Hypertension Pathophysiology

Consistent BP readings >140 mmHg systolic or 90 mmHg diastolic OR taking antihypertensive medications to control BP

Chronic condition: medications are a "treatment" not a "cure".
Major risk factor for the development of cardiovascular and cerebrovascular disease.

Cardiac Output - ejection of blood from the heart during systole. Determined by the blood volume and the ability of the ventricles to fill and effectively pump that blood.

Increased CO or increased PVR cause the BP to rise.

• SNS stimulation. Baroreceptors signal SNS when the MAP changes. Drop in MAP stimulates SNS, increasing HR, CO and constricting arterioles. As a result, BP rises. A rise in MAP has the opposite effect. 
• Circulating epinephrine and norepinephrine have the same effect as SNS stimulation.
• Atrial Natriuretic Peptide (ANP) is released from atrial cells in response to stretching by excess blood volume. It promotes vasodilation and sodium and water excretion, lowering BP.
• RAAS responds to renal perfusion. Angiotensin II is a potent vasoconstrictor. It stimulates adrenal medulla to release Aldosterone, both SVR and CO increase raising BP.
• Adrenomedullin, potent vasodilator.
• Vasopressin or ADH, promotes water retention and vasoconstriction, raising BP.
• Local factors such as inflammatory mediators and various metabolites can promote vasodilation, affecting BP.
• Excess insulin has several effects that potentiall contribute to HTN: 
• sodium retention by the kidneys
• increased SNS activity
• hypertrophy of vascular smooth muscle
• changes in ion transport across cell membranes

Classification	Systolic BP	Diastolic BP
Optimal	<120 mmHg	<80 mmHg
Pre-hypertensive	120-139 mmHg	80-89 mmHg
Stage I HTN	140-159 mmHg	90-99 mmHg
Stage II HTN	≥ 160 mmHg	≥  100 mmHg

Diagnosis:

Systolic blood pressure of 140 mmHg or higher, or diastolic pressure of 90 mmHg or higher, based on the average of three or more readings taken on separate occasions.