Transcript 05.Insufficiency of coronary blood circulation. Cardiac insufficiency

Insufficiency of coronary
blood circulation.
Cardiac insufficiency
Ph.D., MD, Assistant Professor
Hanna Saturska
Functions of the circulatory system
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Transport is the
main function of
circulatory system
Stabilization of
arterial pressure
circulatory system
delivers О2 and
nutrients to the tissues
circulatory system
carries waste products
to the kidneys and
other exceatory organs
Heart insufficiency (Heart failure)
Heart failure (HF),
often called congestive
heart failure (CHF)
or congestive cardiac
failure (CCF), occurs
when the heart is
unable to provide
sufficient pump action
to distribute blood
flow to meet the needs
of the body.
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Heart failure is a global term for
the physiological state in which
cardiac output is insufficient in
meeting the needs of the body
and lungs.
Often termed "congestive heart
failure" or CHF, this is most
commonly caused when cardiac
output is low and the body
becomes congested with fluid
due to an inability of heart output
to properly match venous return.
Heart failure
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Heart failure may be caused by
myocardial failure but may also
occur in the presence of nearnormal cardiac function under
conditions of high demand.
myocardial failure
conditions
of high demand
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To maintain the
pumping function of
the heart,
compensatory
mechanisms increase
blood volume, cardiac
filling pressure, heart
rate, and cardiac
muscle mass.
However, despite
these mechanisms,
there is progressive
decline in the ability of
the heart to contract
and relax, resulting in
worsening heart
failure.
Reasons
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Myocardium injury
Myocardium hypoxia or
ischemia
Infectional-toxical
myocardium damage
Metabolism disorder
Nervous-trophical and
hormonal influences on
the organism
Myocardium overload
Increase of heart outflow
resistance (heart aperture
stenosis, arterial
hypertension)
Increase of diastolic inflow
(hypervolemia, heart
aperture insufficiency)
Mixed
Mixed heart insufficiency variant. It arises at
combination of myocardium damage and its
overload, for example at rheumatism, when of
inflammatory myocardium damage and valvular
heart violations are combined.
Acute pulmonary edema.
 Note enlarged heart size, apical
vascular redistribution ( circle ), and
small bilateral pleural effusions
(arrow ).
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This chest radiograph shows an enlarged
cardiac silhouette and edema at the lung
bases, signs of acute heart failure.
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A 28-year-old woman
presented with acute
heart failure
secondary to chronic
hypertension. The
enlarged cardiac
silhouette on this
anteroposterior (AP)
radiograph is caused
by acute heart failure
due to the effects of
chronic high blood
pressure on the left
ventricle. The heart
then becomes
enlarged, and fluid
accumulates in the
lungs (ie, pulmonary
congestion).
Heart failure can be classified
into 4 classes
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Class I patients have no limitation of
physical activity
Class II patients have slight limitation
of physical activity
Class III patients have marked
limitation of physical activity
Class IV patients have symptoms even
at rest and are unable to carry on any
physical activity without discomfort
Heart failure can be divided into 4 stages, as
follows:
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Stage A patients are
at high risk for heart
failure but have no
structural heart
disease or symptoms
of heart failure
Stage B patients have
structural heart
disease but have no
symptoms of heart
failure
Stage C patients have
structural heart
disease and have
symptoms of heart
failure
Stage D patients have
refractory heart
failure requiring
specialized
interventions
STAGES
Compensation
1. Crash phase
(main sense - compensative hyperfunction)
2. Stable adaptation phase
(main sense - compensative hypertrophy)
Decompensation
3.
Exhaustion
Crash phase
(St. of compensation)
Cardial mechanisms
1.
HB increase (in 2,5
time)
2. Systolic volume
increase
3. Heart index increase
4. Heart work increase
Extracardial
mechanisms
1. Increase of O2
utilization by the
tissues
2. Reduce of
peripheral vessels
resistance
Crash phase
(St. of compensation)
Reason
increase of every cardiomyocytes load
Physiological
mechanisms
* adequate excitement
*relation of excitement and contraction
* adequate contraction
*energy provision
Crash phase
Immediate adaptation mechanisms
1. Adequate excitement
Is based on selective penetration of
Na+, K+, Са2+ due to difference between
the extracellular ions concentration and
intracellular one
Result - depolarization
Crash phase
Immediate adaptation mechanisms
2. Relation of excitement and shortening
*diffusion of depolarization wave inside the
cardiomyocytes
* Са2+ penetration in to cytoplasma from SPR
* Са2+connection with troponin and release of
myosin
3. Shortening
*actin and myosin interaction
Crash phase
Immediate adaptation mechanisms
4. Energy provision
*Glycolisis activation
*Mitochondria activation
*CrPh reserve, glycogen reserve(are localized on
SPR membrane)
-most sensitive - depolarization ( Na,K-АТPаse
and Са- АТPаse control of ions transposition
athwart concentration gradient
Excessive Са concentration causes its
accumulation in mitochondrias and block of
АТP synthezise!!!
Crash phase (pathogenesis)
Heart beat increase
Functional changes
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Increased penetration of Na and
Са cytoplasma inside
Decrease of depolarization
interval
Is possible if:
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activity of Na,K-ATPase and Са ATPase is high
CrPh reserve and ATP reserve is
adequate
ATP synthezise in mitochondrias
is adequate
Na,Са-regulative mechanism is
adequate
Crash phase (pathogenesis)
Increase of shortening power
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( heterometric mechanism and homeometric
mechanism)
Activation of adenilatcyclase by catecholamines
cАМP synthesis
Increase of Са concentration in cytoplasma
Increase of free myosin fibers amount (Са
blockades troponin)
Increased amount of myosin-actin interaction
Using of ATP, CrPh, glycogen
Crash phase (pathogenesis)
Limitation mechanisms
1. Accumulation of Na (because is limited Na,К-АТPase
activity)
2. Violation of Na,Са-exchanged mechanism
3. Са accumulation (because limitation of Ca-АТPase
activity)
after-effect: cardiomyocyte relaxation deficit (diasole
deficit)
Са accumulation in mytochondrias
(dissociation of oxidation and phocphorilation)
4. Energy deficit (deficit of АТP 40-60 % causes
shortening depression)
5. Lactic acid accumulation (causes shortening depress ion
because Н+ions interact with troponin)
Crash phase (pathogenesis)
Resume
Limitation mechanisms cause condition when
heart load is more than heart work.
It is the sense of heart insufficiency.
So, compensative hyperfunction as an adaptation
mechanism is depleted
Stable adaptation phase
(stage of compensation)
Gist: compensative hypertrophy
Mechanisms
* RNA synthesis activation in
cardiomyocites
* Increase of ribosome quantity in
cardiomyocites
* Structural proteins synthesis (at first
mitochondrial proteins and SPR
ones)
* activation DNA and RNA synthesis in
connective tissue cells of the heart
(fibroblasts and endotheliocytes)
* Controlled proliferation of the
connective tissue cells (they are the
donors of RNA and structural
proteins)
Result: heart stable adaptation to load
Myocardium hypertrophy
Signs of hypertrophy
Sick person
1. Continuous heart load
2. Heart hypertrophy is
inadequate
to body weight
3. Decrease of capillaries amount
in
weight unit
4. Inadequate activity of MCh
5. Inadequate activity of SPR
6. Decrease of nervous structures
amount in weight unit (decrease
of
NA concentration)
Sportsman
1. There are periods of heart
load and
restoring
2. Heart hypertrophy is
adequate to
body weight
3. Increase of capillaries
amount in
weight unit
4. Adequate activity of MCh
5. Adequate activity of SPR
6. Increase of nervous
structures
amount in weight unit
(adequate
concentration of NA)
Signs of hypertrophy
Sick person
Results
Heart insufficiency is
compensated by the
hypertrophy (bigger heart mass).
But this change limits maximal
heart work.
Sportsman
Results
Heart insufficiency, which is
compensated by the
hypertrophy,
increases of heart muscles
contraction power and speed
one.
Heart work is increased and
human endurances is
increased too
Exhaustion (stage of decompensation)
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Decrease of correlation between square
cardiomyocyte surface and
cardiomyocyte volume (unbalance of
ions pumps)
Decreased Na,K-АТPase activity
(violation of repolarisation ,
appearance of arrhythmias)
Decreased activity of SPR and СаАТPase (heart relaxes slowly, some
time arise diastole defect at Са
accumulation)
Exhaustion (stage of decompensation)
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Decreased MCh activity and
energy deficit because Са is
accumulated in MCh and it
causes dissociation of
oxidation and phosphorilaion
Depression of contractil
function
Exhaustion of connective tissue
cells donors function
Decrease of coronary blood
flow reserve
Decrease of NА concentration
decrease of maximal speed
shortening of the heart and
maximal force one
Exhaustion
(stage
right-sided heart failure
of
decompensation)
left-sided heart failure
Pathological signs
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Violations of blood circulation
Reduce of systole output
(increase of diastole excess
blood volume, myogene dilation)
Decrease of heart output
Decrease of systole arterial
pressure
Increase of diastole arterial
pressure
Increase of veins pressure
(causes the HR increase)
Slowdown of blood flow (main
sign of decompensation)
Erythrocytosis (compensation)
Breathing violations
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Dyspnoea (reflective irritation of breathing center by the СО2)
Attacks of cardiac asthma at night (blood overflow of the
atriums and central veins, which causes barro-receptors
irritation and breathing center reflexes)
Pathological signs
Violation of waterelectrolyte balance
(edema)
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Blood circulation violation
(slowdown blood flow in
capillaries, intravenous
blood pressure increase)
Reflexes of blood
circulation dumping (blood
retention in depot : liver,
veins)
Deficit of blood circulation
in the arteries
Irritation of the vessels
Renin-angionensin-aaldosterone system
Myocardial infarction
Ischemic heart disease
occurs when there is
a partial blockage of
blood flow to the
heart.
When the heart does
not get enough
blood it has to work
harder and it
becomes starved for
oxygen.
If the blood flow is
completely blocked
then a myocardial
infarction (heart
attack) occurs.
Myocardial infarction
Ischaemical necrosis of the
myocardial tissue, which is resulted
from coronary blood supply
insufficiency
Statistics
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Morbidity increases
Patients which suffer from
myocardial infarction are younger
year by year
Mortality of the patients which suffer
from myocardial infarction increases
year by year
(30-40 %)
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Coronary artery disease is currently the
leading cause of death in the United
States. Despite the increasing
sophistication of surgical techniques, the
introduction of new techniques such as
balloon angioplasty, and a number of new
drugs (e.g. beta blockers, calcium
antagonists), it is estimated that over 1
million heart attacks will occur this year,
resulting in 500,000 deaths. In short, we
do not have an adequate therapeutic
solution to the problem of myocardial
infarction (heart attack).
ЕТHІОLOGY
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Atherosclerosis of the
coronary arteries (in 90-95
% died people at section
was found)
Trombosis of the coronary
arteries :
*at the 4 stage of
atherosclerosis
*arterial hypertension
(because it causes blood
coagulation hyperactivity)
Trombembolism (septic
endocarditis, thrombus
lyses)
Spasm of the coronary
arteries
Risk factors
1. Stress
(at trauma,
operation,
cold, negative
emotions)
BECAUSE IT CAUSES:
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Increase of the
heart activity
Stimulation of
the heart
metabolism
Increase of О2
Risk factors
2. Age (most often
appears in 40 – 59
years old person).
3. Hypokinesia
(activation of the
sympathetic-adrenal
system)
4. Obesity
(hypercholesterolem
ia)
Risk factors
5. MAIL SEX
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Morbidity of the men in 2-3 time more
Mortality of the men in 3-4 time more
Men 45-59 years old - mortality 37 %
Woman 45-59 years old – mortality 17 %
Men 60-74 years old - mortality 55 %
Woman 60-75 years old – mortality 78,4 %
Risk factors
6. Heredity
7. Arterial hypertension
8. Diabetes mellitus
9. Infection (chlamydia pneumonia)
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Pathogenesis
1.
Initial
mechanisms
As a result of atherosclerotic
disease of the coronary
arteries
2.
Mechanisms of the
cardiomyocites
necrosis
As a result of cardiomyocytes
ischemia
Initial mechanisms
1.
Increase of the atherosclerotical
plaque size:
Vessel narrowing---ischemia---necrosogenic ATP
deficit
vessels narrowing on 95 % (“critical stenosis”) causes
АТP deficit (less than 40-60 %) which results in
cardiomyocytes necrosis
Initial mechanisms
2. Increase of injured vessel sensitivity to
vasospastic effects
Damage of endothelium ----decrease of NО-synthetase activity---decrease of NО concentration (which is
powerful vasodilator)
Initial mechanisms
3. Thrombosis
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Anticoagulants blood activity decrease
(heparin is used for activation of lipoprotein lipase at
hyperlipoproteinemia)
Decreased antithrombosis properties of the injured
endothelium
Unmasked collagen fibers cause activation of the
Villebrand’s factor
Cardiomyocytes necrosis mechanism
1. ATP deficit
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Decrease of the
cytochromoxydase
activity
Violation of electrons
transfer in MCh
Violation of Krebs-cycle
Accumulation of
acetylcoensime-A, fat
acids
Deficit of ATP and CPh
Cardiomyocytes necrosis mechanism
2. Acidosis
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Accumulation of Crebscycle metabolits
Accumulation of AcetylCo-A
Accumulation of fatty
acids
Accumulation of piruvate
acid
Accumulation of lactic
acid
Cardiomyocytes necrosis mechanism
Acidosis after-effects
**depression of cardiomyocytes
contractility
(main sign of ischemical area)
Mechanisms
1. Н+-ions interact with troponin.
It causes of myosin releasing
impossibility. So, as a result,
interaction of actin and myosin
becomes impossible
2. Са deficit in cytoplasma occurs
because Ca can be accumulated
in Mch
very often it is complicated by the
“reperfusion syndrome”
Cardiomyocytes necrosis mechanism
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3. Са accumulation
Reasons:
1. Deficient of Ca return in
to SPR (ATP deficit
decreases Ca-ATPase
activity)
2. Violation of Na,Саexchange mechanism
Consequences:
Ca deposit in Mch and АТP
deficit
Damage of cardiomyocytes
membranes
Cardiomyocytes necrosis mechanism
4. “Lipid triade”
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1. Phospholipase activation
(is caused by catecholamines
and Ca)
2. Lipids peroxidation
(accumulation of the free
radicals, relative insufficiency
of the antioxidants)
3. Fat acids (damage of the
membrane’s lipids and
violation of the ion channel’s
functions)
necrosis
Hibernal myocardium
Especial condition of the heart which is
characterized by the sharply decreased pump
function of the heart (at human absolute rest)
without cardiomyocytes cytolysis as a result of
blood supply reducing
(protective reaction)
Hibernal myocardium
Sings
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Decreased left ventricle output at increased O2
need of the organism (physical activity, fever,
hyperthyroidism)
Decreased using of ATP
Retardation of the cardiomyocytes necrosis
Renewal of Н+ concentration, creatinphosphate
level, рСО2 (during 1-3 hour)
Hibernal myocardium
Finishing
Spontaneous recurrent process
after blood supply restoring !!!
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1 stage – hypokinetic and asynchronous
cardiomyocytes contruction
2 stage – renewal of synchronous
cardiomyo-cytes contruction and left
ventricle output rising at increased O2
need of the organism (physical activity)
(Panel A): Light micrograph of normal myocardium. (Panel B):
Representative light micrograph of hibernating myocardium. The myolytic
cytoplasm is filled with PAS-positive material typical of glycogen.
Magnification ´320.
Myocardial Infarction Prevention
Strophanthin comes from
an extract of an African
plant called
strophanthus gratus.
Since 1991 it was
discovered as an
endogenous substance
that research shows
can prevent angina
pectoris and myocardial
infarction by 80-100
percent without major
side effects.
strophanthus gratus