An accurate study of LV function requires obtaining several positions from the parasternal and apical approaches. Initially, the LV image is usually obtained from parasternal access along its long (Fig. 2.1) and short (Fig. 2.9, 2.10) axes. Two-dimensional LV images make it possible to accurately direct the ultrasound beam for M-modal examination (Fig. 2.3, 2.4).
From apical access, LV visualization is performed in two-dimensional mode in four and two-chamber positions (Fig. 2.11, 2.12, 2.14). It is also possible to study LV from subcostal access (Fig. 2.16, 2.18).
Of the parameters of the LV function obtained using M-modal echocardiography, the most informative are the following: anteroposterior shortening of the short axis of the LV, the distance from the E-peak of the anterior valve of the mitral valve to the interventricular septum , the amplitude of motion of the aortic root.
Anteroposterior shortening characterizes the ratio of the diastolic (coinciding with the top of the R wave of the electrocardiogram) and systolic (end of the T wave) sizes of the left ventricle. Normally, the anteroposterior size of the LV short axis decreases by 30% or more. In fig. 2.4 shows the record of the M-modal study of LV with its normal anteroposterior shortening, in Fig. 5.15C – for dilated cardiomyopathy.
If we focus only on M-modal measurements, serious errors can be made in assessing LV function, since these measurements take into account only a small part of the LV at its base. In coronary heart disease, segments with impaired contractility can be removed from the base of the LV; in this case, anteroposterior shortening of the left ventricle will create a false idea of the global systolic function of the left ventricle.
The distance from the E-peak of the movement of the anterior mitral valve leaflet to the interventricular septum is the distance between the point of greatest opening of the mitral valve (in the early diastole phase) and the closest portion of the interventricular septum (during systole). Normally, this distance does not exceed 5 mm. With a decrease in global LV contractility, the amount of blood remaining in its cavity at the end of systole increases, which leads to LV dilatation.
At the same time, a decrease in stroke volume leads to a decrease in transmitral blood flow. The mitral valve in this case does not open as wide as normal. The amplitude of movement of the interventricular septum also decreases. As global LV contractility worsens, the distance between the E-peak of the anterior mitral valve leaflet movement and the interventricular septum increases more and more.
The amplitude of aortic movement at the base of the heart should also be evaluated only qualitatively. It is proportional to the stroke volume. The behavior of the aorta depends on the filling of the left atrium and the kinetic energy of the blood that is released by the left ventricle into the systole. Normally, the aortic root is displaced anteriorly in the systole by more than 7 mm.
Caution should be taken with this indicator, since a low stroke volume does not necessarily mean a decrease in LV contractility. If the cusps of the aortic valve are well visualized with the aorta, it is easy to calculate systolic time intervals. The degree of opening of the valves of the aortic valve and the form of their movement are also indicators of LV systolic function.
In recent years, there have been many publications devoted to computer processing methods for LV M-modal images. But we will not dwell on them, since in most clinical laboratories of echocardiography computers are not used for these purposes, and in addition, with the development of echocardiographic techniques, more reliable methods for assessing global LV contractility have appeared.
In a two-dimensional echocardiographic study, both a qualitative and a quantitative assessment of global LV contractility are performed. In everyday practice, echocardiographic images are evaluated in the same way as ventriculograms: they determine the approximate ratio of systolic and diastolic sizes of the heart.
The most accurate way to assess the global contractility of the left ventricle is quantitative two-dimensional echocardiography. This method, of course, is not without errors, but it is still better than visual assessment of images. In all likelihood, Doppler studies of the global systolic function of the left ventricle are even more accurate, but so far they have a supporting role.
For a quantitative assessment of global LV contractility, the choice of a stereometric LV model is important [29, 31, 32, 33, 34, 39, 42, 43]. After choosing a model, LV volumes are calculated based on its planimetric measurements according to the algorithm corresponding to the selected model. There are many algorithms for calculating LV volumes that we will not dwell on in detail.
In the Laboratory of Echocardiography, UCSF use a modified Simpson algorithm, which is more correctly called the disk method (Fig. 5.1). When using it, the measurement accuracy is practically independent of the shape of the LV: the method is based on reconstruction of the LV from 20 discs – sections of the LV at different levels. The method involves obtaining mutually perpendicular LV images in two- and four-chamber positions.
In several centers, the disc method was compared with radiopaque and radioisotope ventriculography. The main disadvantages of the disk method are that it underestimates (by approximately 25%) LV volumes and involves the use of computer systems. Over time, the cost of computer systems will decrease, and image quality will improve; therefore, quantitative methods for assessing LV contractility will be more accessible.
- Basic diagnostic methods
- Causes of violation of diastolic left ventricular function
- Medical events
- Myocardial infarction and its complications
- Pathology Development Scheme
- Pathological formations
- AIDS heart disease
- Diastolic dysfunction of the left ventricle. Diagnosis and treatment approaches
- Treatment of the disease
- 1 How does the heart rest?
- What is systolic and diastolic heart failure?
Basic diagnostic methods
There are several mathematical algorithms for calculating the left ventricular PV during echocardiography, each of which gives its own result. In other words, if you measure the PV of one patient during one study using the three algorithms Teichholz, Simpson and area-length, you will get three different numbers. Interestingly, the most reputable publications do not indicate how PV is obtained in the presented data.
The ancient Teichholz algorithm, although it is on the menu of probably all existing devices for echocardiography today, is not recommended for use, since it gives a result that is not related to reality. This algorithm is very popular because it gives a quick result. The problem is that the operator sets the device to only the end-diastolic and end-systolic size of the left ventricle (CRC and CRC).
The fact is that the left ventricle is really a bit like a uniformly contracting ellipse, only normal. In most pathological cases associated with a decrease in EF, the left ventricle has a rather spherical shape and can contract unevenly. For example, the basal segments may be hyperkinetic (here we measure the CRC and CSB), and the middle and apical segments can form a large dyskinetic post-infarction aneurysm. As a result, the Teichholz algorithm will produce an inadequate high PV when it is actually low.
So, the Teichholz algorithm is not recommended.
I have never seen a comparison of Simpson algorithms and the area is long. Probably their value is similar. The inhomogeneity of LV contractility creates the problem of measuring PV when using them. This problem is partially solved by using two mutually intersecting planes during measurements (the left ventricular endocardium is circled in the four-chamber and two-chamber positions), or by three-dimensional echocardiography.
Asynchrony of ventricular contraction is even more difficult, as, for example, with blockade of the left bundle branch block. This problem has no solution today. This means that with asynchronous LV contraction, its PV will be determined less accurately, and there is nothing to be done.
The second problem: poor reproducibility of PV. Measure FV three times to one patient with one algorithm for one study and get three numbers. What to do?
The most reproducible results are given by cardiac contrast MRI and three-dimensional echocardiography. The latter is recommended for serial measurements of PV, if it has clinical significance (for example, with cardiotoxic chemotherapy).
The use of echo contrasts increases accuracy. It is believed that they are needed in 10-15% of studies, but it depends on the quality of ultrasound systems.
Reproducibility increases if:
- repeated studies are carried out by the same operator
- using the same apparatus and PV calculation algorithm
- need to be measured with breath held in the exhale
- cycles following a long pause, such as post-extrasystolic, should be avo >
For a thin assessment of the dynamics of systolic function, a global longitudinal strain is better than PV, but more on that below.
After the patient complains to the doctor about the symptoms characteristic of dysfunction of the left ventricle, a number of studies are prescribed. In most cases, a narrow cardiologist is working with the patient.
First of all, the doctor prescribes general tests, on the basis of which the work of the body as a whole will be evaluated. They pass biochemistry, a general analysis of urine and blood, determine the level of potassium, sodium, hemoglobin. The doctor will evaluate the work of the most important human organs – the kidneys and liver.
In case of suspicion, thyroid studies will be prescribed to detect hormone levels. Often, hormonal disorders have a negative effect on the entire body, while the heart muscle must cope with double work. If the cause of the dysfunction lies precisely in violations of the thyroid gland, then the endocrinologist will deal with the treatment. Only after adjusting the level of hormones does the heart muscle return to normal.
An ECG study is the main method for diagnosing problems of this nature. The procedure lasts no more than 10 minutes, electrodes that read information are installed on the patient’s chest. During ECG monitoring, the patient must observe several rules:
The breath should be calm, even.
You can not clamp, you need to relax the whole body.
It is advisable to undergo the procedure on an empty stomach, after eating it should take 2-3 hours.
If necessary, the doctor can prescribe an ECG according to the Holter method. The result of such monitoring is more accurate, because the device reads information during the day. A special belt with a pocket for the device is attached to the patient, and electrodes are installed and fixed on the chest and back. The main task is to lead a normal lifestyle. An ECG is able to detect not only DFID (diastolic dysfunction of the left ventricle), but also other heart diseases.
Simultaneously with the ECG, an ultrasound of the heart is prescribed, it is able to visually assess the state of the organ and track blood flow. During the procedure, the patient is placed on the left side and the sensor is guided through the chest. No preparation for ultrasound is required. The study is able to detect many heart defects, explain chest pain.
The doctor makes the diagnosis on the basis of general analyzes, the results of ECG monitoring and ultrasound of the heart, but in some cases an extended study is required. The patient can be prescribed an ECG after exercise, chest x-ray, MRI of the heart muscle, coronary angiography.
Among the additional measures, it is not excluded the study of thyroid function (determining the level of hormones), chest x-ray, coronarography, etc.
Diastolic dysfunction is detected mainly during an instrumental examination method such as echocardiography. With the introduction of this method into clinical practice, the diagnosis of diastolic dysfunction began to be made at times more often. Echocardiography, as well as Doppler-Echocardiography allows you to identify the main violations that occur during myocardial relaxation, the thickness of its walls, evaluate the ejection fraction, stiffness and other important criteria to determine the presence and type of dysfunction.
Heart diseases are increasingly found in medical practice. They must be carefully studied and examined in order to be able to prevent negative consequences. Diastolic dysfunction of the left ventricle is a common disease that can cause heart failure, accompanied by pulmonary edema or cardiac asthma.
Ventricular dysfunction is more often an age-related disorder and occurs mainly in older people. Women are especially susceptible to this pathology. Diastolic dysfunction of the left ventricle causes hemodynamic disturbances and atrophic changes in the structure of the myocardium. The period of diastole is characterized by muscle relaxation and the filling of the ventricle with arterial blood. The process of filling the heart chamber consists of several stages:
- relaxation of the heart muscle;
- under the influence of the pressure difference from the atrium, the blood passively flows into the ventricle;
- with atrial contraction, the remaining blood is abruptly expelled into the ventricle.
In case of violation of one of the stages, insufficient blood flow is observed, which contributes to the development of left ventricular failure.
The second problem: poor reproducibility of PV. Measure FV three times to one patient with one algorithm for one study and get three numbers. What to do?
Myocardial ischemia causes local disturbances in LV contractility, impaired global LV diastolic and systolic function. In chronic coronary heart disease, two factors have the greatest prognostic value: the severity of coronary artery disease and global systolic function of the left ventricle.
With a transthoracic echocardiographic examination, one can judge about coronary anatomy, as a rule, only indirectly: only in a small number of patients the proximal sections of the coronary arteries are visualized (Fig. 2.7, 5.8). Recently, a transesophageal study has been used to visualize coronary arteries and study coronary blood flow [252, 254] (Fig. 17.5, 17.6, 17.7).
However, this method has not yet received wide practical application for the study of coronary anatomy. The methods for assessing global LV contractility have been discussed above. An echocardiographic study conducted at rest, strictly speaking, is not a diagnostic method for coronary heart disease. The use of echocardiography in combination with stress tests will be discussed later in the chapter “Stress echocardiography”.
Figure 5.8. Aneurysmal expansion of the trunk of the left coronary artery: parasternal short axis at the level of the aortic valve. Ao is the aortic root, LCA is the trunk of the left coronary artery, PA is the pulmonary artery, RVOT is the efferent tract of the right ventricle.
Despite the limitations mentioned, an echocardiographic study at rest provides valuable information for coronary heart disease. Chest pain can be of cardiac or non-cardiac origin. Recognition of myocardial ischemia as a cause of chest pain is of fundamental importance for the further management of patients both in an outpatient study and when they are admitted to an intensive care unit.
Local contractility of the LV is assessed by a two-dimensional echocardiographic study conducted from various positions: most often these are the parasternal positions of the long axis of the LV and the short axis at the level of the mitral valve and the apical positions of the two- and four-chamber heart (Fig. 4.2). To visualize the posterior-basal parts of the left ventricle, the apical position of the four-chamber heart with the deviation of the scan plane downward is also used (Fig. 2.12).
When assessing local LV contractility, it is necessary to visualize the endocardium as best as possible in the study area. To make a decision on whether local LV contractility is impaired or not impaired, one should take into account both the myocardial movement of the study area and its degree of thickening. In addition, local contractility of different LV segments should be compared, and the echo structure of myocardial tissue in the study area should be investigated.
You can not rely solely on assessing myocardial movement: impaired intraventricular conduction, ventricular pre-excitation syndrome, electrical stimulation of the right ventricle, are accompanied by asynchronous contraction of various LV segments, therefore these conditions make it difficult to assess local LV contractility. The paradoxical movement of the interventricular septum, observed, for example, with volume overload of the right ventricle, also complicates it.
Disorders of local LV contractility are described in the following terms: hypokinesia, akinesia, dyskinesia. Hypokinesia means a decrease in the amplitude of movement and thickening of the myocardium of the studied area, akinesia – the absence of movement and thickening, dyskinesia – the movement of the studied LV area in the opposite direction to normal. The term “asynergy” means the simultaneous contraction of various segments; LV asynergy cannot be identified with violations of its local contractility.
Causes of violation of diastolic left ventricular function
To cope with a violation of the left ventricular diastolic function is possible only if it is caused by a cardiac surgical pathology, which can be completely eliminated by surgery. In other cases, problems with heart diastole are corrected medically.
Therapy is primarily aimed at correcting circulatory disorders. The quality of his future life depends on the timeliness, correctness of treatment and the strict implementation of medical recommendations by patients.
The goals of therapeutic measures:
- elimination of cardiac arrhythmias (normalization of the pulse);
- blood pressure stabilization;
- correction of water-salt metabolism;
- elimination of left ventricular hypertrophy.
The heart is a hollow muscular organ consisting of four parts (right and left ventricle and atria, respectively). It has the shape of a dome and, while working with the intrauterine life, never takes breaks for rest, like other organs. That is why some disturbances sometimes occur in the heart.
The most significant in the heart is the left ventricle. The large circle of blood circulation, supplying oxygen to all organs and tissues except the lungs, begins in the left ventricle.
- IHD (cardiac ischemia), which occurs due to insufficient oxygen supply to the myocardium and causes the death of cardiomyocytes. As you know, the role of blood in the body is very large, it is a carrier of the necessary elements: hormones, oxygen, trace elements.
- Sclerosis of the heart, which appeared as a result of a heart attack (post-infarction cardiosclerosis). Sclerosis is not a violation of memory, as is commonly believed in the people. This is hardening of tissues. If scars appear on the organ, this interferes not only with the normal metabolism, but also disrupts the stretching function. Even the myocardium is not protected from such a disease. Different disorders are distinguished depending on the location of the disease leading to cardiosclerosis. And one of them is a disorder of the diastolic function of the left ventricle.
- Hypertrophic cardiomyopathy – thickening of the left heart also leads to pathology of diastolic function.
- Primary arterial hypertension.
- Stenosis or aortic valve insufficiency.
- Inflammation of the pericardium (the outer membrane of the heart) with the application of fibrin filaments – fibrinous pericarditis. Fibrin tightens the heart muscle and prevents it from working fully.
Therapy depends on the stage and severity of the disease, it is absolutely contraindicated to prescribe one or another drug to yourself, because the heart is a vital organ, therefore it is better not to harm your health with incorrect actions.
If there are no symptoms of insufficiency, the doctor may advise taking angiotensin-converting enzyme (ACE) inhibitors. It is a regulator of blood pressure and protects target organs in this disease.
Target organs are those that suffer primarily from dysfunction of the cardiovascular system, that is, they are the first “targets” that are in the way of blood failure. These include the kidneys, brain and spinal cord, heart, blood vessels, and retina.
Taking ACE inhibitors daily at a dose prescribed by a doctor can reduce the risk of complications in target organs and prevent the development of chronic heart failure. Such drugs include enalapril, quadropril, lisinopril. It is difficult to say which is better, everything is discussed at the appointment with a therapist or cardiologist and is prescribed based on the symptoms and past experience of taking the medicine.
If you are intolerant of ACE inhibitors or for some objective reasons, the doctor decided that they will not help you, ARA II (angiotensin receptor antagonists) are prescribed. They have exactly the same properties. These include Losartan, Valsartan and others.
With severe signs of the disease, even more drugs are prescribed to relieve symptoms:
- diuretics (diuretics) – reduce the volume of circulating blood due to the withdrawal of excess fluid;
- beta-blockers – make heart rate less often, reducing the burden on the organ;
- cardiac glycosides – increase the force of contractions of the heart;
- Aspirin – is prescribed to reduce the risk of blood clots and, consequently, ischemia;
- statins – carry out lipid control in the blood due to the normalization of cholesterol fractions that are harmful to blood vessels.
Violation of the diastolic function of the ventricular myocardium can occur due to an increase in its mass – hypertrophy, or a decrease in elasticity, myocardial compliance. It should be noted that almost all heart diseases to one degree or another affect the functions of the left ventricle. Most often, diastolic dysfunction of the left ventricle occurs in diseases such as hypertension, cardiomyopathy, coronary artery disease, aortic stenosis, arrhythmias of various types and origin, pericardial disease.
It should be noted that loss of elasticity and increased rigidity of the muscle wall of the ventricles is observed during the natural aging process. Women over sixty are more prone to this disorder. High blood pressure leads to an increase in the load on the left ventricle, due to which it increases in size, the myocardium hypertrophies. And the altered myocardium loses its ability to normal relaxation, such violations initially lead to dysfunction, and then to failure.
Left atrial enlargement
Three types of left ventricular dysfunction are distinguished.
Type I – diastolic dysfunction of the left ventricle of type 1 is classified as mild in severity. This is the initial stage of pathological changes in the myocardium, its other name is hypertrophic. In the early stages, it is asymptomatic, and this is its insidiousness, since the patient does not suggest a malfunction in the heart and does not seek medical help. With type 1 dysfunction, heart failure does not happen, and this type is diagnosed only with the help of echocardiography.
Type II – dysfunction of the second type is characterized as moderate. In type II, due to insufficient relaxation of the left ventricle and a reduced volume of blood ejected from it, the left atrium takes on a compensatory role and begins to work “for two”, which causes an increase in pressure in the left atrium, and subsequently its increase. The second type of dysfunction can be characterized by clinical symptoms of heart failure and signs of pulmonary stasis.
Type III – or restrictive type dysfunction. This is a serious violation, which is characterized by a sharp decrease in the compliance of the walls of the ventricle, high pressure in the left atrium, a vivid clinical picture of congestive heart failure. In type III, sharp deterioration of the condition with access to pulmonary edema, cardiac asthma is frequent. And these are severe life-threatening conditions that, without proper emergency treatment, often lead to death.
Should diastolic dysfunction be treated if there are no symptoms of the disease and the clinic? Many patients are wondering. Cardiologists agree: yes. Despite the fact that in the early stages there are no clinical manifestations, the dysfunction is capable of progression and the formation of heart failure, especially if the patient has a history of other heart and vascular diseases (AH, CHD).
- ACE inhibitors – this group of drugs is effective both in the early and late stages of the disease. Representatives of the group: enalapril, perindopril, diroton;
- AK – a group that helps to relax the muscle wall of the heart, causes a decrease in hypertrophy, dilates the blood vessels of the heart. Calcium antagonists include amlodipine;
- b-blockers can slow down heart rate, which is why diastole lengthens, which favors heart relaxation. This group of drugs includes bisoprolol, nebivolol, nebilet.
Left ventricular enlargement on ECG (hypertrophy)
Left atrial dilatation: causes and treatment
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The diastolic function of the heart muscle is its ability to relax after the stage of blood expulsion. The effectiveness of the diastole of the heart depends on its condition and the work of the entire cardiovascular system. Therefore, the development of pathologies in the heart affects its entire work, including the ability to relax.
The main reasons for the development of diastolic dysfunction include coronary heart disease, valvular defects and cardiomyopathy. In coronary disease, a violation of diastolic function occurs as a result of a decrease in the ability of muscle cells to relax. Valvular defects first overload the heart muscle, which ultimately violates its trophic functions and also contributes to increased rigidity – poor relaxation. Cardiomyopathies are the result of certain pathological processes.
Violation of diastolic function begins to manifest itself as its decrease in various parts of the heart. Of these, the left ventricle is the most significant. This is primarily due to the fact that he throws blood into a large circle, which ensures its movement through the vessels of internal organs. As is known from the Frank-Starling Act, to which the heart obeys, the amount of blood pushed into the great circle of blood circulation depends on its amount received during diastole.
Violation of the ability of muscle cells of the left ventricle to relax can be of two types. This is a violation of the diastolic function of the left ventricle according to type 1 and type 2. Although, some cardiologists suggest the second type to be divided into two independent ones.
The basis for the violation of the relaxation function of the left ventricle of the first type is a change in blood flow velocity during diastole. At the first stage, it slows down and then increases. This negatively affects the work of the left atrium. Disturbed blood circulation in the vessels of the lungs (pulmonary circulation). And since violation of the diastolic function of the left ventricle of type 1 is often found in patients with coronary heart disease, it becomes clear why stagnation in the pulmonary circulation is most often found in this category of people. This is manifested by a tendency to shortness of breath, the development of chronic lung diseases.
If the work of the left ventricle is impaired by type 1, the doctor begins to treat the patient. At first, the disease does not make itself felt, therefore, they begin active actions later.
Timely prescribed treatment and the implementation of simple preventive rules in many cases can save the patient from chronic problems with blood circulation in the heart muscle. A doctor prescribes a complex of drugs, each of which performs its function.
In case of violation of LV diastolic function according to type 1, the doctor prescribes ACE inhibitors – these are drugs aimed at lowering pressure, they are often prescribed for patients with hypertension. This medical group of drugs has been used for several decades, which confirms its safety and effectiveness.
With pronounced symptoms, in case of heart dysfunction of 4 degrees or 3 degrees, the doctor prescribes serious medications of different groups. Diuretic drugs are used, they normalize the body’s water balance, as a result of which the blood volume is adjusted. It can be Uregit, Mannitol, Ethacrinic acid.
Prescription drugs that reduce the number of heart contractions, but at the same time increase the strength of each stroke, are glycosides. This is a strong group of drugs, an overdose threatens with serious side effects, the patient may begin to suffer from auditory and visual hallucinations, bleeding, temporary clouding of the mind, headaches.
Prevention of thrombosis is carried out with the help of Aspirin Cardio. In patients with cardiovascular diseases, there is a high risk of blood clotting, resulting in clogging of vessels – thrombosis.
Often with ventricular dysfunction, elevated blood cholesterol levels are recorded, which increases the chance of myocardial infarction and stroke. The doctor conducts therapy with statins, they affect the liver, as a result, it reduces the production of cholesterol. The most popular statins are Atorvastatin, Lovastatin, Niacin.
The necessary treatment, how long it needs to be carried out, whether it is possible to completely recover.
Diastolic dysfunction of the left ventricle (abbreviated as DLJ) is an insufficient filling of the ventricle with blood during diastole, i.e., a period of relaxation of the heart muscle.
This pathology is more often diagnosed in women of retirement age, suffering from arterial hypertension, chronic heart failure (abbreviated heart failure) or other heart diseases. In men, left ventricular dysfunction is detected much less frequently.
With such a violation of the functions, the heart muscle is unable to completely relax. From this, the filling of the ventricle with blood decreases. Such a violation of the function of the left ventricle affects the entire period of the heart contraction cycle: if with diastole the ventricle was insufficiently filled with blood, then with systole (myocardial contraction) it will also be pushed into the aorta.
This pathology is treated by a cardiologist. It is possible to involve other narrow specialists in the treatment process: a rheumatologist, a neurologist, and a rehabilitologist.
It will not be possible to completely get rid of such a violation, because it is often provoked by the underlying disease of the heart or blood vessels or their age-related wear. The prognosis depends on the type of dysfunction, the presence of concomitant diseases, the correctness and timeliness of treatment.
Myocardial infarction and its complications
its appearance is explained by a local change in the shape of the LV in the area with impaired contractility. The border between the akinetic and normal myocardium is sometimes well visualized. The presence of LV diastolic deformity with a pronounced demarcation line indicates the formation of aneurysm. In fig. 5.9, 5.10 presents echocardiographic manifestations of myocardial infarction of the anterior-septal apical localization with the formation of LV aneurysm; in fig. 5.11 – antero-septal myocardial infarction, in Fig. 5.12 – posterior myocardial infarction.
Figure 5.9. Left ventricular akinesia of antero-septal apical localization. Left ventricular segments with impaired contractility are indicated by arrows. LAX is the position of the parasternal long axis of the left ventricle, SAX is the position of the parasternal short axis of the left ventricle at the level of the papillary muscles, 4-ch is the apical position of the four-chamber heart, 2-ch is the apical position of the two-chamber heart, LV is the left ventricle, RV is the right ventricle, Ao is the ascending aorta, LA is the left atrium.
Figure 5.10. Aneurysm of the left ventricle of septal apical localization (arrows): the apical position of the four-chamber heart, diastole (A) and systole (B). Myocardial thinning and diastolic deformity are signs of a true aneurysm. LV – left ventricle, RV – right ventricle, LA – left atrium, RA – right atrium.
Figure 5.11. Dyskinesia of the left ventricle of antero-septal localization: the apical position of the four-chamber heart, diastole (A) and systole (B). Left ventricular segments with impaired contractility are indicated by arrows. LV – left ventricle, RV – right ventricle, LA – left atrium, RA – right atrium.
Figure 5.12. Aneurysm of the left ventricle of the posterior basal localization (arrow): the apical position of the bicameral heart. Left ventricular deformity and myocardial thinning in the area of aneurysm. LV – left ventricle, LA – left atrium.
Echocardiography can be used to diagnose and determine the prognosis for acute myocardial infarction. Normal local LV contractility in a patient with chest pain helps to rule out acute myocardial infarction. Schemes for quantitative characterization of violations of local LV contractility have been developed. It was shown that the index of violation of local LV contractility in acute heart attack is an independent prognostic sign.
With the help of an echocardiographic study conducted directly at the patient’s bedside, many complications of myocardial infarction can be quickly recognized. We have already talked about true LV aneurysms. Pseudo-aneurysms are similar in appearance to true aneurysms, but myocardial rupture is the cause of their appearance. An aneurysmal sac of pseudo-aneurysm with an external rupture consists of a pericardium and the remains of a torn wall.
Only small pseudo-aneurysms are compatible with life, therefore pseudo-aneurysms diagnosed with echocardiography have a thin isthmus; this allows them to be distinguished from true aneurysms, in which the isthmus is as wide as the tip. Often it is echocardiography that allows you to detect pseudo-aneurysms [22, 26]. Without surgical treatment, the prognosis for LV pseudo-aneurysm is extremely unfavorable.
Massive rupture of the LV wall is usually not compatible with life. With small ruptures of the LV wall, an echo-negative space between the leaves of the pericardium and signs of cardiac tamponade can be detected. In the vast majority of cases, the appearance of fluid in the pericardial cavity during myocardial infarction is, fortunately, not associated with myocardial rupture, but with epistenocarditis pericarditis or post-infarction pericarditis (Dressler’s syndrome).
Rupture of the interventricular septum leads to blood discharge from left to right at the level of the ventricles (Fig. 5.13), rupture or dysfunction of the papillary muscle leads to the appearance of a flailing valve of the mitral valve and severe mitral insufficiency (Fig. 5.14). In patients with a throttling valve of the mitral valve, an eccentric jet of regurgitation is detected, which spreads circularly along the periphery of the left atrium from the affected valve .
Figure 5.13. Rupture of the interventricular septum (complication of myocardial infarction of the posterior localization): intraoperative transesophageal echocardiographic study. A – before the operation, B – after the operation of suturing the defect of the interventricular septum. A ventricular septal defect is indicated by an arrow. LV – left ventricle, RV – right ventricle, t – thrombus, patch – patch.
Figure 5.14. The threshing posterior cusp of the mitral valve is the result of dysfunction of the papillary muscles (complication of left ventricular myocardial infarction). The posterior cusp of the mitral valve in the systole sags in the cavity of the left atrium. Non-closure of the cusps of the mitral valve leads to severe mitral regurgitation.
With a defect in the interventricular septum, a contrast study can detect the appearance of air bubbles in the left heart, using Doppler studies you can calculate the pressure gradient between the left and right ventricles, the volume of shunted blood.
LV thrombosis will be discussed below in the section “Pathological formations in the LV cavity”.
Ventricular dysfunction is a violation of the ability of the heart muscle to contract with the systolic type to expel blood into the vessels, and relax with diastolic to take blood from the atria. In any case, these processes cause a violation of normal intracardiac hemodynamics (movement of blood through the heart chambers) and stagnation of blood in the lungs and other organs.
Both types of dysfunction are associated with chronic heart failure – the more ventricular function is impaired, the higher the severity of heart failure. If heart failure can be without heart dysfunction, then dysfunction, on the contrary, does not occur without heart failure, that is, in every patient with ventricular dysfunction, there is a chronic heart failure of the initial or severe stage, depending on the symptoms.
Pathology Development Scheme
More often, a combination of several factors acts as the causes:
- elderly age;
- arterial hypertension;
- chronic heart pathologies: arrhythmias or other rhythm disturbances, myocardial fibrosis (replacing muscle tissue with fibrous tissue that is unable to contract and conduct electrical impulses), aortic stenosis;
- acute cardiac abnormalities, such as a heart attack.
Violation of blood flow (hemodynamics) can cause:
- pathology of the circulatory system and coronary vessels: thrombophlebitis, ischemia of the vessels of the heart;
- constrictive pericarditis with a thickening of the outer lining of the heart and compression of the heart chambers;
- primary amyloidosis, in which myocardial elasticity decreases due to the deposition of special substances that cause atrophy of muscle fibers;
- post-infarction cardiosclerosis.
Diastolic ventricular dysfunction can be caused by certain diseases that can significantly disrupt the hemodynamics of the heart:
- Diastolic dysfunction of the left ventricle is a consequence of thickening of the heart muscle tissue (myocardial hypertrophy). As a rule, hypertrophy develops in people with hypertension, aortic stenosis and hypertrophic cardiomyopathy.
- It can develop under the influence of pericarditis, due to which the thickened walls of the pericardium compress the chambers of the heart.
- With pathological changes in the coronary vessels that cause coronary heart disease due to coarsening of the heart tissue and the appearance of scars.
- Amyloidosis causes a decrease in muscle elasticity and atrophic changes in the heart fibers.
Especially often, the disease develops in people with diabetes or obesity. In this case, the pressure on the heart chambers increases, the organ cannot fully function and ventricular dysfunction develops.
There are three types of cardiomyopathies, each of which has characteristic echocardiographic signs: dilated, hypertrophic and restrictive cardiomyopathies.
It is rarely possible to diagnose dilated cardiomyopathy in the early stages of its development. However, severe forms of dilated cardiomyopathy have vivid echocardiographic signs. These signs include: spherical LV shape, LV dilatation with normal or reduced thickness of its walls, systolic movement of all segments in the LV.
The left atrium is almost always enlarged, often all the chambers of the heart are enlarged. An increase in the right heart can be either secondary (due to pulmonary hypertension) or primary (due to the involvement of the myocardium of the right ventricle in the pathological process). LV volume often exceeds 250 ml, and left atrium – 125 ml.
The ejection fraction is often below 20%, but most often it is from 20% to 30%. Cardiac output may be normal or almost normal. This is due to the fact that, firstly, dilated cardiomyopathy is often accompanied by sinus tachycardia, and secondly, a large end-diastolic volume can provide an almost normal stroke volume, despite the low ejection fraction. In fig. 5.15 presents some characteristic signs of dilated cardiomyopathy.
with dilated cardiomyopathy, this ratio approaches unity. The distance from the E-peak of the movement of the anterior valve of the mitral valve to the interventricular septum normally does not exceed 5 mm, with dilated cardiomyopathy it is much larger. LV – left ventricle, RV – right ventricle, LA – left atrium, RA – right atrium, IVS – interventricular septum.
If cardiomyopathy is diagnosed, there is no need to repeat the echocardiography frequently, except when it is done to monitor pulmonary artery pressure and parameters of the LV global contractility, its volume and mass.
Doppler study reveals a decrease in the velocity and acceleration of blood flow in the ascending aorta and a decrease in the integral of the linear velocity of blood flow in the outflow tract of the left ventricle and pulmonary artery.
Diagnosing dilated cardiomyopathy, especially accompanied by severe heart failure, is not difficult. Paradoxically, echocardiography provides very little opportunity to judge the genesis of cardiomyopathy. The UCSF Echocardiography Laboratory has attempted to develop criteria for differential diagnosis of ischemic and idiopathic dilated cardiomyopathy using echocardiography and magnetic resonance imaging.
For this purpose, the wall thickness, their structure, local contractility and LV shape were determined. In patients with ischemic cardiomyopathy, local contractility disorders, heterogeneity of the echo structure, and the presence of segments with normal contractility were more pronounced, but these changes were also found in a significant number of young patients who did not have angiographic signs of coronary heart disease. This suggests that echocardiography cannot be a reliable method for identifying the causes of dilated cardiomyopathy.
Another diagnostic method with the use of echocardiography is now becoming more widespread: endocardial myocardial biopsy under echocardiographic control. With the accumulation of experience, this elegant combination of an invasive method with a non-invasive method can become the standard method for the diagnosis of cardiomyopathy.
Chagas disease is common in South America; this disease is accompanied by cardiomyopathy, which may be segmental in nature . The cause of Chagas disease is the ingestion of Trypanosoma cruzi (when bitten by insect vectors) into the human body with massive myocardial invasion. Cardiomyopathy, developing with this disease, is clinically similar to other far-reaching myocardial lesions.
Hypertrophic cardiomyopathy is an increase in the thickness of the walls of the LV and its mass of unknown etiology; in other words, it is LV hypertrophy in the absence of aortic stenosis or arterial hypertension. LV hypertrophy can be symmetric or asymmetric. Usually, with asymmetric hypertrophic cardiomyopathy, the basal divisions of the interventricular septum are maximally hypertrophied.
Echocardiography is a reliable method for the diagnosis of hypertrophic cardiomyopathy. In the clinic of this disease, the three leading syndromes determine the severity of the lesion and prognosis: this is obstruction of the LV efferent tract, LV diastolic dysfunction, and ventricular heart rhythm disturbances. Echocardiography, in particular Doppler study, can reliably assess the severity of the first two syndromes.
The classic echocardiographic picture with hypertrophic cardiomyopathy is as follows: maximum hypertrophy in the region of the basal divisions of the interventricular septum, varying degrees of severity of involvement in the process of the remaining LV walls; antero-systolic movement of the cusps of the mitral valve, mid-systolic aortic valve cover, dynamic pressure gradient in the LV outflow tract, impaired LV diastolic filling, mitral regurgitation (Fig. 5.16, 5.17, 5.18, 5.19, 5.21). Mitral ring calcification is observed in hypertrophic cardiomyopathy in more than half of cases .
Figure 5.16. Hypertrophic cardiomyopathy: asymmetric hypertrophy of the left ventricle, anterior systolic movement of the mitral valve. The parasternal long axis of the left ventricle. Localization of hypertrophy is typical for hypertrophic cardiomyopathy: it is an interventricular septum, the thickness of which in the diastole reaches 20 mm.
Figures 5.17, 5.18. Hypertrophic cardiomyopathy. Anterosystolic movement of the mitral valve, in which both valve flaps participate. The apical position of the four-chamber heart. Fig. 5.17 – diastole, Fig. 5.18 – systole. LV is the left ventricle, LA is the left atrium, RV is the right ventricle, RA is the right atrium.
Figure 5.19. Hypertrophic cardiomyopathy: subcostal access, long axis of the heart, diastole. The thickness of the interventricular septum reaches 35 mm in the most hypertrophied area. LV – left ventricle, RV – right ventricle, LA – left atrium, RA – right atrium.
The antero-systolic movement of the mitral valve (Fig. 5.17), in which one or both valves can be involved, does not serve as a pathognomonic sign of hypertrophic cardiomyopathy (Fig. 5.20). The antero-systolic movement of the mitral valve can be associated with lengthening of the chords, sometimes it is observed with mitral valve prolapse, it also happens in healthy people.
However, prolonged systolic contact of the mitral valve with the interventricular septum (more than 1/3 of systole) is always associated with high-speed blood flow in the LV efferent tract: with hypertrophic cardiomyopathy, hypertensive heart, and sometimes with aortic stenosis. With pronounced anterior systolic movement of the mitral valve, a thickening of the endocardium of the interventricular septum at the point of contact of the mitral valve with it is often found.
Figure 5.20. Anterosystolic movement of the mitral valve in a patient who underwent reconstructive surgery on the mitral valve (due to rupture of the chords). The antero-systolic movement of the mitral valve appeared after surgery and led to dynamic obstruction of the outflow tract of the left ventricle. The apical position of the four-chamber heart: on the left is diastole, on the right is systole. LV – left ventricle, LA – left atrium.
The causal relationship of the anterior-systolic movement of the mitral valve and the dynamic obstruction of the LV is not fully understood. It is believed that a high-speed blood stream in the LV outflow tract attracts the mitral valve cusps (Venturi effect). The antero-systolic movement of the mitral valve reduces the lumen of the LV outflow tract and causes its dynamic obstruction. Mitral valve contact with the interventricular septum appears on average 30 ms earlier than the maximum intraventricular pressure gradient.
It is more difficult to make a correct diagnosis of atypical, apical LV hypertrophy, since the myocardium of the apex of the LV is the least accessible to study. Diagnosis of hypertrophic cardiomyopathy is also made difficult by the absence of obstruction of the LV outflow tract; in these cases, special tests are needed that provoke its appearance;
these tests not only help identify obstruction, but also determine its severity. Methods that provoke or aggravate obstruction of the LV outflow tract include: Valsalva test, amyl nitrite inhalation (Fig. 5.21, physical exercise tests. They should be performed simultaneously with registration of blood flow in the LV outflow tract in a constant-wave Doppler mode.
Figure 5.21. Hypertrophic cardiomyopathy: a study of blood flow in the outflow tract of the left ventricle in a constant-wave Doppler mode in two patients. A – obstruction of the outflow tract of the left ventricle at rest: the intraventricular pressure gradient reaches 100 mm Hg. Art. B – there is no obstruction at rest; after inhalation of amyl nitrite, the intraventricular pressure gradient is 36 mm Hg. Art.
In about 45% of cases, DFD is asymptomatic for a long time, especially with the hypertrophic and pseudo-normal type of pathology. Over time and with the most severe, restrictive type, the following manifestations are characteristic:
- Dyspnea. Appears at first only with intense physical activity, later at rest.
- Weakness, fatigue, decreased exercise tolerance.
- Violation of the heart rhythm, more often its acceleration or atrial fibrillation.
- Lack of air, compression in the chest area.
- Heart cough, worse when lying down.
- Swelling of the ankles.
At the initial stages of diastolic dysfunction, the patient is unaware of the impaired heart function, and the weakness and shortness of breath are attributed to banal fatigue. The duration of this asymptomatic period is different for each person. A visit to a doctor occurs only when tangible clinical signs appear, for example, shortness of breath at rest, leg swelling, affecting a person’s quality of life.
LV thrombosis is a common finding with echocardiographic examination. In most cases, it is associated with a recent myocardial infarction of the anterior apical localization. Echocardiography is very effective in detecting left blood clots; this inspired a number of researchers to study the structure of blood clots, the time of their formation and disappearance, and the likelihood of thromboembolism. In fig. 5.
24 presents the aneurysm of the apex of the left ventricle, completely filled with a thrombus. Most often, LV thrombosis appears on the third or fifth day of anterior apical myocardial infarction, the likelihood of LV thrombosis increases with age and directly depends on the size of the myocardial lesion. The risk of thromboembolism is maximum from the 5th to the 20th days of the disease with a significant decrease in it at a later date.
Pancreatic tumors can be primary or metastatic, benign or malignant. Tumors that affect the pancreas are similar in histology to left ventricular tumors. The study of the echo structure of the tumor alone does not allow one to judge its origin, but by comparing the data of echocardiography with the clinic, it is almost always possible to predict the data of histological examination.
Not only the echo structure of the tumor is important, but also its mobility and the place of attachment. Among benign tumors, myxomas are most often found, among malignant ones, melanomas and lymphosarcomas. It is also possible the germination of a tumor in the pancreas through the inferior vena cava and the right atrium. Such tumors most often turn out to be hepatomas, but tumors of the kidneys and adrenal glands can similarly grow into the right heart. Malignant thymomas grow into the cavity of the right ventricle through the superior vena cava and sometimes create an obstacle to blood flow.
Among the formations that enter the pancreas through the inferior vena cava, thrombi formed in the veins of the lower extremities have the greatest clinical significance. Thromboembolism migration routes were studied in detail [67, 68, 77]. Once in the pancreas, they are sometimes adjacent to its wall and look like mobile tumor-like formations. Their echo density is lower than that of tumors.
Having passed the tricuspid valve, blood clots can pass through the valve of the pulmonary artery and end its path in the pulmonary artery. Blood clots from the right atrium can enter through the open oval into the left heart and cause “paradoxical” thromboembolism [67, 71, 78]. In all cases of detection of thrombosis of the right heart and in most cases of pulmonary thromboembolism, we recommend the administration of a contrast agent during echocardiography.
AIDS heart disease
pulmonary heart, myocarditis, dilated cardiomyopathy and pericarditis [16, 19, 50]. Among AIDS patients with cardiac symptoms, people who use intravenous drugs, women, as well as hospitalized patients with a variety of infectious diseases and a low number of T-lymphocytes predominate.
The most likely cause of dilated cardiomyopathy in AIDS is infectious myocarditis. Data from pathological and anatomical studies have shown that focal myocarditis in AIDS is common, but is asymptomatic. Many possible causative agents of myocarditis in AIDS were identified: cytomegaloviruses, tuberculosis mycobacteria, Toxoplasma gondii, Cryptococcus neoformans, Candida albicans, Histoplasma capsulatum.
Until a connection has been established between a specific pathogen and the severity of heart damage. Damage to myocytes and the AIDS virus itself is not ruled out. The effusion in the pericardial cavity in AIDS is associated with hypoalbuminemia, infectious damage to the heart and lungs, malignant neoplasms or damage to the pericardium itself.
The development of heart failure in AIDS means a very poor prognosis for the very near future, although at first heart failure responds well to conventional treatment. Exudation in the pericardial cavity with AIDS almost never leads to cardiac tamponade.
When identifying the causes of shortness of breath in an AIDS patient, one should always bear in mind the possibility of heart damage along with lung diseases. Echocardiography is indicated for all AIDS patients with severe shortness of breath, not corresponding to the severity of lung damage, and for all AIDS patients with cardiac symptoms.
Diastolic dysfunction of the left ventricle. Diagnosis and treatment approaches
After the examination, the attending physician will select a suitable complex of drugs that can maintain normal all indicators. Heart failure also plays an important role, the treatment of which requires compliance with a large number of medical recommendations.
So, at an early, asymptomatic stage of the course of dysfunction, ACE inhibitors or, if intolerant, angiotensin II receptor antagonists (ARA II) must be prescribed. These drugs have organoprotective properties, that is, they protect the organs that are most vulnerable to the adverse effects of constantly high blood pressure, for example.
These organs include the kidneys, brain, heart, blood vessels, and the retina. A daily intake of the drug in a dose prescribed by a doctor significantly reduces the risk of complications in these structures. In addition, ACE inhibitors prevent further myocardial remodeling, slowing the development of heart failure. Of the drugs prescribed are enalapril, perindopril, lisinopril, quadripril, from ARA II losartan, valsartan and many others. In addition to them, treatment of the underlying disease that caused ventricular dysfunction is prescribed.
At the stage of severe symptoms, for example, with frequent shortness of breath, nightly attacks of suffocation, swelling of the limbs, all the main groups of drugs are prescribed. These include:
- Diuretics (diuretics) – veroshpiron, diuver, hydrochlorothiazide, indapamide, lasix, furosemide, torasemide eliminate blood stasis in organs and lungs,
- Beta-blockers (metoprolol, bisoprolol, etc.) reduce the heart rate, relax peripheral vessels, helping to reduce the load on the heart,
- Calcium channel inhibitors (amlodipine, verapamil) – act similarly to betablockers,
- Cardiac glycosides (digoxin, corglycon) – increase heart rate,
- Combinations of drugs (noliprel – perindopril and indapamide, amosartan – amlodipine and losartan, lorista – losartan and hydrochlorothiazide, etc.),
- Nitroglycerin under the tongue and in tablets (monochinque, pectrol) with angina pectoris,
- Aspirin (thromboass, aspirin cardio) to prevent thrombosis in blood vessels,
- Statins – to normalize blood cholesterol levels with atherosclerosis and coronary heart disease.
In the absence of treatment, as well as in the case of significant dysfunction, accompanied by severe heart failure, the prognosis is poor, since the progression of the process without treatment invariably ends in death.
If the patient complies with the doctor’s recommendations and takes medication, the prognosis is favorable, since modern drugs not only help eliminate severe symptoms, but also prolong life.
Violation of the diastolic function of the left ventricle cannot be completely stopped, but with adequate medication correction of circulatory disorders, treatment of the underlying disease, proper nutrition, work and rest, patients with such a disorder live a full life for many years.
Despite this, it is worth knowing that such a violation of the heart cycle is a dangerous pathology that cannot be ignored. With a poor course, it can lead to a heart attack, stagnation of blood in the heart and lungs, and edema of the latter. Complications are possible, especially with a severe degree of dysfunction: thrombosis, pulmonary embolism, ventricular fibrillation.
In the absence of proper treatment, severe dysfunction with severe heart failure, the prognosis for recovery is poor. In most such cases, it all ends with the death of the patient.
With regular proper treatment, nutrition adjustment with salt restriction, monitoring of the state and level of blood pressure and cholesterol, the patient can count on a favorable outcome, prolonging life, and moreover, active.
Given the severity of the disease, you can not run it. Remember that postponing a trip to the doctor, you only harm your health. There are so many drugs in the world that you can find one that will reduce unpleasant symptoms. By following a healthy lifestyle, eating right, and following the advice of your doctor, you significantly reduce the risk of complications and aggravation of the condition.
Treatment of the disease
- Type 1 – a violation of relaxation, which reduces the amount of blood needed to enter the ventricle. Deficiency of relaxation leads to atrial hypertrophy due to their increased work;
- Type 2 is pseudo-normal, relaxation is even worse than type 1. The contribution of the atria is important, which with the help of increased pressure in their cavities compensate for the insufficiency of “their brother”;
- Type 3 – a restrictive, more severe stage of the disease, indicates a severe violation of diastolic function, and has an extremely poor prognosis with the subsequent development of chronic heart failure.
This disorder leads to the development of symptomatic arterial hypertension, that is, secondary, and is manifested by the following symptoms:
- at the first stages of diastolic dysfunction, dyspnea during heavy and moderate physical exertion, which was not previously observed, and subsequently difficulty breathing even with little work, and sometimes at rest;
- dysfunction of the ventricle can manifest itself as a dry nagging cough, which intensifies at night or in the afternoon while resting in a prone position;
- a feeling of interruption in the heart, pain in the chest;
- fatigue and decreased performance compared to the previous, “healthy” life.
It is worth remembering that diastolic dysfunction due to the left part of the heart in 45% does not manifest itself.
Diastolic dysfunction of the left ventricle over time may practically not bother the patient. However, this pathology is accompanied by certain symptoms:
- cough, manifested more often in a horizontal position;
- fatigue with habitual physical exertion;
- shortness of breath at first accompanies only during physical exertion, then sharply arises even at rest;
- heart rhythm disturbances, manifested by atrial fibrillation;
- difficulty breathing (dyspnea) at night.
If such symptoms are found, it is necessary to seek medical help and undergo an examination to identify the cause of the discomfort and eliminate the disease at the initial stage.
To avoid the development of most cardiac pathologies, it is necessary to adhere to a healthy lifestyle. This concept includes regular healthy nutrition, sufficient physical activity, the absence of bad habits and regular body tests.
Diastolic dysfunction of the left ventricle, the treatment of which requires high professionalism of the doctor and strict adherence to all his prescriptions, is rare in young active people. That is why, with age, it is important to maintain activity and periodically take vitamin complexes that help to saturate the body with the necessary trace elements.
Diastolic myocardial dysfunction of the left ventricle, which is detected in time, will not do much harm to human health and will not cause serious atrophic changes in the heart tissue.
LG has for some time begun to delight very interesting smartphones. At first, she began to collaborate with Google, having gained invaluable experience in working with the Android operating system. And then very curious flagships began to appear. Now in stores you can easily find the LG G3. This is one of the most advanced smartphones.
On its front panel is a touchscreen display, the resolution of which reaches 2560 x 1440 pixels. The screen of this device contains more points than most computer monitors. And the device surprises with a 13-megapixel laser-guided camera. Permanent memory can be expanded with a microSD card.
In this article we will try to give seven tips for improving the smartphone LG G3. After all, buyers of this device do not use 20% of the opportunities provided. These are the people we want to help. We’ll talk about the features of the LG G3 that you may not be familiar with.
1 How does the heart rest?
The heart is a unique organ, if only because it works and rests at the same time. The thing is that the chambers of the heart of the atrium and ventricles contract in turn. At the time of atrial contraction (systole), the ventricles relax (diastole), and vice versa, when the turn of the ventricular systole comes, the atria relax.
So, the diastole of the left ventricle is the moment when it is in a relaxed state and is filled with blood, which, with further cardiac contraction of the myocardium, is expelled into the vessels and carried throughout the body. The functioning of the heart depends on how fully relaxation or diastole occurs (the amount of blood flowing into the chambers of the heart, the amount of blood ejected from the heart into the vessels).
What is systolic and diastolic heart failure?
Impaired diastolic function
The volume of blood flowing into the lower chambers of the heart decreases, due to which the load on the atria increases, filling pressure increases compensatory in them, pulmonary or systemic stasis develops. Violation of diastolic function leads to the development of diastolic insufficiency, but often diastolic heart failure occurs with preserved systolic function of the left ventricle.
In simple words, the earliest pathological manifestation of the work of the ventricles is their dysfunction in diastole, a more serious problem against the background of dysfunction is diastolic insufficiency. The latter always includes diastolic dysfunction, but far from always with diastolic dysfunction there are symptoms and a clinic of heart failure.
If you read the article “What is chronic heart failure”, then you already know that the stage of the disease and the functional class are always indicated in the diagnosis.
In addition, if an ultrasound of the heart was performed, then the type of insufficiency is also established – systolic or diastolic.
What is systolic heart failure or systolic function?
To answer this question you need to talk a little about the heart cycle.
The heart cycle consists of diastole (relaxation) and systole (contraction) of the ventricles. In diastole, the ventricles collect blood from the atria, and in systole they expel it throughout the body. Depending on how well the heart contracts, its systolic function is determined. At the same time, they are guided by such an indicator obtained by ultrasound of the heart as the ejection fraction.
If the ejection fraction is normal, but the symptoms of heart failure are obvious, then it will be diastolic heart failure or heart failure with preserved systolic function, the last statement is more true if diastolic dysfunction is not confirmed by a special Doppler study.
With diastolic dysfunction, the heart contracts well, but it fills poorly with blood. In diastole, the ventricle should be almost doubled to draw more blood and provide a good discharge, and if it loses this ability, then even with good contractility, the effectiveness of this work will be low.
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