This document discusses hypertension (high blood pressure) including its definition, causes, clinical presentation, assessment, and management. It notes that hypertension is defined as blood pressure above 140/90 mmHg and risks of cardiovascular disease double for every 20/10 mmHg rise. Common complications include stroke, myocardial infarction, heart failure, and renal failure. Treatment involves lifestyle modifications and medication, starting with ACE inhibitors, calcium channel blockers, or thiazides. The goals are to lower blood pressure and reduce cardiovascular risk based on individual patient factors.

1. Pharmacotherapy
Hypertension
RVS Chaitanya koppala

2. Defined as:
Condition where blood pressure is elevated to an extent that
clinical benefit is obtained from blood pressure lowering
&
140/90 mmHg is considered the upper limit of normal
(treatment threshold or targets)

3. • Hypertension is largely a condition of older individuals
• Diastolic pressure peaks at age of 50
• Systolic pressure continues to increase with advancing age
• Risk of cardiovascular disease double for every 20/10mmHg rise in
blood pressure

4. Most common and important cardiovascular complications associated
with hypertension are stroke and myocardial infarction
↑5mmHg in usual diastolic blood pressure is associated with 35-40%
↑ risk of stoke
Risk of heart failure is increased with six fold in hypertensive subjects
↓ blood pressure of 10/6mmHg associated with 38% ↓ stoke and 16%
↓ coronary events
↓5 mmHg blood pressure is associated with 25% ↓ renal failure

5. Complications of hypertension:
Myocardial infarction
Stroke
Cerebral/brainstem infarction
Cerebral haemorrhage
Lacunar syndromes
Multi infarct disease
Hypertensive encephalopathy/ malignant hypertension
Dissection aortic aneurysm
Hypertensive nephroscelrosis
Peripheral vascular disease

6. Epidemiology
10-25% population are expected to benefit from the drug treatment
90-95% of cases of hypertension , there is no underlying medical illness to
cause high blood pressure= essential hypertension
Essential = compensation mechanism to maintain adequate circulation
Genetic factors also clearly plays a role, but not a single gene is responsible
for hypertension except in Polycystic kidney disease /Liddle’s syndrome
More common in black people of African (Caribbean origin)

7. Causes of hypertension
PRIMARY HYPERTENSION : Essential hypertension
SECONDARY HYPERTENSION
Renal diseases Drugs:
Endocrine disease Sympathomimetic amines
Steroid excess: hyperaldosteronism, hypercorticoidism
Growth hormone excess
Catecholamine excess
Pre clampsia
Oestrogens (?)
Ciclosporin
Erthyropoietin
NSAIDS
Steroids
Vascular causes: Renal artery stenosis: fibromuscular
hyperplasia, renal artery atheroma
High salt
Alcohol intake
Obesity

9. Regulation of Blood pressure
Mean blood pressure is the product of Cardiac output and total
peripheral resistance
In most hypertensive individuals no change in cardiac output but
increase in peripheral resistance (?)
Control of blood pressure is important and number of homeostatic
reflexes are evolved to provide the BP homeostatis

10. Minute to minute increase in BP – baroreceptor reflex
Longer term regulation – renin-angiotensin- aldosterone system(salt,
water and blood pressure control)
Long term increase in shear stress also causes the vascular remodeling
Nitric oxide overcome by increased sensitivity to vasoconstrictor
endothelin (increases peripheral resistance)
Atrial natriuretic peptide
Bradykinin
Antidiuretic hormone

12. Clinical presentation
• Severe cases may present – Headache, visual disturbance or evidence
of target organ damage ( stroke, ischaemic heart disease or renal
failure)
• Malignant hypertension : accelerated/uncommon/ emergency, usually
>220/120mmHg evidence of Small vessel damage

13. • Fundoscopy: papilloedema (optic disc swelling), haemorrhages and
exudates
• Renal damage: haematuria, proteinuria and impaired renal function
• Hypertensive encephalopathy: small vessel damage in brain/ cerebral
oedema- confusion, headache, visual loss, seizures and coma
• MRI shows extensive white matter changes
• Requires hospital admission and rapid control of blood pressure over
12-24h towards normal levels

14. Management of hypertension
Diagnosis of hypertension:
All adults have their blood pressure check for every 5 years
Those with high blood pressure 130-139mmHg systolic and 85-89 mmHg
diastolic should have annual measurement
Measurement of blood pressure:
Well maintained sphygmomanometer of validated accuracy
Measured in both arms
In sitting and standing positions
In relaxed condition
Accurate sized cuff should be used
White coat hypertension (?)

15. Assessment of hypertensive patient
Secondary causes
Contributing factors:
Evidence of end organ damage
Determination of cardiovascular risk

16. Secondary causes
Renal damage (haematuria, polyuria)
Phaeochromocytoma (headache, postural dizziness, syncope)
Physical examination: abdominal bruits (renal artery stenosis)
Radiofemoral delay (coarctation of aorta)
Palpable kidneys (polycystic kidney disease)
Laboratory analysis (full blood count, electrolytes , urea , creatinine
and urinalysis)
Ultrasound of abdomen
Isotope regimen for suspected renal disease

17. • Renin levels suppressed by Beta blockers
• Aldosterone by ACE inhibiotors and receptor antagonists
• Very high aldosterone /renin ratio- conn’s syndrome or primary
hyperaldosteronism, cause by benign adenoma/ simple hyperphlasia
• CT/ MRI scanning shows images of tumours

18. Contributing factors:
Should be assessed for possible contributing factors and possible
factors such as obesity, excess alcohol or excess salt intake and lack of
exercise
Provoked by use of drugs (OTC drugs cold and flu remedies)
Smoking, diabetes and hyperlipidaemia
Family history of cardiovascular disease

19. Evidence of end organ damage:
Optic fundi- retinal damage
ECG – detect left ventricular hypertrophy/ ischaemic heart disease
Urine analysis for microalbuminaria (indicator of higher risk of future
end stage renal disease and overall vascular risk)

20. Determination of cardiovascular risk:
Patients with documented atheromatous vascular disease
(MI/Stroke/angina/ peripheral vascular disease)
Type 2 Diabetes over 40 years of age = coronary equivalent
Non diabetic patients with MI
Non diabetic patients without cardiovascular disease necessary to
estimate the cardiovascular risk (microalbuminuria increase 2-3 folds
cardiovascular risk)

21. Treatment
Non pharmacological approaches
Pharmacological approaches
Ancillary drug treatment

22. Non pharmacological treatment
• Patients with mild hypertension in the range of 140-159/90-100mmHg
offered lifestyle advice
• Over weight- weight loss reduces BP about 2.5/1.5mmHg/kg
• DASH (dietary approaches to stop hypertension) found to lower BP
significantly 4.5/2.7mmHg
• DASH- fruit, vegetables, low fat dairy products, fish, low fat poultry
and whole grains, minimizing red meat, confectionary and sweetened
drinks

23. • Subjects should reduce their salt intake (6g NaCl)
• Significant hidden salt in the processed meat, ready meals, cheese and even
bread
• Control intake of calories and saturated fat
• Regular aerobic exercise (min 30mins)
• Alcohol intake 2 units for females and 3 units for male
• Smoking should be quit, or else reduce the units

24. Pharmacological approaches
Treatment thresholds:
S.NO Blood pressure threshold Approach
01 >220/120mmHg Treated immediately, dual therapy suggested for
>20mmHg increase then target
02 >160-220/100-120mmHg
(severity and end organ damage)
Monitored over several weeks, treated if BP remains
in this stage
03 >140-159/90-99mmHg
(severity and end organ damage)
Monitored annually unless evidence of target organ
damage, CVD, DM
04 >135-139/85-89mmHg Monitored annually/reassessed annually
05 Less then 135/89mmHg Rechecked every 5 years

28. Other agents:
Minoxidil: powerful antihypertensive drug, indicated in severe
peripheral oedema and reflex tachycardia (* women ?)
Hydralazine: add on for resistant hypertension therapy
Sodium nitroprusside: direct acting arterial and venous dilator /
intravenous infusion/ blood pressure during anaesthesia
Aliskiren: ? antagonist
Darusentan: endothelin antagonist undergoing clinical trials in
resistant hypertension.

29. Ancillary treatment
ASPIRIN:
• Use reduces CV events at the expense of an increase in GIT complications
• Blood pressure should be controlled (<150/90mmHg) before aspirin.
• It should be restricted to the patients who have no contraindication and
either :
Evidence of established vascular disease
No evident of CVD but who are over 50 yrs of age
No evident of target organ damage
10 year CVD risk >20%

30. Lipid lowering therapy:
• Increasing evidence from the clinical trials of the benefit of lipid
lowering drug treatment in patients with hypertension
• Atorvastatin 10mg reduction in CHD and stroke
• LLT with statins should be prescribed to patients
Under 80 years of age
With cholesterol >3.5mmol/L,
Pre existing vascular disease,
10 years CV risk of >20%

31. Drug selection:
Drugs should be chosen on the basis of efficacy, safety, convenience and
cost
Efficacy:
Evidence from the large scale clinical trials
Short term studies only generates hypothesis and should be used to change
current strategies
Safety:
Drugs need to take on long term, so should be with long established safety
records
Recognize the importance of symptomatic adverse effects since these may
reduce adherance

32. Convenience:
Once daily preparation is more adherence than more frequent regimens
Conscious of the cost of individual preparations
Combination of low doses of anti hypertensive drugs are often better
tolerated than single drugs taken in large doses

33. Algorithm for antihypertensive therapy
< 55 yrs and non blacks > 55 yrs and non blacks
ACE Inhibitors
(capto/enala/lisino/perindo/rami-PRIL)
Calcium channel blockers (nifedipine, amlodipine,
verapamil, diltiazem)
+
Diuretics (thiazides, loop diuretics)
A+C or A+D
A+C+D
Consider adding alpha/beta blocker, spironolactone
Seek specialist advice

34. Thank you