Normal Blood Pressure
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:
- Preload (volume of blood in left ventricle; LV)
- Afterload (resistance LV contracts against)
- 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
Pathogenesis
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
- Atherosclerotic plaque partially blocks blood flow at the renal artery orifice
- Young to middle aged women
- Fibromuscular hyperplasia occurs in multifocal areas of the renal artery
ii. Pathogenesis
- Decreased renal arterial blood flow activates the renin-angiotensin-aldosterone (RAA) system.
- Angiotensin II vasoconstricts TPR arterioles.
- 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
Atherosclerosis
|
| 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
|
Hypertension -Pathophysiology, Causes and Complications – howMed
Normal Blood Pressure
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:
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
ii. Excess sodium produces vasoconstriction of TPR arterioles
Essential hypertension
Accounts for 95% of cases of hypertension
Pathogenesis
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
ii. Pathogenesis
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.
e. Epigastric bruit
f. Angiography
g. Other causes of secondary hypertension
Causes of Secondary Hypertension
Pheochromocytoma: increased catecholamines
Neuroblastoma: increased catecholamines
11-Hydrocylase deficiency: increased mineralocorticoids (i.e. deoxycorticosterone)
Primary aldosteronism (Conn’s syndrome): increased aldosterone
Elderly: systolic hyperlension due to decreased elasticity of lhe aorta
in young women
Cocaine: increased sympathetic activity
cell contraction
Renal parenchymal disease: e,g,, diabetic nephropathy, adull polycystic kidney disease,
glomerulonephritis; retenlion of sodium
Hypothyroidism: diastolic hypertension due to retention of sodium
RAA. renin-angiotensin-aldosterone
Complications of Hypertension
Acute myocardial infarction: most common cause of death
Atherosclerosis
Berry aneurysm: rupiure produces a subarachnoid hemorrhage
Lacunar infarcts: small infarcts 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
(increased vessel permeability, retinal infarction), papilledema