heart failure. myocardial infarction ph.d., md, assistant professor hanna saturska
TRANSCRIPT
Heart failure.
Myocardial Infarction
Ph.D., MD, Assistant Professor Hanna Saturska
Functions of circulatory system
Stabilization of arterial pressure
Tissue provision by О2
The vital role of the circulatory system in maintaining homeostasis depends on the continuous and controlled movement of blood through the thousands of miles of capillaries that permeate every tissue and reach every cell in the body.
It is in the microscopic capillaries that blood performs its ultimate transport function.
Nutrients and other essential materials pass from capillary blood into fluids surrounding the cells as waste products are removed.
Heart insufficiency (Heart failure)
Heart failure is the pathophysiologic state in which the heart, via an abnormality of cardiac function (detectable or not), fails to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.
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
ReasonsMyocardium 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
Heart failure always causes circulatory failure, but the converse is not necessarily the case, because various noncardiac conditions (eg, hypovolemic shock, septic shock) can produce circulatory failure in the presence of normal, modestly impaired, or even supranormal cardiac function.
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.
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 utiliza-tion by the tissues
2. Reduce of peripheral vessels resistance
Reason increase of every cardiomyocytes load
Physiological mechanisms * adequate excitement *relation of excitement and shortening * adequate shortening *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 increaseFunctional 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 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
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 left-sided
Pathological signs
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
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 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
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.
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 persons at section was found)
Trombosis of the coronary arteries : *at 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
Pathogenesis
1.Initial
mechanisms
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
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
The chronic but reversible myocardial dysfunction seen in patients with severe coronary artery disease is a complex, progressive, and dynamic phenomenon that is initiated by repeated episodes of ischemia. In the early stages, resting perfusion is usually preserved, but flow reserve is significantly reduced. With time, and probably also increases in the physiological significance of the underlying coronary narrowing, some of the dysfunctional segments which initially appeared “chronically stunned” may eventually become underperfused, probably in response to the decrease in myocyte energy demand. This transition from chronic stunning to chronic hibernation is associated with several morphological alterations, which include myofibrillar disassembly, myofibrillar loss, and increased glycogen content. Interestingly, these changes take place similarly in dysfunctional and in normally perfused remote regions of the dysfunctional heart, which suggests that they may be more a response to chronic elevations in preload or stretch than the direct consequences of ischemia.
(Panel A): Light micrograph of a 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