HYPERTENSION

EU MBCHB 4

DR D M KILLINGO
 A systolic blood pressure ( SBP) >139 mmHg
and/or
 A diastolic (DBP) >89 mmHg.
 Based on the average of two or more
properly measured, seated BP readings.
 On each of two or more office visits.
 Both systolic and diastolic pressures do not

have to be out of range

 Only Systolic or Diastolic must be out of

range to qualify as hypertension

 The equipment should be regularly inspected and
validated.
 The operator should be trained and regularly
retrained.
 The patient must be properly prepared and
positioned and seated quietly for at least 5 minutes
in a chair.
 The auscultatory method should be used.
 Caffeine, exercise, and smoking should be avoided
for at least 30 minutes before BP measurement.
 An appropriately sized cuff should be used.
 At least two measurements should be made
and the average recorded.
 Clinicians should provide to patients their

specific BP numbers and the BP goal of their

treatment.
 Asymptomatic (unless with complications)
 Life long disease requiring life long treatment

 Relationship btn BP & CVD events is continuous,

consistent & independent of other CVD risk factors

assoc with target organ damage
 CVS risk doubles with every 20/10mmHg rise BP

from 115/75mmHg between 40-70 yrs

 Isolated systolic hypertension carries similar risk
 White coat hypertension is also associated with
increased cardiovascular risk
 Complications include stroke, coronary artery
disease, heart failure, renal failure, retinopathy and
peripheral vascular disease.
Category Systolic Blood Diastolic Blood
Pressure Pressure
Normal < 120 <80

Pre-hypertension 120-139 80-89

Hypertension – 140-159 90-99

Stage 1
Hypertension – >160 >100
Stage 2
 SBP >120 mmHg and <139mmHg and/or

 DBP >80 mmHg and <89 mmHg.

 Prehypertension is not a disease category

rather a designation for individuals at high
risk of developing HTN.
 Individuals who are prehypertensive are not
candidates for drug therapy but
 Should be firmly and unambiguously
advised to practice lifestyle modification
 Those with pre-HTN, who also have
diabetes or kidney disease, drug therapy is
indicated if a trial of lifestyle modification
fails to reduce their BP to 130/80 mmHg or
less.
 Not distinguished as a separate entity as far
as management is concerned.
 SBP should be primarily considered during
treatment and not just diastolic BP.
 Systolic BP is more important cardiovascular
risk factor after age 50.
 Diastolic BP is more important before age 50.
 Hypertensive Urgencies: No progressive
target-organ dysfunction. (Accelerated
Hypertension)

 Hypertensive Emergencies: Progressive end-

organ dysfunction. (Malignant Hypertension)
 Severe elevated BP in the upper range of
stage II hypertension.
 Without progressive end-organ dysfunction.
 Examples: Highly elevated BP without severe
headache, shortness of breath or chest pain.
 Usually due to under-controlled HTN.
 Severely elevated BP (>180/120mmHg) With
progressive target organ dysfunction.
 Require emergent lowering of BP.

Examples: Severely elevated BP with:

 Hypertensive encephalopathy
 Acute left ventricular failure with
pulmonary edema
 Acute MI or unstable angina pectoris
 Dissecting aortic aneurysm
 Primary HTN:
also known as  Secondary HTN:
essential HTN. less common
accounts for 95% cause of HTN ( 5%).
cases of HTN. secondary to
no universally other potentially
established cause rectifiable causes.
known.
 Common  Uncommon
◦ Intrinsic renal ◦ Pheochromocytoma
disease ◦ Glucocorticoid
◦ Renovascular disease excess
◦ Mineralocorticoid ◦ Coarctation of Aorta
excess ◦ Hyper/hypothyroidis
◦ Sleep Breathing m
disorder
 Onset: at age < 30 yrs ( Fibromuscular
dysplasi) or > 55 (athelosclerotic renal
artery stenosis), sudden onset (thrombus
or cholesterol embolism).
 Severity: Grade II, unresponsive to
treatment.
 Episodic, headache and chest
pain/palpitation (pheochromocytoma,
thyroid dysfunction).
 Morbid obesity with history of snoring and
daytime sleepiness (sleep disorders)
 Pallor, edema, other signs of renal disease.
 Abdominal bruit especially with a diastolic

component (renovascular)
 Truncal obesity, purple striae, buffalo hump

(hypercortisolism)
 Increased creatinine, abnormal urinalysis
( renovascular and renal parenchymal
disease)
 Unexplained hypokalemia
(hyperaldosteronism)
 Impaired blood glucose

( hypercortisolism)
 Impaired TFT (Hypo-/hyper- thyroidism)
www.nhlbi.nih.gov
 Common cause of secondary HTN (2-5%)
 HTN is both cause and consequence of renal
disease
 Multifactorial cause for HTN including
disturbances in Na/water balance,
vasodepressors/ prostaglandins imbalance
 Renal disease from multiple etiologies.
 Atherosclerosis 75-90% ( more common in
older patients)
 Fibromuscular dysplasia 10-25% (more
common in young patients, especially
females)
 Other
 Aortic/renal dissection
 Takayasu’s arteritis
 Thrombotic/cholesterol emboli
 CVD
 Post transplantation stenosis
 Post radiation
 Changes in the vessel wall leading to vessel
endothelial injury and arteriosclerosis
throughout the vasculature
 Complications arise due to the “target organ”

dysfunction and ultimately failure.

 Damage to the blood vessels can be seen on

fundoscopy.
 CVS (Heart and Blood Vessels)
 The kidneys
 Nervous system
 The Eyes
 Ventricular hypertrophy, dysfunction and
failure.
 Arrhithymias
 Coronary artery disease, Acute MI
 Arterial aneurysm, dissection, and rupture.
Severe concentric LVH
 Glomerular sclerosis leading to impaired
kidney function and finally end stage kidney
disease.
 Ischemic kidney disease especially when renal

artery stenosis is the cause of HTN

 Stroke, intracerebral and subaracnoid
hemorrhage.
 Arteriolar fibrinoid necrosis leads to lacunar

infarcts may cause hypertensive

leucoencephalopathy
 May later lead to cerebral atrophy and

dementia
 Retinopathy, retinal hemorrhages and
impaired vision.
 Vitreous hemorrhage, retinal detachment
 Neuropathy of the nerves leading to

extraoccular muscle paralysis and

dysfunction
 A B

Normal Retina Hypertensive Retinopathy A: Hemorrhages

B: Exudates (Fatty Deposits)
C: Cotton Wool Spots (Micro
Strokes)
Arteriolar Narrowing
AV
Nicking
 H

E
 Known as the Silent killer
 If BP is very high, you may experience:
 -fatigue
 -decreased activity tolerance
 -dizziness
 -palpitations
 -angina
 -dyspnea
 May present in HTN crises
 (1) To assess lifestyle and identify other
cardiovascular risk factors or concomitant
disorders that may affect prognosis and
guide treatment
 (2) To reveal identifiable causes of high BP
 (3) To assess the presence or absence of

target organ damage and CVD

 Hypertension
 Cigarette smoking
 Obesity (body mass index ≥30 kg/m2)
 Physical inactivity
 Dyslipidemia
 Diabetes mellitus
 Microalbuminuria or estimated GFR <60 mL/min
 Age (older than 55 for men, 65 for women)
 Family history of premature cardiovascular disease
(men under age 55 or women under age 65)
 Microalbuminuria Hypercoagulability

Type 2 diabetes Visceral obesity

CVD Risk
Impaired glucose Hypertension
tolerance

Insulin resistance
Dyslipidemia

Hyperinsulinemia

The high prevalence of hypertension worldwide has contributed to the present pandemic of
cardiovascular diseases (CVD) - responsible for 30% of all deaths worldwide
Adapted from Rutter MK et al. Circulation.
2003;107:458-454
 Sleep apnea
 Drug-induced or related causes
 Chronic kidney disease
 Primary aldosteronism
 Renovascular disease
 Chronic steroid therapy and Cushing’s
syndrome
 Pheochromocytoma
 Coarctation of the aorta
 Thyroid or parathyroid disease
 Heart
Left ventricular hypertrophy
Angina or prior myocardial infarction
Prior coronary revascularization
Heart failure
 Brain - Stroke or transient ischemic attack
 Chronic kidney disease
 Peripheral arterial disease
 Retinopathy
 MANAGEMENT OF HYPERTENSION
 Angina/MI Stroke: Complications of HTN,
Angina may improve with b-blokers
 Asthma, COPD: Preclude the use of some b-
blockers
 Heart failure: ACE inhibitors indication

 DM: ACE preferred

 Polyuria and nocturia: Suggest renal
impairment
 Claudication: May be aggravated by b-
blockers, atheromatous RAS may be present
 Gout: May be aggravated by diuretics
 Use of NSAIDs: May cause or aggravate HTN
 Family history of HTN: Important risk factor
 Family history of premature death: May

have been due to HTN

 Family history of DM : Patient may also be
Diabetic
 Cigarette smoker: Aggravate HTN,

independently a risk factor for CAD and

stroke
 High alcohol: A cause of HTN
 High salt intake: Advice low salt intake
 Appropriate measurement of BP in both
arms
 Optic fundi
 Calculation of BMI ( waist circumference

also may be useful)

 Auscultation for carotid, abdominal, and

femoral bruits
 Palpation of the thyroid gland.
 Thorough examination of the heart and lungs
 Abdomen for enlarged kidneys, masses, and

abnormal aortic pulsation

 Lower extremities for edema and pulses
 Neurological assessment
 EKG.,
 Echocardiogram if indicated,
 Urinalysis.
 Blood glucose,FBC / hematocrit; serum
potassium, creatinine ( or estimated GFR),
and calcium.
 HDL cholesterol, LDL cholesterol, and
triglycerides.
 Optional tests
urinary albumin excretion.
albumin/creatinine ratio.
 Treating SBP and DBP to targets that are
<140/90 mmHg for all patients
 Patients with diabetes or renal disease, the
BP goal is <130/80 mmHg if proteinuria >
1g/day
 Control BP To reduce cardiovascular and
renal morbidity and mortality
 Reductions in stroke incidence, averaging 35–
40 percent
 Reductions in MI, averaging 20–25 percent
 Reductions in HF, averaging >50 percent.
 Antihypertensives
1st choice drugs:
1. diuretics eg Thiazides
2. β-blockers
3. inhibitors of ACE
4. blockers of AT1 receptors (ARB)
5. calcium channel blockers

2nd choice drugs – mainly to drug combinations:

α1-sympatholytics; α2-sympathomimetics; direct
vasodilators; k+ sparing diuretics
Beta blockers : Main Effects of β1- and β2-blockade
Classification:
Therapeutic algorithm of hypertension treatment
 NOTE; Much as Secondary HTN requires medical
therapy;
 Identifying and Treating the cause of Secondary

HTN in some cases may indeed cure the HTN.

 NOTE: HTN crisis is more likely to be associated

with secondary causes of HTN such as

 Renovascular disease

 Primary renal diseases

 Phaeochromocytoma

 Connective tissue disorders

 Sub-classified as hypertensive urgencies or
emergencies, depending on evidence of
ongoing target organ damage.
 In the absence of neurologic, cardiovascular,

or renal deterioration and funduscopic

abnormalities, patients with severely elevated
BPs (>200/120 mm Hg) DO NOT require
immediate BP reduction (HTN urgencies).
 Symptomatic patients with complications eg
hypertensive encephalopathy require prompt
but controlled BP lowering (HTN emergencies)
 However, over-rapid treatment may itself be

hazardous, leading on occasions to ischaemic

complications such as stroke, myocardial
infarction, or blindness.
 It is common to find modestly elevated
blood pressure in patients admitted to
hospital following an acute stroke.
 Cerebral auto regulation is commonly
disturbed in this situation
 Excessive antihypertensive treatment may
only serve to worsen the cerebral damage.
 Such treatment should only be administered
for severe elevation of BP (DBP> 120 mmHg
for ischaemia or SBP > 185mmHg for
haemorrhage))
 Nitrates- iv nitropruside, nitroglycerin *
 Beta blockers-iv labetalol, esmolol
 CCB- iv nicardipine
 ACE- iv Enalaprilat *
 Pentolamine (adrenergic crisis)
 Hydrallazine ( Eclampsia)
Hypertensive urgencies do not require
immediate BP reduction
 BUT rather initiation of maintenance therapy

without acute oral loading for effective and

sustained BP reduction.
The prior practice of immediately reducing BP
with oral loading of clonidine, sublingual
nifedipine or hydrallazine bolus MUST be
DISCOURAGED!
 This exposes the patient to the unnecessary

risk of acute end-organ hypoperfusion

secondary to abrupt, uncontrolled decreases
in BP.
NON- PHARMACOLOGIC THERAPY
FOR HTN
 Increase physical activity such as walking,
biking, aerobic dancing, tennis, soccer,
basketball, etc.
 Decrease time in sedentary behaviors such as
watching television, playing video games, or
spending time online.
 Smoking cessation
 Decrease portion sizes for meals and snacks.
 Reduce portion sizes or frequency of
consumption of calorie containing beverages,
and fats.
 Control Diabetes

The Dietary Approaches to Stop
Hypertension clinical trial (DASH)
 Diet rich in fruits, vegetables, and low fat
dairy foods, can substantially lower blood
pressure in individuals with hypertension and
high normal blood pressure.
Healthy Diets: low in animal fat and a high intake of fish, olive oil,
vegetables, fruits, and full grains
 Combination diet affects comparable to
pharmacological trails in mild
hypertension.
 Population wide reductions in blood
pressure similar to DASH results would
reduce CHD by ~ 15% and stroke by ~27%
 Great potential in susceptible groups:
blacks and elderly.