, metoprolol,
nebivolol) have clinically significant advantages over
nonselective agents (eg, propranolol, nadolol), and are
preferred when using a β-blocker to treat hypertension.
• Cardioselective agents are safer than nonselective
agents for patients with asthma or diabetes who have a
compelling indication for a β-blocker.
• S/E; bradycardia, atrioventricular conduction
abnormalities (eg second- or third-degree heart block),
and the development of acute HF
• Blocking β2-receptors in arteriolar smooth muscle may
cause cold extremities and may aggravate intermittent
claudication or Raynaud’s phenomenon as a result of
decreased peripheral blood flow.
• Abrupt cessation of BB cause cardiac ischemia, a CV
event, rebound hypertension (a sudden increase in BP to
or above pretreatment values). 42
 ACE-Inhibitors
 An ACEi is a first-line therapy option in most patients with
hypertension.
 ACE facilitates production of angiotensin II that has a major
role in arterial BP regulation.ACE is distributed in many
tissues and is present in several different cell types, but its
principal location is in endothelial cells.
 Therefore, the major site for angiotensin II production is in
the blood vessels, not the kidney. An ACEi blocks the ACE,
thus inhibiting the conversion of angiotensin I to
angiotensin II.
• An ACEi also blocks degradation of bradykinin and
stimulates the synthesis of other vasodilating substances
(prostaglandin E2 and prostacyclin).
• ACEi lowers BP in patients with normal plasma renin
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activity.
• Increased bradykinin enhances the BP-lowering effects
of an ACEi, but also is responsible for the side effect of a
dry cough. An ACEi may effectively prevent or regress
LVH by reducing direct stimulation of angiotensin II on
myocardial cells.
• An ACEi reduces CV morbidity and mortality in patients
with HFrEF and decreases progression of CKD.
• An ACEi is a first-line option for patients with diabetes
and hypertension because of demonstrated CV disease
and kidney benefits.
• ACEi therapy is generally well tolerated.
• Patients with CKD or those taking potassium
supplements, potassium-sparing diuretics,
mineralocorticoid receptor antagonists, ARBs, or a direct
renin inhibitor are at highest risk for hyperkalemia.
• S/E; acute kidney injury(worrisome), Angioedema, A 44
persistent dry cough. C/I for pregnancy…
 Angiotensin Receptor Blockers (ARBs)
• Angiotensin II is generated by two enzymatic pathways:
the RAAS, which involves ACE, and an alternative
pathway that uses other enzymes such as chymase
(―tissue ACE‖).
• An ACEi inhibits only the effects of angiotensin II produced
through the RAAS, whereas ARBs inhibit the effects of
angiotensin II from all pathways.
• D/ce from ACE-I= no ↑ kinin level so given for those who
don’t tolerate ACE-I
• ARB therapy directly blocks the AT1 receptor that
mediates the known effects of angiotensin II in humans:
vasoconstriction, aldosterone release, sympathetic
activation, antidiuretic hormone release, and constriction
of the efferent arterioles of the glomerulus.
• They do not block the AT2 receptor.Beneficial effects of
AT2 receptor stimulation (vasodilation, tissue repair, and45
inhibition of cell growth) remain intact with ARB use.
• For patients with type 2 diabetes and CKD, the
progression of kidney disease has been shown to be
significantly reduced with ARB therapy.
• For patients with HFrEF, ARB therapy has been shown
to reduce the risk of hospitalization for HF when used as
an alternative therapy in ACEi-intolerant patients.
• The addition of a CCB or thiazide to an ARB significantly
increases antihypertensive efficacy. Similar to an ACEi,
most ARBs have long enough half-lives to allow for
once-daily dosing. However, candesartan, eprosartan,
losartan, and valsartan have the shortest half-lives and
may require twice-daily dosing for sustained BP
lowering.
• S/E; renal insufficiency, hyperkalemia, and orthostatic
hypotension.
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• C/I; pregnancy
 Calcium Channel Blockers (CCBs)
• Both dihydropyridine CCBs and nondihydropyridine CCBs
are first-line therapies for hypertension.
─ pharmacologically very different from each other.
• CCBs also have compelling indications in stable ischemic
heart disease. However, with this compelling indication,
they are primarily used as an add-on therapy to other
antihypertensive drug classes.
• There are two types of voltage-gated calcium channels: a
high-voltage channel (L-type) and a low-voltage channel
(T-type). Currently available CCBs only block the L-type
channel, which leads to coronary and peripheral
vasodilation.
• Nondihydropyridines (verapamil and diltiazem) decrease
heart rate and slow atrioventricular nodal conduction.
Similar to a β-blocker, these drugs may also treat
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supraventricular tachyarrhythmias (eg, atrial fibrillation).
• Verapamil (and diltiazem to a lesser extent) produces negative
inotropic and chronotropic effects that are responsible for its
propensity to precipitate or cause systolic HF in high-risk
patients.
• All CCBs (except amlodipine and felodipine) have negative
inotropic effects.
• Dihydropyridines do not alter conduction through the
atrioventricular node and thus are not effective agents in
supraventricular tachyarrhythmias.
• Dihydropyridine CCBs are very effective in older patients with
isolated systolic hypertension.
• S/E; Vasodilation related s/e include dizziness, flushing,
headache, and peripheral edema occur more frequently with all
dihydropyridine CCBs than with the nondihydropyridine CCBs
because they are less potent vasodilators.

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 Alternative Agents
• Used as an add-on therapy to provide additional BP lowering in
patients who are already treated with combination therapy consisting
of first-line antihypertensives.
 α1-Blocker
• Selective α1-receptor blockers ( prazosin, and doxazosin) work in
the peripheral vasculature and inhibit the uptake of catecholamines
in smooth muscle cells resulting in vasodilation and BP lowering.
• α1-blockers should only be used in combination with first-line
antihypertensive agents.
• S/E; ―first-dose‖ phenomenon(dizziness or faintness, palpitations),
priapism, orthostatic hypertension.
 Aliskiren
• Aliskiren is the only direct renin inhibitor. This drug blocks the RAAS
at its point of activation, which results in reduced plasma renin
activity and BP lowering.
• The role of this drug class in the management of hypertension is
very limited.
• S/E; Angioedema, C/I ; pregnancy 49
 Centeral α 2- Agonist(.....Sympatholytic Agents)
o Clonidine, guanfacine, and methyldopa lower BP
primarily by stimulating α2-adrenergic receptors in the
brain.
• Clonidine is often used in resistant hypertension, and
methyldopa is commonly used for pregnancy induced
hypertension.
• Chronic use of a centrally acting α2-agonist results in
sodium and water retention, which is most prominent
with methyldopa. Low doses of clonidine and guanfacine
can be used to treat hypertension without the addition of
a thiazide.
• clonidine s/e(sedation, dry mouth, constipation, urinary
retention, and blurred vision).
• Abrupt cessation of a central α2-agonist may lead to 50
rebound hypertension.
Direct Arterial Vasodilator
 Hydralazine and minoxidil directly relax arteriolar smooth
muscle resulting in vasodilation and BP lowering.
 All patients receiving hydralazine or minoxidil for chronic
therapy should first receive both a thiazide and a β-blocker.
 One side effect unique to hydralazine is a dose-dependent
drug-induced lupus-like syndrome.
• slow acetylators‖ are especially prone to develop drug-induced
lupus with hydralazine. This syndrome is more common in
women and is reversible on discontinuation. Drug-induced
lupus may be avoided by using less than 200 mg of hydralazine
daily.
• Minoxidil is a more potent vasodilator than hydralazine and
reserved for resistant hypertension. S/E; hirsutism (hypertrichosis)
• Intravenous nitroprusside can be used to treat malignant
hypertension and life-threatening left ventricular heart failure
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associated with elevated arterial pressure.
 Combination treatment
• Initial therapy with a combination of two antihypertensive
drugs is recommended for patients with stage 2 HTN
particularly if BP is >20/10 mm Hg away from goal.
• Treatment was titrated to a goal BP of <140/90 mm Hg for
most patients and <130/80 mm Hg for patients with
diabetes or CKD.
• Preferred to add a second after moderate dose of the 1st
• When 2 drugs are used make thiazide one of them b/c ↑
response rate to all other drugs.
Hypertensive African Americans tend to have low renin and
may require higher doses of ACEIs and ARBs than whites for
optimal blood pressure control, although this difference is
abolished when these agents are combined with a diuretic.
In black population, including those with diabetes,
evidence supports the use of thiazide diuretics and CCB. 52
53
• Drugs without additive antiHTNsive effect
.ACE-I + BB
.Diuretic + CCB
• Drugs with additice S/E
.BB + nondihydropyridine CCB
• Follow-up & monitoring
.Pre HTN - yearly
.Monthly or less till goal is reached
.More frequent if stage 2 or comorbidity
.After goal is reached- Q 3-6 months
• Serum K & Cr 1-2x/yr

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• Hypertensive complications
Encephalopathy
Cerebral hemorrhage
Left ventricular hypertrophy
Congestive heart failure
Renal insufficiency
Aortic dissection
Retinopathy
• Atherosclerotic complications
Cerebral thrombosis
Myocardial infarction
Coronary artery disease
Claudication syndromes 55
 Hypertensive Urgencies and
Emergencies(crisis)
• BP—greater than 180/120 mmHg.
– Urgencies
• are not associated with acute or
immediately progressing target organ injury
– Emergencies
• Are associated with acute or immediately
progressing target organ injury.
• Are those rare situations that require immediate
BP reduction to limit new or progressing target-
organ damage.
 E.g. encephalopathy, intracranial hemorrhage,
acute left ventricular failure with pulmonary edema,
dissecting aortic aneurysm, unstable angina, acute
renal failure, and eclampsia. 56
Hypertensive Urgencies
• A common error during treatment is initiating overly
aggressive antihypertensive therapy.
• It requires BP reductions with oral antihypertensive
agents to stage 1 values over a period of several hours
to several days.
• Acute administration of a short-acting oral
antihypertensive (eg, captopril, clonidine, labetalol) is an
option for treatment of hypertensive urgency
• Oral captopril is one of the agents of choice and can be
used in doses of 25 to 50 mg at 1- to 2- hour intervals.
The onset of action of oral captopril is 15 to 30 minutes.
• Labetalol can be given in a dose of 200 to 400 mg,
followed by additional doses every 2 to 3 hours. 57
Hypertensive Urgencies cont..
• Oral or sublingual immediate-release
nifedipine for acute BP lowering is
dangerous.
–Rapid lowering of BP… MIs and
strokes risk increase.

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Hypertensive Emergency
• Require immediate BP reduction, parenteral therapy, at
least initially
• The rate of BP reduction is dependent upon whether the
patient has aortic dissection, severe preeclampsia or
eclampsia, or pheochromocytoma with hypertensive
crisis.
• In these life-threatening situations, patients should be
cared for in the intensive care unit, and SBP should be
reduced immediately to <140 mm Hg in the first hour,
with additional BP lowering to <120 mm Hg for patients
with an aortic dissection.
• Severe preeclampsia or eclampsia, pheochromocytoma
with hypertensive crisis, the goal is not to lower BP to
<130/80 mm Hg; rather, the initial target is a reduction in
MAP of up to 25% within over the first hour. 59
 Hypertensive Emergency…
• If then stable, BP can be reduced to 160/100–110 mm
Hg within the next 2 to 6 hours.
• If patients tolerate this reduction well, additional gradual
decreases toward goal BP values can be attempted after
24 to 48 hours.
• The exception for patients with an acute ischemic stroke
where maintaining an elevated BP is needed for a longer
period.

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Drugs for HE
• Sodium nitroprusside 0.25–10 mcg/kg/min
intravenous infusion.
– Caution with high intracranial pressure,
azotemia, or in chronic kidney disease.
– GI side effects and cyanide intoxication.
• Nicardipine hydrochloride 5–15 mg/h
intravenous.
– Most hypertensive emergencies except acute
heart failure
– Caution with coronary ischemia
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Drugs for HE cont….
• Fenoldopam mesylate 0.1–0.3 mcg/kg/min
intravenous infusion.
– Most hypertensive emergencies; caution with
glaucoma
• Nitroglycerin 5–100 mcg/min intravenous
infusion
– Tolerance with prolonged use

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Drugs for HE cont….
• Hydralazine hydrochloride :for eclampsia
– 12–20 mg intravenous.
– 10–50 mg intramuscular
• Esmolol hydrochloride
– 250–500 mcg/kg/min intravenous bolus,
– Then 50–100 mcg/kg/min intravenous
infusion;
– May repeat bolus after 5 minutes or increase
infusion to 300 mcg/min
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 Evaluation of Therapeutic Outcomes

• Routine, ongoing monitoring to assess the

desired effects of antihypertensive therapy
(efficacy, including BP goal attainment),
undesired adverse effects (side effects and
toxicity), and disease progression is needed in
all patients treated with antihypertensive drug
therapy.

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Thank you!!

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