Heart Failure – Acute and Chronic Heart Failures || Pathophysiology of Heart Failures


Questions About Heart Failure – Acute and Chronic Heart Failures

Definition of the concept of heart failure?

Heart failure is the inability of the heart to fill and empty normally, which results in impaired blood supply to the organs in accordance with the body’s needs. The manifestations of heart failure include: First of all, the disease is divided into The first arises suddenly and is characterized by severe symptoms, which must be removed only in a hospital setting.

Heart failure is a typical form of pathology in which the heart does not meet the needs of organs and tissues for adequate blood supply to their functions and the level of plastic processes in them. +Meerson – heart failure – a condition in which the load on the heart exceeds its ability to do work adequate to the load.

What is acute heart failure?

Acute heart failure (AHF) is a condition that occurs as a result of a sharp weakening of the contractile function of the heart muscle, accompanied by stagnant processes in the pulmonary and systemic circulation, as well as a violation of intracardiac dynamics. Acute heart failure leads to extremely serious complications due to dysfunctions of internal organs due to the inability of the myocardium to provide the necessary blood supply. Acute heart failure is a critical change in the work of the body’s cardiovascular system. This dangerous disease manifests itself in both adults and children.

What is metabolic heart failure?

Heart failure is an acute or chronic condition caused by a weakening of the contractility of the myocardium and congestion in the pulmonary or systemic circulation. It manifests itself as shortness of breath at rest or with light exertion, fatigue, edema, cyanosis (cyanosis) of the nails, and nasolabial triangle.

Metabolic heart failure is based on severe metabolic disorders in the myocardium, which lead to the insufficient formation of high-energy phosphorus compounds (creatine phosphate, ATP) or block the use of their energy by cardiomyocytes. A slowdown in the synthesis of macros occurs during myocardial hypoxia of coronary or general origin, restriction of the access of oxidation substrates (fatty acids, glucose, lactic acid), suppression of mitochondrial function, inactivation of creatine kinase, and other enzymes that are involved in the energy supply of the myocardium.

Obstacles to the use of energy by cardiomyocytes are created as a result of dysfunction of membrane ion pumps (N + K + -ATPase, Ca2 + -ATPase) and a violation of the ratio between the contents of sodium, potassium, and calcium ions in the intracellular and extracellular spaces. One of the reasons for this phenomenon is the activation of free radical oxidation of lipids in the membranes of cardiomyocytes and an increase in their permeability. Electrolyte metabolism disorders affect the contractility of cardiomyocytes. In particular, an increase in sodium ions in them causes their swelling. The release of potassium from cells disrupts the interaction between contractile proteins – actin and myosin. The saturation of cardiomyocytes with calcium ions is reflected in the processes of the rhythmic provision of actomyosin with ATP energy. In addition, a violation of the structure of contractile proteins is possible.

What is congestive heart failure?

Congestive heart failure is a condition in which the heart muscle is unable to maintain sufficient blood pressure to adequately supply oxygen to the tissues. It occurs in one out of fifty adults, the prognosis of the condition is unfavorable, since according to statistics, more than half of such patients die from heart failure over the next several years.



List the main non-cardiac mechanisms of adaptation to increasing the burden on the heart.

What is the “emergency” stage of myocardial hyperfunction?

Stage III – Ultimate, dystrophic. Severe circulatory failure, persistent changes in metabolism and functions of organs, irreversible changes in the structure of organs and tissues, pronounced dystrophic changes, complete disability.

Class III – Heart disease leads to significant limitation of physical activity. There are no symptoms at rest. Activity is less than usual causes fatigue, palpitations, or shortness of breath.

Class IV – Heart disease severely restricts all physical activity. Symptoms of heart failure and angina pectoris appear at rest. With any activity, the symptoms worsen.

What is a tonogenic dilatation of the heart?

Tonogenic dilation is called compensatory in another way since at this stage the contractile function of the heart is preserved, and the elimination of the cause of the increased pressure in the left ventricle leads to reverse the development of the process.

Tonogenic dilation is called compensatory in another way since at this stage the contractile function of the heart is preserved, and the elimination of the cause of the increased pressure in the left ventricle leads to the reverse development of the process. The sizes of the atria and ventricles return to normal. Experiencing increased pressure constantly, hypertrophy processes are triggered in the ventricular myocardium. The heart muscle thickens, increasing its muscle mass from the former 300 to 500 grams and even higher. Hypertrophy is often combined with tonogenic dilation.

Why does hypoxia develop in heart failure?

Myocardial hypoxia is a condition characterized by a lack of oxygen in the cells of the heart muscle. Oxygen is necessary to maintain the viability of cells, its deficiency leads to malfunctions in all organs of the body. A state of hypoxia (anoxia) occurs with the inability of the blood vessels to meet the heart’s oxygen demand.

For the heart to work, a constant supply of oxygen is required, a long-term lack of oxygen leads to the death (necrotization) of muscle fibers. In their place, foci of necrosis or scar tissue appear, replacing working cells.

There are two main types of myocardial hypoxia:

  • Acute form – develops with a sharp decrease in oxygen supply.
  • Chronic form – a condition that causes damage to the heart muscle, observed for a long time.

Acute oxygen starvation of the heart can cause a heart attack. The chronic form of oxygen starvation develops for several years and leads to heart failure.

By the nature of development, the following causes of myocardial hypoxia are distinguished:

  • hypoxic – with a decrease in the concentration of oxygen in the air, stay in a polluted air environment;
  • mechanical – in case of injury, a mechanical obstacle to air circulation;
  • respiratory – appear as a result of impaired ventilation of the lungs with pneumonia, bronchitis, edema of the lung tissue;
  • physical – are formed with physical overstrain or weakening of the respiratory muscles;
  • circulatory – occur when blood circulation is disturbed due to vasoconstriction, thrombus formation, heart disease;
  • hemic – develop with a decrease in hemoglobin;
  • histotoxic – provoked by poisoning with toxic substances that block the absorption of oxygen.

What is left ventricular heart failure?

Left-sided AHF manifestations are alveolar and interstitial pulmonary edema ( cardiac asthma ). Interstitial pulmonary edema develops more often against the background of physical and/or nervous tension, but it can also manifest itself during sleep in the form of sudden suffocation, provoking sudden awakening. During an attack, there is a lack of air, a hacking cough with characteristic shortness of breath, general weakness, pallor of the skin. Due to a sharp increase in shortness of breath, the patient takes a forced position, sitting with his legs down. Breathing is hard, the pulse is arrhythmic (gallop rhythm), weak filling.

With the progression of congestion in the pulmonary circulation, pulmonary edema develops – acute pulmonary insufficiency, which is caused by significant sweating of the transudate into the lung tissue. Clinically, this is expressed by suffocation, cough with the release of copious amounts of frothy sputum mixed with blood, wet wheezing, cyanosis of the face, nausea, and vomiting. The pulse is threadlike and the blood pressure drops. Pulmonary edema refers to an emergency that requires immediate intensive care due to the high probability of death.

Acute heart failure leads to extremely serious complications due to dysfunctions of internal organs due to the inability of the myocardium to provide the necessary blood supply.

Acute left ventricular failure may present with syncope due to cerebral hypoxia due to asystole or decreased cardiac output.

List the main manifestations of right ventricular heart failure.

Acute heart failure of the right type develops against the background of pulmonary embolism. Congestion in the systemic circulation is manifested by shortness of breath, cyanosis of the skin, edema of the lower extremities, intense pain in the heart, and right hypochondrium. Blood pressure decreases, the pulse is frequent, weak filling. There is an increase in the liver, as well as (less often) the spleen.
Signs of acute heart failure due to myocardial infarction range from mild pulmonary congestion to a sharp decrease in cardiac output and manifestations of cardiogenic shock.

Peculiarities of development and pathogenesis of heart failure in children.

Causes

Signs of heart failure are observed when the contractility of the myocardium is impaired with its direct or indirect damage. The etiological structure depends on the age of the child. The main causes of the disease in newborns are congenital heart defects, hypoxic myocardial damage in the perinatal period. In older children, cardiac insufficiency occurs under the influence of various factors, the main of which are:

  • Organic heart disease. Most often, pathology becomes a consequence of inflammatory processes – endocarditis, myocarditis, pericarditis. In children, the cause of heart failure is often dilated and hypertrophic forms of cardiomyopathy.
  • Rhythm and conduction disturbances. In children, non-paroxysmal and paroxysmal ventricular tachycardias, complete atrioventricular blocks, atrial or ventricular extrasystoles are predominantly found. Rare causes include Wolff-Parkinson-White syndrome.
  • Acute rheumatic fever. Rheumatism causes cardiac dysfunction in adolescents. The disease is caused by damage to the valve apparatus and hemodynamic disorders. Clinical symptoms of myocardial failure develop after one attack of rheumatic fever.
  • Extracardiac pathology. Among the causes of heart failure, the proportion of systemic lesions of the connective tissue and vasculitis is increasing. Occasionally, signs of HF are found in neuromuscular diseases, mitochondrial diseases, and genetic syndromes.

Pathogenesis

In the development of heart failure in children, basic pathophysiological mechanisms are distinguished, which are triggered regardless of the etiological factors of the disease. At the initial stage of myocardial damage, compensatory processes are included. The heart rate and peripheral vascular resistance increase. The cavity of the left ventricle of the heart expands, and its wall hypertrophies. The older the child is, the more active his adaptation mechanisms are.

With the depletion of the body’s compensatory capabilities, the patient’s condition worsens. There are three hypotheses of impaired myocardial contractility: “energy hunger” of cardiomyocytes, suppression of excitation processes, decreased fiber sensitivity to calcium ions. As a result, the cardiac cavities expand, the effective release of blood into systole decreases.

Further, the renin-angiotensin-aldosterone system is activated, the release of catecholamines and atrial natriuretic peptide is enhanced. Children develop symptoms of central and peripheral hemodynamic disorders. In chronic heart failure, the restructuring of the immune and neuroendocrine systems occurs, and cellular apoptosis increases.

What principal causes of heart failure?

Among the most common causes of heart failure, occurring in 60-70% of patients, are myocardial infarction and coronary artery disease. They are followed by rheumatic heart defects (14%) and dilated cardiomyopathy (11%). In the age group over 60, in addition to coronary heart disease, heart failure is also caused by hypertension (4%). In older patients, type 2 diabetes mellitus and its combination with arterial hypertension are a common cause of heart failure.

Risk factors

The factors provoking the development of heart failure cause its manifestation with a decrease in the compensatory mechanisms of the heart. Unlike causes, risk factors are potentially reversible, and reducing or eliminating them can delay the worsening of heart failure and even save the patient’s life.

These include:

  • overstrain of physical and psycho-emotional capabilities
  • arrhythmias, PE, hypertensive crises, the progression of coronary artery disease;
  • pneumonia, SARS, anemia, renal failure, hyperthyroidism
  • taking cardiotoxic drugs, drugs that promote fluid retention (NSAIDs, estrogens, corticosteroids), increase blood pressure (sardine, ephedrine, adrenaline)
  • pronounced and rapidly progressive increase in body weight, alcoholism
  • a sharp increase in the BCC with massive infusion therapy
  • myocarditis, rheumatism, infective endocarditis
  • non-compliance with recommendations for the treatment of chronic heart failure.

How the myocardium affects the raised work at the first (“emergency”) stage of compensatory hyperfunction?

An increase in the load on the myocardium leads to an increase in the intensity of the functioning of myocardial structures, that is, an increase in the number of functions per unit of heart mass.

If a large load unexpectedly falls on the heart (which is rare with defects), for example, with myocardial infarction, tearing of the papillary muscles, rupture of tendon chords, with a sharp rise in blood pressure due to a rapid increase in peripheral vascular resistance, then in these cases there is a well-pronounced short-term t .n. “emergency” phase of the first stage.

With such an overload of the heart, the amount of blood entering the coronary arteries decreases, the energy of oxidative phosphorlation for heart contractions is not enough and wasteful anaerobic glycolysis joins. As a result, the content of glycogen, creatine phosphate decreases in the heart, under-oxidized products (pyruvic, lactic acids) accumulate, acidosis occurs, and the phenomena of protein and fatty degeneration develop. The sodium content in the cells increases and the potassium content decreases, electrical instability of the myocardium occurs, which can provoke the occurrence of arrhythmias.

Explain the mechanism of wear of heart at excessive hypertrophy of a myocardium.

single process. The mechanism of decompensation of a hypertrophied myocardium includes the following links:

1. The process of hypertrophy does not extend to the coronary vessels, therefore the number of capillaries per unit volume of the myocardium in the hypertrophied heart decreases. Consequently, the blood supply to the hypertrophied heart muscle is insufficient for performing mechanical work.

2. Due to the increase in the volume of hypertrophied muscle fibers, the specific surface of the cells decreases, in connection with this, the conditions for the entry of nutrients into the cells and the release of metabolic products from cardiomyocytes deteriorate.

3. In a hypertrophied heart, the ratio between the volumes of intracellular structures is disturbed. Thus, an increase in the mass of mitochondria and SPR lags behind an increase in the size of myofibrils, which contributes to a deterioration in the energy supply of cardiomyocytes and is accompanied by a violation of Ca2 accumulation in the SPR. There is a Ca2 + overload of cardiomyocytes, which ensures the formation of cardiac contracture and contributes to a decrease in stroke volume. In addition, Ca2 + overload of myocardial cells increases the likelihood of arrhythmias.

4. The conducting system of the heart and the autonomic nerve fibers that innervate the myocardium do not undergo hypertrophy, which also contributes to the occurrence of dysfunction of the hypertrophied heart.

5. Apoptosis of individual cardiomyocytes is activated, which contributes to the gradual replacement of muscle fibers with connective tissue (cardiosclerosis).

Physiological hypertrophy occurs when the heart is exposed to significant periodic loads with pauses. Such hypertrophy develops, for example, in the heart of an athlete, in which periods of training alternate with periods of rest. Physiological hypertrophy forms slowly, gradually. Capillaries and nerves have time to grow along with the growth of muscle fibers, i.e. normal blood supply and nervous trophism are preserved. In the myocardium, the number of mitochondria increases, the activity of the enzymes of the respiratory chain and the ATPase activity of myosin heads increases, the content of myoglobin increases, the power of membrane ion pumps increases, and the ratio of the nucleus volume to the cytoplasm volume remains normal (1: 5). Physiological hypertrophyЇ is balanced growth of cardiomyocytes, allowing them to effectively cope with the increased load.

Explain the mechanism of development of centralization of circulation of a heart failure?

Insufficiency of blood circulation develops in stages. Under the influence of damaging factors, the functions of any of the main links of the circulatory system are disrupted: the heart, blood vessels, the volume of circulating blood, and regulatory mechanisms. Following the above-mentioned attacks, a complex of defensive reactions arises. The mechanisms underlying them are usually subdivided into emergency and slowly developing ones. As a result, blood circulation can be restored, that is, return to the stage of compensation.

With prolonged exposure to damaging factors, compensation mechanisms can provide long-term adequate functioning of the circulatory system. However, in the case of their exhaustion, the phase of compensation disorder begins – decompensation with the development of a clinical picture of circulatory failure.

In the case of acutely developed circulatory failure due to a drop in the minute volume of blood, systemic circulation, the blood supply to the brain immediately deteriorates, and the functions of the central nervous system are impaired. As a result, defense mechanisms immediately turn on due to the influences of the central subcortical formations, reflex effects from the receptors of the carotid sinus zones, the aortic arch, and the heart itself. Sympathetic influences on the heart and blood vessels sharply increase. The main purpose of such shifts is to restore the adequacy and stabilization of the blood supply to the brain and heart, including through the redistribution of circulating blood. This mechanism is called “centralization of blood circulation”.

Name the development causes left ventricular heart failure?

cute failure of this type is most often observed in patients over 60 years of age. But there are cases when the disease affects people over 40 years of age. The development of this ailment is provoked by myocardial infarction and coronary heart disease. Heart defects and cardiomyopathy are considered less likely causes of the disease. Often in older patients, the development of the disease is caused by type 2 diabetes mellitus, in combination with high blood pressure.
Among the reasons provoking pathology can also be attributed: acute viral diseases that a person carries on his feet; advanced pneumonia; taking drugs that can be toxic to the heart and the body as a whole; abuse of coffee and energy drinks, which contain large doses of caffeine.
A person who is overweight and does not follow a healthy lifestyle is at risk. Also, people who abuse alcohol or smoke are more likely to develop heart disease. Left ventricular heart failure can result from myocardial infarction as well as severe arrhythmias. With this pathology, the minute output and the amount of blood that must enter the arterial vessels are sharply reduced. With the development of the disease, the load on the heart increases, because it is trying with all its might to compensate for the changes occurring in the vascular system. The heart muscle begins to contract more strongly, its rhythm becomes more frequent, capillaries and arterioles expand, tissue perfusion increases. The development of pathology leads to stretching of the myocardial muscles.

What mechanism of development of dyspnea at a heart failure?

Dyspnea in heart failure has a mixed mechanism, in which the predominant role belongs to the stimulation of the respiratory center in the medulla oblongata by impulses from the volume and baroreceptors of the vascular bed. They, in turn, are caused mainly by circulatory failure and stagnation of blood in the pulmonary veins, increased blood pressure in the pulmonary circulation.

  • When the left side of the heart is affected, the volume of ejected blood decreases. Stagnation forms in the area of ​​the lungs, as they are overfilled with blood.
  • Congestion contributes to the disruption of gas exchange in the airways, which leads to a deterioration in their ventilation.
  • The body stimulates respiratory function, increases the frequency of breaths and their depth. Therefore, the person experiences shortness of breath.
  • Interstitial pulmonary edema develops.

The brain receives a signal that the lungs are suffering from hypoxia. It activates the respiratory center, forcing a person to breathe more often and deeper.

Why patients with heart failure there can be ascites?

Ascites can develop due to heart failure , or due to constrictive pericarditis. Heart failure can be the result of almost all cardiac diseases.

Heart failure can develop in humans due to the progression of a number of ailments or the presence of age-related changes in the body. This disease negatively affects the ability of the myocardium to contract, organs cannot be supplied with blood in sufficient volume. With heart failure, congestion is often observed, causing ascites – the accumulation of fluid in the abdominal cavity.
The mechanism of ascites formation in heart failure resembles the formation of edema in any part of the body: there is an imbalance between internal and external pressure. The pathogenesis of the disease can be a number of conditions, including –

  • oncological diseases;
  • liver disease;
  • heart failure in a neglected state;
  • pancreatitis;
  • renal failure.

In heart disease, ascites develops as a result of blood stagnation in the heart chambers. When the organ ceases to cope with excess fluid, its accumulation occurs, which is most often observed in the veins of the lower extremities and the peritoneum.

Explain the possibility of the appearance of a diapulse in patients with heart failure?

Why during attacks of warm asthma of the patient takes over the forced position?

A forced position during an attack of bronchial asthma (the patient sits in bed, resting his hands on the edge of the bed) is taken by the patient in order to fix the shoulder girdle. This makes it possible for auxiliary muscles to participate in the act of breathing.

Forced position is a position that relieves pain and improves the patient’s condition. This position is forced by this or that feature of the disease. For example, in the event of an asthma attack, a patient with bronchial asthma sits in bed, leaning forward, rests on the bed, table, thereby including the auxiliary muscles in the act of inhalation. During an attack of cardiac asthma, the patient sits, leaning back somewhat, and rests his hands on the bed, his legs are lowered. In this position, the mass of circulating blood decreases (part of it is retained in the lower extremities), the diaphragm falls slightly, the pressure in the chest decreases, the excursion of the lungs increases, gas exchange and the outflow of venous blood from the brain improve.

What mechanism of development of unloading Parin reflex at dextral ventricular a heart failure?

What causes of transferring of the compensated heart failure in a decompensation stage?

These processes lead to decompensation of heart failure, characterized by the inability of the damaged heart to cope with the function of providing blood in the optimal volume of organs and tissues and to compensate for circulatory disorders. Heart failure in the stage of decompensation is divided into acute, chronic, and also left and right ventricular.

Decompensated heart failure occurs for the following reasons:

  • Hypertensive disease, or rather, an irreversible process can be triggered by a hypertensive crisis.
  • Congenital heart defects. These are abnormalities of the heart valves, due to which heart failure occurs.
  • Myocarditis.
  • Stable tachyarrhythmia.
  • Hypertrophic cardiomyopathy.

What pathogeny of warm edemas?

What signs of heart failure are caused by retardation of the rate of blood flow? What their mechanisms of development?

Insufficient blood circulation is characterized by a different combination of the following symptoms: shortness of breath, fatigue, swelling, especially of the lower extremities, cyanosis, increased heart rate.

Two main factors lead to the development of INSUFFICIENCY OF BLOOD CIRCULATION : impairment of the pumping function of the heart and the tone of peripheral vessels. In this regard, cardiac and vascular forms of circulatory failure are distinguished. Often they are combined, so the term “cardiovascular failure” is often used.

HEART INSUFFICIENCY develops under the influence of various factors, of which the most frequent are overload of the heart, myocardial damage due to the inflammatory process or deep metabolic disorders.

Distinguish between energetic-dynamic and hemodynamic. or congestive, form of heart failure.

Energetic-dynamic heart failure (according to Hegglin) is manifested by a shortening of the mechanical systole and is diagnosed by the premature appearance of the II tone on the PCG. It develops as a result of metabolic disorders in the myocardium and is observed in severe infections, hypokalemia, diabetic coma, etc. This form of heart failure is not accompanied by an increase in the size of the heart and impaired circulation in the pulmonary and systemic circulation, but it can be combined with congestive heart failure (CHF ).

What is Bouveret’s disease? Explain its mechanism of occurrence?

Decompression sickness (Latin prefix de- extraction, destruction + compressio compression, squeezing) is a pathological condition that develops as a result of the formation of gas bubbles in the blood and tissues of living organisms with a decrease in external pressure (in humans, when leaving the caisson, surfacing from depth to the surface, when climbing to a height).

Bouveret’s disease is characterized by sudden attacks of acceleration of the heart rate – paroxysmal tachycardia. By the suddenness of the beginning and end of the crisis, this disease is considered in connection with the nervous system, that is, with the instrument of the astral body. This leads us to the idea that at the moment of this paroxysm there is a sudden and short-lived cessation of the impulses of the nervous system, while the astral body seems to be separated – in a certain place of the nervous system, for example, sudden and transient paralysis of the vagus nerve occurs. This lability of the astral body allows for minimal reasons to cause a crisis.

What is the extrasystole? Name principal views an extrasystole.

Extrasystole is a variant of a heart rhythm disorder, characterized by extraordinary contractions of the whole heart or its individual parts (extrasystoles). It is manifested by a feeling of a strong heart beat, a feeling of sinking heart, anxiety, lack of air. It is diagnosed by the results of ECG, Holter monitoring, stress cardio tests. Treatment includes elimination of the root cause, medication correction of the heart rate; in some forms of extrasystole, radiofrequency ablation of arrhythmogenic zones is indicated.

Classification of extrasystole

The extrasystoles are divided according to the location of the pulse generator, the activity of which causes from the appearance of:

  • Supraventricular extrasystoles – if an extraordinary impulse is generated in any part of the atria, but not in the sinus node
  • Ventricular extrasystoles – if an extraordinary impulse is generated in any part of the ventricles of the heart.

nother classification indicates an extrasystolic heart rhythm:

  • A single extrasystole is one extrasystole that occurs haphazardly relative to the normal rhythm.
  • Bigeminia is an extrasystole following each normal contraction.
  • Trigeminia is an extrasystole that occurs after two normal contractions.
  • Quadrigeminia is an extrasystole that occurs after every three normal contractions.

Features of development and a pathogeny of a heart failure at children.

In the development of heart failure in children, basic pathophysiological mechanisms are distinguished, which are triggered regardless of the etiological factors of the disease. At the initial stage of myocardial damage, compensatory processes are included. The heart rate and peripheral vascular resistance increase. The cavity of the left ventricle of the heart expands, and its wall hypertrophies. The older the child is, the more active his adaptation mechanisms are.

With the depletion of the body’s compensatory capabilities, the patient’s condition worsens. There are three hypotheses of impaired myocardial contractility: “energy hunger” of cardiomyocytes, suppression of excitation processes, decreased fiber sensitivity to calcium ions. As a result, the cardiac cavities expand, the effective release of blood into systole decreases.

Further, the renin-angiotensin-aldosterone system is activated, the release of catecholamines and atrial natriuretic peptide is enhanced. Children develop symptoms of central and peripheral hemodynamic disorders. In chronic heart failure, the restructuring of the immune and neuroendocrine systems occurs, and cellular apoptosis increases.