Surgery heart defects are used for both congenital and acquired heart defects. Indications are set depending on the degree of circulatory disorders. The volume and nature of the intervention depend on the type of heart disease.

In congenital heart defects with an obstruction to blood flow, operations are performed to remove the obstruction: for example, dissection of the valvular constriction of the pulmonary trunk, excision of the narrowed portion of the aorta during its coarctation (narrowing). In case of heart defects with overflow of the pulmonary circulation, operations are performed that eliminate the discharge of blood from one channel to another: ligation of the arterial duct, suturing of a defect in the cardiac septum. Until recently, it was believed that surgical treatment of congenital heart defects is best done at the age of three, five years and later. Currently, the development of anesthesiology, resuscitation and surgical intervention techniques allows the correction of many congenital heart defects to be performed at the age of up to 3 years, in the first years and even months of life.

With acquired heart defects - with stenosis of the mitral or aortic openings - operations are used to restore their patency (see Commissurotomy). Elimination of insufficiency of the mitral or aortic valves is carried out by replacing them with artificial or taken from animals (see Valvuloplasty).

Contraindications to surgical treatment of heart disease are abrupt changes in the myocardium, severe decompensation, persistent changes in the lungs, endocarditis in the acute and subacute stages, and severe concomitant diseases.

Surgical treatment of congenital heart defects

Currently, many of the heart defects are completely eliminated by surgery, and for some defects, surgery reduces suffering, increases the patient's resistance to physical activity, and significantly prolongs their life. But the problem of surgical treatment of congenital heart defects has not yet been fully resolved; surgery is still powerless in the face of such defects as the common arterial trunk. tricuspid atresia. Ebstein's disease, etc.

Some existing methods of surgical correction of congenital heart defects are still very dangerous and risky and are under development. Therefore, conservative treatment of congenital heart defects has not lost its significance even now. Certainly, none drug treatment will not be able to change the existing anatomical defects, but in cases of cardiac decompensation of acute attacks of cardiovascular insufficiency, properly carried out symptomatic treatment leads to an improvement in the patient's condition.

The first attempts at surgical treatment of congenital heart defects date back to the end of the last and the beginning of the present century. The idea of ​​ligation of the patent ductus arteriosus first originated with Monroe. Doyen tried to dissect the stenosed orifice of the pulmonary artery with a tenotomy knife passed through the right ventricle. The patient died in a few hours; on the section, stenosis of the arterial cone of the right ventricle was found. This bold operation for that time was preceded by the work of Carrel, in which the operation of dissection of stenotic valves of the pulmonary artery was experimentally developed. This essentially ended the first unsuccessful attempts at surgical treatment of congenital heart defects.

In fact, the era of surgery for congenital heart defects begins on August 9, 1938, when the American surgeon Gross successfully ligated the open ductus arteriosus. The next very important date in cardiac surgery was November 29, 1944, when, at the suggestion of one of the leading American pediatricians Taussig, the surgeon Blalock successfully performed a bypass anastomosis between the subclavian and pulmonary arteries end to side on the left (Taussig-Blalock operation) with tetralogy of Fallot.

In the Soviet Union, A. N. Bakulev, Yu. Yu. Dzhanelidze and P. A. Kupriyanov were the first to operate on children with congenital heart defects.

Currently, operations for congenital heart defects are being undertaken more and more widely and with great success. Surgery for congenital heart defects has ceased to be the property of the leading surgical clinics. Hundreds of surgeries are performed for congenital heart defects.

The leading place in cardiac surgery is occupied by the Research Institute of Cardiovascular Surgery of the Academy of Medical Sciences.

Cardiac surgery, especially surgery for congenital heart defects, is the youngest and at the same time the most difficult branch of surgery. Proper success in the surgical treatment of patients with congenital heart defects can only be achieved through close contact between a cardiac surgeon and an experienced pediatrician and radiologist.

Children with congenital heart defects in the vast majority are very seriously ill. Some of them, due to severe hemodynamic disturbances, cannot tolerate physical activity. Therefore, surgery for congenital heart defects is a difficult test for patients, and the surgical risk remains very high. In this regard, operations in patients with congenital malformations should be accompanied by a number of conditions that increase the body's resistance to possible cardiopulmonary disorders at the time of surgery.

Advances in anesthesiology in recent years have determined the effectiveness of many surgical interventions for congenital heart defects. Currently, all surgeons use only intratracheal anesthesia (most often ether) with continuous oxygen supply and blockade of reflexogenic zones. For some heart defects, in which there is no severe hypoxemia, nitrous oxide can be used. Most surgeons use barbituric acid derivatives for induction anesthesia.

The most common access to the heart is transpleural - through the left pleural cavity, sometimes through the right one (in cases of intervention on the superior vena cava, interatrial septum). With radical surgical interventions ah, associated with the use of extracorporeal circulation devices, some surgeons use pleural access to the heart, when both pleural cavities are widely opened along the third or fourth intercostal space with a transverse intersection of the sternum at the level of the incision.

Pleural access often causes severe cardiopulmonary changes in patients who already have congenital hemodynamic disorders, which ultimately causes sharp violation gas exchange. Therefore, in recent years, more and more often used transsternal access to the heart and great vessels, when the sternum is dissected longitudinally without opening the pleural cavities.

At one time, to a large extent, it was possible to reduce gas exchange disorders by using artificial cooling of patients according to the method proposed by the Canadian surgeon Bigelov. Artificial cooling in conditions of sharp inhibition of the central nervous system inhibits metabolic processes in the body, which reduces the need for oxygen in tissues. Against this background, changes in gas exchange at the time of surgery were less pronounced. Especially noticeable in the state of hypothermia is the resistance of the nervous tissue to oxygen starvation, which was clearly shown by the experiments of V. I. Burakovsky, E. V. Gubler and G. A. Akimov. Under conditions of normal temperature, the dog cannot tolerate the shutdown of cerebral circulation for more than 5 minutes, as the cells of the cerebral cortex die. If the dog's body temperature is lowered to + 28-26 °, then the cessation of cerebral circulation for a period of 15-20 minutes does not cause noticeable changes in the function of the central nervous system.

Artificial hypothermia also has negative aspects, it adversely affects the function of the heart, which, even under conditions low temperature does a great job. downgrade metabolic processes in the myocardium is a favorable hypoxemic background for the occurrence of various disturbances in the functions of excitability and its conduction. It has been experimentally proven that under conditions of general cooling, the arteriovenous difference in healthy dogs higher than at normal temperature, while the arteriovenous difference of the coronary circulation does not change in them.

Fearing cardiac dysfunction under conditions of hypothermia, many surgeons have narrowed the scope of its use. Now shallow hypothermia (lowering the patient's body temperature to 32-30°C) is used by some surgeons to create conditions for turning off the heart from circulation for 6-8, maximum 10 minutes. This time is usually sufficient for suturing a secondary atrial septal defect or dissecting a stenosing valvular ring of the pulmonary artery or aorta on an open heart. Those changes in gas exchange that occur during heart surgery can be compensated to a certain extent by increased oxygen supply, which is achieved by artificial respiration under intratracheal anesthesia (“controlled breathing”). When artificial respiration is performed, the patient's independent breathing should be turned off, which is achieved by giving curare-like drugs (most often ditilin). The very introduction of these drugs somewhat reduces the basal metabolism, reducing muscle tone.

Intratracheal anesthesia with continuous oxygen supply and blockade of reflexogenic zones under conditions of potentiation and controlled breathing allows complex surgical interventions to be performed with minimal consumption of the main drug and ensuring proper gas exchange.

In cases of terminal conditions and clinical death, intratracheal anesthesia makes it possible to most successfully deal with these severe complications by providing a continuous supply of oxygen and the most effective artificial respiration. Without this, heart massage, intra-arterial and intra-aortic blood transfusion do not bring success. However, intratracheal anesthesia with various methods of intervention has its own characteristics. With congenital heart defects with normal and increased blood flow through the lungs, intratracheal ether anesthesia with a mild degree of potentiation can be successfully used. But during manipulations on the main vessels with high pressure (isolation in some cases of the arterial duct, resection of the narrowed isthmus of the aorta), the so-called controlled hypotension can contribute to the successful operation of the operation, when the use of short-acting antihypertensive drugs reduces the maximum arterial pressure to 70-60 mm Hg. Art. Especially valuable is the method of controlled hypotension during operations for coarctation of the aorta, when in most cases blood pressure in the area of ​​surgical intervention is sharply increased.

All operational methods corrections of congenital heart defects are divided into three types: non-cardiac operations (ligation of the arterial duct, resection of the narrowed portion of the aorta, the imposition of bypass anastomoses), intracardiac operations closed heart and intracardiac, performed under direct vision on the heart turned off from the blood circulation.

If the first two types of surgical interventions are feasible under conditions of normal blood circulation for the patient, then intracardiac operations on a heart that is switched off from blood circulation require special conditions for stopped or artificial (extracorporeal) blood circulation. These operations are the most radical and most effective, but their risk is still very high.

The idea of ​​correcting congenital heart disease under direct vision is very tempting and has attracted the attention of many surgeons for several decades. Indeed, it is possible to radically eliminate the defect only under direct vision on the opened heart. But there are many obstacles to this, it is sometimes extremely difficult to overcome them. Blood circulation in the body can be stopped for 2-3, maximum 5 minutes. Therefore, if the heart is turned off from the blood circulation under conditions of normal body temperature of the patient, then surgical intervention on it should be performed for 1-2 minutes, and the rest of the time will be spent on clamping the vessels (turning off the heart from the blood circulation). During this time, there is little that can be done. If the heart is turned off for a longer time, the cells of the cortex, and then the entire brain, die.

The second insurmountable obstacle is the risk of air embolism of the vessels of the brain or heart muscle when opening the heart that is switched off from the blood circulation. The possibility of intracardiac thrombosis after intervention on the heart can also lead to very serious complications.

The first proposals were to perform intracardiac operations on the heart that was switched off from the blood circulation at normal body temperature of the patient. Such operations were carried out very quickly, but the heart was not completely switched off from the blood circulation, but only partially, with the cessation of the outflow, when the aorta and pulmonary artery were clamped. For obvious reasons, these operations have not found clinical application.

In the 20s and 30s of the current century, experiments were successfully carried out in our country to turn off the heart under conditions of artificial (extracorporeal) circulation. In these cases, by clamping the superior and inferior vena cava, as well as the aorta and pulmonary artery, the heart was switched off from the circulation. Blood from the vena cava was sent to a special apparatus - an oxygenator, where it was enriched with oxygen, and returned to the body through one of the branches of the aortic arch or through the femoral artery.

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Women's magazine www.BlackPantera.ru: F.Kh. Kutushev

I. CONGENITAL HEART DEFECTS

1.1 Introduction

1.2.1 Open ductus arteriosus.

1.2.2 Atrial septal defect

1.2.3 Ventricular septal defect

II. ACQUIRED HEART DEFECTS

2.1 Introduction

2.2 Classification of chronic heart failure

2.3 Mitral valve defects

LIST OF ABBREVIATIONS

ASD - ventricular septal defect

VSD - atrial septal defect

coronary artery disease - ischemic disease hearts

MK - mitral valve

I. CONGENITAL HEART DEFECTS

1.1 Introduction

More than 40 thousand children with pathology are born in our country every year. of cardio-vascular system. About half of them die in the first months of life, although with modern diagnosis of the disease, cardiac surgeons could help most patients. Other patients for a long time do not know about heart disease, they come to specialists in advanced and complicated stages of the disease, when surgical treatment is no longer possible or ineffective. Such patients can meet a doctor of any specialty - an obstetrician-gynecologist, pediatrician, therapist, rheumatologist, cardiologist, etc. therefore, every doctor should be able to recognize congenital heart disease in a timely manner, provide the necessary assistance and refer the patient to a specialized medical institution. This requires a solid knowledge of the clinic and diagnosis of heart defects and indications for their surgical treatment.

Frequency and natural flow congenital heart defects

According to the World Health Organization (1974), 8 out of 1,000 live births have malformations of the circulatory system.

There are more than a hundred variants and combinations of congenital heart defects, the most common are the following: ventricular septal defect, tetralogy of Fallot, transposition of the great vessels, coarctation of the aorta. They account for approximately 80% of all congenital heart defects.

The clinic and the natural course of defects are very diverse and depend on the nature and severity of anatomical changes, concomitant diseases. About 70% of patients with congenital heart defects die in the first year of life, although many of them can be helped by emergency surgery.

Some patients survive to adulthood, often without knowing they have congenital pathology hearts. Against the background of already severe degenerative and sclerotic changes in the myocardium, lungs and other internal organs, patients develop cardiac arrhythmias, pulmonary hypertension develops, and heart failure progresses. Surgical treatment of adult patients does not lead to complete recovery, as is usually the case in childhood Therefore, the timeliness of diagnosis and early surgical intervention are of great importance.

In most patients with heart defects, functional disorders appear from childhood - a lag in physical development, increased fatigue and shortness of breath during exercise, cyanosis, liver enlargement, and other manifestations of circulatory failure. Some congenital heart defects (small defects of the interventricular and interatrial septum, moderate narrowing of the valves of the aorta and pulmonary artery, a small open ductus arteriosus) do not cause noticeable functional changes for a long time, but patients remain at an increased risk of infectious and other complications (endocarditis, cardiac arrhythmias and etc.). Heart defects, accompanied by hypoxemia and cyanosis, are more severe, the probable life expectancy with them is always significantly reduced.

1.2 Classification of congenital heart defects

There are several classifications of congenital heart defects, taking into account embryological, anatomical, hemodynamic disorders. It is most convenient in practical terms to divide all congenital malformations into three groups depending on the state of the pulmonary circulation: with increased, normal and reduced pulmonary blood flow. This simple classification is convenient to use in everyday practice: at the very first x-ray examination, it is possible to establish the nature of changes in blood flow in the lungs.

Among congenital heart defects with increased pulmonary blood flow, the most common are patent ductus arteriosus, atrial and ventricular septal defects. As a rule, these are heart defects of the "pale" type - with arteriovenous shunting of blood. Poor oxygen venous blood begins to be discharged in such cases into the arterial bed, leading to hypoxemia and cyanosis.

Pulmonary hypertension is a severe complication of congenital heart defects of the hypervolemic type. It develops in 10-15% of patients, predominantly of school age and adults. There are many classifications of pulmonary hypertension based on the magnitude of pressure in the pulmonary artery, the ratio of general pulmonary resistance to general peripheral resistance (ARR / OPS), the magnitude and direction of blood shunt. The most complete and convenient of them is the classification adopted at the Institute of Cardiovascular Surgery. A.N. Bakuleva (Table 1)

After listening to the symptoms you describe, medical card, the doctor will measure your pulse, blood pressure and use a stethoscope to listen to your heart.

If your doctor suspects that you have a heart condition, he may ask you to undergo a series of special diagnostic tests to help make an accurate diagnosis and prescribe the necessary treatment.

One of these research methods is non-invasive method, i.e. which does not require any internal intervention.

Another type of research is invasive: with the help of instruments introduced into the body, which, as a rule, causes only minor inconvenience to the patient.

x-ray chest
This study allows the doctor to obtain valuable information about the size of the heart, heart chambers and the condition of the lungs.

Treatment of heart valve disease

Under proper medical supervision, taking the necessary medications Many people with heart disease live normal lives.

However, when medications are ineffective or even dangerous, a doctor may recommend surgery to repair or replace the damaged valve or valves.

In some cases, it is possible to restore the valve with the help of a surgical operation - valvotomy (dissection of fused leaflets of the heart valves), valvuloplasty (restoration of valve function). Some valves can be repaired, but those that are severely deformed or damaged must be removed and replaced with artificial heart valves.

There are two main types of artificial valves.

Bioprostheses or biological artificial valves are made up of biological tissue (human or animal).

Mechanical valves made of metal, carbon and/or synthetic materials.

Your doctor will determine which type of valve is best for you based on many factors, including your age, lifestyle, and the nature of your heart disease.

Before the operation

If there is still time before the operation, the doctor will help prepare for it, give the necessary advice, including even exercises and medical preparations.

One of the most important moments is the preparation of the lungs. Smokers should quit smoking as early as possible. Smoking narrows the coronary arteries, promotes blood clotting, increased flow of mucus into the lungs, increases blood pressure and makes the heart chalice. All of these conditions potentially increase the risk of complications after surgery.

Your admission to the hospital can be scheduled the day before your surgery or in the morning of the same day.

Such a schedule allows the medical staff to conduct additional research, give the necessary instructions and prepare for the operation.

Your medical staff consists of a surgeon, cardiologist, anesthetist, nurses. Sometimes the help of other doctors is also required. The surgeon can discuss the details of the operation and the expected results with you.

The necessary care instructions will be given by the nurses, and the exercise therapy therapist will teach you how to breathe and cough properly after the operation. For the necessary tests and selection of donor blood, you will donate blood.

Modern methods surgeries greatly reduce the need for blood transfusions. If necessary, a blood bank with carefully screened blood will be at the ready. Family donors or own blood are preferred if there is sufficient time to prepare the bank.

On the eve of the operation, after midnight, you should not eat or drink liquids. It is very important that you follow all the instructions, otherwise the doctor will have to reschedule the operation for another day. The duration of heart valve surgery can vary. It usually lasts 3 hours minimum.

Operation

In the operating room, measuring devices will be attached to your arms and legs. Thin tubes will be inserted into the vein and artery. Usually this procedure is painless. The anesthesiologist will administer an anesthetic; you will fall asleep deeply, will not feel pain and will not remember the progress of the operation. During the operation, the heart-lung device will take over the functions of your heart and lungs, allowing the surgeon to replace or reconstruct the heart valve.

After operation

After the operation, you will be admitted to the ward intensive care or recovery room. While you are there, highly professional medical staff will constantly monitor your condition and take the necessary control measurements.

The duration of action of painkillers is different. Someone comes to their senses in an hour or two, but for most people it takes more time. At first you will only be able to hear or see, before you gain the ability to move, gradually you will be able to fully control your body.

When you wake up, you will find a breathing tube in your mouth connected to a respirator. The respirator will help you breathe until you can't breathe on your own. If you are unable to speak due to this obstacle, qualified personnel will be nearby to whom you can communicate using various oral and written signs.

The breathing tube, other tubes and wires will be removed at various times after surgery as needed. Drainage tubes coming from the chest prevent the accumulation of fluid around the heart. A urinary catheter will allow urine tests to be performed to monitor kidney function. Intravenous catheters are used to administer fluids and drugs.

Other devices, which can be attached to the neck or wrist, will measure blood pressure and monitor the heart. Electrode patches and leads will be used to measure heart rate and rate. Once the breathing tube has been removed, you will be able to take deep breaths and cough to clear secretions from your lungs. A nurse or therapist will help you.

It is essential that the lungs are clear to avoid pneumonia; it is also an important condition for your recovery. In the intensive care unit, you will be given medication at set intervals. This and other factors can cause some disorientation. If this happens, don't worry, it's not unusual and it won't last long.

Most patients complain about pain and stiffness, but usually they do not experience severe pain.

After intensive care unit

If the doctor decides that you no longer need to stay in the intensive care unit, you will be transferred to another area of ​​the hospital where you can rest better. You will start walking and your recovery process will continue. Then you will be sent home. As your health improves, you will need fewer medications and in smaller doses. The stitches will be removed 7-10 days after the operation. After a few days, you may be allowed to shower or bathe.

With regard to the movements below, the necessary instructions will be given by the doctor and medical staff. Some of our tips will also help you:

Getting out of bed- roll to the side and lower your legs off the bed, using your upper body and arms, try to sit up.

Getting up from a chair- move to the edge of the chair, put your feet under you, try to stand up using the leg muscles. In the same way, in reverse order, try to sit down.

seat- Sit straight with both feet on the floor. The knees should be at the level of the hips. Don't cross your legs.

Picking up objects from the floor- without bending at the waist. Bend your knees, keeping your back straight.

Recovery

The degree of recovery is different in each case, but every day you will gradually feel better.

A doctor who is closely monitoring your recovery will determine when you can return home. The degree of activity, diet, medications, what can be done and what - will not be determined by the medical staff who worked with you.

Ask questions and strictly follow the advice. Everyone wants to get home as soon as possible, but it is not unusual for you to feel fear when leaving the hospital. Knowing what to expect when you return home will help you and your family cope with this change. Successful valve surgery will change your life in a qualitative way and allow you to engage in activities that were not available before the operation.

Your recovery will depend on your age, general health, and the condition of your heart. How you follow all medical advice, exercise and lead a healthy lifestyle will be the envy of your recovery.

Gradually you will feel better and stronger. An echocardiogram should be taken approximately 6 to 12 weeks after surgery to monitor the performance of your new prosthetic valve. The echo results will be the base data for comparison with subsequent changes. In the event of any problems with a prosthetic heart valve, echocardiography is the most readily available diagnostic tool.

Often a comparison with a baseline echo can be helpful for early diagnosis. If the doctor did not refer you to a baseline echo, check if you need to undergo this study. Problems rarely occur after heart valve surgery, but sometimes they do. There are some signs and symptoms that you need to be aware of that require immediate attention. If a problem is detected early, it can be easily resolved.

Seek medical attention immediately if you experience the following symptoms:

1. Chest pain or severe pressure that does not go away within a few minutes.
2. Sudden or gradually increasing shortness of breath.
3. Temporary blindness in one eye or gray veil before the eyes.
4. Weakness, awkwardness or numbness in the face, legs on one side of the body, even if they are temporary.
5. Slurred speech, even for a short period of time.
6. Unusually rapid weight gain, fluid retention, swollen feet at the ankles (weigh every day to control).
7. Weakness, especially if it is accompanied by a fever that does not go away within a few days (some doctors recommend taking the temperature twice a day for 2-3 weeks).
8. Chills or fever with a temperature above 40 degrees.
9. Unusual bleeding or bruising.
10. Dark or even black stools, dark urine. Also pay attention to the presence of blood in them.
11. Loss of consciousness even for a short period of time.
12. A sudden change or absence of a normal sound or sensation in your heart valve as it opens and closes, and in your heart rate and rate.
13. Redness, swelling, discharge or discomfort in the incision area.
14. Burning sensation or change in the frequency of urination.

Medications

You should only take medicines prescribed or approved by your doctor. Aspirin, for example, should not be taken without consulting a doctor.

If you have had a mechanical valve implanted, medications such as anticoagulants or "blood thinners" (usually Phenylin and Warfarin) may be prescribed by your doctor to help prevent blood clots. These drugs prolong the period of time during which your blood clots.

The action of anticoagulants must be carefully monitored using a blood test called prothrombin time (Quick time). The doctor may prescribe a dosage to keep the prothrombin time within certain parameters.

The drug is usually taken once a day at the same time. It is important to take it strictly in accordance with the prescription of the doctor. Your doctor will also tell you how often you need to check your prothrombin time. Your treatment will be adjusted from time to time based on the results of your examination.

Treatment with anticoagulants limits the body's natural ability to stop bleeding. For this reason, you must be especially careful about activities that may cause cuts or bruising. Any head injury can result in serious injury. If this happens, you may experience dizzy spells, headache, weakness or numbness in the limbs, changes in vision, or loss of consciousness.

Discuss any problems that arise with your doctor.

Precautions while taking acticoagulants

If you are taking anticoagulant drugs, you should definitely notify your dentist or doctor about this. In some cases, before this or that treatment, it is necessary to adjust the dosage or stop taking these drugs for a while in order to avoid heavy bleeding.

Infection Prevention

Talk to your doctor or surgeon about the possibility of infection and how to avoid it. For this purpose, it is essential that you receive pre-treatment with antibiotics before visiting the dentist (even for the purpose of cleaning), before any urological procedure (such as a cystoscopy), colon examination, or implantation of any medical device. During all these procedures, bacteria can enter the bloodstream and cause an infectious disease called bacterial endocarditis. Antibiotics are used to prevent this type of infection. Check with your doctor if you notice any signs of infection, including an infection on the surface of the skin.

Activity

Only your doctor can advise you to limit this or that type of activity. Only you can know better than anyone about your general condition. We provide some basic guidelines for your daily activities: Do not push, pull, or lift heavy objects weighing more than 5 kg for 6-8 weeks after surgery

Car driving

You should check with your doctor about when you can drive again. You should not do this before you are sure of complete safety. You can be in the car as a passenger, during a long layover you need to stop every hour and take a short walk. As both a passenger and a driver, you must always fasten your seat belt.

Diet

Your doctor or healthcare team may recommend a diet, avoid certain foods, or supplement your diet. You should stick to weight according to your ages and reduce your salt intake. Proper nutrition is very important for your recovery. Any significant changes to your diet should be discussed with your doctor or healthcare team.

Physical exercise

Do all the exercises your doctor recommends. They help restore health and strength, as well as relieve stress. Your doctor will recommend a cardiac rehabilitation program that will teach you how to properly exercise and lead a healthy lifestyle.

Return to work

After surgery, many patients will be able to return to work and normal work activities. The doctor will advise when it is better to do this, and what you need to limit yourself to.

Smoking

Smoking increases the amount of mucus in the lungs, contributes to the formation of blood clots and increases the workload on the heart. In addition, it contributes to the formation of atherosclerosis (hardening of the arteries). Smoking prevents the necessary amount of oxygen from reaching the tissues and heart muscle. The surgeon usually warns that smoking or any tobacco product is bad for your health. As a rule, people who smoke find it very difficult to quit. If you need help, see a doctor.

sexual activity

Some people who have had heart surgery worry that they will not be able to have a normal sex life after the operation. They will usually be able to return to normal sexual activity within a few weeks. You should discuss this issue with your doctor and let him know if you have any problems.

Trips

Traveling is not contraindicated, but it is necessary to rid yourself of any stressful situations in this regard. Organize your trip in such a way as to distribute rest and physical activity equally. Talk to your doctor about possible deviations from your medication schedule. Always have medicines on hand, always carry prescriptions with you in case you lose your medicines.

emotional changes

Many people are depressed for several days or weeks after surgery. It will take a lot of strength to overcome fear, anxiety and bad mood. You can be irritable, whiny. Some may be tormented by nightmares, while others have a weakening of memory or an inability to concentrate their attention. These are normal reactions and usually go away after a few days or weeks. Discussing all these problems with your doctor and your loved ones will help you a lot.

Remember that heart surgery is not the best time in your life. Only a frank discussion of all questions and problems with doctors, medical personnel, your loved ones is the key to your recovery.

In most cases, valvular heart disease is acquired in nature, as it occurs as a result of rheumatic or infective endocarditis. Valvular defects can also be congenital, however, due to the much greater prevalence of acquired defects, all types of valve damage are described in this chapter.

Acquired heart defects are more often formed in young and middle-aged people. IN recent decades in connection with a decrease in the incidence of acute rheumatic fever, a trend towards a decrease in the proportion of patients with acquired heart defects among cardiac patients is noted.

CLASSIFICATION

Cassification of valvular heart disease is presented in Table. 8-1.

Table 8-1. Classification of valvular heart disease

Acquired defects often affect the mitral valve, less often - the aortic valve, even less often - the tricuspid and pulmonary valve. Multivalvular defects are characteristic of rheumatic heart disease. In complex defects, the overall clinical picture consists of lesions of individual valves, although some manifestations may become uncharacteristic. In general, multivalvular malformations are worse prognostically than single valve malformations.

Sometimes valve dysfunction is not associated with damage to the valve apparatus itself, but with a significant stretching of the heart cavities. In this case, excessive expansion of the valve ring and so-called relative valve insufficiency can occur. In other cases, the normal lumen of the valvular orifice is insufficient to ensure the unhindered passage of blood between the enlarged chambers and dilated vessels, and the situation is regarded as relative stenosis of the valvular orifice.

PATHOGENESIS

If, as a result of valvulitis, the valve leaflets are deformed, shortened, or destroyed, valve closure becomes incomplete and valvular insufficiency occurs. The subsequent fibrosing process and often calcification can fix or intensify the resulting deformities and/or lead to narrowing of the valvular ring - stenosis. In many cases of rheumatic disease, valve insufficiency and stenosis of the same valve opening are combined. Significant destruction of the valves and the occurrence of valvular insufficiency without any signs of stenosis is more characteristic of a defect resulting from infective endocarditis.

In most cases, the formation of rheumatic valvular disease occurs during the period of activity of both primary and recurrent acute rheumatic fever, which in adults is often asymptomatic. The formation of the defect, apparently, continues for 1-3 years after the relief of clinical signs of activity, due to subclinical minimal activity of inflammation, the continuation of fibrosing processes, and later - due to a slow increasing calcification. A defect in infective endocarditis is formed faster (with acute endocarditis - sometimes within a few days).

DIAGNOSTICS

Valvular defects can last for years, decades and occur without subjective symptoms. However, even during this period, early diagnosis is possible, mainly on the basis of auscultation of the heart and echocardiography data.

It should be emphasized that auscultation by an experienced physician often makes it possible to suspect a defect at an early stage. The sensitivity of phonocardiography is much less. It can be useful mainly as a method of recording, documenting sound symptoms at points selected during auscultation.

EchoCG (including Doppler mode) is the main method for objective diagnosis of defects. In its specificity and sensitivity, it significantly surpasses physical and radiological studies. Echocardiography allows early detection of the presence and severity of stenosis or insufficiency, assess the features of intracardiac hemodynamics, the degree of myocardial hypertrophy, the volume of cavities, and characterize the function of the heart. EchoCG is indispensable for multivalvular lesions. This method is also useful for recognizing infective endocarditis, as it makes it possible to detect its characteristic vegetations longer than 4 mm, which are better visualized with transesophageal access.

TREATMENT

In many patients, the main method of treating the defect is partial or complete surgical correction. The exception is patients with advanced stages of the disease, with active carditis, with severe concomitant pathology. The question of the optimal timing of the operation should be decided jointly with the cardiac surgeon. With the improvement of surgical technique, there is a noticeable trend towards expanding the indications for surgical treatment, covering more severe patients. The operated patients, even with excellent immediate results of the operation, still cannot be considered completely healthy, they are subject to systematic observation by a cardiologist.

PREVENTION

Prevention of rheumatic heart disease is reduced to the prevention and early treatment of any streptococcal infection. Prevention with antibacterial drugs is necessary to prevent recurrent attacks of acute rheumatic fever and the progression of the existing defect. Valve damage of any nature predisposes to the development of infective endocarditis. Therefore, any intervention that can lead to at least a short-term bacteremia (dental, surgical, etc.) should be performed one hour after taking the antibiotic.

8.1. MITRAL STENOSE

Mitral stenosis - narrowing of the left atrioventricular orifice.

ETIOLOGY

This defect is almost always due to acute rheumatic fever, usually transferred to young age although the disease may not have been diagnosed in the past. The prevailing mitral stenosis is noted in approximately 40% of patients with rheumatic heart disease (65% of them are women). In the rare Lutembasche syndrome, rheumatic mitral stenosis is associated with birth defect interatrial septum (ASD). Congenital mitral stenosis is extremely rare. Narrowing of the mitral orifice may be due to left atrial myxoma or a large thrombus in it. In aortic insufficiency, auscultatory signs of relative mitral stenosis are occasionally noticeable.

PATHOGENESIS

If the area of ​​the mitral orifice, which is normally about 4 cm 2, becomes less than 2 cm 2, then to maintain cardiac output, the pressure in the left atrium increases, its hypertrophy and dilation occur (the diameter according to EchoCG is more than 4 cm). Subsequently, venous stasis develops in the lungs and reflexively increases the pressure in the pulmonary artery system, which leads to overload and an increase in the right heart. Pulmonary hypertension, initially labile and reversible, later, as fibrosis develops and the pulmonary vascular wall thickens, becomes stable and irreversible (Fig. 8-1).

Rice. 8-1. Hemodynamics in mitral stenosis: a - diastole (blood flow through the narrowed opening of the mitral valve); b - systole. LP - left atrium; LV - left ventricle; A - aorta.

The pressure drop (gradient) at the level of the valvular orifice depends on the area of ​​the orifice and the amount of volumetric blood flow during diastole. The smaller the hole and the more blood passes per unit time through the narrowed opening, the greater the pressure drop and the greater the overload of the left atrium and the worse the hemodynamic consequences of stenosis. The pressure drop especially increases in conditions of increased cardiac output, for example, during exercise, fever, pregnancy. The relationship of hemodynamic disturbances with the magnitude of volumetric blood flow explains the poor tolerance of tachycardia of any nature by these patients, especially if rhythm disturbance occurs suddenly, for example, with the development of a tachysystolic form of atrial fibrillation, with fever, heavy exercise, childbirth. The shortening of diastole further complicates the filling of the left ventricle and leads to a further increase in atrial pressure. Under these conditions, stagnation in the pulmonary circulation, up to pulmonary edema, occurs more often.

The redistribution of blood worsens the conditions of external respiration, predisposes not only to the development of pulmonary edema, but also to respiratory infections. Stretching of the left atrium can be accompanied by the formation of parietal thrombi and embolism of the vessels of the brain, kidneys, spleen and other organs, as well as the almost natural development of atrial fibrillation, after which the tendency to thrombosis and the risk of thromboembolism increases. The narrowing of the mitral orifice, and then hypertension of the pulmonary circulation, cause a decrease in cardiac output, a decrease in perfusion of the organs of the large circle and muscles, which is manifested by weakness, a decrease in working capacity even before development of CHF, dizziness, cold extremities, a tendency to arterial hypotension.

After a period of compensation, which, if acute rheumatic fever does not recur and the defect does not progress, can last decades, right ventricular failure develops with stagnation in the systemic circulation.

CLINICAL PICTURE

COMPLAINTS

65% of patients have a history of rheumatic attacks.

If the defect is mild and there are no excessive loads, then the state of health can remain satisfactory for many years. The asymptomatic period is shortened if streptococcal infections recur.

In typical cases, an early complaint is shortness of breath when climbing uphill, stairs. In severe cases, shortness of breath is provoked by any load, excitement, fever and other factors that increase blood circulation. Attacks of cardiac asthma can occur in the supine position, at night, forcing the patient to sit down. Palpitations, cough, hemoptysis, heaviness in the chest are possible. Angina pectoris is not characteristic of mitral stenosis, but occasionally it is observed in patients with significant hypertension in a small circle. A decrease in cardiac output can lead to symptoms of vertebrobasilar insufficiency (dizziness, fainting), gradually increasing general weakness, especially aggravated after exercise. To weakness, due to its slow increase, patients, gradually reducing household loads, imperceptibly adapt to themselves. Therefore, it may not appear among the active complaints.

With an asymptomatic course of the disease, worsening of the condition may occur with a relapse of acute rheumatic fever, and then part of the complaints (an additional decrease in exercise tolerance, arrhythmias, etc.) may be due to carditis. In relatively rare cases, the first noticeable manifestation of an existing defect may be complications - atrial fibrillation, thromboembolism.

OBJECTIVE EXAMINATION

The appearance of the patient in most cases is without features. In severe mitral stenosis, it can be characteristic: peripheral cyanosis, a sharply defined cyanotic flush, a visible pulsation of the precordial and epigastric region is possible due to an increase in the right ventricle. Draws attention to the tendency to tachycardia and arterial hypotension.

Auscultatory signs of malformation usually precede other symptoms.

In typical cases, a loud (clapping) 1st tone and a jerky tone (click) of the opening of the mitral valve at the beginning of diastole, 0.04-0.12 s after the start of the 2nd tone, are heard above the apex of the heart. As left atrial pressure increases, the valve opens earlier, the interval shortens, and the opening tone may not be perceived separately on auscultation. The opening tone disappears with significant calcification of the valves.

The most specific for mitral stenosis is a rumbling low-frequency diastolic murmur, beginning after the mitral valve opening tone, with protodiastolic and presystolic amplification. Sometimes protodiastolic and presystolic murmurs are heard separately, sometimes only presystolic murmurs are heard. The latter is associated with atrial systole, and therefore it disappears with atrial fibrillation or already in the period preceding the rhythm disturbance. Noise may be accompanied by palpable trembling of the chest wall. The combination of presystolic murmur and mitral valve opening tone is pathognomonic for rheumatic mitral stenosis. In some patients, systolic murmur is also heard, which may be associated either with simultaneously existing mitral insufficiency, or with relative tricuspid insufficiency (especially with a significant increase in the right ventricle).

All the described sound symptoms of mitral stenosis, as well as trembling of the chest wall, are better detected when the patient is on the left side, with a slightly increased rhythm (for example, after a slight load - undressing), while holding the breath on exhalation. The volume of sound symptoms depends on many factors and does not always reflect the severity of the defect.

Above the pulmonary artery, an accent and sometimes splitting of the II tone is revealed, which is associated with hypertension of the small circle. Later, an independent soft protodiastolic murmur associated with relative insufficiency of the pulmonary valve can be heard there.

Phonocardiography is less sensitive than the auscultation of an experienced physician, but allows you to objectify and sometimes more clearly understand the auscultatory picture.

The ECG may remain close to normal. In sinus rhythm, signs of overload of the left atrium are sometimes noticeable [wide (about 0.12 s) double-humped teeth P, especially in I and II standard leads, biphasic teeth P with a wide negative phase in lead V 1] and the right ventricle (an increase in the R, segment reduction ST, negative asymmetrical teeth T in lead V 1), sometimes with the development of incomplete or complete blockade right leg bundle of His. Often noted sinus tachycardia, atrial extrasystole. Significant deformation and expansion of the tooth P allow predicting the rapid development of atrial fibrillation, first paroxysmal, and then permanent, which almost always complicates severe mitral stenosis.

Echocardiography (including Doppler mode) easily and reliably detects mitral stenosis and makes it possible to judge its severity. It allows you to clarify the structure of the valve (the presence of fibrosis, calcification) and a characteristic feature of the movement of the anterior and posterior cusps: being fused, they move concordantly during diastole, and not discordantly, as is normal. With echocardiography, you can measure the size of the cavities of the heart (including the left atrium), calculate the area of ​​the mitral orifice, assess the pressure in the pulmonary circulation, determine the condition of other valves, and sometimes detect parietal blood clots.

X-ray examination is inferior to echocardiography in terms of informativeness. In direct and oblique projections with contrasting of the esophagus, the characteristic features of the configuration of the heart are determined. With a small mitral stenosis, the silhouette of the heart may not change. As the defect progresses, an increase in the left atrium is detected, which leads to straightening of the left contour of the heart ("smoothing the waist") and then to its bulging. In oblique projections, the esophagus is pushed back by the left atrium, along an arc of small radius (no more than 6 cm). The shadow of the pulmonary artery expands. With advanced disease, an increase in the right heart, filling of the retrosternal space with the right ventricle, expansion of large pulmonary vessels and superior vena cava, venous plethora of the lungs are found. The left ventricle is not enlarged. On x-ray, calcifications are sometimes seen in the moving leaflets of the mitral valve.

Cardiac surgery (cardiac catheterization, angiocardiography) is sometimes performed to rule out other cardiac pathology (if this fails when using non-invasive methods) in preparing the patient for surgical treatment of the defect.

COMPLICATIONS

With severe mitral stenosis and in the later stages of the disease, atrial arrhythmias are often observed, especially atrial fibrillation in the form of fibrillation and, less often, atrial flutter: first, a paroxysmal form, and then permanent. Equally natural is the development in the later stages of CHF with stagnation in a large circle, sometimes after the appearance of atrial fibrillation. Among other complications, we note embolism in the organs of the systemic circulation (in patients who have had an embolism, repeated embolism is very likely), a spherical thrombus in the atrium, and repeated infections of the respiratory tract. As with all rheumatic malformations, relapses of acute rheumatic fever with further progression of valvular disease are not uncommon. Infective endocarditis can complicate mitral stenosis, although it is rare in isolated mitral stenosis.

DIAGNOSTICS

Early diagnosis of the defect (at the asymptomatic stage) is possible on the basis of anamnesis, auscultatory signs (diastolic murmur at the apex of the heart, at least weak) and EchoCG data in a polyclinic setting. Examination in a hospital is necessary only in a part of patients, if it is difficult to exclude a complex defect, acute rheumatic fever, and to resolve the issue of surgical treatment.

DIFFERENTIAL DIAGNOSIS

Differential diagnosis is rarely difficult.

Primary hypertension of the small circle is characterized by the absence of an auscultatory picture characteristic of mitral stenosis and signs of enlargement of the left atrium.

Tricuspid stenosis, which also almost always has a rheumatic nature and gives auscultatory symptoms similar to mitral stenosis, is very rare as an isolated defect. It is usually associated with mitral stenosis and aortic valve disease. This defect is characterized by an increase in the right atrium and stagnation in the systemic circulation. With severe tricuspid stenosis, there is no significant stagnation in the small circle, even with the simultaneous presence of mitral stenosis. Careful echocardiography usually makes it possible to diagnose this malformation against the background of a multivalvular lesion.

Relative mitral stenosis in aortic insufficiency (see section 8.5 "Aortic insufficiency"), although it gives auscultatory symptoms consistent with mitral stenosis, there is no opening tone, and signs of aortic insufficiency, including left ventricular enlargement, come to the fore and precede signs of mitral stenosis.

The narrowing of the mitral orifice due to left atrial myxoma can give a picture typical of stenosis, but also without an opening tone. The auscultatory picture, especially the loudness and duration of the murmur, can change immediately when the patient's position changes. The disease may initially be asymptomatic, but is sometimes accompanied by fever, anemia, increased ESR, and weight loss. In the future, with significant obstruction, signs of stagnation in the lungs and a decrease in blood pressure come to the fore. The duration of the disease is usually several weeks or months. There are no signs of other defects. Echocardiography (see Fig. 8-2) and angiocardiography are of decisive importance in the diagnosis, which allow assessing the presence, size and position of the tumor.

Rice. 8-2. Echocardiogram in mitral stenosis. a - in one-dimensional mode: 1 - right ventricle, 2 - left ventricle, 3 - U-shaped curve of oscillation of the anterior leaflet of the mitral valve; b - in two-dimensional mode: 1 - left ventricle, 2 - left atrium, 3 - "sailing" phenomenon of the anterior leaflet of the mitral valve.

TREATMENT

GENERAL ACTIVITIES

Poorly tolerated loads are excluded, i.e. provoking prolonged shortness of breath, palpitations, weakness. Work associated with physical or significant emotional stress, cooling is contraindicated. With a small mitral stenosis, the patient usually tolerates pregnancy and childbirth satisfactorily (during pregnancy, patients should also be observed by a cardiologist). With a pronounced defect, and even more so if there are symptoms at rest, the issue of pregnancy and childbirth should be considered one year after successful surgical treatment. With the development of complications, patients, as a rule, are unable to work, the preservation of pregnancy is not indicated. All patients with mitral stenosis should be observed by a cardiorheumatologist and hospitalized for complications.

MEDICAL THERAPY

Drug therapy is carried out with complications and for the prevention of relapses of acute rheumatic fever and infective endocarditis. Any infectious disease should be treated as soon as it is detected and more aggressive treatment tactics should be applied. If atrial fibrillation is observed in a patient not subject to surgery, recovery sinus rhythm, as a rule, do not produce; are limited to a decrease in the frequency of ventricular contractions (with the exception of rare cases when flicker occurs as an early complication). With tachysystolic flicker, β are useful - adrenoblockers and / or digoxin in small doses, antiplatelet agents. Anticoagulants (warfarin) are also prescribed after a thromboembolic complication. In CHF, an ACE inhibitor, diuretic drugs are additionally prescribed, starting with small doses. Arterial hypotension may complicate the treatment with these drugs. Sinus tachycardia with mitral stenosis is not an indication for the use of cardiac glycosides.

SURGERY

In each case, the feasibility of surgical treatment should be determined.

Optimal candidates are considered patients with isolated uncomplicated mitral stenosis with shortness of breath, but without persistent atrial fibrillation, without significant enlargement of the left atrium, without the development of persistent pulmonary hypertension, and without signs of acute rheumatic fever. They should be referred to a cardiac surgeon, together with whom they decide on the possibility and duration of the operation.

The type of operation (mitral commissurotomy, valvuloplasty, valve replacement) is determined by the cardiac surgeon. They are also trying to use balloon valvuloplasty. Recently, there has been a noticeable trend towards expanding indications for surgical treatment towards more severe patients with combined and multivalvular defects, with some complications. Calcifications, parietal thrombi are not considered contraindications to surgery, although they complicate surgical treatment.

In patients with atrial fibrillation, sinus rhythm may spontaneously recover during surgery or in the immediate postoperative period. If this does not happen, then the normalization of the rhythm with the help of drugs or electropulse treatment is advisable at a later date, after prophylaxis of embolism with anticoagulants for 2-3 weeks.

FORECAST

Mitral stenosis, even slight, may progress due to relapses of acute rheumatic fever, to which such patients are very prone. Most untreated patients die from complications: thromboembolism, CHF. Surgical treatment improves the prognosis, although progression of the disease with the development of restenosis and other complications is possible even with excellent immediate results of the operation. Operated patients should be observed by a cardiologist.

8.2. MITRAL INSUFFICIENCY

Mitral insufficiency (mitral valve insufficiency) can be caused by damage to the valve leaflets, as well as damage to the chords, adjacent myocardium, and valve ring.

ETIOLOGY

The etiology of this defect is diverse.

Mitral insufficiency is often caused by rheumatic endocarditis, leading to deformation and shortening of the leaflets, fibrosis and rigidity of the entire valvular apparatus. Often, rheumatic mitral insufficiency is combined with mitral stenosis, and mitral insufficiency precedes the development of stenosis.

The development of mitral insufficiency is also possible due to deformation and destruction of the valves in infective endocarditis.

Mitral insufficiency as a result of inflammatory damage to the valves sometimes occurs with SLE, rheumatoid arthritis, ankylosing spondylitis, systemic scleroderma.

This defect may be the result of mitral valve prolapse (see Chapter 10 "Mitral valve prolapse") due to myxematous degeneration and stretching of the chords, as well as due to stretching of the papillary muscles during ischemia, infarction, left ventricular aneurysm, trauma and other processes with weakening (sometimes rupture ) papillary muscles; with obstructive hypertrophic cardiomyopathy(due to its characteristic forward displacement of the anterior leaflet of the mitral valve). Mitral insufficiency in Marfan syndrome is associated with increased extensibility of both the chords and the valve ring.

Congenital mitral regurgitation is rare. Calcification of the valve leaflets and valve ring contributes to mitral regurgitation.

Any significant distension of the left ventricle, such as dilated cardiomyopathy, in advanced stages hypertension, aortic insufficiency, can lead to stretching of the valve ring and relative mitral insufficiency.

With all these diseases, we are usually talking about chronic mitral insufficiency, which forms over weeks, months and gradually increases over a longer period. Calcification of the valve leaflets and valve ring contribute to mitral regurgitation.

PATHOGENESIS

With mitral insufficiency, almost all parts of the heart are involved in the pathological process.

Due to the lack of a phase of complete closure of the mitral valve, part of the blood is uselessly moved from the left ventricle to the left atrium and back, causing a volume overload of the left heart: during ventricular systole, atrial overflow occurs, during diastole, the ventricle overflows. Useful ejection is significantly less than the systolic volume, and with severe insufficiency the volume of regurgitation (return) can be equal to the volume of useful emission. Due to the hypertrophy of the left sections and the absence of an obstruction at the level of the aortic valve, the ejection into the aorta remains normal until the development of left ventricular failure. An increase in the left heart contributes to the stretching of the valvular ring and further slow progression of mitral insufficiency, regardless of the recurrence of the underlying disease.

In the later stages, due to the weakening of the left ventricle, the pressure in the left atrium increases, which leads to overflow of the pulmonary veins and reflexively to hypertension in the pulmonary artery system, which further causes overload in the right sections, but usually significantly less than with mitral stenosis.

In some patients with long-term mitral insufficiency, the left atrium, due to the great compliance of its wall, increases especially significantly. In these patients, atrial pressure does not reach a high level, and hypertension of the small circle is moderate. Cardiac output is reduced. Atrial distension predisposes to the development of arrhythmias and the formation of parietal thrombi, which can be a source of thromboembolic complications. However, in general, with mitral insufficiency, atrial fibrillation and thromboembolism occur somewhat less frequently than with mitral stenosis.

CLINICAL PICTURE

COMPLAINTS

Some patients have a history of acute rheumatic fever (which may be asymptomatic) or another disease that can lead to mitral insufficiency. A long-term asymptomatic course is characteristic, when the defect does not affect daily activity. Only in the later stages, with an increase in pressure in the left atrium, the patient begins to be disturbed by gradually increasing weakness, palpitations, shortness of breath during exercise, and later - nocturnal attacks of cardiac asthma. Hemoptysis and complaints associated with thromboembolism in the organs of a large circle are possible, but less characteristic than with stenosis.

OBJECTIVE EXAMINATION

The appearance of the patient in most cases has no characteristic features. Only with severe mitral insufficiency in some patients can peripheral cyanosis and cyanotic "mitral flush" be detected. Heart rate and blood pressure with uncomplicated defect are close to normal. With long-term mitral insufficiency, one can notice signs of an increase in the left ventricle: an increase in the apex beat and its displacement laterally. With severe regurgitation, it is sometimes possible to observe a pulsation of the left parasternal region associated with the filling of the left atrium during blood regurgitation during ventricular systole. In the later stages, a cardiac impulse is also noticeable - a pulsation of the entire precordial region, reflecting an increase in the right ventricle.

The auscultatory picture is less specific than with mitral stenosis.

In typical cases, a weakening or disappearance of the first tone is detected above the apex of the heart, a decreasing systolic murmur of various timbre, duration and volume, conducted to the axillary region and to the base of the heart (to a lesser extent). Occasionally, the noise is accompanied by palpable trembling. The duration of the noise reflects the severity of the defect and is quite constant in different cycles, even in the presence of an arrhythmia. With a severe defect, the murmur is pansystolic, and its decreasing character is not noticeable.

With mitral insufficiency associated with mitral valve prolapse, the murmur usually occurs after an additional systolic tone and increases towards the end of systole.

In the later stages, sometimes 0.12-0.17 s after the onset of the aortic component of the II tone, the III tone is detected.

Sound symptoms are better determined after a small load, with the patient positioned on the left side, with holding the breath at full exhalation. II tone over the pulmonary artery in the later stages is increased and can be split.

INSTRUMENTAL EXAMINATION METHODS

Use the following methods.

The ECG has no abnormalities or shows signs of overload of the left atrium, later - the left ventricle. In the later stages, paroxysmal or constant atrial fibrillation is possible.

Echocardiography allows assessing the condition and movement of the valvular leaflets, the presence and severity of regurgitation (Fig. 8-3, 8-4), the size of the left atrium and other chambers of the heart. Sometimes fibrosis and calcifications are noticeable, with infective endocarditis - vegetation on the valves.

When using the X-ray method (with contrasting of the esophagus), signs of an increase in the left atrium are found in the form of smoothing, and then bulging of the "waist" of the heart. In oblique projections, one can see a decrease in the retrocardial space and pushing back the esophagus along an arc of a large radius (more than 6 cm) by an enlarged atrium. Dilatation of the left atrium in some untreated cases is unusually large. With fluoroscopy, additional expansion of the left atrium (displacement of the esophagus) is sometimes noted during ventricular systole, and occasionally moving calcifications are visible in the region of the valve or valve ring. The left ventricle is usually enlarged. In the later stages, there are signs of an increase in the right parts of the heart, an increase in the vascular pattern in the lungs due to venous plethora and hypertension of the small circle.

Special research methods, including angiocardiography, are appropriate in some patients if surgical treatment is discussed, for a more accurate assessment of the severity of regurgitation and judgment about possible availability other pathology (malformations of other valves, coronary sclerosis).

Rice. 8-3. Echocardiogram with initial mitral insufficiency: a - echo Doppler cardiogram. Regurgitation corresponds to the spectrum of flow velocity in systole. b - color Doppler mapping. Regurgitation corresponds to a mosaic spot in the middle. Different colors reflect the different speed and direction of blood particles within the turbulent flow of regurgitation. Designations: LV - cavity of the left ventricle; LP - left atrial cavity; MR - stream of mitral regurgitation. At the bottom of the figures - ECG. The figure shows the measured characteristics of the regurgitation flow.

Rice. 8-4. Echocardiogram with severe mitral insufficiency: a - echo Doppler cardiogram. Regurgitation corresponds to the spectrum of flow velocity in systole. b - color Doppler mapping. Regurgitation corresponds to a mosaic spot in the middle. Different colors reflect the different speed and direction of blood particles within the turbulent flow of regurgitation. Designations: LV - cavity of the left ventricle; LP - left atrial cavity; MR - stream of mitral regurgitation. At the bottom of the figures - ECG. The figure shows the measured characteristics of the regurgitation flow. Severe mitral insufficiency is distinguished by a more intense systolic shadow in the upper figure, a large color spot and, most importantly, the calculated characteristics of the regurgitation flow shown in the figure.

COMPLICATIONS

Mitral insufficiency is somewhat less common than mitral stenosis, complicated by atrial fibrillation and thromboembolism in the systemic circulation. Atrial fibrillation is better tolerated than with stenosis. At any stage of the disease, infective endocarditis is possible, in the later stages - cardiac (initially left ventricular, later right ventricular) insufficiency. If the defect is of a rheumatic nature, relapses of acute rheumatic fever are possible with further progression of the defect.

DIAGNOSTICS

Adults with a systolic murmur at the apex of the heart, despite the presence or absence of episodes of acute rheumatic fever in history and complaints, should be referred for echocardiography, which provides an early diagnosis of the defect. In most cases, this is possible in a polyclinic setting.

DIFFERENTIAL DIAGNOSIS

Due to the low specificity of auscultatory symptoms, a tendency to overdiagnosis of mitral insufficiency is noted.

This diagnosis was erroneously made to persons with a systolic murmur at the apex of the heart, not associated with a defect. Such noise is often found in healthy people, especially in young people and adolescents. Systolic murmur of non-valvular origin can be with anemia, thyrotoxicosis, vegetative dystonia. In most cases, the noise is not loud, soft timbre, short. These individuals have no other auscultatory changes, the size of the heart chambers is not significantly increased. With echocardiography, a normally functioning valve is found.

Systolic murmur without mitral regurgitation and left atrial enlargement (according to echocardiography and x-ray) is not evidence of a defect. A small mitral regurgitation, sometimes detected near the leaflets during Doppler echocardiography, apparently, may have a different origin. Allow for the possibility of physiological minimal mitral regurgitation in healthy individuals, which may be accompanied by a systolic murmur.

Diagnostic difficulties may arise with a combination of mitral stenosis and mitral insufficiency, tk. the symptoms of both defects are summed up. Usually, signs of one of the defects predominate, which should be reflected in the diagnosis. If, with undoubted mitral insufficiency, some increase (flapping) of the first tone and the opening tone of the mitral valve are detected (even in the absence of diastolic murmur at the apex), then in most cases this indicates a simultaneously existing mitral stenosis. With stenosis, a weakening of the first tone and instrumental signs of at least a slight increase in the left ventricle may also indicate in favor of simultaneously existing mitral insufficiency. Diagnosis is easily established by echocardiography. The detection of a combination of mitral stenosis and insufficiency undoubtedly indicates the rheumatic nature of the disease.

Tricuspid valve insufficiency is also accompanied by systolic murmur, but the point at which it is maximum is located more medially than with mitral insufficiency, and it is heard better when holding the breath while inhaling. There may be a systolic pulsation of the cervical veins and liver. Echocardiography shows tricuspid regurgitation. The right parts of the heart are always significantly enlarged.

With relative mitral insufficiency, attention is drawn to a significant increase in the left ventricle and only a moderate increase in the left atrium (with valvular mitral insufficiency, the relationship is rather reversed).

TREATMENT

Patients are subject to systematic observation by a cardiorheumatologist. With uncomplicated mitral insufficiency, patients are usually active and tolerate moderate exercise satisfactorily. Large loads are contraindicated. The occurrence of complications usually leads to temporary or permanent disability.

MEDICAL THERAPY

Drugs are prescribed for the underlying disease (acute rheumatic fever, infective endocarditis, SLE, etc.), with the development of complications (in these cases, hospitalization is necessary), for the prevention of relapses of acute rheumatic fever, infective endocarditis. In case of development of heart failure, treatment is carried out according to the usual principles (see Chapter 11 "Heart failure"). ACE inhibitors are used, which contribute to some increase in useful output in these patients by reducing blood regurgitation. With the development of persistent atrial fibrillation, β - blockers or digoxin to reduce heart rate, as well as anticoagulants or antiplatelet agents.

SURGERY

Severe mitral regurgitation with initial signs weakening of the left ventricle - an indication for surgical treatment (valvuloplasty or valve replacement). The optimal time for the operation and its type is chosen by the cardiac surgeon. The operation is usually ineffective in the later stages, with a significant increase in the chambers of the heart (end diastolic size more than 7 cm) and a decrease in function (ejection fraction less than 30%) of the left ventricle. The results of the operation are worse in patients with mitral insufficiency associated with dysfunction of the papillary muscle as a result of coronary artery disease. With a pronounced narrowing of the coronary arteries, coronary artery bypass grafting is sometimes performed simultaneously. Patients undergoing surgery are subject to the supervision of a cardiologist.

FORECAST

Mitral insufficiency remains compensated for a long time. Severe defect is prone to slow progression, regardless of the presence of complications. Complications accelerate the development of the disease. Untreated patients die mainly from CHF.

8.4. AORTIC STENOSE

Aortic stenosis - stenosis of the aortic mouth at the level of the aortic valve.

ETIOLOGY

The etiology of aortic stenosis is different.

Rheumatic aortic stenosis is usually associated with aortic insufficiency and mitral valve disease, and this disease is several times more common in men.

Congenital aortic stenosis is often seen in patients with bicuspid aortic valve disease and is usually not associated with other malformations. The hemodynamic consequences of such stenosis may be noticeable already at birth, but more often they appear gradually over the first decades of life.

Acquired non-rheumatic calcific aortic stenosis is often found in the elderly.

Extension ascending aorta of different nature (more often with atherosclerosis of the aorta, aneurysm of the ascending part, stretching of the aorta due to aortic insufficiency, etc.) can lead to relative stenosis of the aortic orifice.

The valvular apparatus in rheumatic or congenital aortic stenosis is particularly prone to calcification, which leads to further progression of the stenosis.

PATHOGENESIS

With significant aortic stenosis, the pressure drop between the left ventricle and the aorta increases during systole, sometimes exceeding 100 mm Hg, an overload of the left ventricle occurs, and the ejection period lengthens. Cardiac output at rest remains normal for a long time due to significant compensatory capabilities of the left ventricle, its overload and gradual concentric hypertrophy. A long period of full compensation is a characteristic feature of this defect (Fig. 8-5).

Rice. 8-5. Hemodynamics in valvular stenosis of the aortic orifice: a - diastole; b - systole. LP - left atrium; LV - left ventricle; A - aorta.

The following mechanisms are involved in the pathogenesis of the disease.

As concentric hypertrophy increases, the compliance of the left ventricular wall decreases, which can lead to an increase in the end-diastolic pressure in it even before the violation of the contractile function of the ventricle and the development of heart failure (diastolic dysfunction). The consequence of this may be an increase in the load on the left atrium ("mitralization" of aortic stenosis).

In the later stages, the force of contraction of the myocardium of the left ventricle decreases, its dilatation occurs, and the increase in cardiac output during exercise decreases. Then, cardiac output decreases at rest, blood supply to organs worsens, and left ventricular failure develops. Later joins and right ventricular failure.

Some patients may experience atrial fibrillation. Arrhythmia is poorly tolerated by these patients, provokes or significantly increases heart failure. Severe left ventricular hypertrophy predisposes to ventricular arrhythmias.

Owing to increased work of the heart and significant hypertrophy of the left ventricle, oxygen consumption by the heart is increased. The stenosis-related increase in left ventricular systolic pressure can lead to mechanical compression of the coronary vessels during systole, making coronary perfusion difficult. As a result, coronary insufficiency, especially subendocardial ischemia, occurs relatively easily in these patients, even without atherosclerotic lesions of the coronary vessels. In the later stages, a decrease in cardiac output further reduces coronary blood flow. At the same time, there may be signs of ischemia of the brain, other organs, limbs.

Relapses of acute rheumatic fever, coronary insufficiency, along with the progression of stenosis, worsen the state of the myocardium, accelerate the development of decompensation.

CLINICAL PICTURE

Aortic stenosis is characterized by a long (for decades) asymptomatic course. Isolated aortic stenosis manifests itself clinically only when the cross-sectional area of ​​the aortic orifice is four times less than normal.

COMPLAINTS

Shortness of breath, angina pectoris, dizziness and fainting, general weakness occur with long-term and severe aortic stenosis and are mainly due to insufficient cardiac output, i.e. actually starting left ventricular failure. At first, they are only noticeable during physical exertion.

OBJECTIVE EXAMINATION

Appearance, pulse, blood pressure remain normal for a long time. Only at a late stage, with a decrease in cardiac output, pallor, a decrease in systolic and pulse pressure are characteristic. The pulse during this period of small filling is flat, which is better seen on the sphygmogram, where the serration of the ascending part of the curve is typical.

Examination reveals signs of left ventricular hypertrophy in the form of amplification and some displacement of the apex beat. Significant expansion of the heart is already noticeable with the development of CHF.

Auscultatory symptoms are the earliest sign to diagnose aortic stenosis.

Above the aorta, a rough systolic murmur is heard with a maximum in the middle of systole (on the phonogram, the noise has diamond shape), carried out on both common carotid arteries, sometimes towards the apex of the heart. The noise is louder when holding the breath on exhalation. With the development of CHF, the noise weakens.

An important diagnostic sign of severe stenosis is systolic trembling over the aorta.

It is possible to increase the I tone above the aorta - an ejection tone or aortic valve opening tone. The aortic component of the II tone is delayed (approaching the pulmonary component or merging with it), weakened or absent. Calcification of the valves contributes to the weakening of tones.

In general, the severity of the defect is judged mainly by the severity of complaints and the size of the left ventricle. Auscultatory data and features of blood pressure are of lesser importance.

INSTRUMENTAL METHODS

The following instrumental studies are used.

The ECG may remain normal for a long time. Later, signs of enlargement of the left ventricle are found. Perhaps a gradually increasing violation of conduction along the left leg of the bundle of His. Changes in the terminal part of the ventricular complex may be associated with coronary insufficiency. In severe stenosis in the later stages, signs of an increase in the left atrium are sometimes determined, and in some patients - atrial fibrillation. The development of atrial fibrillation even before left ventricular failure is uncharacteristic for this defect and usually indicates a simultaneously existing mitral defect.

Echocardiography determines the thickening of the walls of the left ventricle, incomplete opening of the aortic valve, the presence of calcifications in the valves. The dimensions of the cavities remain normal for a long time. Doppler mode makes it possible to estimate pressure drop and valve orifice area.

X-ray examination with a long-term stenosis, despite pronounced concentric hypertrophy, shows only a moderate increase in the contour of the left ventricle. In severe stenosis, expansion of the ascending aorta, calcifications in the aortic valve cusps are noticeable. In the later stages, signs of stagnation in the pulmonary circulation, an increase in the left atrium, and then an increase in the right parts of the heart are revealed.

Special studies (left heart catheterization, angiocardiography) are useful, mainly if the possibility of surgical treatment is discussed. These methods make it possible to clarify the localization of stenosis relative to the valve, more accurately measure the pressure drop at the level of stenosis, evaluate the function of the left ventricle and the role of the defect in the formation of coronary insufficiency, the presence and severity of other valvular lesions. In patients with angina pectoris and those over 45 years of age, coronary angiography is usually required.

COMPLICATIONS

Complications include left ventricular failure, difficult to treat; violations of the coronary and cerebral circulation; infective endocarditis; relapses of acute rheumatic fever (if the defect is of rheumatic etiology). Valve calcification in elderly patients can progress rapidly, shortening the compensation period; sometimes it causes embolism of vessels of a large circle. Sudden death is possible (apparently, arrhythmic nature) and before the development of CHF. However, most untreated patients with isolated aortic stenosis die over the age of 45 years, on average 2-4 years after the onset of signs of left ventricular failure and one year after the addition of right ventricular failure. Thus, the occurrence of heart failure, as well as a significant increase in the heart, are prognostically unfavorable signs.

DIAGNOSTICS

The diagnosis should be made early, at the asymptomatic stage, on the basis of auscultation and echocardiography. TO early symptoms defects include systolic murmur at the base of the heart with conduction to the neck, clinical and instrumental signs of left ventricular hypertrophy. All these data can be obtained during an outpatient examination. Examination in a hospital is necessary in the development of complications or discussion of the feasibility of surgical treatment and in the presence of difficulties in differential diagnosis.

DIFFERENTIAL DIAGNOSIS

The rheumatic nature of aortic stenosis is established on the basis of anamnesis and combination with aortic insufficiency, with rheumatic damage to the mitral valve. With relative stenosis of the aortic orifice, there is no systolic tremor of the chest wall, no calcifications are detected, signs of aortic insufficiency or any disease accompanied by expansion of the ascending aorta are detected. Aortic stenosis should be distinguished from obstructive hypertrophic cardiomyopathy and the rare congenital subvalvular and supravalvular aortic stenosis due to local fibrous thickening near the valve.

In obstructive hypertrophic cardiomyopathy, the murmur is louder on the left side of the sternum and often does not pass to the common carotid arteries, there is no valve calcification and expansion of the ascending aorta. Echocardiography is critical to the diagnosis, showing significant thickening of the interventricular septum compared to back wall left ventricle.

Congenital subvalvular aortic stenosis does not give an increased tone of ejection into the aorta, calcification is not detected. Clarify the diagnosis during catheterization of the left heart, determining the level of pressure drop.

Supravalvular aortic stenosis (a rare congenital anomaly) is sometimes associated with delayed mental development, the characteristic appearance of the patient's face, hypoplasia of the ascending aorta, narrowing of large peripheral arteries, as well as branches of the pulmonary artery, family distribution. In contrast to aortic stenosis, the aortic component of the II tone is increased, the murmur is better detected over the carotid arteries, there is no ejection tone and post-stenotic expansion of the aorta. Blood pressure on the right and left arms can be different. The final diagnosis is made using left heart catheterization and angiocardiography.

The association of angina pectoris with aortic stenosis usually becomes clear when massive left ventricular hypertrophy and other signs of stenosis are detected. In middle-aged men, one has to resort to coronary angiography in order to reliably exclude simultaneously existing coronary artery disease. It should be borne in mind that exercise tests in the presence of severe aortic stenosis are contraindicated due to the risk of provocation of ventricular arrhythmias and ventricular fibrillation.

TREATMENT

GENERAL ACTIVITIES

Patients are subject to the supervision of a cardiorheumatologist. They can remain able-bodied for a long time if the work is not associated with great physical stress. Large loads, such as sports, should be excluded, even if subjectively they are well tolerated (which is not uncommon). Prevention of infective endocarditis is important, with rheumatic disease - prevention of acute rheumatic fever.

MEDICAL THERAPY

Complications are forced to resort to drug therapy. Developed CHF is difficult to treat and quickly becomes refractory. Cardiac glycosides are generally contraindicated. ACE inhibitors are ineffective. Diuretic drugs should be used with great caution as they reduce preload and can markedly reduce an already reduced cardiac output. Nitroglycerin and other drugs containing nitric oxide may be effective for angina. In the event of atrial fibrillation, which usually sharply worsens the patient's condition, a temporary effect can be achieved by restoring sinus rhythm.

SURGERY

The main treatment is surgical (usually valve replacement). The consultation of a cardiac surgeon should be directed primarily to young patients with severe aortic stenosis, even if it does not give significant symptoms, and older individuals in whom the defect, being isolated or sharply predominant, limits activity. In these individuals, if necessary, coronary artery bypass grafting is also performed at the same time. In the presence of contraindications to surgery, not related to the state of the heart, sometimes resort to balloon valvuloplasty. After a successful operation, along with an improvement in the general condition and expansion of functionality, a partial regression of left ventricular hypertrophy is usually noted. Operated patients should remain under the supervision of a cardiologist.

8.5. AORTIC INSUFFICIENCY

Aortic insufficiency - the inability to completely close the aortic valve, usually due to structural changes, destruction or wrinkling of the valves.

ETIOLOGY

Aortic insufficiency can be caused by the following diseases.

Acute rheumatic fever is one of the most common causes of this defect. Rheumatic aortic insufficiency is often associated with aortic stenosis and mitral valve disease.

Other causes, as a rule, lead to isolated aortic insufficiency, which is much more common in men: infective endocarditis, syphilitic and other aortitis, rheumatoid arthritis and other rheumatic diseases, especially ankylosing spondylitis.

Rarely, aortic insufficiency may be congenital [including bicuspid aortic valve, sometimes associated with ventricular septal defect (VSD), aortic sinus aneurysm].

Severe hypertension, atherosclerosis of the aorta due to stretching of the aortic orifice sometimes lead to relative aortic insufficiency. Apparently, the inferiority of the middle layer of the aorta plays a significant role in the development of relative aortic insufficiency. This is the same nature of relative aortic insufficiency in ascending aortic aneurysm, Marfan's syndrome.

With infective endocarditis, trauma, dissecting aortic aneurysm, acute aortic insufficiency may develop, which differs in some pathophysiological and clinical features.

PATHOGENESIS

Incomplete closure of the aortic valve during diastole causes some of the blood to return from the aorta to the left ventricle, resulting in diastolic ventricular overload and peripheral circulatory deficit. The volume of regurgitation approximately corresponds to the severity of the valvular defect. An increase in regurgitation is facilitated by a rare rhythm and an increase in peripheral vascular resistance. With a pronounced defect, the volume of regurgitation can reach the volume of useful ejection. Systolic output from the left ventricle (useful output and volume of regurgitation) is increased. The result is an increase in systolic and pulse blood pressure and a decrease in diastolic (Fig. 8-6).

Rice. 8-6. Hemodynamics in aortic valve insufficiency: a - diastole; b - systole. LP - left atrium; LV - left ventricle; A - aorta. The light arrow indicates the jet of blood regurgitation from the aorta into the left ventricle.

Large compensatory capabilities of the left ventricle, its hypertrophy allow in most cases to maintain a useful output at a normal level for many years. Load tolerance is initially normal. With a compensated defect during exercise due to tachycardia with a shortening of diastole and a slight decrease in peripheral vascular resistance, the volume of regurgitation even decreases. Hypertrophy of the wall of the left ventricle is less pronounced than in aortic stenosis. In the later stages, an increase in end-diastolic pressure in the left ventricle (diastolic dysfunction) can lead to overload of the left atrium, and dilatation of the left ventricle - to relative mitral insufficiency ("mitralization" of the aortic defect). With the exhaustion of the compensatory capabilities of the left ventricle, exercise tolerance worsens, left ventricular failure develops. Later joins and right ventricular failure.

Aortic insufficiency adversely affects the coronary circulation. On the one hand, increased heart work and left ventricular hypertrophy increase oxygen consumption. On the other hand, an increase in left ventricular end-diastolic pressure as a result of diastolic regurgitation impedes coronary blood flow during diastole.

The defect can progress due to the activity of the underlying disease (acute rheumatic fever, infective endocarditis, aortitis, etc.), as well as due to the gradual stretching of the aortic orifice by excessive ejection.

CLINICAL PICTURE

COMPLAINTS

Characterized by a long (often decades) asymptomatic existence of the defect, when the patient is able to perform even significant physical activity. Complaints come later.

Early symptoms include a feeling of increased heart contractions in the chest and a feeling of pulsation of blood vessels (in the head, in the limbs, along the spine), especially after exercise and when lying on the left side. In severe aortic insufficiency, general weakness, dizziness, and a tendency to tachycardia at rest are possible.

Later, with the weakening of the left ventricle, shortness of breath during exercise, nocturnal cardiac asthma joins. CHF, having arisen, is poorly amenable to drug therapy and progresses relatively quickly.

Attacks of angina pectoris are possible, even in young people, occurring during exercise or at rest, at night, usually difficult to stop with nitroglycerin.

OBJECTIVE EXAMINATION

Many patients are pale, limbs are warm. On examination, symptoms associated with high pulse pressure are sometimes noticeable early: increased pulsation of the cervical and other peripheral arteries, arterioles of the nail bed (when the nail tip is pressed), pulsation of the pupils, movements of the limbs and head, respectively, for each systole. Hypertrophy of the left ventricle is manifested by an increase in the apical impulse and its displacement to the left and down. The apex beat can become diffuse. In the anterior region of the neck above the sternum and in the epigastrium, an increased pulsation of the aorta is palpated.

Characterized by an increase in systolic (sometimes up to 200 mm Hg) and pulse pressure, as well as a decrease in diastolic (sometimes up to 0 mm Hg). On large arteries (brachial, femoral) you can listen (sometimes this requires a stronger pressing of the stethoscope) double noise. The pulse is fast and high. On the sphygmogram, the dicrotic notch, reflecting the closure of the aortic valve, is partially or completely smoothed out. In the later stages, diastolic BP may increase slightly, reflecting a significant increase in end-diastolic pressure in the weakening left ventricle and is partly due to the vasoconstriction characteristic of severe CHF.

The auscultatory picture has the following characteristic features.

Mandatory auscultatory sign of aortic insufficiency is a low-pitched high-frequency decreasing diastolic murmur, starting immediately after the second tone, occupying the initial part or the entire diastole, with a maximum in the third intercostal space on the left near the sternum or above the aortic valve. This noise, due to its high frequency, is sometimes poorly recorded on the phonocardiogram. The duration of the murmur is proportional to the severity of the regurgitation, and is best heard while holding the breath after a full expiration, with the patient in a sitting position with an inclination forward or in the supine position and on the elbows, as well as during isometric exercise.

In patients with severe aortic insufficiency, a systolic murmur over the aorta is often heard, usually due to increased systolic output and relative aortic stenosis. In rheumatic patients, this noise may also be associated with organic stenosis of the aortic orifice. The systolic murmur, regardless of its nature, is usually louder than the diastolic murmur.

The aortic component of the II tone is weakened. I tone is sometimes also weakened. With a significant expansion of the mouth of the aorta, a loud tone of expulsion into the aorta is possible, almost coinciding with the I tone. III and rarely IV sounds can be heard (if they are not overlapped by diastolic murmur).

Relatively rarely, an independent diastolic murmur is heard above the apex - protodiastolic or presystolic (Flint's murmur), associated with displacement of the anterior leaflet of the mitral valve by a regurgitant jet and the occurrence of relative mitral stenosis. This phenomenon is not accompanied by a mitral valve opening tone and any noticeable increase in the left atrium. In such cases, echocardiography is necessary to rule out organic mitral stenosis.

FLOW

Repeated episodes of acute rheumatic fever are possible. After a long asymptomatic period, left ventricular failure develops, which usually progresses rapidly in the future. Infective endocarditis is the cause of aortic insufficiency and at the same time can complicate aortic insufficiency of any nature, at any stage. Often there is insufficiency of the coronary arteries.

INSTRUMENTAL METHODS

Conduct the following instrumental studies.

The ECG usually shows sinus rhythm and signs of left ventricular hypertrophy. Changes in the terminal part of the ventricular complex may be partly associated with coronary insufficiency. Quite often blockade of the left leg of a ventriculonector is gradually formed.

Echocardiography reveals increased systolic movement of the left ventricular wall and trembling of the anterior leaflet of the mitral valve caused by a jet of regurgitation. Sometimes the absence of closure of the aortic valve leaflets during diastole is found. Deformation of the valves may be noticeable. Signs of vegetation on them indicate infective endocarditis, which complicates this defect relatively often. Two-dimensional echocardiography allows you to better assess the increase in the left ventricle and features of its systolic function. With Doppler echocardiography, the severity of regurgitation can be measured (Fig. 8-7).

An X-ray method reveals an increase in the left ventricle, sometimes significant. The "waist" of the heart is underlined. Only at a late stage, when increased pressure in the left atrium and relative mitral insufficiency lead to an increase in the left atrium, does the "waist" become flattened. Calcifications are possible in the leaflets of the aortic valve. Noticeable increased pulsation of the ascending aorta, the shadow of which is expanded. With the development of left ventricular failure, signs of stagnation in the lungs are revealed. If the defect is small, then the radiograph, as well as the ECG, may remain close to normal.

Special cardiological examinations (cavity probing, angiocardiography) make it possible to more accurately measure the volume of regurgitation, assess the effect of the defect on hemodynamics, and clarify whether there are other defects. With the help of coronary angiography, the condition of the coronary arteries is assessed. These studies are sometimes performed in preparation for surgery.

Rice. 8-7. Doppler echocardiogram in aortic valve insufficiency. The arrow indicates abnormal turbulent diastolic flow under the aortic cusps in the outflow tract of the left ventricle.

DIAGNOSTICS

Early diagnosis is usually not difficult. It is based on the characteristics of the peripheral circulation, auscultatory signs [protodiastolic murmur in the third intercostal space on the left (even if short and weak)] and echocardiography data.

DIFFERENTIAL DIAGNOSIS

Required differential diagnosis with the following diseases.

Features of the peripheral circulation, characteristic of aortic insufficiency, can be observed with open ductus arteriosus. In therapeutic practice, this defect is found in adolescents and young adults. Auscultatory for him is typical continuous systolic-diastolic murmur at the base of the heart, ie. higher than in aortic insufficiency. Indirect signs of hypertension of the small circle are noticeable. Sometimes the anamnesis (noise heard from childhood, frequent pneumonia) allows us to clarify the diagnosis.

A high rapid pulse by itself is not specific to aortic insufficiency. It can be observed with fever, anemia, thyrotoxicosis.

A decrease in diastolic blood pressure, sometimes to zero, occasionally occurs with severe autonomic dystonia, especially in adolescents.

In all these cases, echocardiography allows us to clarify the structure and function of the aortic valve.

TREATMENT

GENERAL ACTIVITIES

Many patients with aortic insufficiency are able to perform a lot of physical activity and even play sports, but since the diagnosis is known, excessive exercise should be avoided, as they hasten the depletion of compensation reserves.

MEDICAL THERAPY

To slow down the progression of the defect, the treatment of the underlying disease is of decisive importance: acute rheumatic fever, infective endocarditis, rheumatoid arthritis, etc. Additional drug treatment is necessary, mainly in the event of complications. As a rule, hospitalization is indicated for such patients. In the treatment of CHF (unless it is partially associated with a relapse of acute rheumatic fever), it is usually possible to achieve only a limited and temporary effect. ACE inhibitors, by reducing afterload, may slightly reduce the amount of regurgitation. Rational treatment with diuretics is important. Cardiac glycosides, β - blockers in these patients should be used with caution, because. a decrease in heart rate under their influence can significantly worsen peripheral circulation. Therefore, it is more beneficial to keep them moderate tachycardia, about 80-90 per minute.

SURGERY

For surgical treatment (valve replacement), patients with severe isolated aortic insufficiency, without an exacerbation of the underlying disease, with the very initial signs of decompensation, are more suitable. Both before and after surgery, prevention of infective endocarditis is important.

8.6. ACUTE AORTIC INSUFFICIENCY

Etiology. Acute aortic insufficiency is associated with infective endocarditis (cusp perforation), dissecting aortic aneurysm, or trauma.

Clinical painting. The left ventricle is usually almost not enlarged, but its volume overload is especially great. Therefore, in the clinical picture, against the background of signs of the underlying disease, acute left ventricular failure (shortness of breath, cardiac asthma, pulmonary edema) often predominates.

The patient has tachycardia. Typical for chronic aortic insufficiency changes in blood pressure and other features of the peripheral circulation are usually less pronounced. The auscultatory picture is consistent with chronic aortic insufficiency, often showing a protodiastolic gallop rhythm. There are usually no characteristic changes on the ECG. Doppler echocardiography allows you to verify aortic regurgitation and assess its severity. An X-ray method reveals an increase in the movements of the left ventricle, which has normal or slightly enlarged dimensions. There is no expansion of the ascending aorta (alterations of the aorta may be associated with a dissecting aneurysm or trauma). Signs of venous congestion in the lungs (sometimes pulmonary edema) contrast with the size of the left ventricle close to normal.

Treatment. Patients are treated similarly to patients with acute mitral insufficiency. In the case of infective endocarditis, if against the background of therapy with diuretics, ACE inhibitors, as well as antibiotics, rapid positive effect, then the surgical treatment of the defect that has arisen is postponed until the maximum stabilization of hemodynamics and suppression of infection. In the absence of a quick effect, an emergency operation is resorted to - valve prosthetics. With dissecting aneurysm and trauma, the time of possible surgical intervention, including aortic valve replacement, is determined in connection with the underlying disease.

Forecast. The prognosis is determined by the underlying disease, the volume of regurgitation and the severity of left ventricular failure.

8.7. TRICUSPITAL STENOSE

Tricuspid stenosis is a relatively rarely diagnosed defect, usually, as a rule, combined with tricuspid insufficiency, mitral stenosis, and defects of other valves. This defect is somewhat more common in women.

ETIOLOGY AND PATHOGENESIS

Tricuspid stenosis is caused by the following diseases.

Usually the defect is of rheumatic origin.

Very rarely, tricuspid stenosis may be due to carcinoid syndrome, endocardial fibroelastosis.

The defect leads to an overload of the right atrium and stagnation in the systemic circulation.

CLINICAL PICTURE

Characterized by peripheral cyanosis, severe stagnation in the systemic circulation, especially significant swelling of the jugular veins, high wave A phlebogram (if sinus rhythm is preserved). The auscultatory picture is similar to that of mitral stenosis:

Diastolic murmur with protodiastolic and presystolic enhancement;

Tricuspid valve opening tone.

Auscultatory signs are heard more clearly over bottom sternum, while holding the breath while inhaling. Palpable trembling is uncharacteristic due to the low pressure gradient. Unlike mitral stenosis, there are no signs of hypertension of the small circle, venous plethora of the lungs and a significant increase in the right ventricle.

On the ECG, signs of overload of the right atrium are noted: a high pointed tooth P, especially in II and III standard leads, often atrial fibrillation. Echocardiography detects the thickening of the leaflets and allows you to evaluate the pressure drop across the valve. The X-ray method determines the increase in the right atrium and the expansion of the superior vena cava. Valve calcification is rare. If surgical treatment is discussed, then the severity of tricuspid stenosis is clarified by probing the right heart: the pressure gradient at the valve level in tricuspid stenosis is 3-5 mm Hg, rarely more (normally up to 1 mm Hg. ).

DIAGNOSTICS

When combined with severe mitral stenosis (as often happens) and other defects, tricuspid stenosis is diagnosed with great difficulty. Right atrial enlargement is a relatively specific finding, suggesting tricuspid stenosis even in multivalvular lesions. Severe tricuspid stenosis prevents venous plethora of the lungs, due to the simultaneous presence of mitral stenosis.

TREATMENT

Usually treated for CHF. In rare cases, surgical treatment is resorted to - tricuspid commissurotomy, or, more often, valvuloplasty or valve replacement (since stenosis is usually combined with insufficiency). The decision on surgical treatment to a large extent depends on the presence and severity of other valvular lesions, the state of the myocardium.

8.8. TRICUSPITAL INSUFFICIENCY

ETIOLOGY AND PATHOGENESIS

The causes of tricuspid insufficiency are listed below.

Tricuspid insufficiency in most cases is relative and is associated with significant dilatation of the right ventricle of various origins (valvular, congenital malformations, chronic cor pulmonale, later stages heart failure with hypertension, atherosclerotic cardiosclerosis, with dilated cardiomyopathy and other myocardial diseases), usually already against the background of severe right ventricular or total heart failure.

Organic tricuspid insufficiency may be rheumatic in nature and is usually associated with tricuspid stenosis and other valvular defects.

Other causes of organic tricuspid insufficiency include infective endocarditis (eg, in intravenous drug users), Ebstein anomaly, carcinoid syndrome, and endocardial fibroelastosis.

Tricuspid insufficiency is accompanied by regurgitation of blood from the right ventricle into the right atrium during systole, which causes an overload of the right heart and a decrease in cardiac output (Fig. 8-8). Atrial dilatation contributes to the development of atrial fibrillation.

Rice. 8-8. Hemodynamics in tricuspid valve insufficiency: a - diastole; b - systole. LA - pulmonary artery; RV - right ventricle; PP - right atrium; IVC - inferior vena cava; SVC - superior vena cava. The light part of the arrow indicates a stream of blood regurgitation into the right atrium and vena cava.

CLINICAL PICTURE

Characterized by significant weakness, diffuse cardiac impulse, severe right ventricular failure with systolic pulsation of the liver and jugular veins (the most specific clinical sign). The pulsation of the jugular veins is noticeable to the eye (not palpable) and can be confirmed by the phlebogram (increased V wave). A systolic murmur is heard with a maximum medial to the apex, aggravated by inhalation. While maintaining sinus rhythm (which is uncharacteristic), a presystolic gallop rhythm is possible.

On the ECG, signs of overload of the right heart and almost always atrial fibrillation are noted; there may be changes associated with the underlying disease. EchoCG and X-ray method reveal an increase in the right heart, increased motor activity of the right ventricle; there may be signs of additional expansion of the right atrium during ventricular systole. Doppler echocardiography allows early visualization of regurgitation.

TREATMENT

Treatment of the underlying disease, CHF, and reduction of pulmonary hypertension can lead to some reduction in heart size and a decrease in the severity of relative tricuspid insufficiency. In rare cases, surgical treatment is used - valvuloplasty or valve replacement as part of the treatment of multivalvular disease. In cases of surgical treatment, success is usually limited.

FORECAST

In most cases, relative tricuspid insufficiency occurs already with significant changes in the myocardium, so the prognosis is generally unfavorable. If the defect was preceded by left ventricular failure, then shortness of breath, especially painful for the patient, slightly decreases due to the deposition of fluid in peripheral edema, i.e. there is some subjective improvement, despite further deterioration of hemodynamics.

8.9. PULMONARY VALVE DEFECTS

Pulmonary stenosis is almost always congenital (see Chapter 9, Congenital Heart Disease).

Valve insufficiency is usually relative due to stretching of the orifice of the pulmonary artery caused by severe hypertension of the pulmonary circulation of any nature. Rarely, the defect is associated with rheumatic valve disease, infective endocarditis.

The hemodynamic consequences of valve insufficiency (both relative and organic) are usually small. The most characteristic is a high-frequency soft decreasing diastolic murmur in the second intercostal space on the left near the sternum, in combination with radiographic and echocardiographic signs of an enlarged right ventricle and dilated pulmonary artery. Pulmonary hypertension corresponds to the emphasis of the II tone over the pulmonary artery. Possible right ventricular failure.

Treatment should be carried out in order to stop the underlying disease and reduce pressure in the pulmonary artery. The severity of heart failure and the overall prognosis depend more on the severity of pulmonary hypertension than on the amount of regurgitation.

8.10. COMPLEX FAULTS

Defects involving various valves, with a combination of stenosis and insufficiency at the level of one valve, are quite common, and they are especially characteristic of rheumatic heart disease, although they can occur after infective endocarditis. Symptoms consist of signs and syndromes of damage to individual valves (hypertension of the small circle, coronary insufficiency, heart failure, etc.). EchoCG allows you to judge the structure and function of individual valves. The diagnosis should list the existing lesions and, if possible, highlight the predominant, hemodynamically most significant, which is important when discussing surgical treatment. Treatment approaches are similar to those for isolated valvular disease. Complex defects, as a rule, have a worse prognosis than isolated ones, and their surgical treatment is technically more difficult.

an arrhythmia characterized by sudden attacks increased heart rate, in medicine is called paroxysmal tachycardia. In this case, the heart rate per minute is from 140 to 250 beats per minute. The main cause of the pathology is the repetition of the input impulse and circular circulating excitation through the myocardium, which disrupts the heart rhythm.

A pathological cardiac condition is preceded by extrasystole, which must be treated in order to avoid complications.

Classification

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Forms of pathology

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Reasons for development

The pathogenesis of the disease has not been reliably elucidated. The main causes of paroxysmal tachycardia include:

• increased tone of the sympathetic department of the NS (nervous system);
• prolonged stress;
• violations in the work of organs and their systems;
• osteochondrosis;
• neurosis;
• dystrophy of the heart muscle (heart disease, cardiosclerosis, infectious diseases, etc.);
• severe alcohol intoxication;
• the negative impact of toxic substances;
• congenital and acquired cardiac anomalies;
• narcotic substances;
• smoking;
• high blood pressure.

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Course of the disease

The development of a continuously relapsing form of paroxysmal tachycardia can last for years. The basis of development is a repeated impulse and a constant circular circulation of excitation. As a rule, attacks overtake a person unexpectedly, without any preliminary symptoms. Their duration can vary from a few seconds to 2-3 hours, in rare cases - up to several days. Atrial paroxysmal tachycardia differs from supraventricular tachycardia in less pronounced negative symptoms and is considered less dangerous. With serious blood flow disorders, arrhythmia attacks occur. The disease provokes a serious risk to the health and life of the patient.

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Symptoms and signs

Trembling in the hands and feet is one of the symptoms of the disease.

In the intervals between paroxysmal attacks, the patient feels quite healthy. Description chronic course diseases will have symptoms depending on the type and form of pathology. Paroxysmal tachycardia has the following symptomatic features:

• trembling in hands and feet;
• sudden loss of body weight;
• increased irritability;
• fragility and hair loss.

If the cause of paroxysmal tachycardia is congenital or acquired heart disease, or chronic heart failure, the following symptoms appear:

• severe shortness of breath;
• increased fatigue;
• noise in ears;
• bouts of nausea;
• flatulence;
• increased sweating;
• fainting state;
• heart pains.

The attack is characterized by tremors in the chest and subsequent strong heartbeat. Patients feel physically how their heart is pounding. At the same time it is felt great weakness, shortness of breath, vision and speech may be impaired, sensitivity in the limbs may be lost. Paroxysmal ventricular tachycardia can cause loss of consciousness. May happen clinical death in which there is no pulse and breathing.

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Consequences of paroxysmal tachycardia

Pathology is dangerous without the necessary therapy. It can lead to serious problems with health, and in the worst cases, even death. Often there are problems with the respiratory organs, thrombosis of the renal vessels, during the examination, atrial fibrillation is noted. There is a risk of myocardial infarction, acute heart failure and pulmonary edema. Paroxysm of supraventricular tachycardia rarely causes serious complications with timely diagnosis and a properly selected course of therapy.

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Diagnostic methods

If necessary, 24-hour monitoring of the heart rate is carried out using an electrocardiogram.

The doctor makes the primary diagnosis based on the history of the disease and characteristic symptoms. When listening to heart beats, tachycardia is detected. There is severe hypotension when measuring pressure or reduced systolic pressure. Electrocardiography is prescribed to confirm the preliminary diagnosis of "paroxysmal tachycardia". Atrial and ventricular tachycardia on the ECG have clear differences. The doctor, after conducting basic research, may prescribe such additional methods for diagnosing the heart:

• ultrasonography;
• multislice computed tomography;
• echocardiography;
• coronarography;
• electrophysiological examination through the esophagus;
• magnetic resonance imaging.

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treating doctor

Paroxysmal tachycardia is treated by a cardiologist. He specializes in diseases of the cardiovascular system. It studies the influence of the work of the heart on the internal organs and their systems. A timely visit to a cardiologist if paroxysmal tachycardia is suspected increases the chances of saving a life and avoiding health problems in the future.

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Treatment of the disease

The main goal in paroxysmal tachycardia is to prevent further occurrence of attacks and to stop the disease during periods of remission. The treatment was aimed at reducing the number of PT attacks by taking medications. The action of drugs is aimed, among other things, at preventing serious complications that provoke paroxysmal tachycardia. First health care carried out by healthcare workers.

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Medications

The pathology treatment regimen is prescribed by a cardiologist.

Medicines, their dosage and duration of treatment are prescribed by a cardiologist, based on the clinical picture of the disease. For the treatment of paroxysmal tachycardia, drugs with a sedative effect are used. These include barbiturates, tranquilizers and bromine. At the beginning of treatment, beta-blockers Atenolol and Metoprolol are often used. If the myocardium is not affected and there is no heart failure, the doctor may prescribe a therapeutic course with Quinidine. For treatment, tablets, droppers, injections are used, depending on the professional choice of the doctor.

If a diagnosis of paroxysmal tachycardia has been made and myocardial damage has developed, heart failure has been diagnosed or seizures have occurred during pregnancy, Isoptin is used. The main component of the drug is foxglove. An effective effect is produced by a combination of digitalis and Quinidine drugs, it is often used when an attack of paroxysmal tachycardia occurs.

It should be remembered that self-medication for heart disease is extremely dangerous and can lead to very serious consequences both for the health and for the life of the patient.

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Surgery

Severe course of the disease and lack of positive results from exposure medicines calls for drastic measures. In such cases, surgical treatment is recommended. The operation is aimed at the destruction of abnormal cardiac sources of rhythm and rupture of existing, additional paths conducting impulses. It may be necessary to install a pacemaker.

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Treatment with folk remedies

Tincture is consumed daily half an hour before meals.

Alternative methods of treating paroxysmal tachycardia include taking Eleutherococcus extract. The extract should be drunk daily, 20 drops half an hour before meals. It is also recommended to eat a lot of fresh fruits and vegetables. A good calming effect is produced by hot baths with the addition of a decoction of valerian officinalis.

To reduce the heart rate caused by paroxysmal sinus tachycardia with folk remedies, you can prepare a decoction of calendula. To prepare, follow these steps:

1. Take 2 teaspoons of dry calendula and pour 1 cup of boiling water.
2. Infuse for 40 minutes, then strain.
3. Decoction to take half a cup 4 times a day.

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Prevention methods

To reduce the risk of developing paroxysmal tachycardia, you should give up alcoholic beverages and tobacco products. It is not recommended to drink coffee in large quantities. You should reduce strong physical exertion, active sports and avoid stressful situations. In order for the heart and blood vessels to be healthy, it is necessary to eat properly and rationally. It is recommended to exclude fatty and fried foods from food, replacing it with vegetables and fruits. Patients diagnosed with paroxysmal supraventricular tachycardia should regularly take medications prescribed by their doctor.

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Possible forecast

Supraventricular tachycardia has a favorable prognosis in the absence of organic damage hearts. At ventricular tachycardia the prognosis is much worse, especially if the pathology is of a coronagenic nature. Fatal outcome may cause paroxysmal ventricular tachycardia due to acute attack heart attack, which in the first month is up to 35% of cases, and in the first year - up to 55%. Taking regular medications and implanting a pacemaker reduces the risk lethal outcome and improve prognosis.

Symptomatic arterial hypertension

Symptomatic (secondary) arterial hypertension is a persistent increase in blood pressure due to the presence of diseases of various organs and systems. Symptomatic arterial hypertension is, according to various sources, from 10 to 15% of cases of arterial hypertension. However, more than 50 different diseases lead to its development.

If the cause of the frequent increase in blood pressure cannot be established using all methods of examination, then the diagnosis of "arterial hypertension" is made, and this is up to 85-90% of cases, respectively.

What diseases lead to the development of symptomatic hypertension?

The causes of symptomatic arterial hypertension can be a variety of diseases, the spectrum of which is quite wide. The most common among them:

• congenital and acquired malformations of the heart and blood vessels;
• congenital and acquired renal pathology, including renal vessels (pyelonephritis, glomerulonephritis, polycystosis, tumors);
• diseases of the endocrine system (diabetes mellitus, thyroid pathology, dysfunction of the adrenal cortex and pituitary gland, menopause);
• diseases of the nervous system (encephalitis, trauma, tumors);
• systemic diseases (rheumatoid arthritis, systemic lupus erythematosus);
• iatrogenic drug hypertension(occurs due to side effects of drugs);

This classification is far from complete, often the cause of hypertension is a combination of several factors. So, in the official classification, the group “other reasons” is singled out.

What are the symptoms of symptomatic hypertension?

Signs of hypertension: headache and dizziness, a feeling of fullness in the head, blurred vision in the form of flickering in the eyes, hearing impairment in the form of noise, weakness, insomnia, pain in the heart area.

The presence of a disease that can lead to an increase in pressure, symptoms characteristic of this disease.

The use of drugs, the side effect of which is an increase in pressure.

The development of hypertension at a young age (up to 27 years).

Blood pressure is poorly reduced to normal numbers with the help of antihypertensive drugs.

The severity of hypertension develops rapidly, with the transition to a malignant form.

Whom should I contact with a persistent increase in blood pressure?

If within a month there are drops in systolic blood pressure over 140 mm Hg. Art., it is necessary to consult a doctor and find out the cause of the ailment, in order to choose the right treatment tactics.

Understanding the etiology of increased pressure is not an easy task and is not quickly solved. To do this, you will have to undergo a series of consultations and a lot of examinations. First you need to contact a therapist who, after talking with the patient, will choose an examination program to determine the cause of the disease. After analyzing the required minimum of examinations, if necessary, the therapist will refer the patient to a specialist for further, in-depth research, this may be:

• cardiologist;
• nephrologist;
• endocrinologist;
• neurologist;
• gynecologist;
• ophthalmologist

What research methods are used to clarify the cause of arterial hypertension?

Based on the wide range of diseases that contribute to the development of arterial hypertension, a thorough investigation is necessary to identify the cause. various systems and organs. The most commonly used methods are:

• regular measurement of blood pressure;
• general analysis of blood, urine;
• biochemical blood and urine tests;
• a blood test for hormone levels;
• electrocardiogram and echocardiogram;
• electroencephalogram;
• ultrasound examination of the kidneys;
• computed tomography of the skull and kidneys;
• renal angiography.

When establishing a primary disease, additional in-depth research methods are prescribed. narrow specialists, to clarify the degree and localization of the lesion, as well as determine the tactics of treatment.

What risk factors contribute to the development of symptomatic hypertension?

In addition to the presence of an underlying (primary) disease that contributes to the development of secondary hypertension, symptomatic hypertension is exacerbated by the presence of common risk factors:

• smoking;
• alcoholism and domestic drunkenness;
• obesity;
• stress;
• improper use of drugs (exceeding the dosage, exceeding the duration of the course of therapy, self-medication).

Can birth control drugs cause secondary hypertension?

Yes, they can, this is due to the high content of estrogen in drugs. The use of hormonal contraceptives was common cause development of hypertension in women 15–20 years ago.

IN modern preparations the content of estrogen is reduced and balanced, so the risk of developing hypertension is minimized.

However, in women after 35 years, in the presence of a hereditary predisposition and other risk factors, in 5% of cases it is possible to develop this condition. side effects. If this happens, you need to contact a gynecologist for examination and selection of another drug.

What determines the severity of symptomatic hypertension?

The severity of symptomatic hypertension is due to the underlying cause - the underlying disease. Depending on the duration of the increase in pressure, the magnitude of blood pressure, the presence of changes in the fundus and the degree of change (cardiac hypertrophy), 4 degrees of hypertension are distinguished by severity:

• transient - temporary, the most common, often passes on its own, there are no pathological changes in the heart and fundus;
• labile - a moderate increase in pressure, rarely decreases on its own, there are minor changes in the heart and fundus;
• stable - a steady increase in pressure, moderate hypertrophy of the heart, vasoconstriction of the fundus;
• malignant - the most dangerous and unfavorable form; most often found in renal pathology, appears suddenly, immediately with high numbers of systolic and, which is characteristic, diastolic pressure; develops rapidly, has pronounced complications of the heart and blood vessels of the fundus; The malignant form accounts for about 1-3% of arterial hypertension, respectively, from 10 to 30% of the number of symptomatic hypertension.

How is symptomatic hypertension treated?

The tactics of treatment is completely determined by the etiology of hypertension. That is, first of all, it is necessary to treat the primary disease that causes hypertension. Symptomatic treatment is mandatory. It is also necessary to eliminate all risk factors that contribute to the aggravation of hypertension.

Etiological treatment:

• conservative therapy with the use of medications, more often used for infectious and hormonal etiology;
• surgical treatment, especially for congenital and acquired defects of the kidneys, renal vessels, heart and tumors;
• for tumors in the brain, including the pituitary gland, radiation treatments are used (laser and X-rays, radiotherapy);
• if the cause of hypertension was drugs (glucocorticosteroids, contraceptives, and others), adjustment of therapeutic regimens or drug withdrawal is applied.

Symptomatic treatment - selection of antihypertensive drugs:

• drugs of centralized and peripheral action on the sympathetic nervous system(clofelin, methyldopa, adreno- and ganglionic blockers);
• ACE inhibitors (captopril and others);
• vasodilators - dilating vessels (apressin);
• the use of diuretics.

Elimination of other factors contributing to the development of hypertension:

• proper nutrition, with restriction of salt and fat;
• how to get rid of excess weight rational nutrition, and physical activity;
• quitting smoking (including "passive" - ​​when someone smokes nearby);
• reducing the consumption of alcoholic beverages to a minimum or complete rejection of alcohol;
• development of stress tolerance.

Given the complexity of the etiology and pathogenesis of the development of arterial hypertension, the selection of the correct treatment tactics is difficult even for a specialist, so it is absolutely impossible to self-medicate.

Acquired heart disease (ACD)- this is a group of diseases in which the structure and function of the heart valves are disturbed, which causes a restructuring of hemodynamics, as a result of which there is an overload of the corresponding parts of the heart, hypertrophy of the heart muscle, circulatory disorders in the heart and in the body as a whole. If, as a result of a pathological process, deformation of the valve tissues occurs and the hole through which blood enters the next section of the heart narrows, then such a defect is called stenosis. Deformation can lead to non-closure of the heart valves due to a change in shape, shortening them as a result of scarring of the affected tissues, this defect is called insufficiency. Valve insufficiency can be functional, resulting from the expansion of the chambers of the heart, the area of ​​​​the unchanged valve is not enough to close the enlarged hole - the valves sag (prolapse).

The work of the heart is rebuilt depending on the changes that have occurred and the needs of the blood flow in the body.

Causes of acquired heart defects

In most cases, the defects are caused by rheumatic diseases, in particular rheumatic endocarditis (about 75% of cases). The development of atherosclerosis may also be the cause, systemic diseases connective tissue, trauma, sepsis, infection, overload, autoimmune reactions. These pathological conditions cause disturbances in the structure of the heart valves.

Classification of acquired heart defects

There are four chambers in the human heart: the left and right atria and ventricles, between which there are heart valves. The aorta comes out of the left ventricle, and the pulmonary artery comes out of the right ventricle.

Between the left heart chambers is a bicuspid valve, the mitral valve. And between the right departments - a tricuspid valve, another name is tricuspid. In front of the aorta is the aortic valve, in front of the pulmonary artery is another one, the pulmonary valve.

The performance of the heart muscle depends on the functioning of the valves, which, when the heart muscle contracts, allow blood to pass to the next section without obstruction, and when the heart muscle relaxes, they do not allow blood to flow back. If the function of the valves is impaired, then the function of the heart is also impaired.

For reasons of formation, defects are classified as follows :

• degenerative, or atherosclerotic, they occur in 5.7% of cases; more often these processes develop after forty-fifty years, calcium is deposited on the leaflets of the affected valves, which leads to the progression of the defect;
• rheumatic, forming against the background rheumatic diseases(in 80% of cases);
• malformations resulting from inflammation inner shell heart (endocarditis);
• syphilitic (in 5% of cases).

According to the type of functional pathology, defects are divided into the following types:

• simple - valve insufficiency or stenosis;
• combined - insufficiency or narrowing of two or more valves;
• combined - both pathologies on one valve (stenosis and insufficiency).

Depending on the localization, the following pathologies are distinguished :

• mitral defect;
• tricuspid defect;
• aortic defect.

Hemodynamics can be impaired to varying degrees:

• slightly;
• moderately;
• expressly.

The mitral valve is affected more often than the aortic valve. Pathologies of the tricuspid valve and the pulmonary artery valve are less common.

Symptoms of acquired heart defects

mitral stenosis. It is manifested by sealing or fusion of the leaflets, a decrease in the area of ​​​​the opening of the mitral valve. As a result, the blood flow from the left atrium to the left ventricle is difficult, the left atrium begins to work with increased load. This leads to an increase in the left atrium. Less blood enters the left ventricle.

Due to the decrease in the area of ​​the mitral orifice, the pressure in the left atrium increases, and then in the pulmonary veins, through which oxygen-enriched blood from the lungs enters the heart. Usually, the pressure in the pulmonary arteries begins to rise when the diameter of the opening becomes less than 1 cm, compared with the normal 4-6 cm, a spasm occurs in the arterioles of the lungs, which aggravates the process. Thus, the so-called pulmonary hypertension is formed, the long existence of which leads to sclerosis of arterioles with their obliteration, which cannot be eliminated even after the stenosis has been eliminated.

With this defect, the left atrium is hypertrophied and expanded, first of all, and then the right parts of the heart.

At the beginning of the formation of this defect, the symptoms are not noticeable. In the future, shortness of breath, cough during physical exertion, and then at rest come out on top. There may be hemoptysis, persistent pain in the region of the heart, rhythm disturbances (tachycardia, atrial fibrillation). If the process goes far, then pulmonary edema may develop during exercise.

There are physical signs of mitral stenosis: a diastolic murmur in the heart, a chest trembling corresponding to this noise (“cat's purr”) is felt, the boundaries of the heart change. An experienced specialist can often make a diagnosis already with a careful examination of the patient.

Mitral insufficiency. Valve insufficiency is expressed in the ability of blood to return back to the atrium during the contraction of the left ventricle, since a message remains between the left atrium and the ventricle that is not closed by the valve leaflets at the time of contraction. Such insufficiency is caused either by deformation of the valve as a result of a tissue-changing process, or by its sagging (prolapse), due to stretching of the heart chambers when they are overloaded.

Compensated mitral insufficiency usually lasts for several years, in the affected heart the work of the left atrium and left ventricle increases, first hypertrophy of the muscles of these departments develops, and then the cavities begin to expand (dilation). Then, due to the decrease in stroke volume minute burst blood from the heart begins to decrease, and the amount of blood returned (regurgitation) to the left atrium increases. Stagnation of blood begins in the pulmonary circulation (pulmonary), the pressure in it increases, the load on the right ventricle increases, it hypertrophies and expands. This leads to rapid decompensation of cardiac activity and the development of right ventricular failure.

If compensatory mechanisms do not have time to develop with acute mitral valve insufficiency, then the disease can debut with pulmonary edema and lead to death.

Clinical manifestations of mitral insufficiency in the compensated stage are minimal and may not be noticed by the patient. Beginning decompensation is characterized by shortness of breath, poor exercise tolerance, then, when stagnation in the pulmonary circulation increases, attacks of cardiac asthma appear. In addition, pain in the region of the heart, palpitations, interruptions in the work of the heart may be disturbing.

Right ventricular heart failure leads to stagnation of blood in the systemic circulation. The liver increases, cyanosis of the lips, extremities, edema in the legs, fluid in the abdomen, and heart rhythm disturbances appear (50% of patients have atrial fibrillation).

Make a diagnosis of mitral regurgitation at the present time with available instrumental methods research: ECG, ECHO-KG, radiation diagnostic methods, ventriculography and others - not difficult. However, an examination by an attentive cardiologist based on anamnesis, auscultation, percussion, palpation will make it possible to draw up the correct examination algorithm and take timely measures to prevent further development of the defect formation process.

aortic stenosis. This defect among PPS is detected quite often, in 80--85% of cases it is formed as a result of rheumatism, in 10-15% of cases it is acquired against the background of an atherosclerotic process, followed by calcium deposition in atherosclerotic plaques (calcinosis). There is a narrowing of the aortic orifice at the site of the aortic semilunar valve. For many years, the left ventricle has been working with increasing tension, however, when the reserves are depleted, the left atrium, the pulmonary circle, and then the right sections of the heart begin to suffer. The pressure gradient between the left ventricle and the aorta increases, which is directly related to the degree of narrowing of the orifice. The ejection of blood from the left ventricle becomes less, the heart's blood supply worsens, which is manifested by angina pectoris, low blood pressure and pulse weakness, cerebral circulatory failure with neurological symptoms, including dizziness, headache, loss of consciousness.

The appearance of complaints in patients begins when the area of ​​the orifice of the aorta decreases by more than half. When complaints appear, this indicates a far advanced process, a high degree of stenosis and a high pressure gradient between the left ventricle and the aorta. In this case, it is necessary to talk about treatment already taking into account the surgical correction of the defect.

Aortic insufficiency- this is a pathology of the valve, in which the exit from the aorta is not completely blocked, the blood has the ability to return to the left ventricle in the phase of its relaxation. The walls of the ventricle thicken (hypertrophy) as more blood has to be pumped. With hypertrophy of the ventricle, the insufficiency of its nutrition gradually manifests itself. Larger muscle mass requires more blood flow and oxygen supply. At the same time, due to the fact that part of the blood in diastole returns to the left ventricle, the aortic-left ventricular gradient decreases (it determines the coronary blood flow) and, as a result, less blood enters the arteries of the heart. There is angina pectoris. There are sensations of pulsation in the head, neck. Characteristic neurological manifestations such as: lightheadedness, dizziness, sudden fainting, especially during physical exertion, with a change in body position. The hemodynamics of the systemic circulation in this defect is characterized by: high systolic pressure, low diastolic pressure, compensatory tachycardia, increased pulsation large arteries, including the aorta. In the stage of decompensation, dilatation (expansion) of the left ventricle develops, the efficiency of systole decreases, the pressure in it increases, then in the left atrium and the pulmonary circulation. There are clinical signs of stagnation in the pulmonary circulation: shortness of breath, cardiac asthma.

A thorough examination by a cardiologist may allow the doctor to suspect or even make a diagnosis of aortic insufficiency. So-famous symptoms such as "dance of the carotid" - increased pulsation carotid arteries, "capillary pulse", which is detected when pressing on the nail phalanx, de Musset's symptom - when the patient's head sways to the beat of the phases of the cardiac cycle, pulsation of the pupils and others are already detected at the stage of a far advanced process. But palpation, percussion, auscultation and a thorough history taking will reveal the disease for more early stages and prevent disease progression.

Tricuspid stenosis. This defect rarely occurs as an isolated pathology. It is expressed in the contraction available holes between the right ventricle and the right atrium, which are separated by the tricuspid valve. Most often, it occurs with rheumatism, infective endocarditis, and other systemic diseases of the connective tissue; sometimes there is a narrowing of the hole as a result of the formation of a myxoma-tumor that has formed in the right atrium, less often there are other reasons. Hamodynamics is disturbed as a result of the fact that not all blood from the atrium can enter the right ventricle, which should normally occur after atrial systole. The atrium is overloaded, stretched, blood stagnates in the systemic circulation, the liver enlarges, edema of the lower extremities appears, fluid in the abdominal cavity. Less blood flows from the right ventricle to the lungs, which causes shortness of breath. IN initial stage there may be no symptoms, these hemodynamic disorders occur later - heart failure, atrial fibrillation, thrombosis, cyanosis of nails, lips, yellowness of the skin.

Tricuspid insufficiency. This pathology most often accompanies other defects, manifests itself in the form of tricuspid valve insufficiency. Due to venous stasis, ascites gradually develops, the liver and spleen increase in size, high venous pressure is noted, liver fibrosis develops and its function decreases.

Combined defects and a combination of pathological conditions

The most common combination is mitral stenosis and mitral insufficiency. With such a pathological combination, cyanosis and shortness of breath are noted already in the early stages.

Aortic valve disease is characterized by stenosis and valve insufficiency at the same time, usually has a faint pronounced signs two states.

With combined defects, several valves are affected, and in each of them there can be both isolated pathologies and their combination.

Methods for diagnosing heart defects

In order to establish a diagnosis of heart disease, anamnesis is collected, the presence of diseases that could lead to deformation of the heart valve is detected: rheumatic diseases, infectious, inflammatory processes, autoimmune diseases, injury.

Be sure to examine the patient, revealed the presence of shortness of breath, cyanosis, edema, pulsation of peripheral veins. Percussion reveals the boundaries of the heart, listens to tones and murmurs in the heart. Determine the size of the liver and spleen.

The main method for diagnosing valvular pathology is echocardiography, which allows you to identify a defect, determine the area of ​​\u200b\u200bthe opening between the atrium and ventricle, valve sizes, cardiac fraction, and pressure in the pulmonary artery. More accurate information about the state of the valves can be obtained by performing transesophageal echocardiography.

Also used in the diagnosis of electrocardiography, which allows you to assess the presence of atrial and ventricular hypertrophy, to identify signs of overload of the heart. 24-hour Holter ECG monitoring reveals rhythm and conduction disturbances.

Highly informative methods for diagnosing heart defects are MRI of the heart or MSCT of the heart. Computed tomography provides accurate and numerous cuts, which can be used to accurately diagnose the defect and its appearance.

An important role in the diagnosis is occupied by laboratory tests, among which are urine, blood tests, determination of blood sugar, cholesterol levels, and rheumatoid tests. Lab tests allow to identify the cause of the disease, which plays an important role for the subsequent treatment and behavior of the patient.

Prevention and prognosisat PPP

There are no such preventive measures that would save one hundred percent from acquired heart disease. But there are a number of measures that will reduce the risk of developing heart defects. The following are meant:

• timely treatment of infections caused by streptococcus (in particular tonsillitis);
• bicillin prophylaxis in case of rheumatic attack;
• taking antibiotics before surgical and dental procedures if there is a risk of infective endocarditis;
• prevention of syphilis, sepsis, rheumatism: sanitation infectious foci, proper nutrition, mode of work and rest;
• rejection of bad habits;
• the presence of moderate physical activity, accessible physical exercises;
• hardening.

The prognosis for the life and working capacity of people with heart defects depends on the general condition, fitness of the person, and physical endurance. If there are no symptoms of decompensation, a person can live and work as usual. If circulatory failure develops, work should be either facilitated or stopped, sanatorium treatment at specialized resorts is indicated.

It is necessary to be observed by a cardiologist in order to monitor the dynamics of the process and, with the progression of the disease, determine in time the indications for cardiac surgical treatment of heart disease.

Treatment of acquired heart defects can be conservative and surgical.

Conservative treatment is effective only in the early stages of the development of heart disease and requires mandatory dynamic monitoring by a cardiologist.

PPS should be treated surgically when:

1. Progressive heart failure.
2. Pathological changes in the valve significantly affect hemodynamics.
3. Conducted conservative therapy does not have the desired effect.
4. And there are fears of serious complications.

Types of operations for heart defects

Open heart surgery is performed under cardiopulmonary bypass through a median sternotomy. The median sternotomy creates optimal conditions for the cardiac surgeon to work - to perform the necessary surgical interventions in case of various pathologies and for connecting a heart-lung machine. The soft tissue incision is approximately equal in length to the length of the sternum (about 20 cm), and the sternum is dissected along the entire length.

The main two types of operations that are currently used for PPS are the reconstruction of the affected valves (plastic) or their prosthetics.

Valve-preserving surgery is performed to correct the cause of valve dysfunction.

If the valves do not close (valve insufficiency), then the cardiac surgeon during the operation achieves normalization of the closure of the valve leaflets, performing resection of the valve leaflets, annuloplasty, commissural plastics, chord prosthetics. If there is a valvular stenosis, then the separation of those sections of the valves that have grown together due to the pathological process is carried out - an open commissurotomy is performed.

If it is impossible to perform plasty, when there are no conditions for this, valve-replacing operations for prosthetic heart valves are performed. In case of intervention on mitral valve prosthetics is performed with full or partial preservation of the anterior or posterior leaflets of the valve, and if impossible, without their preservation.

During valve replacement operations, prostheses are used.

1. Prostheses can be made from animal or human tissue. Such prostheses are called biological. Its main advantage is that the patient does not need to take anticoagulant drugs during the subsequent years of life, and their main disadvantage is their limited service life (10-15 years).
2. Prostheses consisting entirely of mechanical elements (titanium and pyrolytic carbon) are called mechanical prostheses. They are very reliable and able to serve without failure for many years, without replacement, but after such an operation, the patient must always take anticoagulants for life, this is a negative aspect of using a mechanical prosthesis.

Minimally invasive surgeries.

Modern surgery, thanks to the creation of new instruments, has been able to modify online access to the heart, which leads to the fact that operations become minimally traumatic for the patient.

The meaning of such operations is that access to the heart is carried out through small incisions in the skin. In minimally invasive operations on the mitral valve, a right-sided lateral minithoracotomy is performed, while the skin incision is made no more than 5 cm, this allows you to completely abandon the dissection of the sternum and provides convenient access to the heart. To improve visualization, endoscopic video support with multiple magnification is used. With minimally invasive access to the aortic valve, the incision on the skin is approximately two times smaller (the length of the incision is 8 cm), and the sternum is dissected along the length in its upper part. The advantage of this method is that the non-incised area of ​​the sternum provides greater stability after surgery, as well as a better cosmetic effect due to the reduction in the size of the suture.

Endovascular surgery - transcatheter aortic valve replacement (TAVI).

Transcatheter aortic valve implantation methods:

1. The entire operation is performed through a blood vessel (femoral or subclavian artery). The meaning of the procedure is to puncture the femoral or subclavian artery with a guide catheter and deliver the stent valve against the blood flow to the site of its implantation (aortic root).
2. through the aorta. The essence of the method is to cut the sternum over a short distance (ministernotomy) and puncture the aortic wall in the ascending section and implant the stent valve into the aortic root. The method is used when it is impossible to deliver the valve through the femoral and subclavian arteries, as well as when there is a pronounced bending of the arc of the artery.
3. Through the top of the heart. The meaning of the procedure is to make a small incision in the fifth intercostal space on the left (minithoracotomy), puncture the apex of the heart with a guide catheter and install a stent valve. Once the new valve is implanted, the catheter is removed. The new valve starts working immediately.

There are two types of stent valves:

1. Self-expanding stent valve expands up to right size after removing the restrictive shell of the coupling from it.
2. A balloon dilatable stent valve that expands to the desired size when the balloon is inflated; after the final installation of the stent valve, the balloon is deflated and removed.