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Hypertension

Hypertension: Definition
Persistent elevation of
 Systolic blood pressure ≥140 mm Hg
or
 Diastolic blood pressure ≥90 mm Hg
Classification
Prehypertension: Definition

• Systolic blood pressure:


120–139 mm Hg
or
• Diastolic blood pressure:
80–89 mm Hg
Prevalence

• National Health and Morbidity Survey


Age 2006 2011

Age >18 years old 32.2% 32.7%

Age > 30 years old 42.6% 43.5%


Pathophysiology
Cardiac
•Heart rate
•Inotropic state
•Neural (pons and medulla)
•Humoral (hormones)

Cardiac Output

Renal Fluid Volume Control


•Renin–angiotensin
•Aldosterone
•Atrial natriuretic factor
Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.
Mechanism of Action of
Aldosterone

.
Etiology of Hypertension

• Primary (essential or idiopathic)


hypertension
 Elevated BP without an identified
cause
 90% to 95% of all cases
Risk Factors for - Primary Hypertension
• Age (>55)
• Alcohol
• Cigarette smoking
• Genetic factors
• Diabetes mellitus
• Elevated serum lipids
• Excess dietary sodium
• Gender ed to
 SBP rises with age Alcohol – excessive use strongly correlat
hypertension
 Smoking – increases risk for cardiovascular disease ; vasoconstriction
 Diabetes – along with hypertension greater risk for target organ disease and
usually more severe
 Hyperlipidemia elevated in people with hypertension; increases risk of
atherosclerosis
Secondary hypertension
 Elevated BP with a specific cause
• 5% to 10% of adult cases
Clinical Manifestations
• Usually symptomatic
• Symptom often secondary to
target organ disease
• Can include:
 Fatigue, reduced activity tolerance
 Dizziness
 Palpitations, angina, headaches
 Dyspnea ( LVH or cardiac failure)
Complications
• Target organ diseases occur most
frequently in:
 Heart
 Brain
 Peripheral vasculature
 Kidney
 Eyes
Complications
• Cerebrovascular disease
 Stroke
• Peripheral vascular disease
• Nephrosclerosis
• Retinal damage
• Atherosclerosis most common cause of cerebrovascular disease;
hypertension major risk factor for cerebral atherosclerosis and stroke
• Atherosclerosis in peripheral blood vessels too; can lead to PVD, aortic
aneurysm, aortic dissection
• Hypertension one of leading causes of end-stage renal disease, esp. in
African-Americans; some degree of renal dysfunction usual in person with
even mild BP elevations
• Retina is only place blood vessels can be directly visualized; if see damage
there then indicates damage in brain, heart, & kidney too; Can cause
blurring, retinal hemorrhage and blindness
Assessment
• History and physical examination
• BP measurement in both arms
 Use arm with higher reading for subsequent
measurements
 BP highest in early morning, lowest at
night
History
Hypertension
BP Measurement
• Use auscultatory method with a properly calibrated
instrument
• Patient seated quietly for 5 min in a chair and arm
supported at heart level

• Appropriate-sized cuff is necessary to ensure accurate reading

• At least two measurements should be obtained

• Allow at least 1 minute between readings. If one arm higher


than other; take BP in higher arm for subsequent
measurements
Hypertension
Diagnostic Studies
• Urinalysis, creatinine clearance
• Serum electrolytes, glucose
• BUN and serum creatinine
• Serum lipid profile
• ECG
• Echocardiogram
Hypertension
Diagnostic Studies
• “White coat” phenomenon may precipitate the need
for ambulatory blood pressure monitoring (ABPM)
 Noninvasive, fully automated system that
measures BP at preset intervals over a 24-hour
period
 Also used when suspect drug resistance,
hypotensive symptoms with drug therapy,
episodic hypertension, or SNS dysfunction
Risk restratification
Benefits of Lowering BP

Average Percent Reduction


Stroke incidence 35%–40%
Myocardial infarction 20%–25%

Heart failure 50%


Management
• Non pharmacological
• Pharmacological
Lifestyle Modifications

• Wt. reduction
 10 kg (22 lb) loss; SBP by 5-20 mm Hg
• Na reduction
 <2.4 g of sodium/day
• Avoid alcohol intake
Lifestyle Modifications

• Physical activity:
 Regular physical (aerobic) activity,
 At least 30 min, most days of week

• Avoidance of cigarette smoking

• Stress management
Content
• Pharmacological treatment
• Hypertensive urgency
• Hypertensive emergency
Types of
ANTI-HYPERTENSIVE Agents
• A - Angiotensin converting enzyme inhibitors (ACEIs)
Angiotensin receptor II blockers (ARBs)
• B - Beta blockers
• C - Calcium channel blockers
• D - Diuretics
Direct vasodilators
• S - Sympatholytics
• (alpha blockers, alpha & beta blockers,
• central sympathoplegic agents)
ANGIOTENSIN CONVERTING
ENZYME INHIBITORS / ACEI :
Captopril, Enalapril, Lisinopril, Perindopril

• Prevent the onset of microalbuminuria


• Reduce proteinuria
• Retard the progression of renal disease

Inhibition of ACE ---- decrease Ag II formation (active vasoconstrictor) ---- vasodilation of


both arteries and veins ---- reduce preload and afterload of the heart
Inhibition of Renin Angiotensin Aldosterone system ---- reduced synthesis & secretion of
aldosterne ---- reduced sodium & water retention

Untoward effects:
• - first dose phenomenon (start with low dose at bed time)
• - dry cough, angioedema (due to bradykinin)
• - renal impairment
• - increase foetal and neonatal mortality
ANGIOTENSIN RECEPTOR BLOCKERS /
ARBs : Losartan, Valsartan

• Specifically block angiotensin II receptors


• Recommended in ACEI intolerant patients
BETA-BLOCKERS / ß-BLOCKERS
Non-selective – Propranolol
Beta-1 selective – Atenolol, Metoprolol

Untoward effects:
• - Cardiac depression → ↓ HR (bradycardia); ↓FOC (LV insufficiency);
precipitates heart failure
• - Bronchospasm: beta-2 blockade. Contraindicated in asthma, COPD
• - CNS depression, lethargy, depression
• - Peripheral vasoconstriction: cold extremities; precipitates peripheral
vascular disease (Contraindication)
• - Abrupt withdrawal after long-term, high dose therapy: rebound
hypertension, precipitate angina, tachyarrhythmia
• - Dyslipidaemia, effect on carbohydrate meta (hypo or hyperglycemia)–
caution with diabetes
CALCIUM CHANNEL BLOCKERS (CCBs)
Dihydropyridine : Nifidipine, Amlodipine
Non- Dihydropyridine : Diltiazem, Verapamil

• CCBs prevent entry of calcium via “L” channels → reduced


intracellular calcium → reduced action potential and activity of
vascular smooth muscle → vasodilatation → antihypertensive
action

Untoward effects:
• - Hypotension, salt & water retension, reflex tachycardia,
headache, flushing, giddiness
• - Bradycardia, heart block, LV insufficiency, worsen Congestive
heart failure
DIURETICS
Thiazides and related compounds: Hydrochlorothiazide, Chlorthalidone, Indapamide,
spironolactone (K+ sparing diuretics)
Loop Diuretics: Furosemide, Bumetanide

Untoward effects:
• - Related to diuretic action (electrolyte
depletion; hypokalaemia)
• - Not-related to diuretic action
(Hyperglycaemia, hyperuricemia,
dyslipidaemia↑cho,Tg)
• - Hypersensitive reaction (sulphonamide
allergy)
DIRECT VASODILATORS
Sodium Nitroprusside: both arterial and venous vasodilator
- onset 30 sec., peak 2 min, duration 3 min
Untoward effects:
• - Excessive hypotension with toxicity
• - Cyanide poisoning (if treatment continues > 24-48 hr)

Minoxidil & Hydralazine: arterial vasodilator


- act directly on blood vessels, independently of sympathetic system.

Untoward effects:
• - Minoxidil – more potent than Hydralazine (Na & water retension, Hirsutism)
• - Hydralazine – use during pregnancy (eg. Preechlampsia), and adjunct to other
antihypertensive, long-term high dose → associated with drug induced lupus
syndrome
SYMPATHOLYTICS
Selective α1blocker - Prazosin
Selective alpha-1 and nonselective beta-blocker – Labetelol, Carvedilol

Action: vasodilation → decreased PR → decreased BP

Untowards effects:
-postural hypotension (avoid upright position within 3 hr after IV), weakness,
headache
-scalp tingling, difficulty in micturition, epigastric pain, nausea, vomiting, liver
damage
CENTRALLY ACTING AGENTS
Clonidine, alpha-Methyldopa

• Act on α2 receptor → reduced central


sympathetic outflow → reduced BP

Untowards effects:
• Depression, drowsiness
• Hypertensive crisis on withdrawal (clonidine)
Summary of antihypertensive drug treatment
Aged over 55 years or
Aged under
black person of African
55 years
or Caribbean family A – ACE inhibitor or
origin of any age angiotensin II
receptor blocker
(ARB)
C – Calcium-channel
blocker (CCB)
Step 1 A C D – Thiazide-like
diuretic

Step 2 A+C

Step 3 A+C+D

Step 4 Resistant hypertension


A + C + D + consider further Diuretic or Alpha- or Beta-blocker
Consider seeking expert advice

NOTE: Thiazide-like diuretic, such as chlortalidone or indapamide in preference to a conventional thiazide


diuretic such as bendroflumethiazide or hydrochlorothiazide.
Hypertension and Elderly
• In the very elderly (>80 years old) who can
tolerate treatment, a target of <150 mmHg/90
mmHg is acceptable.
• In the very elderly, thiazide-like diuretics
based treatment with or without ACEIs
reduced not only stroke but also total
mortality.
Hypertension and Diabetes Mellitus

• Pharmacological treatment should be initiated in


patients with diabetes when the BP is persistently
>140 mmHg systolic and/or >80 mmHg diastolic.
SBP should be targeted to<140 and DBP <80
mmHg
• The presence of microalbuminuria or overt
proteinuria should be treated even if the BP is not
elevated. An ACEI or ARB is preferred.
• In a proportion of patients, microalbuminuria
may be normalised by higher doses of ACEIs and
ARBs.
Hypertension and Cardiovascular
Disease
• In post-infarction patients, ACEIs and beta-
blockers (especially in patients with LV
dysfunction), help to reduce future cardiac
events which include cardiac failure, cardiac
mortality and morbidity.
Hypertension and Stroke

• Blood pressure is the most consistent and powerful


predictor of stroke and is also the most important
modifiable cause from stroke
• Calcium channel blockers in particular, provided
significantly better primary protection against stroke
compared with diuretics and/or beta-blockers in Asian
and Caucasian populations.
• Combination of an ACEI and diuretic has been shown
to reduce stroke recurrence in both normotensive and
hypertensive patients when treatment was started at
least two weeks after the stroke.
Severe hypertension
• persistent elevated SBP >180 mmHg and/or
DBP >110mmHg
• Patients are then categorised as having:-
(a) asymptomatic severe hypertension,
(b) hypertensive urgencies, or
(c) hypertensive emergencies
(b) and (c) are also referred to as hypertensive
crises.
Severe Hypertension
• Presents with:
– Non-specific signs: Lethargy, Giddiness, Headache

– Acute target organ damage. E.G acute heart failure, acute


coronary syndromes, acute renal failure, dissecting aneurysm,
subarachnoid haemorrhage and hypertensive encephalopathy.

– Incidental Finding/asymptomatic

** RP, CXR, ECG, UFEME should be done to assess organ damage


• Cause:
– Commonest cause is due to longstanding poorly controlled
essential Hypertension
– Other Causes are:
Hypertensive Urgencies
• Include patients with grade III or IV retinal
changes (also known as accelerated and
malignant hypertension), but no overt acute
target organ damage/complication.
• Must be admitted. BP measurement should be
repeated after 30 minutes of bed rest. Initial
treatment should aim for about 25% reduction
in BP over 24 hours but not lower than 160/90
mmHg.
Oral drug for hypertensive urgency
Hypertensive Emergencies
• Patients with complications of severe
hypertension such as acute heart failure,
dissecting aneurysm, acute coronary syndromes,
hypertensive encephalopathy, subarachnoid
haemorrhage and acute renal failure.
• The BP needs to be reduced rapidly. It is
suggested that the BP be reduced by 25%
depending on clinical scenario over 3 to 12 hours
but not lower than 160/90mmHg.
Summary
• In patients with newly diagnosed uncomplicated
hypertension and no compelling indications,
choice of first line monotherapy includes ACEIs,
ARBs, CCBs, diuretics and beta blockers.
• Combination therapy is often required to achieve
target and may be instituted early in patients
with stage II hypertension and in high risk stage I
hypertension.
• A patients whose BP is not controlled on three or
more drugs (including a diuretic) is by definition
having resistant hypertension.
Reference
• Kumar and clerk
• CPG : Management of Hypertension
• Oxford handbook
• NICE guideline
• 2017 ACC Hypertension guideline
Thank you

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