Date post: | 26-Dec-2015 |
Category: |
Documents |
Upload: | caitlin-fleming |
View: | 225 times |
Download: | 0 times |
Regulation of arterial pressure (АP)
Formula: АP = CO · PRCO – cardiac output
PR – peripheral resistance (depended to arterioles tone)
CO leads to PR and АP normalizes finally
PR leads to CO and АP normalizes finally
AP normal range:
Systolic – 100 - 125 (equilibration 100 - 139) mm Hg
Diastolic – 70 - 80 (equilibration 60 - 89) mm Hg
Regulative systems
1. Barroreceptors of aorta arch and sinus caroticus
Barroreceptors of the vessels
Medulla oblongata (vessel’s active center)
Afferent impulses
Heart (CO increase at decreased АP)
Arterioles (spasm) Еfferent і impulses
Regulative systems
2. Renin–angiotensin system
АPActivation of kidney
JGA (juxta glomerular apparatus)
Excretion of the RENIN
(it is enzyme)
Conversation
angiotensin 1 into angiotensin 2
Conversation angiotensinogen into angiotensin 1
Angiotensin converting enzyme (АCE)
Regulative systems
3. Renin–angiotensin-aldosteron system
Renin Actination of suprarenal glangs
(cortical layer)
Na reabsorbtion
in kidney increase
Angiotensin 2
Aldosteron excretion
Na concentration in blood increase,
blood osmotic pressure increase
Move of extravascular fluid inside the
vessels
Increase of circulative blood volume
(CBV)
CО increase
Classification
Arterial hypotension
Arterial hypertension
AcuteChronic
Secondary
AP above 139/89 mm Hg
Primary
AP less than 100/60 mm Hg
AP elevation (value above 139/89 mm Hg), which is resulted from rising
of peripheral vessels resistance
(one of the most common cardiovascular disorders)
Arterial hypertension (АH)Arterial hypertension (АH)
Classification
Primary AH (essential, hypertonic disease)
Secondary AH (that is happened in 5 - 10 % cases).
It’s a symptom of some disease course
Reason is unknown.AH is polyetiological disease.
AH arises on the ground of genetically peculiarities of metabolism.
That is possible to have genetically defect of the systems, which control relaxation of the smooth
muscle cells of the arterioles.
Etiology (primary AH) Etiology (primary AH)
Contributing factorsFamily history
Age-related changes in blood pressureHigh salt intake
Stress
Hyperinsulinemia:
causes high activity sympathetic link of ANS and its effect on cardiac output, peripheral vascular resistance and renal sodium retention;
stimulates sodium and calcium transport across the cell membrane of vascular smooth muscle, thereby sensitizing blood vessels to vasopressor stimuli
Obesity (because hyperinsulinemia)Excess alcohol consumption
(mechanism in unclear)
Race
(for example: AH isn’t only more prevalent in African Americans than whites, it is also more severe).
Possible explanation: due to evolutionary adaptation to the severe environment (western Africa and Western hemisphere) in condition of salt and water deprivation survival is possible due to retention of sodium and water in organism. That leads to conserve sodium.
There is little information about other racial groups
1. Renal (resulted from kidney pathology)
Etiologysecondary АHEtiologysecondary АH
GlomerulonephritisGlomerulonephritis
Kidney damage at collagenosis
Kidney damage at collagenosis
Kidney amiloidosisKidney amiloidosis
Glomerulosclerosis because diabetes mellitus
Glomerulosclerosis because diabetes mellitus
Nephropathy of the pregnant
Nephropathy of the pregnant
Hereditary defect of renal vessels
Hereditary defect of renal vessels
Renal vessels atherosclerosis, embolism or thrombosis
Renal vessels atherosclerosis, embolism or thrombosis
Kidney tumorKidney tumor
Uri stone diseaseUri stone disease
3. Angiogene(is caused by vessels pathology)
2. Renoprive (arises after kidney remove)
Etiologysecondary АHEtiologysecondary АH
Aorta damageAorta damage Arteries carotids damage
Arteries carotids damage
4. Endocrinopathy (develops in the result of endocrine glands pathology)
Etiologysecondary АHEtiologysecondary АH
Cushing's disease (Adrenocorticotropin over production by
the pituitary gland anterior part)
Cushing's disease (Adrenocorticotropin over production by
the pituitary gland anterior part)
Acromegaly (Somatotropin over production by
the pituitary gland anterior part)
Acromegaly (Somatotropin over production by
the pituitary gland anterior part)
Hyperaldosteronism (aldosteron over excretion by suprarenal
glands)
Hyperaldosteronism (aldosteron over excretion by suprarenal
glands)
Menopause(age-depended decrease of female
gonads activity – estrogens excretion decrease)
Possible mechanism – deficit of NO synthesis by endotheliocytes
Menopause(age-depended decrease of female
gonads activity – estrogens excretion decrease)
Possible mechanism – deficit of NO synthesis by endotheliocytes
5. Neurogene (is accompanying to nerves system pathology)
Etiologysecondary АHEtiologysecondary АH
Brain hemorrhageBrain hemorrhage
EncephalitisEncephalitis
Brain tumorBrain tumor
Brain traumaBrain trauma
Brain ischemiaBrain ischemia
7. Drug-induced
6. Cardiac
Etiologysecondary АHEtiologysecondary АH
Heart failureHeart failureHeart defectHeart defect
Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives
Drugs, which cause vessels spasm (influent on kidney), hormonal contraceptives
Emotional excitement (SNS activation)
Emotional excitement (SNS activation)
Increase of circulative blood volume (CBV)Increase of circulative blood volume (CBV)
Cardiac output (CО) increaseCardiac output (CО) increase
Kidney functions violationKidney functions violation
Peripheral vessels resistance increasePeripheral vessels resistance increase
Pathogenesis
Increase of circulative blood volume (CBV)Increase of circulative blood volume (CBV)
Pathogenesis
Reasons
NaCl (intake more 5 g/day) NaCl (intake more 5 g/day)
Decrease Na excretion by kidney
(kidney diseases)Decrease Na excretion by kidney
(kidney diseases)
1. CBV increase1. CBV increase
Na retention in bloodNa retention in blood
Blood osmotic pressure increase
Blood osmotic pressure increase
HypervolemiaHypervolemia
Cardiac output increaseCardiac output increase
AP elevationAP elevation
Na accumulation in vessels smooth muscle wall and increase of its
osmotic pressure
Na accumulation in vessels smooth muscle wall and increase of its
osmotic pressure
Vessels wall edemaVessels wall edema
Vessels narrowingVessels narrowing
Peripheral vessels resistance increasePeripheral vessels
resistance increase
Vessels smooth muscle sensitivity to
vasoconstrictive influences increase
(noradrenalin, adrenalin, endothelin, angiotensin)
Vessels smooth muscle sensitivity to
vasoconstrictive influences increase
(noradrenalin, adrenalin, endothelin, angiotensin)
Formula: АP = CO · PRFormula: АP = CO · PR
Pathogenesis
Vessels spasm
Vessels spasm
2. Cardiac output increase (CO)2. Cardiac output increase (CO)
Reasons
Circulative blood volume increase (CBV)
Circulative blood volume increase (CBV)
physical (overload) stress
physical (overload) stress
Emotional stress Emotional stress
HyperthyreosisHyperthyreosis
Pathogenesis
2. Cardiac output increase2. Cardiac output increase
SAS activationSAS activation
Adrenalin excretionAdrenalin excretion
Increase of cardiac contractility force
Increase of cardiac contractility force
Increase of cardiac output
Increase of cardiac output
Increase of heart beats Increase of heart beats
AP elevationAP elevation
Pathogenesis
Formula: АP = CO · PRFormula: АP = CO · PR
3. SAS activation3. SAS activation
Interaction adrenalin and alpha-adrenoreceptors
Interaction adrenalin and alpha-adrenoreceptors
Arterioles smooth muscles spasm
Arterioles smooth muscles spasm
Suprarenal glands activation
Suprarenal glands activation
Venues smooth muscles spasm
Venues smooth muscles spasm
Increase of circulative blood in big blood
circle
Increase of circulative blood in big blood
circle adrenoreceptors of
heartadrenoreceptors of
heart
АdrenalinАdrenalinNoradrenalinNoradrenalin
Increase of CBVIncrease of CBV
CO increaseCO increase
Arterioles narrowing
Arterioles narrowing
alpha-adrenoreceptors of vessels
alpha-adrenoreceptors of vessels
CO increaseCO increase
AP increaseAP increase
SAS activationSAS activation
Arterioles narrowing Arterioles narrowing
PR increasePR increase
Pathogenesis
Formula: АP = CO · PRFormula: АP = CO · PR
4. Kidney functions violation4. Kidney functions violation
Long time spasm of kidney’s arteries
Long time spasm of kidney’s arteries
AP increaseAP increase
AP decrease in renal capillaries
AP decrease in renal capillaries
Activation of JGAActivation of JGA
Renin excretionRenin excretion
Angiotensin 2 synthesis
Angiotensin 2 synthesis
Angiotensin 2 effects
• Smooth muscles contraction in the vessels
• Stimulation of the vasoactive center in brain
• Noradrenalin excretion increase• Adrenalin excretion increase from
suprarenal glands• Aldosteron excretion increase from
suprarenal glands (Na retention due to kidney)
Angiotensin 2 effects
• Smooth muscles contraction in the vessels
• Stimulation of the vasoactive center in brain
• Noradrenalin excretion increase• Adrenalin excretion increase from
suprarenal glands• Aldosteron excretion increase from
suprarenal glands (Na retention due to kidney)
Pathogenesis
Depressive function of kidney – synthesis of the substances for AP reduce
Depressive function of kidney – synthesis of the substances for AP reduce
PG Е 2PG Е 2
Phospholipid Renin Inhibitor
Phospholipid Renin Inhibitor
AngiotensinaseAngiotensinase
Phosphatydilcholin alkali ethers
Phosphatydilcholin alkali ethers
! ! !
Exhaustion of kidney depressive function
leads to arterial hypertension stabilization
dilates renal arteries, reduces renin synthesis and reduces Na
reabsorbing in kidney
dilates renal arteries, reduces renin synthesis and reduces Na
reabsorbing in kidney
1st period
functional violations
(heart hypertrophy)
2d periodPathological changes in arteries and arterioles (dystrophy):- Arterioles sclerosis
- Arteriole’s wall infiltration by plasma (leads to dystrophy)
- Arterioles necrosis (hypertonic crisis arises in clinic)
- Vein’s wall thickening
Arterial hypertension after-effects
3d period
Secondary changes in organs and systems
Kidney
(nephrosclerosis and chronic kidney insufficiency)
Kidney
(nephrosclerosis and chronic kidney insufficiency)
CNS
– brain hypoxia
– neurons destruction
– apoplexy (because vessels destruction and rupture leads to brain hemorrhages and brain destruction)
CNS
– brain hypoxia
– neurons destruction
– apoplexy (because vessels destruction and rupture leads to brain hemorrhages and brain destruction)
Heart
Decompensate heart failureHeart
Decompensate heart failure
Organs of vision- retinopathy (retina’s vessels injury)- hemorrhages and separation (exfoliation) of
retina, that leads to blindness
Organs of vision- retinopathy (retina’s vessels injury)- hemorrhages and separation (exfoliation) of
retina, that leads to blindness
Endocrine system
Glands atrophy and sclerosisEndocrine system
Glands atrophy and sclerosis
Arterial hypertension after-effects