Normal BP - 120/80 mmHg
Types
Pre-hypertension : 140/90 mmHg
Hypertension I : 160/100 mmHg
Hypertension II : more than 160/100 mmHg
Etiology
Primary Hypertension : Cause is unknown
Secondary Hypertension : BP is elevated due to some other
condition. Exact cause is known.
The causes of secondary hypertension: Congenital narrowing
of aorta, Renal disease, Cushing's syndrome, Sleep apnea, Cirrhosis of
liver
Other factors : Alcohol, Smoking, Stress, Family history and
Obesity.
Pathophysiology
Activities of Sympathetic Nervous System
When BP is decreased
SNS is activated. It increases the heart rate and cardiac output thus pressure
on the peripheral arteries is increased.
Activities of Vascular Endothelium
Single cell layer lining the blood vessels,
produce vasoactive substances like
nitric acid, endothelin. These substances
are potent vasoconstrictors and causes increase in blood pressure level.
Activities of RAAS (Renin - Angiotensin - Aldosterone)
On low blood volume / pressure, RAAS system gets activated.
Angiotensinogen is converted to angiotensin I by renin. Then, A I is
converted to active Angiotensin II by Angiotension converting enzyme. A-II
act on AT1 receptors, aldosterone is released. Sodium and water retention
takes place leading to increased blood volume and blood pressure.
Clinical Features
Severe head ache, Blurred vision, Dizziness, Nausea and Vomitting, Fatigue,
Irregular heart beat, Chest pain
Management
Lifestyle modifications
Reduce alcohol and smoking
Excercise
Stree management
Dietary sodium retention
Medications
Many anti-hypertensive drugs are used,
Diuretics : Inhibits sodium reabsorption. Eg:
Furosemide
ACE Inhibitors : Inhibits the
coversion of A-I to A-II. Eg: Captopril
Beta blockers : Eg: Propanolol
Vasodilators: Eg: Nitroglycerin
Calcium channel blocker (CCB) :
Inhibits movements of extracellular calcium into the cells and causing
vasodilation and decreased heart rate.
