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MindMap Gallery Disease causing cardiac insufficiency
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Disease causing cardiac insufficiency
This is a mind map about cardiac insufficiency, including causes, triggers, classifications, functional and metabolic changes, and mechanisms.
Edited at 2023-11-11 20:48:51- bacteria
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Disease causing cardiac insufficiency
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- Outline
cardiac insufficiency
Cause
Myocardial damage
primary
myocardial infarction
Refers to the disease caused by myocardial ischemia and necrosis due to sudden coronary artery obstruction. Other causes include coronary embolism, arteritis, and ruptured aneurysm.
Symptoms of myocardial infarction include substernal pain, fever, tachycardia, etc., which may be accompanied by nausea, vomiting, hypotension, etc. Treatment methods for myocardial infarction include drug therapy, interventional therapy, and surgical treatment.
myocarditis
It refers to a disease in which localized or diffuse inflammatory lesions of the myocardium are the main manifestations.
The treatment of myocarditis is mainly symptomatic, auxiliary and supportive treatment, mainly comprehensive treatment of shock, heart failure and arrhythmia, especially the treatment of patients with fulminant myocarditis.
Primary myocardial damage refers to the structural and functional abnormalities of the myocardium due to various reasons, resulting in severe impairment of myocardial systolic and diastolic function.
Secondary
coronary atherosclerosis
It refers to a disease in which atherosclerosis occurs in the coronary arteries, causing coronary artery stenosis or occlusion, thereby causing insufficient blood supply to the myocardium or myocardial necrosis.
The treatment of coronary atherosclerosis requires different treatments according to the degree of the disease, including drug treatment, stent implantation, and coronary artery bypass grafting.
Secondary myocardial damage refers to damage to the myocardium due to other diseases or causes.
ventricular overload
capacity load
Volume overload in ventricular overload means that the heart needs to receive too much blood during diastole, resulting in an increased workload on the heart.
heart valve insufficiency
Heart valve insufficiency means that the valves do not close tightly and blood flows back. This may be due to abnormal heart valve structure and function caused by various reasons. According to the location of the heart valve, the disease can be divided into types such as mitral valve insufficiency, tricuspid valve insufficiency, aortic valve insufficiency, and pulmonary valve insufficiency. The onset of the disease is associated with ventricular abnormalities, congenital valvular disease, rheumatic valvular disease, and degenerative valvular disease. Typical symptoms are dyspnea, palpitations, chest pain, edema of both lower limbs, etc.
pressure load
The pressure load of ventricular overload means that the heart needs to resist resistance such as excessive blood pressure or pulmonary hypertension during systole, resulting in an increased burden on the heart.
hypertension, arterial hypertension
Hypertension refers to the excessive lateral pressure of blood on the blood vessel wall, which is usually caused by factors such as decreased elasticity of the blood vessel wall and smaller blood vessel diameter. Pulmonary hypertension refers to an increase in pulmonary artery pressure beyond the normal range, usually caused by increased resistance in the pulmonary artery itself or lesions in the pulmonary circulatory system.
Ventricular overload refers to an increase in the resistance that the heart needs to overcome during pumping, resulting in an increase in cardiac workload.
preoccupation disorder
Thick
Refers to the increase in the size of myocardial cells and the thickening of myocardial fibers, resulting in thickening of the ventricular wall. This kind of hypertrophy is usually caused by genetic, endocrine and other factors, and may also be related to diseases such as hypertension and myocarditis. Hypertrophy may cause a decrease in the pumping function of the heart, causing symptoms such as difficulty breathing, palpitations, and chest pain.
Fibrosis
It refers to the replacement of heart muscle cells by scar tissue, causing the ventricular walls to become stiffer and lose elasticity. This kind of fibrosis is usually caused by diseases such as myocardial ischemia and myocarditis, and may also be related to long-term hypertension, diabetes, etc. Fibrosis may lead to a decrease in the pumping function of the heart, leading to symptoms such as heart failure and arrhythmias.
Ventricular filling disorders are usually caused by myocardial hypertrophy, increased cardiac load, etc. When myocardial hypertrophy occurs, the compliance of myocardial expansion decreases, and the resistance of blood entering the left ventricle increases, leading to filling dysfunction. Following filling dysfunction, a reduction in left ventricular end-diastolic volume results.
Arrhythmia
Acute (functional)
Common causes of acute arrhythmias include being overly excited or drinking a lot of alcohol, which may also be related to infection, electrolyte imbalance and other factors. Patients may have symptoms such as angina pectoris, fatigue, dizziness, and chest tightness.
Chronic (structural)
Chronic arrhythmias refer to diseases characterized by slowing of heart rate, including sinus bradyarrhythmia, atrioventricular junctional heart rate, ventricular autonomic rhythm, conduction block, etc. This type of disease can cause patients to experience symptoms such as shortness of breath, fatigue, chest tightness, dizziness, and chills.
It is a general term for symptoms such as all or part of the heart activity becoming too fast, too slow or irregular due to abnormalities in the origin, frequency, rhythm, conduction pathway or speed of cardiac activation.
inducement
Infect
Cardiac insufficiency caused by infection is mainly due to the infection involving the heart, causing damage to cardiac function, thereby affecting myocardial function. This condition may lead to acute heart failure, such as acute left heart failure.
Fever, infection
Arrhythmia
Long-term bradycardia or tachycardia can lead to reduced heart function and, in severe cases, heart failure.
pregnancy and childbirth
Increased blood volume and sympathetic excitement
During pregnancy, the pregnant woman's heart needs to bear a greater load, because the growth and development of the fetus and the increase in amniotic fluid will increase the burden on the pregnant woman's heart. During delivery, the mother needs to experience physiological changes such as uterine contractions, exertion during labor, and blood loss, all of which will have an impact on heart function. In particular, emergency labor, prolonged labor, or difficult labor may increase the burden on the heart and lead to cardiac insufficiency.
Water and electrolyte disorders, acid-base imbalance
Water and electrolyte disorders, such as hyponatremia or hypernatremia, may affect the electrophysiological activity of the heart, leading to arrhythmia or decreased myocardial contractility, thereby causing cardiac insufficiency. Acid-base imbalance may also have an impact on heart function. For example, severe metabolic acidosis may cause a decrease in myocardial contractility, leading to cardiac insufficiency. At the same time, acid-base imbalance may also affect the electrophysiological activity of the heart, leading to arrhythmia.
Generally speaking, patients with cardiac insufficiency have a basis for heart failure, so the triggers of cardiac insufficiency refer to the causes of heart failure in patients.
Classification
According to the location of failure
left heart failure
Coronary heart disease, cardiomyopathy, hypertension
It refers to heart failure caused by left ventricular compensatory insufficiency. It is very common clinically and is mainly characterized by pulmonary circulation congestion. Left heart failure is divided into acute left heart failure and chronic left heart failure. Chronic left heart failure (CHF) is the end result of most cardiovascular diseases and the leading cause of death. Acute left heart failure (AHF) is due to the sudden abnormality of cardiac structure and function, resulting in a significant and sharp decrease in short-term cardiac blood output, tissue and organ hypoperfusion, and acute congestion syndrome.
right heart failure
Pulmonary embolism, pulmonary hypertension, COPD
Right ventricular systolic and diastolic dysfunction can occur due to any structural or functional abnormality in the cardiovascular system, resulting in impaired right ventricular filling or ejection function, which is insufficient to produce the cardiac output required by the body, or cannot form normal filling pressure. A complex clinical syndrome that occurs when Right heart failure is mainly right ventricular stroke dysfunction, seen in cor pulmonale, tricuspid valve or pulmonary valve disease, and is often secondary to left heart failure.
total heart failure
myocarditis
It refers to the simultaneous or sequential occurrence of left heart failure and right heart failure, and related clinical manifestations. Most clinical cases are total heart failure secondary to right heart failure and left heart failure. When right heart failure occurs, the blood output of the right heart decreases, and the symptoms of pulmonary congestion such as dyspnea in left heart failure are alleviated.
By severity of heart failure
Level I
During the compensatory period of cardiac function, patients are not restricted in their daily activities and generally do not experience symptoms such as fatigue and dyspnea.
Level II
Patients do not experience obvious symptoms of discomfort during daily rest, but are prone to symptoms such as chest tightness, asthma, and fatigue during activities.
Level III
The patient's physical activities are significantly limited, and symptoms of heart failure such as fatigue, coughing, dizziness, and profuse sweating may occur during slight activities.
Level IV
It is a more serious condition. The patient cannot engage in any physical work and is prone to symptoms of heart failure even when resting.
Functional and metabolic changes
low cardiac output syndrome
Reduced heart pumping ability
blood pressure changes
Organ blood flow redistribution
Low cardiac output syndrome (referred to as low cardiac output) is a group of clinical syndromes characterized by decreased cardiac output and insufficient peripheral organ perfusion. It is common after cardiac surgery and occurs in various diseases leading to cardiac dysfunction. Obstacles may occur.
venous congestion syndrome
systemic venous congestion
right heart failure
cardiac edema
hypoalbuminemia
jugular venous distention
When myocardial contractility decreases, the neuro-humoral regulation mechanism is overactivated through increased blood volume and volume vasoconstriction, leading to an increase in preload. Instead of effectively increasing cardiac output, it causes a significant increase in filling pressure and causes venous congestion. The main sites of systemic venous congestion include the organs of the head, neck, chest, abdominal cavity and lower limbs.
Pulmonary circulation congestion
paradynamic dyspnea
Muscle contraction squeezes veins
increased oxygen consumption
increased heart rate
Paroxysmal nocturnal dyspnea
Increased reflux in supine position
vagus nerve excitement
Squat breathing
When left ventricular dysfunction occurs, the pressure within the left ventricle increases, impeding pulmonary venous return and causing pulmonary congestion. During pulmonary congestion, the lung volume increases and appears dark red, with foamy red bloody fluid flowing out from the cut surface.
The mechanism
Structural damage to the heart
Decreased number of cardiomyocytes
Structural changes in myocardium
ventricular dilation
Myocardial damage is a common phenomenon in cardiology, which refers to damage to the muscle tissue of the heart.
Myocardial energy metabolism disorder
Myocardial energy metabolism disorder refers to insufficient energy generation or utilization by myocardial cells, which leads to damage to myocardial cell function and affects the pumping function of the heart. The process of energy metabolism in cardiomyocytes mainly includes the oxidation of energy substances such as glucose and fatty acids and the generation of adenosine triphosphate (ATP). When the energy metabolism of myocardial cells is disrupted, it may lead to insufficient energy production in the myocardial cells, resulting in weakened myocardial contractility, thus affecting the heart's pumping function. There are many causes of energy metabolism disorders in myocardial cells, such as hypoxia, vitamin B1 deficiency, myocardial ischemia, etc. For example, when the myocardium is hypoxic, the oxygen demand of the cardiomyocytes cannot be met, resulting in an obstacle to the oxidative process, which in turn causes insufficient energy production in the cardiomyocytes. In addition, when vitamin B1 is lacking, the oxidation of pyruvate is impaired, which can also cause insufficient myocardial energy production.
Myocardial excitation-contraction coupling disorder
Affects the transport distribution and binding of Ca2
Decreased myocardial compliance
Myocardial compliance refers to the ease with which myocardial cells deform under the influence of external forces. When cardiac insufficiency occurs, the pumping function of the heart decreases, and the preload and afterload of the heart increase, causing the myocardial cells to be overstressed and difficult to deform, thus reducing the compliance of the myocardium.
Ventricular wall diastolic coordination disorder
The diastolic and contraction activities of the ventricular walls are uncoordinated, resulting in a decrease in the heart's pumping function. This incoordination may be caused by myocardial ischemia, hypoxia, drug effects, etc. In the case of cardiac insufficiency, the pumping function of the heart decreases, resulting in uncoordinated contraction and relaxation of the ventricular walls. This incoordination can lead to myocardial ischemia and hypoxia, further aggravating heart disease and affecting the heart's pumping function.
compensation
Activation of neuro-humoral regulatory mechanisms
sympathetic nervous system activation
Fast heart rate: increased myocardial oxygen consumption, affecting ventricular filling
Generalized vasoconstriction throughout the body
sodium and water retention
Skeletal muscle fatigue
Activation of sympathetic nerves can increase myocardial contractility, heart rate, and cardiac output, thereby temporarily alleviating symptoms of cardiac insufficiency. However, if this activation is excessive, it can have adverse effects on the heart, such as causing arrhythmias and myocardial damage. Activation of sympathetic nerves can also increase blood flow resistance by promoting vasoconstriction, thereby maintaining circulating blood volume and maintaining normal cardiac output. However, excessive vasoconstriction may increase the burden on the heart and further impair cardiac function.
Activation of the renin-angiotensin-aldosterone system
sodium and water retention
myocardial fibrosis
In cardiac dysfunction, activation of the renin-angiotensin-aldosterone system (RAAS) is an important compensatory mechanism. When the heart's pumping function is impaired, cardiac output decreases, and the body responds to this change by activating the RAAS. Activation of the renin-angiotensin-aldosterone system can promote vasoconstriction and water and sodium retention, thereby increasing circulating blood volume and cardiac output and maintaining the pumping function of the heart. If RAAS is overactivated, it will lead to increased cardiac load and myocardial remodeling, further damaging cardiac function.
Changes in Mars Substances in Other Bodily Fluids
High expression of vasoconstrictor active substances
Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are two important neurohormones, mainly expressed in atrial and ventricular myocytes. When the atrial wall is stimulated by stretch, ANP secretion increases. Its physiological role is to dilate blood vessels, increase sodium excretion, and counteract the pressor effect of epinephrine, renin-angiotensin and other vasoconstrictor substances. BNP is mainly expressed in ventricular myocardium, and its secretion changes with the level of ventricular filling pressure. When heart failure occurs, ventricular wall tension increases, and the ventricular muscles not only increase BNP secretion, but also significantly increase ANP secretion in the plasma. These neurohormones increase with the severity of heart failure and therefore may serve as markers to assess the course of heart failure and determine prognosis. However, even if exogenous neurohormones are infused, it is difficult to achieve the beneficial effects of natriuresis, diuresis, and reduction of vascular resistance due to their rapid degradation and weakened physiological effects. In addition, some growth factors and cytokines are also involved in the regulation of cardiac dysfunction. For example, endothelin is a potent vasoconstrictor that stimulates cardiomyocyte growth and hypertrophy and promotes vascular smooth muscle cell proliferation and migration. Nitric oxide is a gas signaling molecule that relaxes blood vessels and suppresses inflammatory responses. Transforming growth factor is a multifunctional cytokine that promotes cell proliferation, differentiation, apoptosis, and migration. These growth factors and cytokines play important roles in the onset and progression of heart failure.
Compensation of the heart itself
increased heart rate
cardiac tensogenic dilation
Increased myocardial contraction
increased oxygen consumption
ventricular remodeling
Changes in structure, metabolism and function
Performance
concentric hypertrophy
extracardiac compensation
increase blood volume
blood flow redistribution
Increased red blood cells
Increased ability of tissue cells to utilize oxygen
Venous congestion syndrome caused by cardiac insufficiency is due to a decrease in myocardial contractility, which leads to an increase in blood volume and volume vasoconstriction, which in turn leads to an increase in preload and a significant increase in filling pressure, resulting in venous congestion. This condition usually manifests as systemic and pulmonary congestion. Systemic circulation congestion mainly manifests as liver enlargement, liver function decline, portal hypertension, etc.; pulmonary circulation congestion manifests as pulmonary edema, pulmonary congestion, etc. These symptoms will affect the patient's blood circulation, leading to insufficient blood supply to various organs in the body, and in severe cases, may even cause cardiogenic shock.
Myocardial damage is a common phenomenon in cardiology, which refers to damage to the muscle tissue of the heart.
The neuro-humoral regulation mechanism of the body's compensatory response in cardiac insufficiency is the basic mechanism that mediates intracardiac and extracardiac compensatory and adaptive responses, and is also a key pathway leading to the occurrence and development of cardiac insufficiency.