Definition: Elevated arterial pressure is called hypertension.

Diagnosis Systolic Blood Pressure (in mm of Hg) < 130 139 139 Hypertension Stage 1 140 159 90 99 Diastolic Blood Pressure (in mm of Hg) < 85 85 90

Introduction

Normal High Normal

Stage 2
Stage 3

160 -179
> 180

100 109
> 110
Source: Joint National Committee, 6th report

Criteria as per Joint National Committee,7th report

Stage
Normal Prehypertension Stage 1 Stage 2

Systolic BP (mm of Hg)

120 120 - 139 140 159 More than 160

Diastolic BP (mm of Hg)

80 80 - 89 90 -99 More than 100

Why identify and treat hypertension?

Hypertension when unrecognized is associated with higher incidence of:
Coronary artery disease: After 50 years of age, even mild hypertension is associated with 56% increase in cardiovascular deaths Cardiac hypertrophy and cardiac failure. Cerebro-vascular accidents: After 50 years of age, even mild hypertension is associated with 42% increase in stroke

incidence.
Aortic dissection. Renal failure.

 Cerebrovascular diseases Consequences Of Inadequate Treatment of Hypertension

o o o o o o o o Ischemic stroke Hemorrhagic stroke TIA Dementia Myocardial infarction Angina Left ventricular hypertrophy Left ventricular dysfunction

Cardiovascular diseases

Renal disorders Peripheral vascular diseases Aortic aneurysm Retinopathy Malignant hypertension

Complication of Untreated HT

HT is a major risk factors for Coronary Heart Disease

Physiology of Blood Pressure Regulation

Blood pressure is dependent on
Cardiac output and, Peripheral vascular resistance.

Cardiac output is dependent on

Blood volume (in turn regulated by mineralocorticoids and atrial natriuretic
factor).

Cardiac factors like heart rate and contractility.

Peripheral vascular resistance is controlled by neural and humoral influences, which produce vasoconstriction or vasodilatation.

Moment to moment regulation of BP occurs with the help of baroreflexes (via autonomic nerves) and humoral mechanisms. These influences affect arterioles, post-capillary venules (capacitance vessels),
renal vessels and heart.

How Vessel Caliber and Blood Flow Influence BP

Vasoconstrictor Influences Humoral:

Angiotensin, Catecholamines, Endothelin-1, Thromboxane A2 Leukotreines.

Vasodilator Influences Humoral:

Prostaglandins Nitric Oxide

Neural:
2 adrenergic influences (1 adrenergic influences increase heart rate and cardiac contractility, thereby raising BP; hence the role of cardioselective beta 1 blocker drugs for treatment of hypertension)

Neural:
-adrenergic influences.

Cardiac output is dependent on blood volume (in turn regulated by mineralocorticoids and atrial natriuretic factor) and on certain cardiac factors like heart rate and contractility.

Factors controlling peripheral arteriolar resistance

Function of Renin Angiotensin System

Etiological Classification of Hypertension

Primary hypertension (also called idiopathic or essential HT):
o 90 to 95% cases of HT are idiopathic in nature.

Secondary hypertension: When HT is due to some other disease.

o Renal diseases:
o o o o glomerulonephritis, chronic renal failure, renal artery stenosis, polycystic kidney hyperfunctioning adrenal cortex (Cushings syndrome, primary hyperaldosteronism), pheochromocytoma, administration of exogenous hormones (corticosteroids and estrogens) and sympathomimetic drugs. coarctation of aorta.

Endocrinal diseases:
o o o

o o

Cardiovascular disorders:
o

Neurological disorders:
o increased intra cranial pressure.

Classification based on Course of the Disease

o o o o

Benign Hypertension:
This is a chronic disorder with a relatively lesser increase in blood pressure. Usually the diastolic is less than 110 mm of Hg. Clinical manifestations are slow to appear and the disease may remain silent for a long time. Ultimately, however it progresses to severe end organ damage.

o o o o o

Malignant Hypertension:
It marked by acute elevation in blood pressure. Diastolic levels are usually > 130 mm of Hg. It may arise de novo or as a complication of benign hypertension. It is a medical emergency because end organ damage occurs rapidly Complications are papilledema, retinal hemorrhages, encephalopathy, cardiac involvement and renal failure. More likely to occur in toxemia of pregnancy and due to renal diseases.

Mechanism of HT in some important conditions

Complications of Hypertension

Determinants of Hypertension Related Risks

Age of the patient.

Level of blood pressure.
Presence of other cardiovascular

risk factors.
Target organ damage.

Presence of associated clinical conditions.

Pathogenesis of Hypertension
Since BP equals cardiac output (CO) total peripheral vascular resistance (TPR), pathogenic mechanisms of HT must involve increased CO, increased TPR, or both.

In primary hypertension and hypertension due to pheochromocytoma, primary aldosteronism, renovascular disease, and renal parenchymal disease, CO is normal or slightly increased, and TPR is usually increased.
Some disorders that increase CO (thyrotoxicosis, arteriovenous fistula, aortic regurgitation), produce isolated systolic hypertension. Some elderly patients have isolated systolic hypertension, probably due to inelasticity of the aorta and its major branches. Both genetic factors and environmental influences act in concert to produce essential hypertension.

How Aging influences Blood Pressure

Physiological mechanisms perturbed during development of HT

Cardiac output. Peripheral resistance Renin-angiotensin-aldosterone system Autonomic nervous system Other factors
Bradykinin Endothelin Nitric oxide Atrial natriuretic factor

Postulated Abnormalities in Essential HT

Defective Renal Homeostasis
Hyperresponsiveness to Sympathetic stimulation

Others:
o Vascular hypertrophy

and hyperplasia. o Unidentified substance with mineralocorticoid activity. o Increased sensitivity to angiotensin II

Vasodilator Deficiency Abnormal Sodium Transport across Cell membranes

Abnormal Sodium Transport

In many cases of hypertension, Na transport across the cell wall is abnormal, because the Na-K pump (Na+, K+-ATPase) is defective or inhibited or because permeability to Na+ is increased. This results is increased intracellular Na, which makes the cell more sensitive to sympathetic stimulation.

Ca follows Na, so accumulation of intracellular Ca may be responsible for the increased sensitivity.
Because Na+, K+-ATPase may pump norepinephrine back into sympathetic neurons (thus inactivating this neurotransmitter), inhibition of this mechanism could also enhance the effect of norepinephrine, increasing BP.

Defective renal homeostasis

In normal individuals, kidneys can increase Na+ excretion in response to increased Na+ load, volume load or when BP is rising. In contrast, in individuals prone to hypertension, this homeostatic mechanism for Na + excretion is defective. Also genetic factors in such individuals, results in diminished Na+ excretion at normal arterial pressures; however Na+ excretion at higher pressures is normal. Sodium retention produces expansion of blood volume, thereby increasing cardiac output.

Increased cardiac output produces peripheral vasoconstriction due to auto-regulatory influences (Autoregulation: caliber of blood
vessels is also regulated by amount of blood flowing through it. When flow is high, vessel caliber decreases and vice versa).

Hyper-responsiveness to sympathetic stimulation

Sympathetic stimulation increases BP, usually more in patients with prehypertension or hypertension than in normotensive patients. Whether this hyperresponsiveness resides in the sympathetic nervous system or in the myocardium and vascular smooth muscle is unknown. A high resting pulse rate, which may result from increased sympathetic nervous activity, is a well-known predictor of hypertension. In some hypertensive patients, circulating plasma catecholamine levels during rest are higher than normal.

Vasodilator Deficiency
Deficiency of a vasodilator (eg, bradykinin, nitric oxide) rather than excess of a vasoconstrictor (eg, angiotensin,

norepinephrine) may cause hypertension.

If the kidneys do not produce adequate amounts of vasodilators (because of renal parenchymal disease or bilateral nephrectomy), BP can increase. Vasodilators and vasoconstrictors (mainly endothelin) are also

produced in endothelial cells. Therefore, endothelial dysfunction

greatly affects BP.

Other Postulated Mechanisms

Vascular smooth muscle hypertrophy and hyperplasia may be seen in hypertensive individuals due to defective intracellular signaling. In a subset of patients, in spite of low plasma renin levels, sodium retention is seen. This may possibly be due to presence of an unidentified substance with mineralcorticoid activity. Or it may be because of increased sensitivity of adrenals to angiotensin II (angiotensin II produces increase vasoconstriction and aldosterone secretion. This causes sodium retention at DCT).

Prognosis
The higher the BP and the more severe the retinal changes and other evidence of target-organ involvement, the worse is the prognosis. Systolic BP predicts fatal and nonfatal cardiovascular events better than diastolic BP. Without treatment, 1-yr survival is < 10% in patients with retinal sclerosis, cotton-wool exudates, arteriolar narrowing, and hemorrhage (grade 3 retinopathy), and < 5% in patients with the same changes plus papilledema (grade 4 retinopathy). CAD is the most common cause of death among treated hypertensive patients.

Ischemic or hemorrhagic stroke is a common consequence of inadequately treated hypertension.

However, effective control of hypertension prevents most complications and prolongs life.

Lifestyle Modifications to Prevent and Manage hypertension