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Hypertension -Pathophysiology, Causes and Complications

Hypertension Classification

Normal Blood Pressure

<120 mm Hg systolic and <80 mm Hg diastolic


120 mm Hg systolic or 80 to 89 mm Hg diastolic

Stage 1 hypertension

140 to 159 mm Hg systolic or 90 to 99 mmHg diastolic

Stage 2 hypertension

> 160 mm Hg systolic or > 100 mm Hg

Pathophysiology of Hypertension

Systolic blood pressure (SBP):

Correlates with stroke volume (SV) and compliance of aorta

i.    Primary determinants of stroke volume:

  1. Preload (volume of blood in left ventricle; LV)
  2. Afterload (resistance LV contracts against)
  3. Contractility of heart

ii.    Vessel elasticity determines complaince of the aorta

iii.    Increased Preload, increased contractility: SBP; increased preload,   decreased contractility, decreased afterload: increased SBP

iv.    Decreased Elasticity decreased of aorta (old age): increased SBP

Diastolic BP (DBP):

Represents volume of blood in the aorta in diastole

i.    Depends on the vascular tone of the peripheral resistance arterioles.

ii.    Vasoconstriction:  increased DBP; vasodilation:  decreased DBP

Vasoconstriction increases TPR

Increases diastolic blood pressure

Role of sodium in hypertension

i.    Excess sodium increases plasma volume

  • Increases stroke volume and systolic blood pressure

ii.    Excess sodium produces vasoconstriction of TPR arterioles

  • Sodium enters arteriole smooth muscle cells and opens calcium channels, causing vasoconstriction.
  • Increases diastolic blood pressure
Essential hypertension

Accounts for 95% of cases of hypertension


i.    Genetic factors reduce renal sodium excretion

ii.    Unknown factors cause vasoconstriction of arterioles

iii.    Obesity, stress

Secondary hypertension

Accounts for 5% of cases of hypertension

Renovascular hypertension

i.    Causes

  1. Atherosclerotic plaque partially blocks blood flow at the renal artery orifice
  2. Young to middle aged women
    • Fibromuscular hyperplasia occurs in multifocal areas of the renal artery

ii.    Pathogenesis

  1. Decreased renal arterial blood flow activates the renin-angiotensin-aldosterone (RAA) system.
  2. Angiotensin II vasoconstricts TPR arterioles.
  3. Aldosterone increases sodium retention

iii.    Clinical findings

a. Severe, uncontrollable hypertension
b. Increased plasma renin activity (PRA)
c. Involved kidney has increased PRA in the renal vein

d. Uninvolved kidney has decreased PRA.

  • Increased plasma volume due to aldosterone excess suppresses RAA system in normal kidney

e. Epigastric bruit

  • Sound is due to turbulence of blood flow through the narrow renal artery

f. Angiography

  • Involved kidney shows diminished size (atrophy) and delayed emptying
  • Renal artery has “ beaded” appearance in fibromuscular hyperplasia

g. Other causes of secondary hypertension

Causes of Secondary Hypertension
System or source Description
Adrenal Cushing syndrome: increased mineralocorticoids

Pheochromocytoma: increased catecholamines

Neuroblastoma: increased catecholamines

11-Hydrocylase deficiency: increased mineralocorticoids (i.e. deoxycorticosterone)

Primary aldosteronism (Conn’s syndrome): increased aldosterone

Aorta Postductal coarctation: activalion of RAA system

Elderly: systolic hyperlension due to decreased elasticity of lhe aorta

CNS Inlracranial hypertension: release of catecholamines
Drugs Oral contraceptive: increased synthesis of angiotensinogen; most common cause of hyperlension

in young women

Cocaine: increased sympathetic activity

Parathyroid Primary hyperparathyroidism: calcium increases peripheral resistance arteriole smooth muscle

cell contraction

Pregnancy Preeclampsia: increased angiotensin II
Renal Renovascular disease: atherosclerosis (elderly men), fibromuscular hyperplasia (women)

Renal parenchymal disease: e,g,, diabetic nephropathy, adull polycystic kidney disease,

glomerulonephritis; retenlion of sodium

Thyroid Craves’ disease: systolic hypertension from increased cardiac conlraction

Hypothyroidism: diastolic hypertension due to retention of sodium

RAA. renin-angiotensin-aldosterone

Complications of Hypertension
System Complications
Cardiovascular Left ventricular hyperlrophy; most common overall complication

Acute myocardial infarction: most common cause of death


Central nervous Intracerebral hematoma: due to rupiure of Charcot-Bouchard aneurysms

Berry aneurysm: rupiure produces a subarachnoid hemorrhage

Lacunar infarcts: small infarcts due to hyaline arteriolosclerosis

Renal Benign nephrosclerosis: kidney disease of hypertension; due to hyaline arteriolosclerosis;

atrophy of tubules and sclerosis of glomeruli; progresses to renal failure

Malignant hypertension: rapid increase in blood pressure accompanied by renal failure and

cerebral edema

Eyes Hypertensive retinopathy: arteriovenous nicking, hemorrhage of retinal vessels, exudates

(increased vessel permeability, retinal infarction), papilledema

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