HYPERTENSION

INTRODUCTION
• Defined as blood pressure persistently ≥
140/90mmHg
• Hypertension is an important public health
problem worldwide.
• Hypertension is an acknowledged potential risk
factor in the development of cardiovascular
diseases like stroke, coronary heart disease,
renal failure and congestive heart failure .
 INTRODUCTION
• The prevalence of HTN increases with age
• The risk of morbidity and mortality rises with
increasing systolic and diastolic BP
• Patients with isolated systolic HTN have 2-3x
increase in risk of cardiac mortality
 EPIDEMIOLOGY
• Ogah et al documented 43 studies on
prevalent rates of hypertension in Nigeria
between 1960 and 2012. The overall
prevalence of hypertension in Nigeria ranges
from 8%-46.4% depending on the study
target population
 EPIDEMIOLOGY
• The estimated overall prevalence rate of
hypertension in Nigeria is 28.9% (29.5% in
men, 25% among women, 30.6% and 26.4% in
urban and rural areas respectively).
Precautions to take when measuring BP

• The patient should have rested for at lease 5

minutes
• Use appropriate cuff size
• Support the arm
• No stimulants like caffeine, alcohol, etc
• For diabetics and elderly patients, do erect
and supine to exclude orthostatic hypotension
 TYPES OF HYPERTENSION
• PRIMARY (ESSENTIAL) HTN
• Accounts for 90% of cases of HTN
• Cause is unknown
• However its aetiology may be multifactorial
 Genetic factors
• HTN tends to run in families
• Children of hypertensive parents are more
likely to be hypertensive too
• This may be explained by the shared
environmental influences
• However the actual genetic component is yet
to be identified
 Foetal factors
• Low birth weight is associated with
subsequent high BP
• The exact explanation for this is not known
•
 Environmental factors
• Obesity:
• Fat people are more likely to have high BP
than thin people
• However, in obese people, there is a risk of
measuring the BP with a small cuff
• This results to over estimation of the BP
• Obstructive sleep apnoea may also be a
contributing factor to HTN in obese people
 Environmental factors
• Alcohol consumption:
• People who consume large amounts of alcohol
are more likely to be hypertensive ( > 14units
per week for females; > 21 units per week for
males)
• Studies have shown that subjects who drink
small quantities of alcohol are less likely to be
hypertensive compared to those who don’t take
alcohol
 Environmental factors
• Sodium intake:
• Populations who take higher amount of salt have
higher blood pressures than those who consume
less sodium
• The high salt diet consumed by people who
move from rural to urban areas may be a
contributor to the high BP seen in them
• Some studies have shown that high potassium
diet may be protective.
 Environmental factors
• Stress:
• Acute stress and pain can cause elevated BP
• However, the relationship between chronic
stress and HTN is uncertain
 Other risk factors
• Insulin resistance:
• In metabolic syndrome-X, there is
hyperinsulinaemia, glucose intolerance,
reduced HDL cholesterol,
hypertriglyceridaemia, central obesity and
HTN
• All these are related to insulin resistance
 Other risk factors
• Humoral mechanisms:
• The following are involved in short-term
physiologic regulation of BP:
• Autonomic nervous system
• RAAS
• Natriuretic peptide
 SECONDARY HYPERTENSION
• RENAL DISEASE: Chronic glomerulonephritis, Adult
polycystic kidney disease (ADPKD), renal artery
stenosis, Diabetic nephropathy, etc
• COARCTATION OF THE AORTA
• ENDOCRINE DISEASES: Cushings disease, Conns
syndrome, phaeochromocytoma, acromegaly,
congenital adrenal hyperplasia, thyroid disease, etc
• DRUGS: Oral contraceptives, NSAIDS, anabolic
steroids, alcohol, monoamine oxidase inhibitors, etc
CLASSIFICATION
ESC/ESH classification (2013)
Category Systolic Diastolic
Optimal <120 and <80
Normal 120-129 and/or 80-84
High normal 130-139 and/or 85-89
Grade I 140-159 and/or 90-99
Grade 2 160-179 and/or 100-109
Grade 3 ≥ 180 and/or ≥ 110
Isolated ≥ 140 and <90
systolic HTN
 JNC 7
• BP Classification
• SBPmmHg DBPmmHg
• Normal <120 <80
• Pre-hypertension 120-139 80-89
• Stage 1 140-159 90-99
• Stage 2 >160 >100
• Pre-hypertension, a new category designated
emphasizes that patients with pre-hypertension
are at risk for progression to htn and that lifestyle
modifications are important preventive strategies.
 Recommendations by JNC 8
• In patients >18 years with CKD, initial or add-on therapy
should be an ACE inhibitor or ARB, regardless of race or
diabetes status
• JNC 8 recommends treating patients ages 18 to 69years who
have CKD and BP ≥140/90 mmHg.
• JNC 7’s more stringent recommendation treating such
patients with BP≥130/80 mmHg was relaxed because there:
• Is little evidence of a lower mortality rate or
cardiovascular or cerebrovascular benefits as
a result of tighter control.
• White coat hypertension: Elevated office BP,
normal out of office BP

• Masked Hypertension; patient has normal

office blood pressure and elevated out-of-
office blood pressure
 PATHOPHYSIOLOGY
• The pathogenesis of essential HTN is not clear
• BP = Cardiac output (CO) x Total peripheral
resistance (TPR)
• High BP may be due to elevated CO; normal
TPR
• Elevated TPR, normal CO
• Elevated TPR and CO
 Cardiac changes
• 1. Resistance in the blood vessels
• Peripheral resistance is determined by small
arterioles
• The small arterioles have smooth muscle cells
which respond to sympathetic nerve
stimulation
• Stimulation of the sympathetic nerve leads to
vasoconstriction
 Cardiac changes
• In HTN, there is an increase in the muscle wall
thickness and narrowing of the lumen
diameter
• This leads to increased total peripheral
resistance and hence elevated BP with normal
cardiac output
 Cardiac changes
• Changes in large vessels:
• There is thickening of the tunica media with
increased deposition of calcium and collagen
• This leads to reduced compliance of the
arterial wall and hence increased TPR
 Renal changes:
• Renin also has a role in pathogenesis if HTN
• It is secreted by the juxta-glomerular
apparatus of the kidneys
• Renin is released in response to
underperfusion of the glomerulus, response
to salt intake or sympathetic stimulation
• Renin-Angiotensinogen-Angiotensin I-
Angiotensin converting enzyme-Angiotensin II
 Renal changes:
• Angiotensin II is a powerful vasoconstrictor,
causes left ventricular hypertrophy.
• It also stimulates the Zona glomerulosa of the
adrenal gland to release aldosterone
• Aldosterone causes salt and water retention
• Aldosterone also causes fibrosis of the heart
muscle
• This leads to the decreased compliance of the LV
wall
 Others
• Nitric Oxide: Causes vasodilatation
• Bradykinin: Vasodilator
• Endothelin: Causes vasoconstriction and may
cause salt sensitive rise in BP.
• This is usually counteracted by NO.
• However when there is an imbalance with higher
levels of endothelin and reduction in NO, there is
resultant vasoconstriction and thus elevated BP
 Others
• Atrial Natruiretic peptide: Increases salt and
water excretion by in response to increased
blood volume
• Ouabain: It is a naturally occurring steroid-like
agent
• It acts on the vascular smooth muscle to cause
vasoconstriction
 GENETIC FORMS OF HYPERTENSION
• LIDDLES syndrome: HTN, hypokalaemia, low
alsdosterone, low plasma renin
• GLUCOCORTICOID REMEDABLE ALDOSTERONISM
(GRA): hyperaldosteronisn, low renin, low potassium,
high sodium…(like conns syndrome)
• CONGENITAL ADRENAL HYPERPLASIA: Due to
deficiency of 11-beta-hydroxylase
• Gordon’s syndrome: xterized by hyperkalaemia,
familial HTN; due to mutation on the long arm of
chromosome 7
 SYMPTOMS
• Non specific
• Headache
• Blurring of vision
• Or symptoms of complications
 SIGNS
• HEART:
• Displaced , heaving apex due to LVH
• Loud A2
• S4
• KIDNEYS:
• Features of renal failure
 SIGNS
• CNS:
• Transient ischaemic attack
• Stroke
• Hypertensive encephalopathy
• Subarachnoid haemorrhage
 SIGNS
• FUNDI:
• Keith-Wegener classification of hypertensive retinopathy:
• Grade I: Narrowing, sclerosis, increased tortuosity of the
arterioles with increased reflectiveness (silver wiring)
• Grade II: Arterio-venous nipping due to thickened
retinal arteries passing over the retinal veins
• Grade III: Plus flame shaped haemorrhages and soft
exudates (cotton wool) due to small infarcts
• Grade IV: plus papilloedema (blurring of the margins of
the optic disc)
 EVALUATION
• History
• age, sex, occupation, address.
• PMH
• Family history
•           -HT, Diabetes, Heart disease, sudden death.
• Diet history
• - salt
•       -  drugs.
• Height, weight
• Pulse, BP
• Peripheral pulses
• Neck veins, bruits, thyroid
• Heart
• Abdominal mass, bruits.
• Neurologic exam.
• Fundoscopy
• smoking
• alcohol
• obesity
• BMI > 27 
• ­    Blood pressure
• ­    Blood sugar
• ­    Serum cholesterol, triglycerides
• Left ventricular enlargement
• Albuminuria.
 Investigations
• Urinalysis, urine microscopy
• E&U, Creatinine
• CXR
• Fasting blood sugar
• Fasting lipid profile
• ECG
• Echocardiography
• Renal USS
• Urinary metanephrines if phaechromocytoma is
suspected
 BENEFITS OF LOWERING BP
• Stroke reduction- 40%
• MI reduction - 25%
• Heat failure - >50%
 LIFE STYLE MODIFICATION
• Lose weight if overweight. This can be
accomplished with the DASH diet, which is
rich in fruits and vegetables and encourages
the use of fat-free or low-fat milk and milk
products.
• Limit alcohol intake to 14 units per week for
women and 21 units per week in men
 LIFE STYLE MODIFICATION
• Increase aerobic activity (30-45 min most days
of the week).
• Reduce sodium intake to no more than 100
mmol/d (2.4 g sodium or 6 g sodium chloride).
• Maintain adequate intake of dietary
potassium (approximately 90 mmol/d).
• Stop smoking and reduce intake of dietary
saturated fat and cholesterol for overall
cardiovascular health.
TREATMENT
TREATMENT
 NICE GUIDELINES FOR HTN MNGT
Age <55years Age > 55 years
Black of African or
Carrebean descent
STEP 1 A C OR D
STEP 2 A+C A+C
STEP 3 A+C+D A+C+D
STEP 4 Resistant hypertension Resistant hypertension
A+C+D A+C+D
+Diuretic or alpha blocker +Diuretic or alpha blocker
or beta blocker or beta blocker
• The rationale for step 1 is that young
caucasians are more likely to have high renin;
while elderly and black patients have lower
renin levels
 HYPERTENSIVE CRISIS
• Hypertensive emergency is a BP of 220/140 or
greater with target organ damage (TOD).
• Hypertensive urgency is defined as a BP above
180/110 without TOD
• Hypertensive emergencies encompass a
spectrum of clinical presentations in which
uncontrolled BPs lead to progressive or
impending end-organ dysfunction
 HYPERTENSIVE EMERGENCIES
• Acute end-organ damage in the setting of a
hypertensive emergency may include the following
• Neurologic - Hypertensive encephalopathy, cerebral
vascular accident/cerebral infarction. subarachnoid
hemorrhage, intracranial hemorrhage
• Cardiovascular - Myocardial ischemia/infarction,
acute left ventricular dysfunction, acute pulmonary
edema, aortic dissection
• Others - Acute renal failure/insufficiency,
retinopathy, eclampsia, microangiopathic hemolytic
anemia
 HYPERTENSIVE URGENCY
• Severe hypertension in the organ transplant
patient
• Preoperative hypertension
• Hypertension associated with burns
• Severe, uncontrolled hypertension
ACCELERATED/MALIGNANT HYPERTENSION

• Malignant / accelerated HTN occurs when blood

pressure rises suddenly with DBP >120mmHg.
• Clinical lesions are best seen in the retina.
• In accelerated hypertension, there are other
features of HTN retinopathy, but no
papilloedema
• However, in Malignant HTN, there is presence of
papilloedema
ACCELERATED/MALIGNANT HYPERTENSION

• The characteristic histologic change is fibrinoid

necrosis of the vessel wall
• If untreated, it can lead to renal failure, heart
failure, aortic dissection, stroke and may lead
to death.
PAPILLOEDEMA IN MALIGNANT
HYPERTENSION
 HYPERTENSIVE ENCEPHALOPATHY

• An uncommon but serious complication of

HTN
• Poor prognosis if left untreated
• Headache, confusion, blurring of vision,
transient focal neurological deficit
• Prompt response to anti-hypertensives
• It is a diagnosis of exclusion
 PARENTERAL THERAPY FOR HYPERTENSIVE
CRISIS
• SODIUM NITROPRUSSIDE: Rapid onset of action; 0.25-
2mcg/kg/min
• IV LABETALOL: alpha and beta blocker;
0.5-2mcg/kg/min
• IV NICARDIPINE: dihydropyridine calcium channel
blocker; infusion at 5mg/kg/hr
• IV HYDRALAZINE: direct relaxation of the vascular
smooth muscle; unpredictable hypotensive effect
• PHENTOLAMINE: alpha blocker used for
phaeochromocytoma
 Factos responsible for poor BP control

• Non-Compliance Coffee
• Obesity Antidepressant
• NSAID Inadequate doses***
• Renal insufficiency Fear of causing
• Salt intake danger to the
patient***
• Alcohol Faith healing***
• Tobacco Fake drugs
Management of Hypertension in Pregnancy

• Discontinue ACEi or ARBs

• First drug of choice: Methyl dopa
• Second line agents are Nifedipine and
Labetalol
THANK YOU