Transcript 01. Pathophysiology of cardiovasc diseases

Clinical Pathophysiology Of
Cardiovascular Diseases
Ph. D., M D.
Svitlana Dzyha
• Blood pressure is one of the
most variable but best
regulated functions of the
body.
• The purpose of the control of
blood pressure is to keep
blood flow constant to vital
organs such as the heart,
brain, and kidneys.
• The continuous elevation of
blood pressure that occurs
with hypertension is a
contributor to premature death
and disability due to its effect
on the heart, blood vessels,
and kidneys.
• The level of blood
pressure in the healthy
people is the very stable
value.
• The stability of blood
pressure is supported by
regulative systems.
• Hayton (1974) divided
them into two groups –
hemodynamic system
and regulative system.
Arterial blood pressure normal range:
Systolic – 100 - 125 (equilibration 100 - 139) mm Hg
Diastolic – 70 - 80 (equilibration 60 - 89) mm Hg
Regulation of arterial pressure (АP)
by hemodynamic system
Formula: АP = CO · PR
CO – cardiac output
PR – peripheral vascular resistance (depended to arterioles tone)
CO leads to
PR leads to
PR and АP normalizes finally
CO and АP normalizes finally
AP normal range:
Systolic – 100 - 125 (equilibration 100 - 139) mm Hg
Diastolic – 70 - 80 (equilibration 60 - 89) mm Hg
Mechanisms of Blood Pressure
Regulation
• Short-term regulation
• neural mechanisms
• hormonal mechanisms
• Long-term regulation
NEURAL MECHANISMS
Location and innervation of the aortic arch
and carotid sinus baroreceptors and the
carotid body chemoreceptors.
Regulative systems
1. Barroreceptors of aorta
arch and sinus caroticus
Barroreceptors
of the vessels
Afferent impulses
Medulla oblongata
(vessel’s active center)
Heart (CO increase at
decreased АP)
Arterioles (spasm)
Еfferent і impulses
Regulative systems
Role of the vasopressin in arterial
hypertension pathogenesis
Classification
Arterial hypertension
Primary
AP above 139/89 mm Hg
Secondary
AP less than 100/60 mm Hg
Arterial hypotension
Acute
Chronic
Arterial hypertension (АH)
AP elevation
(value above 139/89 mm Hg), which
is resulted from rising of peripheral
vessels resistance
(one of the most common cardiovascular disorders)
Classification
Primary AH
(essential, hypertonic disease)
Secondary AH
(that is happened in 10 - 20 % cases).
It’s a symptom of some disease course
Etiology (primary AH)
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.
Contributing factors
Risk Factors
Family history of hypertension
Race
Age-related increases in blood
pressure
Diabetes mellitus
Contributing factors
Lifestyle Factors
Stress
Excessive calorie
intake and obesity
Excessive alcohol
consumption
High sodium
intake
Physical
inactivity
Oral contraceptive
drugs
Pathogenesis
AP = СO х PR
Increase of circulative blood volume
(CBV)
Emotional excitement
(SNS activation)
Cardiac output (CО) increase
Peripheral vessels resistance
increase
Kidney functions violation
Pathogenesis
Increase of circulative blood volume (CBV)
NaCl (intake more 5 g/day)
Reasons
Decrease Na excretion by kidney
(kidney diseases)
Pathogenesis
1. CBV increase
Na accumulation in
vessels smooth muscle
wall and increase of its
Na retention in blood
osmotic pressure
Blood osmotic pressure
increase
Vessels smooth muscle
sensitivity to
vasoconstrictive
influences increase
(noradrenalin, adrenalin,
endothelin, angiotensin)
Hypervolemia
Vessels wall edema
Vessels
narrowing
Cardiac output increase
Vessels
spasm
AP elevation
Formula: АP = CO · PR
Peripheral vessels
resistance increase
Pathogenesis
2. Cardiac output increase (CO)
Circulative blood volume
increase (CBV)
Reasons
Emotional stress
Physical (overload) stress
Hyperthyroidism
Pathogenesis
2. Cardiac output increase
SAS activation
Adrenalin excretion
Increase of cardiac
contractility force
Increase of heart beats
Increase of cardiac
output
AP elevation
Formula: АP = CO · PR
Pathogenesis
3. SAS activation
SAS activation
Interaction adrenalin and
alpha-adrenoreceptors
Arterioles smooth
muscles spasm
Arterioles narrowing
Suprarenal glands
activation
Venues smooth
muscles spasm
Increase of circulative
blood in big blood
circle
Increase of CBV
PR increase
CO increase
Formula: АP = CO · PR
Noradrenalin
adrenoreceptors of
heart
CO increase
AP increase
Аdrenalin
alpha-adrenoreceptors
of vessels
Arterioles
narrowing
Pathogenesis
4. Kidney functions violation
Long time spasm of
kidney arteries
AP decrease in renal
capillaries
Activation of JGA
Renin excretion
Angiotensin 2
synthesis
AP increase
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)
Depressive function of kidney – synthesis of the
substances for AP reduce
PG Е 2
dilates renal arteries, reduces renin
synthesis and reduces Na
reabsorbing in kidney
Phospholipid Renin
Inhibitor
Angiotensinase
Phosphatydilcholin
alkali ethers
! ! !
Exhaustion of kidney
depressive function
leads to arterial
hypertension
stabilization
Increase of vesseles resistance
• It is the defining mechanism.
Irrespective of first reason, in
the patients with hypertonic
disease almost always
increases peripheral
resistance.
• It is considered, that the
essence hypertonic disease
just is in increase of
peripheral vessels tonus.
Hyperkinetic phase, which is
connected to increase of
cardiac output, happens only
at early stages of disease and
not in all patients.
The hereditary predisposition
Etiology
secondary АH
1. Renal
(resulted from kidney pathology)
Pyelonephritis
Glomerulonephritis
Kidney damage at
collagenosis
Acute renal failure
Acute urinary tract
obstruction
Kidney amiloidosis
Kidney tumor
Diabetic nephropathy
Nephropathy of the pregnant
Hereditary defect of renal
vessels
Polycystic kidney disease
Renal vessels atherosclerosis,
embolism or thrombosis
Etiology
secondary АH
4. Endocrinopathy
(develops in the result of endocrine glands pathology)
Acromegaly
(Somatotropin over production by
the pituitary gland anterior
part)
Cushing's disease
(Adrenocorticotropin over
production by the pituitary gland
anterior part)
Pheochromocytoma
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
Etiology
secondary АH
5. Neurogene
(is accompanying to nerves system pathology)
Encephalitis
Brain tumor
Brain trauma
Brain ischemia
Brain hemorrhage
Etiology
secondary АH
6. Cardiac
Heart defect
Heart failure
7. Drug-induced
Drugs, which cause vessels spasm (influent
on kidney), hormonal contraceptives
Arterial hypertension after-effects
1st period
functional violations
(heart hypertrophy)
2d period
Pathological 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
CNS
Kidney
(nephrosclerosis and chronic
kidney insufficiency)
– brain hypoxia
– neurons destruction
– apoplexy (because vessels destruction and rupture
leads to brain hemorrhages and brain
destruction)
-
Heart
Decompensate heart failure
Organs of vision
retinopathy (retina’s vessels injury)
hemorrhages and separation (exfoliation) of
retina, that leads to blindness
Endocrine system
Glands atrophy and sclerosis