heart failure. myocardial infarction
DESCRIPTION
Heart failure. Myocardial Infarction. Ph.D. , MD , Assistant Professor Ha nna Saturska. Functions of the circulatory system. Transport is the main function of circulatory system Stabilization of arterial pressure circulatory system delivers О 2 and nutrients to the tissues - PowerPoint PPT PresentationTRANSCRIPT
Heart failure.
Myocardial Infarction
Ph.D., MD, Assistant Professor Hanna Saturska
Functions of the circulatory system
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.
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
Heart failure may be caused by myocardial failure but may also occur in the presence of near-normal cardiac function under conditions of high demand.
myocardial failureconditions
of high demand
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.
ReasonsMyocardium injury
- Myocardium hypoxia or ischemia
- Infectional-toxical myocardium damage
- Metabolism disorder- Nervous-trophical and
hormonal influences on the organismMyocardium 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 ).
This chest radiograph shows an enlarged cardiac silhouette and edema at the lung bases, signs of acute heart failure.
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 classifiedinto 4 classes
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:
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
Reason increase of every cardiomyocytes load
Physiological mechanisms * adequate excitement *relation of excitement and contraction * adequate contraction *energy provision
Crash phase (St. of compensation)
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
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 Immediate adaptation mechanisms
Crash phase (pathogenesis)Heart beat increase
Functional changes Increased penetration of Na and
Са cytoplasma inside Decrease of depolarization
interval
Is possible if: 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
Increase of shortening power( 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 mechanisms1. Accumulation of Na (because is limited Na,К-АТPase
activity)2. Violation of Na,Са-exchanged mechanism3. 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)
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 hypertrophyMechanisms
* 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 hypertrophySick person
1. Continuous heart load2. Heart hypertrophy is
inadequate to body weight3. Decrease of capillaries amount
in weight unit 4. Inadequate activity of MCh5. Inadequate activity of SPR6. Decrease of nervous
structuresamount in weight unit (decrease
of NA concentration)
Sportsman1. There are periods of heart
load and restoring2. Heart hypertrophy is
adequate to body weight3. Increase of capillaries
amount in weight unit4. Adequate activity of MCh5. Adequate activity of SPR6. Increase of nervous
structures amount in weight unit
(adequate concentration of NA)
Sick personResults
Heart insufficiency is compensated by the
hypertrophy (bigger heart mass). But this change limits maximal
heart work.
SportsmanResults
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
Signs of hypertrophy
Exhaustion (stage of decompensation) 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 Са-АТPase (heart relaxes slowly, some time arise diastole defect at Са accumulation)
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 of decompensation)
Exhaustion (stage of decompensation) right-sided heart failure left-sided heart failure
Pathological signsViolations 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 violationsDyspnoea (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)
Violation of water-electrolyte balance
(edema) 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 volume receptors
Hypersecretion of aldosteron (Na retention) and vasopressin (water retention)
Hypervolemia, ascytes, edema
Pathological signs
Renin-angionensin-aaldosterone system
Myocardial infarctionIschemic 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.
Ischaemical necrosis of the myocardial tissue, which is resulted
from coronary blood supply insufficiency
Myocardial infarction
Statistics
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 %)
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 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: Increase of the
heart activity Stimulation of
the heart metabolism
Increase of О2
using
2. Age (most often appears in 40 – 59 years old person).
3. Hypokinesia (activation of the sympathetic-adrenal system)
4. Obesity (hypercholesterolemia)
Risk factors
5. MAIL SEX 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. Heredity7. Arterial hypertension
8. Diabetes mellitus9. Infection (chlamydia pneumonia)
Risk factors
Pathogenesis1.
Initialmechanisms
As a result of atherosclerotic disease of the coronary
arteries
2.Mechanisms of the
cardiomyocitesnecrosis
As a result of cardiomyocytes ischemia
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
Initial mechanisms3. Thrombosis
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
1. ATP deficit 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 causes - ineffective Na,К-АТPase
(fatal arrhythmias) - ineffective Са-АТPase
(damage of the Mch)
Cardiomyocytes necrosis mechanism
2. Acidosis
Accumulation of Crebs-cycle metabolits
Accumulation of Acetyl-Co-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)
Mechanisms1. 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
3. Са accumulationReasons:
1. Deficient of Ca return in to SPR (ATP deficit decreases Ca-ATPase activity)
2. Violation of Na,Са-exchange mechanism
Consequences: Ca deposit in Mch and АТP
deficit Damage of cardiomyocytes
membranes
Cardiomyocytes necrosis mechanism
4. “Lipid triade” 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)
Cardiomyocytes necrosis mechanism
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)
Sings 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
FinishingSpontaneous recurrent process after blood supply restoring !!!
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)
Hibernal myocardium
(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