PHARMACOLOGICAL

TREATMENT OF
HYPERTENSION
DR SASI P.G
SAITOTI S.S
 OUTLINE
• Definition
• Classification
• Causes
• Pathophysiology
• Diagnosis
• Drug Treatment
• Hypertensive emergency
• Recent Advances
• Summary
 introduction
• The aims of antihypertensive therapy are to
relieve or forestall symptoms, to prevent
complications, and to prolong life.
• Before drug treatment is started, causes of
secondary hypertension should be looked for,
and factors which tend to raise blood pressure
eliminated.
• Therapy should be individualised rather than
blindly following a sequential list of drugs
• Very high blood pressure when accompanied
by symptoms should be treated without delay,
however the lowering of blood pressure
should be gradual

• Treatment of hypertension is not just a matter

of prescribing drugs, quality of life and
compliance issues must also be taken into
account
 Definition
• Hypertension (HT) is a chronic medical condition
in which systemic arterial blood pressure is
persistently elevated.
• Classified as:
• 1. Primary HT-90-95%, essential HT where no
medical cause is found.
• 2. Secondary HT-5-10% which is a secondary
cause to some pathology, eg. Conditions affecting
kidneys, arteries.
W.H.O DEFINITION OF HT
• HT can be defined as sustained
average levels of BP according to WHO
as follows in mmHg
SBP DBP
NORMALTENSION <140 <90
BORDERLINE HT 140_ 159 90- 94
HT > 160 >95
HT is confirmed after repeated
measurement
 CLASSIFICATION CONT..
Classification according to the Diastolic BP
(mmHg)
• MILD HT 90 – 104 mmHg
• MODERATE HT 105 – 114 mmHg
• SEVERE HT > 115 mmHg
 Subclassification:
Classification of HT Systolic (mmHg) Diastolic (mmHg)

Normal 90–119 60–79

Prehypertension 120-139 80–89

Stage 1 140-159 90–99

Stage 2 ≥160 ≥100

Isolated systolic HT ≥140 <90

 Causes:
Primary hypertension
• 95% cases.
• No direct causes but other factors:
1. Sedentary lifestyle
2. Smoking and alcohol
3. Obesity
4. Family hx
5. Increase intake of salt
 Causes
Secondary HT
• 5% cases.
• Identifiable causes:
1. Renal disease- renal A stenosis
2. Endocrine causes (Cushing’s,
hyperaldosteronism)
3. Congenital defects-coarctation of aorta
 Pathophysiology:
• Not much is understood but what is known
about primary HT is:

- Cardiac output is raised early in the disease

course, with Total peripheral resistance (TPR)
normal

- Over time cardiac output drops to normal levels

but TPR is increased.
 PATHOGENESIS CONT..
3 Theories have been proposed to explain this:
• Inability of the kidneys to excrete sodium,
resulting in natriuretic factors such as Atrial
Natriuretic Factor being secreted to promote salt
excretion with the side effect of raising total
peripheral resistance.
• An overactive Renin-angiotensin system leads
to vasoconstriction and retention of sodium and
water. The increase in blood volume leads to
hypertension.
• An overactive sympathetic nervous system,
leading to increased stress responses.
 PATHOGENESIS…
• The following are the possible mechanisms:
 Damage of vascular endothelium or impaired Nitric
Oxide production,blood vessels become hyper
responsive to VASOCONSTRICTION while
VASODILATATION becomes impaired causing
elevated TPR and tendency to HYPERTENSION

 Endothelium also produces ENDOTHELIN (ET-I)

which is one of the most potent VASOCONSTRICTOR
agents, ET-I is stimulated by Angio II, catecholamines
& insulin. Nitric Oxide inhibits its production

 Patients with HT over secrete ET-I

 PATHOGENESIS..…
• The role of SALT in the pathogenesis of HT is well
documented through experiments with humans &
animal models

• All Studies showed that increased SALT intake was

accompanied by an increase in BP

• These changes were reversed when the SALT intake

was reduced

• Scientific studies have shown that, the HIGH rate of

HT in certain ethnic groups may be caused in part by
an INHERITED tendency to retain SALT
 PATHONESIS..…
• SALT induced HT is due to BLOOD volume expansion
(PRELOAD).

• This is due to high plasma renin (and hence aldosterone)

concentrations in relation to salt intake.

• In a normal individual an increase in blood volume, the

RENAL mechanisms restores blood volume to normal by
excreting the excess volume

• In HT patients this mechanisms is blunted & therefore BP

stabilizes at a higher level when SALT intake rises.
• Salt restriction studies in hypertensive individuals
have been encouraging and salt restriction leads
to an enhanced effect of B-adrenoceptor
blockers, ACE inhibitors and diuretics.

• Blacks have an impaired ability of the kidney to

excrete a Na+ load even at a modest salt intake,
possibly due to:
Inadequate RAAS response to a high SALT intake
Inappropriate sympathetic response or
Reduced Atrial Natriuretic Peptide secretion
• Lifestyle also plays a role in the pathogenesis
of essential hypertension: obesity, alcohol, salt,
fat diet, animal protein diet.
• Finally, some individual may have a genetic
predisposition to the development of
hypertension.
 Diagnosis
• By persistent high BP levels ie. At least on 3
separate checks 1 week apart unless the BP is
significantly raised or is associated with end
organ damage then you can start with
medications ASAP.
 The principal aims of treatment of
hypertension
• Attainment of good blood pressure control in the
community
• Reduction of cardiovascular morbidity and
mortality
• Prevention of arteriosclerosis
• Control of other vascular risk factors
• Avoidance of progression to more severe stages
of hypertension
• Reversal of target organ damage
 Non pharmacological Treatment
• Non pharmacological treatment is to be
preferred but unfortunately is rarely sufficient
to achieve reasonable goal blood pressures in
patients with established sustained
hypertension.

• The exception is the obese person who

consumes too much alcohol, if such
individuals lose weight and reduce their
alcohol intake hypertension may be controlled
• Cessation of smoking
- Smoking should be discouraged
- It raises BP acutely and may be a factor in making
hypertension proceed to the accelerated phase
- Cigarette smoking is a major factor in arterial
complications in hypertensive patients

• Reduction of obesity
- There was a 7-fold difference in the prevalence of
hypertension btn the heaviest and lightest.
• Reduction in Alcohol consumption
-Alcohol abuse plays a role in the maintenance and
progression of hypertension
- Alcohol consumption should therefore be reduced
if it is greater than 3 drinks per day
- In heavy drinkers abstinence can lead to
impressive reductions in blood pressure

• Reducing stress
• Fish oil is shown to lower blood pressure in
hypertensive individuals. The fish oil may increase
sodium and water excretion.
 Clinical pharmacology of Drugs used
in Treatment of Hypertension
• Diuretics
• B-Adrenoceptor Blocking Drugs
• A1-Adrenoceptor Blockers
• Calcium Antagonists
• Angiotensin- Converting Enzyme inhibitors
• Drugs with a central Actions
• Direct-Acting Vasodilators
• Newer Agent
 1.Diuretics
• Diuretics used in the treatment of hypertension
include
Benzothiadiazines(thiazides)
-such as chlorothiazide, hydrochlothiazide
bendroflumethiazide(bendrofluazide),
hydroflumethiazide, methyclothiazide,
cyclopenthiazide and polythiazide

Heterocyclic(thiazide-like) such as chlorthalidone,

clorexolone, quinethazone,metolazone,
clopamide.
Loop diuretics such as furosemide, bumetanide,
piretanide, torasemide
Potassium sparing diuretics such as
spironolactone, amiloride and triamterene.
………
……..
 Mechanism of Action
• The loop diuretics act by inhibiting active chloride
transport in the thick ascending limb of the loop
of henle.

• The benzothiadiazines(thiazides) and related

heterocyclic compounds act on the early distal
tubule

• Potassium sparing diuretics act at the late distal

tubule
 Pharmacodynamic properties
• Thiazide and thiazide-like Diuretics
- The thiazide and thiazide-like diuretics reach their
active site in the early distal tubule of the nephron
via the probenecid-sensitive organic acid
secretory pathway.

- Their natriuretic effect is less than that of the loop

diuretics- 10% versus 20% of filtered sodium
excreted- and their exact molecular basis of action
remains unspecified
• Loop Diuretics
- The loop diuretics like the thiazide are highly
protein bound.
- They reach their active site by tubular secretion
rather than glomerular filtration.
- After secretion they travel with the tubular fluid
to the loop of henle where they exert their effect
by inhibiting the chloride-sodium/potassium
pump.
- Each loop diuretic has the same maximal
response, they differ only in potency, bumetanide
being 10 times more potent than torasemide and
50 times more potent than furosemide
• Potassium – sparing Diuretics
- Spironolactone which structurally resembles
aldosterone, acts by competing with the
mineralocorticoid for the corresponding receptor
protein in the distal nephron

- Triamterene and amiloride act at the cortical

collecting duct of the distal tubule and their
potassium- sparing effect is mediated by reversing
the negatively oriented potential difference in this
part of the nephron, thus preventing secretion of
positively charged potassium ions.
 Clinical Effectiveness
• Diuretics are effective antihypertensive agents
that make major contribution to reducing
cardiovascular mortality.
• There have been many large multicentre trials in
hypertension in which diuretics have been used
as first- line treatment over periods of 25 yrs
• The principal drugs used were thiazides
hydrochlorothiazide, chlorothiazide, and
bendroflumethiazide, chlorthalidone and the
potassium sparing agent amiloride, triamterene
and spironolactone
• No different effect of the various diuretics used
and all have produced positive results

• In studies comparing diuretics and B – blockers,

the 2 types of drugs have similar effects in
protecting against cardiovascular events,
although 1 trial found that diuretics were more
effective than a B- blocker(atenolol) in preventing
myocardial infarction in elderly patients
 Tolerability and Drug interaction
potential
• The most dangerous adverse effect of the
potassium sparing diuretics is hyperkalaemia

• It occur in the presence of deteriorating renal

function, so elderly patient are at risk
• Spironolactone lead into gynaecomastia and this
drug is no longer considered a 1st agent for
treatment of hypertension
• Two of the most adverse effect of diuretics are

Mild hypovolaemia and mild hypokalaemia with

potassium loosing agent.

Elevated LDL cholesterol levels have been

reported in some studies with diuretics (dose
dependent)
 Drug interaction
• Antihypertensive effect of thiazide diuretics is
inhibited by NSAIDS with exception of sulindac,
which appears not to inhibit renal prostaglandin
synthesis,
• The increased incidence of cardiac arrythmias
due to digoxin as a result of diuretics- induced
hypokalaemia.
• The interaction of thiazide diuretics and lithium
leading to lithium toxicity is due to the increased
proximal tubular reabsorption of lithium
• Combination of ACE inhibitors and potassium
sparing diuretics can result in dangerous
hyperkalaemia especially in patients with
impaired renal function
 2.β–Adrenoceptor Blocking Drugs
( B-Blockers)
• The available B-blockers are Acebutolol,
Alprenolol, Atenolol, Betaxolol, Bisoprolol,
Carvedilol, caliprolol,esmolol,nadolol, oxprenolol
Labetalol, Metoprolol, Pindolol, Sotalol, Timolol,

• Although they posses generally similar

antihypertensive effectiveness, the B-blockers
vary in their subsidiary pharmacodynamic effects
and in their pharmacokinetic properties.
 Mechanisms/site of Action
• B-blockers inhibit catecholamine binding at B-
adrenoceptor sites.
• The following physiological effects may be involved
 Reduction in CO
 A central nervous system effect
 Inhibition of renin
 Reduction in venous return and plasma volume
 Resetting of baroreceptor levels
 Reduction in peripheral vascular resistance
 Reduction in noradrenaline ,norepinephrine) release
 Prevention of the pressor response to
catecholamines with exercise and stress
 Pharmacodynamic properties
• All B-blockers are contraindicated in patient with
asthma

• Relatively B1-selactive agents may however be

more appropriate in diabetic patients as they are
less likely to aggravate hypoglycaemia, they may
also be preferable in patients with peripheral
vascular disease, as they do not block peripheral
B2-mediated vasodilatation
• Some B-blockers have vasodilatory activity eg.
Labetalol, carvedilol due to a1-adrenoceptor
blockade and possibly a direct peripheral effect,

• This has theoretical importance in enhancing the

anthypertensive effect and reducing certain
adverse effects such as cold extremities.

• However postural hypotension may be a problem

if the vasodilatation is too marked
 Clinical effectiveness
• B-blockers are contraindicated in patients with
CCF and Asthma and are best avoided in patients
with COPD.

• However this reservation may be outweighed by

benefit where angina coexist.

• In patient with peripheral vascular disease, B-

blockers have shown no benefit or a worsening of
symptoms….
• However drugs with vasodilator activity such as
celiprolol and labetalol have been found to
produce decrease in peripheral vascular
resistance

• B-blockers appear less beneficial in elderly

patients and consequently should not be
considered first line therapy in this age group
 Tolerability and drug interactions
potential
• Adverse cardiac effects of B-blockers include,
bradycardia, heart failure and following an
abrupt withdrawal, worsening angina and even
infarction
• Peripheral vascular effects are more likely with
drugs not possessing vasodilator activity or
relative B1-selectivity and include cold
extremities and even gangrene particularly in
elderly patients who show less ability to tolerate
B-blockers
• Bronchospasm in patient with Asthma or COPD
• Nightmare, vivid dreams and even hallucination
can occur with the more lipophilic B-blockers eg
propranolol and oxprenolol

• Non selective B-blockers without partial agonist

activity appear to cause a definite increase in
VLDL cholesterol and triglycerides, and a decrease
in HDL cholesterol

• Drug that appear to have no or little adverse

effect on plasma lipids include carvedilol,
celiprolol, labetalol and pindolol
 Drug interactions
• Are seen with the lipophilic hepaticaly metabolised
B-blockers eg alprenolol, metoprolol, oxprenolol,
propranolol, thus cimetidine may cause an increase
in plasma conc of these drugs

• Rifampicin and phenobarbital because of enzyme

induction may cause an increase ……

• Lipophilic B-blocker may cause an increase in plasma

conc of chlorpromazine, theophylline and warfarin as
a result of their effect on hepatic enzyme activity
 3.α1-Adrenoceptor Blockers
Includes doxazosin, prazosin, terazosin

• Mechanism/site of Action

The quinazoline derivatives which are selective for

postjunctional a1-adrenoceptors act by causing a
decrease in peripheral resistance
 Pharmacodynamic properties
• Doxazosin is about one- half as potent as
prazosin as a postsynaptic a1-adrenoceptor
inhibitor in animal studies while terazosin is
about a tenth as potent

• Doxazosin and prazosin increase plasma renin

minimally whereas terazosin seems to have a
great effect
 Tolerability and drug interactions
potential
• The adverse effect profile is similar for all 3
agents, consisting mainly of postural dizziness
and headache

• With slightly increase nasal congestion with

terazosin in comparison with prazosin

• Verapamil decrease first pass metabolism of

prazosin and increase its oral bioavailability and
peak plasma conc, there by enhancing its
anthypertensive effect
• Cimetidine cause an increase in plasma conc of
all the a1-blockers and a dose adjustment may be
required when these agents are used
concomitantly

• The a1-blockers are not widely regarded as first

line therapy in hypertension at the present time
 4.Calcium Antagonists
• There are three distinct chemical classes of
calcium antagonist available for the treatment of
hypertension
Phenylalkylamines such as verapamil and
gallopamil

Benzothiazepines such as diltiazem

Dihydropyridines such as nifedipine, felodipine,

amlodipine etc
 Mechanism/site of action
• The calcium antagonist act by blocking the entry
of calcium ions into cells during the depolarised
phase of the action potential.

• Consequently they reduce the amount of calcium

ions available for excitation-contraction, vascular
smooth muscle is most sensitive to such blockade
 Clinical effectiveness
• The antihypertensive effectiveness of the
calcium antagonist is well established both for
conventional and controlled release formulation

• Decreases in left ventricular hypertrophy have

been seen with nicardipine and felodipine

• Isradipine was found to be superior to atenolol

for the treatment of hypertension in one study
• With regard to heart rate, both diltiazem, and
verapamil tend to cause a decrease, isradipine
cause a slight increase and the other calcium
antagonist are neutral in their effect

• Sustained release nicardipine has been observed

to improve quality of life in elderly patients,
while sustained release nifedipine had a
deleterious effect on symptoms
 Tolerability and drug interactions
potential
• Adverse effects with the calcium antagonists appear
to some extent to be class related, the most common
being headache, flushing, ankle oedema and
palpitation precipitated by the vasodilator properties
of these drugs.
• Adverse effect are also dose related and tolerance to
them develops with time.
• In general vasodilatation related adverse effects are
less common with the sustained release formulations
• With verapamil, constipation is commonly
experienced and can be a problem
 Drug interactions
• Calcium antagonists raise plasma digoxin concentrations
when these agents are administered concomitantly
• Also they raise plasma conc of lipophilic B-blockers and
may cause cardiac depression as seen with sustained
release nifedipine and propranolol

• Alcohol raises plasma nifedipine conc while cimetidine

raises plasma conc of all the calcium antagonists
• Thiophylline conc are also increased by some calcium
antagonist

• Diltiazem increase cyclosporin conc, which has implications

for renal transplant recipients in whom lower doses of
cyclosporin can be given
 5.Angiotensin-converting Enzyme
(ACE) Inhibitors
• The currently available ACE inhibitors are
Captopril,
Enalapril, benazepril, cilazapril, fosinopril
Lisinopril, ramipril, fenopril, delapril
 Mechanism/site of action
• ACE inhibitors competitively inhibit the action of
the angiotensin converting enzyme which
catalyses the formation of the high potent
vasoconstrictor angiotensin 2 and the destruction
of the potent vasodilator bradykinin

• The antihypertensive effect of the ACE inhibitors

is due to reduction in total peripheral resistance
an effect that is intensified in sodium depleted
state
 Clinical effectiveness
• They are effective antihypertensive both as
monotherapy and in combination

• An increase antihypertensive response is seen

when ACE inhibitors are combined with
diuretics

• Tolerance to the antihypertensive effect does

not occur over time
• They are beneficial in diabetic patients because of
their anti-proteinuric effect

• They are well tolerated in elderly patients

• The antihypertensive response appears to be

lower with lisinopril, benazepril, enalapril, and
captopril in black patients than in white patients,
but equivalent for fosinopril and quinapril
 Tolerability and drug interactions
potential
• The most frequent adverse effect is cough,
dizziness, headache, fatigue and musculoskeletal
pain
• ACE inhibitors suppress erythropoietin production
in patient with chronic renal failure or in renal
transplant recipients
• Perinatal renal failure, oligohydramnios, delayed
foetal growth and decreased foetal survival have
been described when woman received enalapril
or captopril during pregnancy
 Drug interactions
• Concomitant administration of NSAIDS may
attenuate the antihypertensive effect of ACE
inhibitors.

• Administration of ACE inhibitors with diuretics

has been shown to improve the metabolic
adverse effect profile of diuretics.

• However administration with potassium sparing

diuretics should be avoided because of an
increased risk of hyperkalaemia.
 6.Central acting Antihypertensives
• The most commonly used agents of this class are
methyldopa, clonidine, and moxonidine

• Two older centrally acting drugs which are less

commonly used nowadays are guanabenz and
guanfacine
 Mechanism/ site of action
• Methyldopa
 Acts mainly by dampening down sympathetic outflow
from the central nervous system but may also block
adrenergic nerve terminals on the arteriole
• Clonidine
 Its antihypertensive effect is mainly due to
stimulation of central postsynaptic a2-adrenoceptors,
 It may also interfere with the peripheral regulation of
noradrenaline via its partial agonist activity at
presynaptic a2-adrenoceptors
 also suppress plasma renin activity, the mechanism of
which is uncertain

• Moxonidine- structurally related to clonidine but has

different pharmacological profile
 Pharmacodynamic properties
• Methyldopa reduces BP without causing much
change in HR or CO
• The minimum effective dose is 125mg twice daily
with maximum daily dose of 3g

• Clonidine after a 0.2mg oral dose, renal, hepatic,

and limb blood flow are unaltered, while HR
decrease, systemic vascular resistance is reduced
slightly
• Rebound hypertension can occur on abrupt
cessation of high dose oral clonidine
• Moxonidine
 Moxonidine is an imidazoline receptor agonist
that is highly selective for the I1-imidazoline
receptor with little effect at the central alpha2-
receptor.
Binding at central imidazoline receptors
correlate with the degree of BP reduction
It cause a reduction in plasma
noradrenaline(norepinephrine) and renin
concdiminished sympathetic activity
 Clinical effectiveness
• Methyldopa
- It reduce left ventricular hypertrophy

- Has proved clinically useful as add-on therapy in

refractory hypertension

- It is still the mainstay of maintanance

antihypertensive therapy in pregnancy
• Clonidine
- Transdermal clonidine has proved as effective as
oral clonidine in open comparative clinical trials

- Once wkly administration of the transdermal

formulation may offer advantages in term of
patient convenience

- Meloxinidine 0.2 mg once or twice daily has

proved equivalent to clonidine ,atenolol,
captopril, sustained release nifedipine,
 Tolerability and drug interaction
potential
• Methyldopa
- Adverse effects are prominent especially at the
beginning of therapy

- It include somnolence, depression, sexual

dysfunction, autoimmune haemolytic anaemia,
hepatic dysfunction, drug fever

- The adverse effect of methyldopa on quality of

life appeared to be due to its central action
• Clonidine
- Adverse effect include dry mouth, drowsness,
dizziness, nausea, and impotence

• Mexonidine
- Include dry mouth, tiredness and headache
 7.Direct-Acting vasodilators
• Hydralazine
• Cadralazine
• Minoxidil

• Hydralazine lowers BP by reducing peripheral

vascular resistance as a result of arterial smooth
muscle relaxation.
• In term of hypertensive effectiveness, hydralazine
has proved comparable to diuretics, B-blockers
and centrally acting hypertensive
 8.Newer Agents
• Potassium channel opener (pinacidil)

• Serotonin2(5-HT2) antagonist ketanserin

• Angiotensin 2 receptor antagonist losartan

 Mechanism/site of Action
• Pinacidil
Is a vasodilator belonging to a novel class of drugs
known potassium channel openers

When potassium channels are opened, potassium

leaks from cells, resulting in a negative shift in the
resting membrane potential

The cells hyperpolarise, which result in a decrease

in intracellular calcium and relaxation of smooth
muscle, particularly in the vasculature
 Ketanserin
• Is a serotonin (5-HT) antagonist that binds
primarily to 5-HT2 receptors, but also has weak
a1-adrenoceptor antagonist activity

• It has other action such as depression of the renin

angiotensin aldosterone system and sympathetic
inhibition
• The drug is effective in lowering blood pressure in
essential hypertension. It also inhibits platelet
aggregation. It is well tolerated and is particularly
effective in older patients.
 Losartan
• Is the first of a new class of antihypertensive
agents that act by blocking angiotensin 2, subtype
1 (AT1) receptors
• These receptors are located in vascular and cardiac
tissue and also in the brain, kidney and adrenal
gland
• It is involved in the BP control via
- Direct vasoconstriction of arteriolar smooth
muscle
- Release of aldosterone and cortisol from the
adrenal cortex
- A direct antinatriuretic effect on the kidney
• Blockade of AT1 receptors directly
Causes vasodilation,

Reduces secretion of vasopressin,

Reduces production and secretion of aldosterone,

amongst other actions – the combined effect of
which is reduction of blood pressure
• Eg. Telmisartan
 Clinical effectiveness
• Pinacidil
- Has been evaluated in both non comparative and
comparative clinical trials
- Compared with the placebo, it reduce systolic BP
by up to 19mmHg and diastolic by up to 15mmHg
- Pinacidil has proved well compared to diuretics,
prazosin, methyldopa, and B-blockers in term of
its effectiveness
- It is used in combination therapy for patients who
have refractory hypertension
 Ketanserin
• 40 to 80mg/day has proved superior to placebo in
the treatment of mild to moderate hypertension

• In comparative studies, it has shown similar

effectiveness to several B blockers and diuretics
and it also compares favourably with nifedipine
and captopril
 Losartan
• In dose of 50 to 90mg once daily, losartan
monotherapy has proved effective in lowering
diastolic BP by about 8 to 13mmHg in patient with
mild to moderate Hypertension

• Has shown equivalent effectiveness to enalapril,

atenolol

• Pending acceptable long term effectiveness and

safety result it may find initial use in the
management of patients with mild to severe
hypertension who are unresponsive to or
intolerant of their current therapy
 HYPERTENSIVE EMERGENCIES
• Life-threatening

• Transfer to an ICU

• Evaluate the patient

• Avoid rapid reduction of BP

• Several Drugs may be depending on the

clinical condition of the patient
Drugs that may be used include

1)Sodium nitroprusside ( by IV infusion; 0.5-6

microgm /kg/min

2)Hydralazine ( 5-10mg by intermittent IV

injection; or 200microgm/min by IV infusion)

3) Labetalol ( 20-50mg by intermittent IV injection

@ 15min; or 0.5-6mg/min by IV infusion)

4) Nifedipine (5-10mg orally)

5)Captopril (25mg orally)

 Recent advances in the management
of hypertension
• Recent studies published in the european society
of HT guidelines.
• Consensus in the studies recommend that:
1. In grade 1 hypertensives (systolic blood pressure
[SBP] of 140-159 mm Hg or diastolic blood
pressure [DPB] of 90-99 mm Hg) at low or
moderate risk, drug therapy should be started
after a suitable period with lifestyle changes. A
more prompt initiation of treatment is advisable
if grade 1 hypertension is associated with a high
level of risk or if hypertension is grade 2 or 3.
2.In patients with high normal blood pressure (BP)
(SBP of 130-139 mm Hg or DPB of 85-89 mm Hg)
uncomplicated by diabetes or previous
cardiovascular events, no trial evidence of
treatment benefits, except for a delayed onset of
hypertension (crossing the 140/90 mm Hg cutoff)
is available.
3.Initiation of antihypertensive drug therapy in
diabetic patients with high normal BP is currently
unsupported by prospective trial evidence. For
the time being, it appears prudent to recommend
treatment initiation in high normal BP diabetic
patients if subclinical organ damage (particularly
microalbuminuria or proteinuria) is present.
4. Trial evidence concerning antihypertensive
drug treatment in patients with previous
cardiovascular events in the absence of
hypertension is controversial, and further trials
must be completed before firm
recommendations can be given.

5. Early BP-lowering treatment, before organ

damage develops or becomes irreversible or
cardiovascular events occur, appears to be a
prudent recommendation.
ANY QUESTION?????????
THANK YOU

Dr. Azhar Chishti