HYPERTENSION

INTRODUCTION
High B.P. : condition in which the B.P. is
chronically elevated definition: persistent increase in systolic B.P.

with a consequent increase in diastolic B.P.

normal B.P. 120/80 mmHg (BP= C.O. x t.p.r.)

HT: sys B.P. 140 mmHg; dias B.P. 90 mmHg

CLASSIFICATION
1. Primary (Essential) hypertension (90-95%)

2.

Secondary hypertension (5-10%)

benign malignant

CATEGORY

SYSTOLIC B.P. (mmHg)

DIASTOLIC B.P. (mmHg)

Optimal Normal High normal

< 120 < 130 130-139

< 80 < 85 85-89

HYPERTENSION Mild (stage 1)

moderate (stage 2) severe (stage 3) Very severe (stage 4)

140-159
160-179 180-209 210

90-99
100-109 110-119 120

MALIGNANT HT

200

140

Etiological classification of Hypertension

A. Essential Hypertension (90%)
1. Genetic factors
2. Racial and environmental factors 3. Risk factors modifying the course of essential hypertension

B. Secondary Hypertension
Renal

(10%)

Endocrine

Renovascular hypertension Renal parenchymal hypertension Adrenocortical hyperfunction Hyperparathroidism Oral contraceptives

Coarctation of Aorta Neurogenic

Pathogenesis (Primary HT)

1. High plasma level of catecholamines

2.
3. 4.

Increase in blood volume i.e. arterial overfilling and arteriolar constriction

Increased cardiac output Low-renin essential hypertension (due to altered responsiveness to renin release)

5. High renin essential hypertension (due to decreased adrenal responsivness to angiotensin-II)

Etiology (under four headings)

1. RENAL HT (produced by renal diseases)
- Divided into two groups:
(i) Renal vascular HT e.g. Occlusion of major renal artery, eclampsia, pre-eclampsia etc. (ii) Renal parenchymal HT e.g. In glomerulonephritis, pyelonephritis, interstitial nephritis, polycystic kidney disease, renin producing tumors

PATHOPHYSIOLOGY
1. Overactivation of Sympathetic Nervous System

2. Overactivation of Renin angiotensinaldosterone system (RAAS)

3.

Natriuretic factors

1. Renal HT can be due to 3 inter-related pathogenetic mechanisms:

1. Activation of renin-angiotensin system 2. Sodium and water retention 3. Decreased release of vasodepressor materials

-- release of renin is stimulated by renal ischemia, sympathetic nervous system stimulation, depressed sodium concentration, fluid depletion

Angiotensinogen
Renin

Angiotensin-I
ACE/Kininase-II

Angiotensin-II
Aminopeptidase

Vasoconstriction Na+/H2O retention

BP

Blood
volume

Angiotensin-III
Angiotensinogenase

Aldosterone release

Inactive fragments HYPERTENSION

 RAAS is concerned mainly with 3 functions: Control of blood pressure by altering plasma concentration of angiotensin II and aldosterone Regulation of sodium and water retention Regulation of potassium balance

 Sodium and water retention: - Blood volume and cardiac output determine blood volume -- are regulated by blood levels of sodium
- Blood concentration of sodium is regulated by 3 ways:
(i) Release of aldosterone from activation of RAAS (ii) Reduction in GFR due to reduced blood flow as in reduced renal mass or renal artery stenosis proximal tubular reabsorption of sodium (iii) release of atriopeptin hormone from atria of heart in response to volume expansion these peptides cause increased GFR and inhibit sodium reabsorption

 Decreased release of vasodepressor material: - Many vasodepressor material counterbalance the vasopressor effect of angiotensin II
- These include: PGs (PGE2, PGF2, PGA) -- released from interstitial cells of medulla, urinary kallikrein-kinin system and platelet activating factor

2. ENDOCRINE HYPERTENSION
- Various hormonal secretions produce secondary HT - These are: (i) Adrenal gland e.g. In primary aldosteronism, cushing syndrome, pheochromocytoma (ii) Parathyroid gland hyperparathyroidism e.g. Hypercalcemia in

(iii) Oral contraceptives oestrogen component in contraceptives stimulate hepatic synthesis of renin substrate

3. COARCTATION OF AORTA - Division of aorta that is a local malformation marked by deformed aortic media, causing narrowing of lumen of the vessel

(coarctate- to press close together)

4. NEUROGEINC HT - Are all uncommon causes of HT - Psychogenic, polyneuritis, increased intracranial pressure and section of spinal cord

Symptoms
1. 3. 5. Confusion, Vision problems Cyanosis Fatigue

2. Angina-like chest pain 4. Dizziness, nausea, vomiting 6. Edema

7. Respiratory distress

Pathophysiology of hypertension
INAPPROPRIATELY HIGH SYMPATHETIC OUTFLOW

Increased large arterial stiffness

Abnormal venoconstriction and high venous return

Inappropriately high cardiac output

Increased systemic resistance

INAPPROPRIATELY HIGH RENIN RELEASE

ABNORMAL RENAL SALT/WATER HANDLING