1. SYSTEMIC HYPERTENSION

2. Hypertension is one of the leading causes of the global burden of disease.
Hypertension doubles the risk of cardiovascular diseases, including coronary heart disease (CHD), congestive heart failure (CHF), ischemic and hemorrhagic stroke, renal failure, and peripheral arterial disease.
Although antihypertensive therapy clearly reduces the risks of cardiovascular and renal disease, large segments of the hypertensive population are either untreated or inadequately treated.

3. Definition
Hypertension currently is defined as a usual BP of 140/90 mm Hg or higher, for which the benefits of drug treatment have been definitively established

4. Staging of Office Blood Pressure
BP STAGE
SYSTOLIC BP (mm Hg)
DIASTOLIC BP (mm Hg)
Normal
<120
<80
Prehypertension
80-89
Stage 1 hypertension
90-99
Stage 2 hypertension
≥160
≥100

5. Aetiology Primary (Essential) hypertension
The majority (90–95%) of patients with hypertension have primary elevation of blood pressure, i.e. essential hypertension of unknown cause.
Secondary hypertension (5-10%).

6. Many factors may contribute to development of essential HT
Neural Mechanisms
Baroreflex control of sinus node function is abnormal
Obesity-Related Hypertension
Obstructive Sleep Apnea
Renal Mechanisms
acquired or inherited defect in the kidneys' ability to excrete the excessive sodium load
Low Birth Weight
Genetic Contributions

7. Vascular Mechanisms Hormonal Mechanisms Endothelial Cell Dysfunction
Vascular Remodeling: An increase in the medial thickness relative to lumen diameter (increased media-to-lumen ratio) is the hallmark of hypertensive remodeling in small and large arteries.
Hormonal Mechanisms
Activation of the renin-angiotensin-aldosterone system (RAAS) is one of the most important mechanisms contributing to endothelial cell dysfunction, vascular remodeling, and hypertension

8. Secondary hypertension
Renal diseases
These account for over 80% of the cases of secondary hypertension.
The common causes are:
■ diabetic nephropathy
■ chronic glomerulonephritis
■ adult polycystic disease
■ chronic tubulointerstitial nephritis
■ renovascular disease.

9. Congenital cardiovascular causes
Endocrine causes
These include:
Conn’s syndrome
Congenital adrenal hyperplasia
phaeochromocytoma
Cushing’s syndrome
acromegaly.
Hyperparathyroidism
Primary hypothyroidism
Thyrotoxicosis
Congenital cardiovascular causes
The major cause is coarctation of the aorta

10. Drugs: NSAIDs, oral contraceptives, steroids, carbenoxolone, liquorice, sympathomimetics and vasopressin.
Pregnancy (pre-eclampsia)
Alcohol
Obesity

11. All adults should have blood pressure measured routinely at least every 5 years until the age of 80 years.
Seated blood pressure when measured after 5 minutes’ resting with appropriate cuff size and arm supported is usually sufficient, but standing blood pressure should be measured in diabetic and elderly subjects to exclude orthostatic hypotension.
The cuff should be deflated at 2 mm/s and the blood pressure measured to the nearest 2 mmHg.
Two consistent blood pressure measurements are needed to estimate blood pressure, and more are recommended if there is variation in the pressure.
When assessing the cardiovascular risk, the average blood pressure at separate visits is more accurate than measurements taken at a single visit.

12. Assessment
History
Family history, lifestyle (exercise, salt intake, smoking habit) and other risk factors should be recorded.
The patient with mild hypertension is usually asymptomatic.
Higher levels of blood pressure may be associated with headaches, epistaxis or nocturia.
Attacks of sweating, headaches and palpitations point towards the diagnosis of phaeochromocytoma.
Breathlessness may be present owing to left ventricular hypertrophy or cardiac failure,
symptoms of peripheral arterial vascular disease suggest the diagnosis of atheromatous renal artery stenosis.

13. Examination Findings related to hypertension Loud A2 S4
Forceful sustained apical impulse (heaving)

14. Examination
Secondary causes: Radio-femoral delay (coarctation of the aorta), enlarged kidneys (polycystic kidney disease), abdominal bruits (renal artery stenosis) and the characteristic facies and habitus of Cushing's syndrome are all examples of physical signs that may help to identify causes of secondary hypertension.
Risk factors: Examination may also reveal features of important risk factors such as central obesity and hyperlipidaemia (tendon xanthomas etc.).
Complications:
The optic fundi are often abnormal
and there may be evidence of generalised atheroma or specific complications such as aortic aneurysm or peripheral vascular disease.

15. investigation of all patients
Investigations
investigation of all patients
Urinalysis for blood, protein and glucose
Blood urea, electrolytes and creatinine
N.B. Hypokalaemic alkalosis may indicate primary hyperaldosteronism but is usually due to diuretic therapy
Blood glucose
Serum total and HDL cholesterol
12-lead ECG (left ventricular hypertrophy, coronary artery disease)

16. investigation of selected patients
Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta
Ambulatory BP recording: to assess borderline or 'white coat' hypertension
Echocardiogram: to detect or quantify left ventricular hypertrophy & for the diagnosis ofcoactation of aorta
Renal ultrasound: to detect possible renal disease
Renal angiography: to detect or confirm presence of renal artery stenosis
Urinary catecholamines: to detect possible phaeochromocytoma
Urinary cortisol and dexamethasone suppression test: to detect possible Cushing's syndrome
Plasma renin activity and aldosterone: to detect possible primary aldosteronism

17. Ambulatory blood pressure monitoring
Indirect automatic blood pressure measurements can be made over a 24-hour period using a measuring device worn by the patient.
they are used to confirm the diagnosis in those patients with ‘white-coat’ hypertension, i.e. blood pressure is completely normal at all stages except during a clinical consultation
These devices may also be used to monitor the response of patients to drug treatment and, in particular, can be used to determine the adequacy of 24-hour control with once-daily medication

18. Ambulatory blood pressure recordings seem to be better predictors of cardiovascular risk than clinic measurements.
Analysis of the diurnal variation in blood pressure suggests that those hypertensives with loss of the usual nocturnal fall in blood pressure (‘non-dippers’) have a worse prognosis than those who retain this pattern.

19. Complications

21. Central nervous system
Blood vessels
In larger arteries (> 1 mm in diameter), the internal elastic lamina is thickened, smooth muscle is hypertrophied and fibrous tissue is deposited.
In smaller arteries (< 1 mm), hyaline arteriosclerosis
aortic aneurysm and aortic dissection
Central nervous system
Stroke (due to cerebral haemorrhage or infarction).
Carotid atheroma and transient ischaemic attacks are more common in hypertensive patients.
Subarachnoid haemorrhage is also associated with hypertension.

22. Hypertensive encephalopathy is a rare condition characterised by high BP and neurological symptoms, including transient disturbances of speech or vision, paraesthesiae, disorientation, fits and loss of consciousness. Papilloedema is common.
Retina
central retinal vein thrombosis
Hypertensive retinopathy
Grade I
Arteriolar thickening, tortuosity and increased reflectiveness ('silver wiring')
Grade 2
Grade 1 plus constriction of veins at arterial crossings ('arteriovenous nipping')
Grade 3
Grade 2 plus evidence of retinal ischaemia (flame-shaped or blot haemorrhages and 'cotton wool' exudates)
Grade 4
papilloedema

23. 'Malignant' or 'accelerated' phase hypertension (Diastole>130 mmgh)
Heart
coronary artery disease.
left ventricular hypertrophy
Atrial fibrillation
Diastolic dysfunction
LV failure.
Kidneys
Long-standing hypertension may cause proteinuria and progressive renal failure by damaging the renal vasculature.
'Malignant' or 'accelerated' phase hypertension (Diastole>130 mmgh)
This rare condition may complicate hypertension of any aetiology and is characterised by accelerated microvascular damage and by intravascular thrombosis.
The diagnosis is based on evidence of high BP and rapidly progressive end organ damage, such as retinopathy (grade 3 or 4), renal dysfunction (especially proteinuria) and/or hypertensive encephalopathy .
Left ventricular failure may occur and, if this is untreated, death occurs within months.