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Systemic arterial hypertension
Blood pressure
 BP is defined by physical factors of circulatory system (compliance and elasticity)
 P = Q x R (analogy of Ohm’s law)
P = mean arterial pressure
Q = amount of circulating blood
R = resistance against blood flow in exact part of cardiovascular system
Systolic arterial pressure
Factors affecting its levels:
 Venous return and acquired preload of ventricles
 Contractility of myocardium
 Systolic volume – amount of blood ejected with one ventricular contraction
 Speed/rate of ejection to the large arteries
 Compliance of large arteries of elastic type
 Resistance in the arteries of muscular type
Diastolic arterial pressure
Depends on:
 Systolic pressure
 Peripheral resistance
 Time between two systoles
Arterial HTN
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HTN is BP above 140/90 mm Hg (WHO)
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Pulmonary circulation – upper limits: 30/12 mm Hg
Increase in BP could be the result of:
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Increase in blood volume (Q)
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Increased resistance of vessels (R)
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Combination of both mechanisms (Q + R)
System arterial hypertension
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In 95% of cases cause (or pathogenesis) is unknown
= essential (primary) hypertension
Hypothesis
• Disorders of reabsorption of salt and water in kidneys
• Changes in reactivity of sympathoadrenal system
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In the remaining 5% of cases causes and pathogenesis are know
= secondary hypertension
Primary HTN
Genetic factors + environmental factors + disorders of regulation mechanisms
1. Genetic factors: 30% of those participate in the development of HTN
Familiar predisposition
The responsible gene has not been identified yet
Polygenic and heterogenic inheritance
Changes in polymorphism of gene responsible for angiotenzinogen are often
2. Environmental factors
Increased Na intake: reduction of intake has beneficial effect in HTN management
High caloric intake: HTN is 2-3fold more often in obese patient (increased Na in high food
intake + insulinoresistance)
Increased alcohol intake: ↑ sympathoadrenal activity, ↓ magnesium, etc.
Smoking: mobilization of catecholamines and other vasoconstrictive substances,
activation of atherosclerosis development
Psychological stress
Secondary HTN
Secondary HTN as main result of increased peripheral resistance
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Pheochromocytoma
Renal artery stenosis
Secondary HTN as main result of increased blood volume and its circulation
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Primary hyperaldosteronism (Conn syndrome)
Cushing syndrome (hypercortisolism)
Acromegaly
Hyperthyreosis
Secondary HTN as a result of increased peripheral resistance and blood volume
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End-stage chronic kidney failure
Hypothyreosis
Pressure overload of the heart in HTN (increased
afterload)
Causes:
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Increased peripheral vascular resistance

Narrowing of lumen (acceleration of atherosclerosis)
Pressure overload leads to
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Changes in ejection fraction
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Changes in ejection volume
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With time leads to eventual left-sided heart failure
Volume overload of the heart in HTN (increased
preload)
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Result of hyperkinetic/hyperdynamic circulation
Systolic volume is increased as a result of increased preload
Heart adapts by hypertrophy and dilatation