This document discusses the pathophysiology of cardiovascular system arterial hypertension. It begins by outlining the relevance and prevalence of hypertension as a major health problem. It then describes the main mechanisms that regulate arterial pressure in the immediate, middle, and late term, including baroreceptor and chemoreceptor responses, the renin-angiotensin system, vasopressin secretion, and renal control of fluid volume. Secondary forms of hypertension are discussed which are caused by renal, endocrine, or neurogenic factors. Primary or essential hypertension is described as being caused by genetic and environmental risk factors that disrupt the balance of pressor and depressor influences on the cardiovascular system. Several theories of its pathogenesis are mentioned involving the brain, kid

1. PATHOPHYSIOLOGY OF
CARDIOVASCULAR SYSTEM
ARTERIAL
HYPERTENSION
Associate Professor of Pathophysiology Department
Arsenteva Ekaterina Vladimirovna
Ev.arsenteva@ yandex.ru
1

2. Relevance
 The central problem of modern medicine
 Currently it is the greatest noninfectious
human pandemic
 In economically developed countries it
founds 20-40% of the population
 Persons older than 65 years have the AH
more than 50%
 "Rejuvenation" of the average age of
death
 The mortality rate increased by 1.7 times
in the last year
2

3. The main mechanisms of a regulation of
the arterial pressure (immediate)
The first three from in which the CNS is involved (baroreceptor trigger zone ,
chemoreceptor trigger zone and ischemic reaction of a CNS) join in the first
seconds from the moment of change of the arterial tension — a system of
quick response
1) baroreceptor trigger zone. Decrease AP → depression of
exaltation of the baroreceptors localized in carotid sinus and an
aortic arch → the signals are passed to the spinal bulb vasomotor
center → augmentation of heart work (i.e. to rising of a stroke
output), vasoconstrictions (i.e. to depression of peripheric
resistance) and to return of the arterial tension to normal values.
The functioning of this mechanism is defined by genetic factors.
2) chemoreceptor trigger zone . Decrease AP → hypoxemia,
hypercapnia, acidosis → excitation of the chemoreceptors of
the same zone → same reflectors reaction.
3) ischemic reaction of a CNS. With a significant drop in
blood pressure (40 mm Hg) developed dangerous brain
ischemia. Activation of the vasomotor center, ↑ sympathetic
division of the ANS, vasoconstriction and blood pressure rise.
3

4. The main mechanisms of a regulation of
the arterial pressure (middle-term)
 Autoregulation Mechanism: extension resistive
vessels leads to their constriction and rise in blood
pressure
 Activation of the renin-angiotensin system
 Increased secretion of ADH = vasopressin
hypothalamus (↑ PR and BCV).
 The mechanism of movement of the fluid in the
capillaries: the fall in blood pressure due to
blood loss interstitial fluid enters the blood
vessels (the first 5 minutes can move 10-15% of
normal BCV → ↑ blood pressure).
4

5. Late and long-acting
mechanisms
 Renal system of control over the volume of the
liquid. Even a small increase in blood pressure
is accompanied by a significant ↑ excretion of
fluid by kidneys. Different individuals, this
ability may differ.
 Aldosterone system.The drop in blood
pressure, bcc → activation of the renin-
angiotensin system → angiotensin II-induced
hypersecretion of aldosterone → ↑ tubular
reabsorption of Na (and using ADH-water) →
↑BCV → ↑ MCV, PR
 System vasopressin (ADH). Falling blood
pressure → → ↑ production of ADH → ↑ fluid
reabsorption in the kidneys → ↑ BCV, MCV and
BP
5

6. Depressor mechanisms
 I. Immidiate reflex mechanisms. When ↑ blood pressure
→ activation of the aortic arch and carotid sinus
baroreceptors, appropriate nerve-depressants inhibited
sympathetic, parasympathetic division is activated (↓ HR)
and blood pressure ↓;
 II. Middle-term mechanisms Increased blood pressure →
↑ myocardial wall tension and intracavitary pressure → ↑
secretion of ANP → excretion of sodium and water by the
kidneys → ↓ BCV , MCV, PR and blood pressure;
 III. Long-acting mechanisms. Renal regulation,
depressor humoral substances: NO, kinins, prostacyclin,
prostaglandin E, ANP, locally-metabolites (CO2, lactate),
inflammatory mediators (histamine, bradykinin,
substance P), acetylcholine.
6

7. Arterial hypertension
* permanent increase in arterial pressure
 systolic pressure is more than 140 mm hg.
 diastolic pressure is more than 90 mm hg.
7

8. Arterial hypertension
Mechanisms
VIOLATION dynamic equilibrium between
the pressor and depressor influence on
the cardiovascular system and blood
volume
The increase of pressor effects and / or
Decrease depressor effects
8

9. Secondary
(symptomatic
)
Arterial hypertension
Etiological
classification
Primary
(an essential
hypertensia)
9

10. SECONDARY (SYMPTOMATIC)
HYPERTENSION
 Renal hypertensias
Nephrogenic (connected to a disease of kidneys)
Renovascular (connected to a disease of renal
vessels )
 Endocrine hypertensias
 Neurogenic hypertensias
 The other hypertensias (caused by a
coarctation of an aorta and other anomalies of
vessels, augmentation of a blood circulation
volume during extra transfusion, a polycythemia,
etc). 10

11. Increase: * general peripheral vascular resistanse
* blood volume
* cardiac output
VASORENAL Arterial hypertension
Angiotensin II
The stimulation
of aldosterone
production
in the adrenal
glands
Increased
contractility
heart function
Contraction
myocyte
arterioles,
It’s
remodeling
Hypersensitivity
of the artery
walls to
vasoconstrictor
s
Realization of renal and
extrarenal effects of
aldosterone
ARTERIAL HYPERTENSION
SECONDARY (SYMPTOMATIC) HYPERTENSION
Activation of the
release:
a) atecholamines
from postganglionic
nerve fibers
b) the endothelin
11

12. deficiency of kinins
Deficiency of
prostaglandin -
vasodilators
NEPHROGENIC HYPERTENSIAS
weight reduction of
renal parenchyma
Reduced blood flow
In the kidney
Increased
reabsorption of Na +
Activation of
RAAS
hypernatremia
hypervolemia
SECONDARY (SYMPTOMATIC) HYPERTENSION
Increase: * general peripheral vascular resistanse
* blood volume
* cardiac output
ARTERIAL HYPERTENSION 12

13. ENDOCRINE HYPERTENSIAS
Hormones hyperproduction with
hypertensive action:
•catecholamines
•vasopressin
•ACTH
•mineralocorticoid
•endothelin
•thyroid hormones
Increased heart
sensitivity to hormones
with hypertensive effect
SECONDARY (SYMPTOMATIC) HYPERTENSION
Increase: * general peripheral vascular resistanse
* blood volume
* cardiac output
ARTERIAL HYPERTENSION 13

14. ALDOSTERONISM (ENDOCRINE)
Transport excess Na + into the cells
Stimulation of the reabsorption of
Na +
Renal effects
Activation of synthesis
and incretion of ADH
Extrarenal effects
hyperosmia of blood Hypersensitivity
of the artery
walls to
vasoconstrictor
s
Increased
myocyte
tone of
vessels and
heart
The swelling of
cells (endothelial
and muscle cells
of the vascular
wall)
hypervolemia
Reabsorption of excess fluid
Increase:
* general peripheral vascular
resistanse
* blood volume
* cardiac output
ARTERIAL HYPERTENSION
SECONDARY (SYMPTOMATIC) HYPERTENSION
14

15. Neurogenic:
Activation sympathetic
nervous system
Humoral
NEUROSIS
HYPERTENSIVE STRENGTHENING EFFECTS
Activation of neurons:
•sympathetic posterior hypothalamus
nuclei
•adrenergic structures
•reticular formation
•vasomotor center
Chronic
Stress
SECONDARY (SYMPTOMATIC) HYPERTENSION
NEUROGENIC HYPERTENSIAS
ORGANIC BRAIN DAMAGE
STRUCTURES, regulates the
level of blood pressure
Activation of hormone synthesis with
hypertensive action
Increase: * general peripheral vascular
resistanse
* blood volume
* cardiac output
ARTERIAL HYPERTENSION 15

16. An idiopathic hypertensia (primary or
essential hypertensia) this is a chronic
disease which main clinical implication is
long and resistant increase of an arterial
pressure (hypertensia).
Essential hypertensia
16

17. ETIOLOGY
RISK FACTORS
Hereditary
predisposition
Individual
characteristic
s
Environmental
factors
17

18. ETIOLOGY of EH
HERIDITARY FACTORS
dysfunction
of receptors
Accumulation of
excess Ca2 +, Na
+ ions in
myocytes
Decrease synthesis
of vasodilators
Dominance
effects
hypertensive
agents
system
membranopatiya
Violation of gene
expression of
endothelial cells
18

19. consumptio
n of salt in
great
numbers
ETIOLOGY of EH
Environmental factors
hypodynami
a
a
smoking
intoxicatio
n
Psycho-
emotional
stresses
19

20. obesity
ETIOLOGY of EH
Individual characteristics
cholesterin
level in blood
tolerance
to glucose
and renin
activity
sex
age
20

21. 21

22. Arterial hypertension
Mechanisms
VIOLATION dynamic equilibrium between
the pressor and depressor influence on
the cardiovascular system and blood
volume
The increase of pressor effects and / or
Decrease depressor effects
22

23. Pathogenesis theories of an
essential hypertensia
 Cerebro-ischemic Dickinson’s theory
 Neurogenic theory (G. F. Lang and A. L.
Myasnikov's)
 Theory of A.Guyton (kidney mechanism)
 Membranous theory
23

24. Neurogenic mechanism
Psychological trauma (chronic stress)
Stagnant foci overstimulation in the cerebral cortex
Violation of the brake control function of the cortex of
the subcortical structures
Stagnant focus of excitation in the subcortex
Hyperactivation of sympathoadrenal system
24

25. Increased vascular tone caused by stimulation of alpha 1-adrenergic receptors of smooth
muscle cells by hyperactivation of SAS.
spike
AT II
Adrenalin
histamine
Must cell
Serotonin
Adrenergic
nerve
Smooth
muscle cells
contraction
Cholinergic
nerve
25

26. Kidney mechanism
Hypoxia kidneys,
Excitation SNS
Renin (JGA) АТ I
ACE
АТ II (vessels spasm)
Aldosteron
(reabsorbtion Nа)
BCV
endotelium swealling
sensitivity to
vasoconstrictors
26

27. The role of angiotensin-converting enzyme (ACE) in improving vascular tone and
vascular remodeling in hypertension
angiotensinoge
n
renin
aldosteron
kallikrein
kininogen
Inactivation of
bradikinin
brad
ikini
n
ACE
Contraction of
smooth muscle
Proliferation
,
hypertrophy
Retention
sodium and
water
27

28. Membranous theory
28

29. ARTERIAL HYPERTENSION
Chronic stress
Central disturbance of BP
regulation
Increase activity SAS
Hypersecretion
cathecholamines
Generalized defect of
Ca2+-Na+ transport
Increase Ca2+ content
in cells of vessel wall
vasoconstrictio
n
Defect of sodium
excretion in kidneys
Excess of
consumption of NaCl
Retention sodium and
water
BCV
Cardiac output PVR
29

30. Arterial hypertension
30

31. At arterial hypertension in fine arteries and arterioles of muscular type there
are structural changes, including a hyperplasia and a hypertrophy of cell
smooth muscular, a hyalinosis (sclerosis). It leads to a thickening of a wall
and a diminutions that enlarges peripheral vessel resistance.
31

32. Pathological anatomy
left ventricular
hypertrophy
hyalinosis of
glomeruli
fibrinoid
necrosis of
arterioles
hemorrhagic
stroke
32

33. Stages of AH
The I stage - there is no objective evidence of target
organ damage. ↑ blood pressure does not reach
high numbers, detected by chance.
The II stage - one or more signs of target organ
lesions: left ventricular hypertrophy, narrowing of
the retinal vessels, albuminuria, atherosclerotic
vascular disease.
The III stage - detailed clinical picture of target organ
damage (heart, brain, kidneys, blood vessels,
retina).
33

34. It is characterized by episodes of temporary increase
in arterial pressure (a transitional hypertensia).
-hypertrophy of a muscular layer and elastic structures of arterioles and
their fine branches,
-morphological features of a spastic narrowing of arterioles or their
more profound changes in cases of hypertensive crisis.
-The moderate compensatory hypertrophy of a left ventricle of heart
becomes perceptible.
PRECLINICAL STAGE. I stage
34

35. It characterizes the period of permanent increase in arterial
pressure.
Vicious circles in hypertension:
1. Renin: an increase in blood pressure (arterial spasm) leads to renal ischemia
and activation of the RAAS.
2. Cardiac: hypervolemia (caused by aldosterone and ADH), according to
Anrep's law, causes an increase in heart volume (force of heart contractions is
proportional to pressure) and an increase in blood pressure.
3. Receptor (atherosclerosis reduces the sensitivity of the depressor zones).
4. Vascular: chronic spasm of vascular smooth muscle leads to the
accumulation of Ca + 2 in the cytoplasm of muscle fibers and their hypertrophy
and hyperplasia develop. This leads to an increase in peripheral vascular
resistance.
II STAGE
35

36. In arterioles, arteries of elastic, muscular and elastic
and muscular types, and also in heart there are
characteristic changes.
Changes of arteries of elastic, muscular and elastic and muscular types
are presented elastofibrosis and an atherosclerosis
Elastofibrosis is characterized by a hyperplasia and splitting of an
internal elastic membrane and a sclerosis.
Atherosclerosis is a characteristic for an idiopathic hypertensia, differs
in an originality: atherosclerotic changes have more widespread
character, taking arteries of muscular type that doesn't happen in the
absence of arterial hypertension; fibrous plaques have circular, but not
segmentary character that leads to sharper diminuation of a vessel.
Elastofibrosis and the stenosing atherosclerosis are usually expressed in
arteries of heart, cerebrum, kidneys, pancreas, in somnolent and
vertebral arteries.
II STAGE OF WIDESPREAD CHANGES OF ARTERIES
36

37. Radiologically signs of left ventricular hypertrophy, hypertrophy with its dilation,
aortic atherosclerotic lesions, signs of venous congestion in the lungs identify (Fig.
а, б, в).
In this stage degree of a hypertrophy of a
myocardium accrues, the mass of heart can reach
900 — 1000 g, and thickness of a wall of a left
ventricle - 2 — 3 cm).
There is a relative failure of blood supply of a
myocardium which is aggravated with organic
vascular changes. That leads to development of
dystrophic changes of cardiomyocytes and
myogenic dilation of cavities of heart (an eccentric
hypertrophy of a myocardium), to development of
a diffuse local cardiosclerosis and emergence of
signs of a heart decompensation.
cor bovinum
37

38. Severe hypertrophy of the left ventricle of the heart.
Increasing the R-wave in outlets V5 - V6 and S wave in outlets V1, V2,
R in V4 <R V6, S in VI + R in V5> 35 mm.
The shift of the transition zone to the right to V3.
Shifting the heart's electrical axis to the left, with RI> 12 mm.
Spesific depression segment S-T, and T wave inversion in I, aVL, V5, V6. 38

39. Hemorrhagic cerebral
stroke.
On transaxial tomograms
of the brain revealed a
hematoma (a),
communicating with the
forefoot of the right lateral
ventricle (b).
Ischemic cerebral stroke.
THE STAGE OF CHANGES OF ORGANS
The hyalinosis and a
fibrinoid necrosis with
microaneurysms are often
found in vessels of a
cerebrum, leading to
intracerebral bleedings.
39

40. The changes of kidneys at essential
hypertensia are caused by a hyalinosis of
arteriolas (arteriolosclerosis) which is
followed by collapse of capillaires and a
sclerosis of a glomerules
(glomerulosclerosis), an atrophy of a
canaliculus, a compensatory hypertrophy
of the remained nephrons which gives to
the surface of kidneys a granular look.
The kidneys at the same time diminish in
size, become dense, cortical substance
becomes thinner. Such kidneys are in state
of nephrosclerosis. An arteriolar
nephrosclerosis can lead to development
of a chronic renal failure.
40

41. Hypertensive neuroretinopatia
Patient I., 45 years old. The picture shows the fundus artery unevenly
narrowed, their walls are sometimes sealed, sclerotic, a symptom of "copper
wire". Vienna expanded, crimped, a symptom of pathological arteriovenous
Cross (Salus I, II, III). optic disc waxy, its fuzzy boundaries. In the retina,
mainly around the optic nerve, multiple bleeding (hemorrhage in the layer of
nerve fibers) and white "cotton-like" foci (areas of retinal ischemia).
41

42. Consequences of AH
42

43. Outcome of the hypertension
Apoplexy
Heart
failure
Pulmonary
edema
Myocardial
infarction
Encephalopathy
43

44. Thank you for your
attention!
To your success!
Send me your question
EV.Arsenteva@yandex.ru
44