Beta-blockers are the group of choice in the treatment of hypertension in people with tachycardia, heart failure. The drugs work well with diuretics, which enhance the antihypertensive effect. The use of Nebival reduces the likelihood of developing severe cardiovascular diseases, the risk of sudden death. The medicine is prescribed by a doctor according to strict indications.
Mechanism of action
The biologically active substance of the drug is nebivalol, which consists of two parts that are different in chemical composition and mode of action. The drug belongs to the group of selective beta-blockers, acts mainly on beta1-adrenergic receptors. After taking Nebival, the heart rate decreases, vasodilatation occurs, and myocardial oxygen demand decreases. The drug does not affect beta2-adrenergic receptors, therefore the risk of bronchospasm, increased uterine tone is minimal.
Distribution in the body
After taking the drug, it is rapidly absorbed in the gastrointestinal tract. A notable advantage is that the medicine can be taken with or without food. Food does not affect the absorption process or the activity of Nebival. Metabolism occurs in the liver, the drug is excreted equally by the kidneys and intestines.
When choosing an antihypertensive agent, attention should be paid to the patient's metabolism. People with a slow metabolism need to be prescribed low doses, since the bioavailability of the drug is high. If the metabolism is fast, the dose must be increased.
Indications and contraindications
The drug is used to reduce blood pressure in hypertension. In the complex treatment of chronic heart failure, mainly in the elderly (over 70 years old), these tablets have a good effect.
In some cases, it is not recommended to take Nebival tablets. To avoid side effects, worsening of the condition, you must carefully read the instructions.
- Allergic reaction to one of the components of the drug.
- Acute disruption of the liver or kidneys.
- Lowering blood pressure (systolic< 90 мм рт. ст.).
- Bradycardia (pulse less than 60).
- Atrioventricular block II-III degree, weakness of the sinus node.
- The drug should not be taken in case of acute heart failure, collapse, when it is necessary to inject drugs that increase the strength of heart contractions.
- Patients with bronchial asthma should stop taking the medication. It is necessary to select analogues of Nebival or another antihypertensive agent.
- Lactase deficiency is a direct contraindication; it is also not recommended to use the medicine for people with impaired absorption of galactose, glucose.
- The drug is not used in children (under 18 years of age).
- Pregnancy. Nebival negatively affects the development of the child. Before prescribing the remedy, you need to make sure that the woman is not pregnant. When breastfeeding, the drug is contraindicated.
Note! The day before the proposed operation with the use of anesthesia, Nebival is canceled!
Release form and method of administration
The tablets are round in shape, with slightly beveled edges. The pack contains 2 blisters of 10 white tablets each. It is recommended to store at a temperature not exceeding 25 degrees.
The dosage and frequency of administration directly depends on the pathology, the condition of the kidneys, liver, the presence of concomitant diseases.
Arterial hypertension
To reduce blood pressure, it is recommended to use 5 mg (1 tablet) of Nebival 1 time per day, the effectiveness will increase if the hours of admission are unchanged (for example, every day in the morning at 9.00). The drug acts gradually, the pressure will normalize in 1-2 weeks after the start of the intake. Nebival is prescribed alone or in combination with other medicines, it goes well with diuretics (hydrochlorothiazide).
Chronic heart failure
In case of heart disease, the dose is selected by the doctor individually. You should start with 1.25 mg (a quarter of a tablet) per day. After 14 days, the dose is gradually increased. The maximum dose is 10 mg. After each dose increase, it is necessary to monitor the patient's condition for 2-3 hours. Periodically, you need to measure the pressure, heart rate, pay attention to the general condition of the patient, the presence of complaints.
The drug is also canceled gradually, a one-stage cancellation often leads to a worsening of the condition.
In case of renal failure, do not take more than 2.5 mg of the drug per day.
Adverse Reactions
After you start taking Nebival, side reactions may occur, therefore, before buying, you must read the instructions. If the condition worsens, any of the following symptoms occur, you should consult a doctor.
- A sharp drop in blood pressure, slowing of atrioventricular impulse conduction, bradycardia (decrease in pulse< 60), возникновение аритмии, боли в сердце.
- Headache, sleep disturbance, dizziness, mood deterioration.
- Nausea (less often vomiting), decreased appetite, bloating, problems with stools (constipation or diarrhea).
- An allergic reaction is manifested by a rash on the body, itching, sometimes - Quincke's edema.
- In rare cases, shortness of breath, bronchospasm occurs.
- Increased fatigue, the occurrence of edema or pasty limbs.
special instructions
Nebival can cause dizziness, it increases fatigue, therefore it is used with caution in patients whose work is associated with precise actions, driving vehicles. Before using the drug, it is recommended to read the instructions or ask your doctor questions of interest.
The drug often causes exacerbation of allergic reactions, psoriasis.
Nebival does not affect glucose metabolism, but patients with diabetes mellitus, thyroid pathology should take the drug under the supervision of a doctor. The medicine masks the manifestations of hypoglycemia, thyrotoxicosis: heart palpitations, breathing.
The drug is prescribed with caution to patients with depression, myasthenia gravis.
Interaction
- It is forbidden to take Nebival with floktaphenin and sultopride, in which case the risk of ventricular arrhythmia increases.
- Simultaneous administration with antiarrhythmic drugs, calcium channel blockers leads to conduction disturbances (AV-blockade), a decrease in the contractile function of the heart, hypotension.
- Central antihypertensive drugs (clonidine, methyldopa) in combination with Nebival increase heart failure by decreasing heart rate and strength.
- Care must be taken when prescribing Nebival in conjunction with insulin and other antihyperglycemic drugs. Beta-adrenal locator masks the symptoms of hypoglycemia.
- It is recommended to reduce the dose of the antihypertensive drug if the patient is taking baclofen or amifostine. The risk of hypotension increases significantly.
- Antidepressants, antipsychotics enhance the effect of the drug.
- Alcohol does not affect the metabolism of the drug.
Overdose
When the maximum allowable dose (10 mg) is increased several times, the following symptoms occur: a sharp decrease in pressure, pulse, nausea, vomiting, cyanosis is possible. In severe cases, there is loss of consciousness, signs of heart failure, coma, cardiac arrest.
First aid
The main task is to neutralize excess nebivalol in the body. For this purpose, gastric lavage is carried out, activated charcoal or other sorbents are prescribed. Further treatment is symptomatic. With severe hypotension, bradycardia, beta-adrenostimulants are administered, if the effect is not achieved, the use of dopamine, norepinephrine is necessary. In case of ventricular arrhythmia, it is necessary to administer lidocaine, if there are convulsions - diazepam.
Among the most common diseases in our time are diseases associated with the heart. Most often, with diseases of the heart muscle, the doctor states the diagnosis - arrhythmia.
And no one will be afraid of such a type of arrhythmia as sinus tachycardia. It is interesting that at the present time these words do not shock a person. He accepts the diagnosis and begins to fight his disease.
- What do you need to know about the disease?
- Forms of manifestation
- Signs and danger of the disease
- How dangerous is all this?
- Diagnostics
- Prevention and treatment
What do you need to know about the disease?
Everyone knows that before starting a fight against something or someone, it is necessary to study the situation from the inside, and only then to rebuff the problem. So what is sinus tachycardia? Before dealing with this issue, it is worth making a reservation: many, speaking about this disease, use the term "sinus". But, even using the wrong meaning of the word, you will always be understood.
Tachycardia is a type of arrhythmia. It should be noted that at its core, this disease is only a symptom of problems in the body.
Thus, most often it is not the disease that is treated - tachycardia, but what caused it is treated.
By its nature, the problem is a rapid heartbeat. The maximum value of heart contraction within the normal range is 90 beats per minute. Anything that is at least 10 beats higher than this is considered abnormal and such a deviation is tachycardia.
There is an international classification of diseases 10 revision, or simply ICB 10. All diseases have their own code ICB 10, which will equally denote a disease in any country in the world. Thus, if you have been diagnosed with sinus tachycardia, then in whatever country you are in America, Russia, England or Israel, this disease will have the same indicator for μb 10 - I49.5.
Forms of manifestation
It occurs due to strong physical exertion, and the disease can also manifest itself due to great emotional experiences in a person's life, or due to an increased body temperature.
Signs and danger of the disease
Of course, sinus tachycardia, like any other disease, can be identified by symptoms. Signs of this disease include:
How dangerous is all this?
Sinus tachycardia is striking in its unusualness. Initially, it is not a disease. It would seem, what is it if the heart beats faster. Logically, this should be even more useful, but even here not everything is so smooth.
The more often the heart contracts, the less it manages to saturate the blood with oxygen, therefore, such contractions are more harmful and dangerous. The longer the illness lasts, the more oxygen is lacking in the body and heart. Each time, more and more the likelihood of organ damage due to lack of oxygen.
As a result, tachycardia, which is not a sign of heart disease, can lead to ischemia of the heart muscle and life-threatening consequences.
Diagnostics
Such a disease is diagnosed by carrying out the following actions:
Prevention and treatment
As a rule, in order to get rid of a rapid pulse, it is initially necessary to overcome the diseases and problems that cause it.
To reduce the rapid heart rate itself, in addition to the medications prescribed by the doctor, you can also use a set of additional measures to prevent the disease.
It is necessary to exclude all contacts with harmful substances that can poison the body. It will be necessary to quit bad habits.
To get a better effect, you need to use light physical activity, such as race walking. But at the same time, it is very dangerous to overextend the body. It is worth making a healthy menu, and excluding foods that affect the heartbeat from the diet.
The whole range of measures should be discussed with the doctor and only he can determine what will be useful in your case. Discuss with the treating specialist the possibility of using such folk methods as decoctions, tinctures, aromatherapy and massages.
- Do you often experience discomfort in the area of the heart (pain, tingling, constriction)?
- You may suddenly feel weak and tired ...
- Increased pressure is constantly felt ...
- Shortness of breath after the slightest physical exertion and there is nothing to say ...
- And you have been taking a bunch of medications for a long time, dieting and monitoring your weight ...
What is an ischemic attack?
TIA (transient ischemic attack) is an acute but short-term episode of neurological dysfunction caused by damage to the blood supply to one part of the brain.
If we talk about the concept of ischemia in general, then this is a violation of blood flow in a certain part of the body or in the entire organ. This pathology can suddenly occur in the intestines, in cartilaginous and bone structures, but the most difficult cases are noted in the heart and brain.
TIA is popularly called a microstroke for the similarity of symptoms, but this is not entirely true. The average duration of an ischemic attack is 12 minutes, and if the symptoms persist within a day, then this is a different diagnosis - ischemic stroke. The difference between the two is well documented in various medical literature. Ischemic attack symptoms are obvious.
It is most correct to call a transient ischemic attack a harbinger of an acute stroke, which can occur very soon, within a couple of months.
TIA classification - frequency, severity, ICD-10
By how easy or difficult the disease is, the following types are distinguished:
- mild course of TIA (after 10 minutes the patient feels as usual);
- a form of moderate severity (manifestations of TIA do not go away for several hours);
- severe form of TIA (signs persist for a day).
According to the frequency of TIA, the following types are distinguished:
- rare (no more than 2 times a year);
- average in frequency (every 2 months);
- frequent (more than 1 time per month).
According to the ICD-10 (this is an international classification system of diseases, in which a code is assigned to each type of disease), TIA has the following classification:
- G 45.0 - syndrome of the vertebrobasilar arterial system.
- G 45.4 - TGA syndrome. This syndrome, by the way, is considered by many researchers to be part of epileptic disorders and is not attributed to ischemia.
- G 45.1 - carotid artery syndrome (in the carotid basin).
- G 45.2 - multiple and bilateral arterial syndromes.
- G 45.3 - transient blindness syndrome.
- G 459, unspecified TIA.
- G 45.8 - other TIAs pass under this code.
Symptoms of the disease
The manifestations of an ischemic attack will depend on the region of which artery there was a violation. Common symptoms are:
- weakness, paralysis of the face or limbs, usually on one side of the body;
- distorted slurred speech;
- blindness in one or both eyes, split eyes;
- dizziness;
- difficulty swallowing;
- tinnitus and severe hearing impairment.
Symptoms by type of TIA
If there is a violation of the passage of the vessel in the basin of the carotid arteries (TIA in the carotid basin), then this will result in the following manifestations:
- lack or reduced ability to control limbs (usually one side);
- slurred speech, misunderstanding of addressed speech (dysarthria and aphasia);
- violation of fine motor skills;
- severe visual impairment;
- constant desire to sleep;
- confusion of consciousness.
TIA in the vertebral artery system (in the vertebrobasilar basin) is manifested in the following:
- vomit;
- dizziness;
- lack of coordination;
- hemianopsia, photopsia;
- split before the eyes;
- paralysis of the face.
Transient monocular blindness is manifested by the sensation of a curtain in front of the eyes, covering one eye for a short time. This form of TIA can occur suddenly, or it can be caused by bright light, too hot a bath or bath, a sharp turn. In addition, there may be impaired coordination and motor skills.
Transient global amnesia is another type of TIA. She has only one symptom - loss of memory for recent events. Moreover, the patient remembers what happened a long time ago. In this case, the person is confused, repeats the same questions, disoriented in time and space.
Causes of TIA
Blood clots are the most common culprit in transient ischemic attack. Blood clots can form as a result of atherosclerosis or diseases of the cardiovascular system (myocardial infarction, atrial fibrillation, atrial myxoma). A blood clot can block blood flow to part of the brain. The brain cells suffer from blockages within seconds. This causes symptoms in the parts of the body that are controlled by these cells. After that, the blood flow returns and the symptoms disappear.
Violation of blood flow can occur in one of the vascular reservoirs, which in the human body are divided into two types:
- vertebrobasilar;
- carotid.
The first is located between the vertebral arteries. It supplies blood to the brain stem. The second is located between the two carotid arteries. It supplies blood to the cerebral hemispheres.
Sometimes TIA is caused by a sharp drop in blood pressure, which reduces blood flow to the brain.
Well, the undoubted "satellites" of any vascular pathology, dramatically increasing the chances of a transient ischemic attack:
- smoking;
- high cholesterol;
- excessive consumption of alcohol;
- diabetes;
- overweight.
Diagnosis of TIA
TIA is insidious in that it lasts a few minutes, and when the ambulance arrives, the patient, as a rule, refuses to be hospitalized, since all the symptoms have passed. But you must definitely go to the hospital, as the ischemic attack may recur.
The following tests are considered urgently:
- biochemical blood test with determination of glucose and cholesterol levels;
- complete blood count;
- analysis of the level of electrolytes in the blood serum (iron, calcium, potassium, sodium, magnesium, chlorine, phosphorus);
- coagulation studies, or coagulogram;
The following tests are helpful and can often be performed urgently:
- erythrocyte sedimentation rate;
- heart enzymes - proteins that are released into the blood when the heart is disrupted;
- lipid profile, or lipidogram - a special blood test that reflects the level of concentration of fats and lipoproteins.
Additional laboratory tests ordered as needed (based on medical history) include the following:
- screening for hypercoagulable conditions (especially in young patients without known vascular risk factors);
- serological reaction to syphilis;
- analysis for the presence of antiphospholipid antibodies;
- electrophoresis of hemoglobin;
- serum protein electrophoresis;
- examination of cerebrospinal fluid.
The following examinations must be carried out within 24 hours:
- Magnetic resonance imaging (MRI) is a modern, but already very well-studied and widely used, safe method of radiation diagnostics.
- Non-contrast computed tomography is a type of CT scan, but is done without an intravenous infusion of radiopaque contrast agents.
- Carotid Doppler ultrasonography of the neck, also called duplex scanning or ultrasonography, is an accurate, completely painless and harmless procedure that examines the shape of blood vessels.
- CT angiography (CTA) - this use of computed tomography gives good visibility of blood vessels and features of blood flow.
- Magnetic resonance angiography (MRA) - a type of MRI to obtain an image of the lumen of blood vessels for the presence of plaques.
- Doppler ultrasound (ultrasound dopplerography), today it is one of the safest methods that give maximum information about the state of the vascular system.
- Echocardiography, to check your heart shape and blood flow, is a method of ultrasound examination of the heart and heart valve apparatus.
- PET of the brain, stands for Positron Emission Tomography. This is the latest diagnostic method used to assess not the structure of brain tissue, as is done by magnetic resonance imaging and computed tomography, but the functional work of the brain.
Various types of treatment for ailment
Many doctors agree that it is not TIA that should be treated, but the main culprit - atherosclerosis. The disease must be treated with medication, sometimes surgically.
It is also imperative to change your lifestyle in favor of a healthy one.
Drug treatment, i.e. drug treatment should be started urgently and include taking the following groups of drugs:
- drugs that lower the level of "bad" cholesterol (Caduet, Mevacor);
- nootropics and neuroprotectors (Baclofen, Pronoran, Cinnarizin, Pantogam);
- blood thinning medications (Curantil, Trental);
- drugs that lower blood pressure (Enalapril, Mikardis, Valsakor);
- antioxidants (Mexidol);
- metabolites (Cytoflavin);
- sedatives (Pipolfen, Validol, Proroxan);
- sleeping pills (Melaxen, Donormil);
- drugs to reduce sugar (Maninil, Siofor).
After completing a comprehensive course of treatment, the patient must be under the supervision of a local doctor.
Surgical treatment may be warranted if the person has a narrowing of the carotid artery, which is located in the neck. When medications don't work, your doctor may recommend an operation called carotid endarterectomy. What this operation is can be described quite simply. Such an intervention is the process of cleansing the carotid arteries from fatty deposits and plaques. Thus, blood flow is restored, and the risk of recurrence of an ischemic attack is significantly reduced. This operation is very effective, but it also has risks: stroke and re-blockage of the carotid artery, bleeding, infections.
Surgical treatment of ischemic stroke cannot be prescribed to everyone.
There are quite a few contraindications for its implementation, including hypertension, acute heart failure, Alzheimer's disease, advanced oncology, and recent myocardial infarction.
Disease prevention
How can TIA be prevented? If you look for data on the topic of "ischemic attack treatment", then almost every medical manual says about the necessary prevention of ischemic stroke. It is imperative to take precautions to prevent TIA. If you have already been the victim of an ischemic attack, then you are doubly at risk of stroke.
You can do the following to prevent transient ischemic attack:
- avoid active and passive smoking;
- follow the principles of proper nutrition: vegetables and fruits with a minimum of unhealthy fatty foods;
- be physically active;
- limit or eliminate alcohol consumption;
- limit salt intake;
- control sugar levels;
- control blood pressure;
- eliminate stressful situations.
Consequences of an ischemic attack
The forecast here is rather unfavorable. Usually, more than 2-3 ischemic attacks do not occur, then a severe stroke necessarily occurs, which can lead to disability or even death. 10% of those who have experienced an ischemic attack during the first or second days receive a stroke in the form of a cerebral stroke or myocardial infarction. Unfortunately, a huge number of people after suffering an ischemic stroke do not go to doctors, which makes the prognosis of recovery sharply negative and subsequently leads to serious problems.
TIA is not dangerous to human life, but it is a formidable warning before a more serious problem. If this pathology is not treated, then in the near future the most powerful ischemic attack of the brain may occur again.
Short description
Chronic systolic heart failure- a clinical syndrome that complicates the course of a number of diseases and is characterized by the presence of shortness of breath during exercise (and then at rest), rapid fatigue, peripheral edema and objective signs of dysfunction of the heart at rest (for example, auscultatory signs, echocardiography - data).
Code for the international classification of diseases ICD-10:
- I50 Heart failure
Statistical data. Chronic systolic heart failure occurs in 0.4-2% of the population. With age, its prevalence increases: in people over 75 years old, it develops in 10% of cases.
Causes
Etiology... Heart failure with low cardiac output .. Myocardial damage: ... IHD (postinfarction cardiosclerosis, chronic myocardial ischemia) ... Cardiomyopathies ... Myocarditis ... Toxic effects (eg alcohol, doxorubicin) ... Infiltrative diseases (sarcoidosis , amyloidosis) ... Endocrine diseases ... Nutritional disorders (vitamin B1 deficiency) .. Myocardial overload ... Arterial hypertension ... Rheumatic heart defects ... Congenital heart defects (eg, aortic stenosis) .. Arrhythmias. .. Supraventricular and ventricular tachycardias ... Atrial fibrillation. Heart failure with high cardiac output .. Anemia .. Sepsis .. Arteriovenous fistula.
Risk factors... Refusal of the patient from pharmacotherapy. Prescribing drugs with a negative inotropic effect, and their uncontrolled intake. Thyrotoxicosis, pregnancy and other conditions associated with an increase in metabolic requirements. Overweight. The presence of chronic pathology of the heart and blood vessels (arterial hypertension, ischemic heart disease, heart defects, etc.).
Pathogenesis... The pumping function of the heart is impaired, which leads to a decrease in cardiac output. As a result of a decrease in cardiac output, hypoperfusion of many organs and tissues occurs. A decrease in cardiac perfusion leads to the activation of the sympathetic nervous system and an increase in the heart rate. A decrease in renal perfusion causes stimulation of the renin-angiotensin system. Renin production increases, while excessive production of angiotensin II occurs, leading to vasoconstriction, water retention (edema, thirst, increased BCC) and a subsequent increase in preload on the heart .. A decrease in peripheral muscle perfusion causes the accumulation of under-oxidized metabolic products in them, as well as hypoxia. to severe fatigue.
CLASSIFICATIONS
Classification of the XII All-Union Congress of Physicians in 1935 (ND Strazhesko, V.Kh. Vasilenko).
Stage I (initial) - latent heart failure, manifested only during physical exertion (shortness of breath, tachycardia, fatigue).
Stage II (pronounced) - prolonged circulatory failure, hemodynamic disturbances (stagnation in the large and small circulatory systems), organ and metabolic dysfunctions are also expressed at rest .. Period A - the beginning of a long stage, characterized by mild hemodynamic disturbances, cardiac dysfunctions or only parts of them .. Period B is the end of a long stage, characterized by profound hemodynamic disturbances, the whole CVS is involved in the process.
Stage III (final, dystrophic) - severe hemodynamic disturbances, persistent changes in metabolism and functions of all organs, irreversible changes in the structure of tissues and organs.
New York Heart Association classification(1964). Class I - normal physical activity does not cause severe fatigue, shortness of breath or palpitations. Class II - slight limitation of physical activity: feeling good at rest, but normal physical activity causes fatigue, palpitations, shortness of breath or pain. Class III - a pronounced limitation of physical activity: a satisfactory state of health at rest, but less than usual load leads to the appearance of symptoms. IV class - the inability to perform any physical activity without deteriorating health: symptoms of heart failure are present even at rest and intensify with any physical activity.
Heart Failure Society Classification(OSNN, 2002) adopted at the All-Russian Congress of Cardiology in October 2002. The convenience of this classification is that it not only reflects the state of the process, but also its dynamics. The diagnosis must reflect both the stage of chronic heart failure and its functional class. It should be borne in mind that the correspondence between the stage and the functional class is not quite clear - the functional class is displayed in the presence of slightly less pronounced manifestations than is necessary to expose the corresponding stage of heart failure.
. Stages of chronic heart failure(may worsen despite treatment) .. Stage I - the initial stage of heart disease (lesions). Hemodynamics is not impaired. Latent heart failure Asymptomatic left ventricular dysfunction .. Stage IIA - a clinically pronounced stage of heart disease (lesion). Disturbances of hemodynamics in one of the circles of blood circulation, expressed moderately. Adaptive remodeling of the heart and blood vessels .. Stage IIB - severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels .. Stage III - the final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in organs - targets (heart, lungs, blood vessels, brain, kidneys). The final stage of organ remodeling.
. Functional classes of chronic heart failure(may change during treatment both in one and the other direction) .. FC I - there are no restrictions on physical activity: habitual physical activity is not accompanied by rapid fatigue, shortness of breath or palpitations. The patient suffers an increased load, but it may be accompanied by shortness of breath and / or slow recovery of strength .. FC II - slight restriction of physical activity: there are no symptoms at rest, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations .. FC III - a noticeable restriction of physical activity: at rest there are no symptoms, physical activity of lower intensity in comparison with the usual loads is accompanied by the appearance of symptoms. IV FC - inability to perform any physical activity without discomfort; symptoms of heart failure are present at rest and are worse with minimal physical activity.
Symptoms (signs)
Clinical manifestations
. Complaints- shortness of breath, attacks of suffocation, weakness, fatigue .. Shortness of breath in the initial stage of heart failure occurs during exercise, and with severe heart failure - at rest. It appears as a result of an increase in pressure in the pulmonary capillaries and veins. This reduces the elasticity of the lungs and increases the work of the respiratory muscles. For severe heart failure, orthopnea is characteristic - a forced sitting position taken by the patient to facilitate breathing with severe shortness of breath. The deterioration of well-being in the supine position is due to the deposition of fluid in the pulmonary capillaries, leading to an increase in hydrostatic pressure. In addition, in the supine position, the diaphragm rises, which makes breathing somewhat difficult. For chronic heart failure, paroxysmal nocturnal dyspnea (cardiac asthma) is characteristic, due to the occurrence of interstitial pulmonary edema. At night, during sleep, an attack of severe shortness of breath develops, accompanied by coughing and wheezing in the lungs. With the progression of heart failure, alveolar pulmonary edema may occur .. Rapid fatigue in patients with heart failure appears due to insufficient oxygen supply to skeletal muscles .. Patients with chronic heart failure may be disturbed by nausea, decreased appetite, abdominal pain, abdominal enlargement (ascites) due to blood stagnation in the liver and the portal vein system .. From the side of the heart, pathological III and IV heart sounds can be heard. Moist wheezing is determined in the lungs. Characterized by hydrothorax, often right-sided, resulting from an increase in pleural capillary pressure and extravasation of fluid into the pleural cavity.
. The clinical manifestations of heart failure significantly depend on its stage... Stage I - signs (fatigue, shortness of breath and palpitations) appear during normal physical activity, at rest there are no manifestations of heart failure .. Stage IIA - there are unexpressed hemodynamic disturbances. Clinical manifestations depend on which parts of the heart are predominantly affected (right or left) ... Left ventricular failure is characterized by stagnation in the pulmonary circulation, manifested by typical inspiratory dyspnea with moderate exercise, attacks of paroxysmal nocturnal dyspnea, rapid fatigue. Edema and enlargement of the liver are uncharacteristic ... Right ventricular failure is characterized by the formation of congestion in the systemic circulation. Patients are worried about pain and heaviness in the right hypochondrium, a decrease in urine output. An enlarged liver is characteristic (the surface is smooth, the edge is rounded, palpation is painful). A distinctive feature of stage IIA heart failure is considered to be complete compensation of the condition during treatment, i.e. reversibility of manifestations of heart failure as a result of adequate treatment .. Stage IIB - there are deep hemodynamic disturbances, the entire circulatory system is involved in the process. Shortness of breath occurs with the slightest physical exertion. Patients are worried about a feeling of heaviness in the right hypochondrium, general weakness, sleep disturbance. Characterized by orthopnea, edema, ascites (a consequence of an increase in pressure in the hepatic veins and veins of the peritoneum - extravasation occurs, and fluid accumulates in the abdominal cavity), hydrothorax, hydropericardium .. Stage III - the final dystrophic stage with deep irreversible metabolic disorders. As a rule, the condition of patients at this stage is severe. Shortness of breath is expressed even at rest. Characterized by massive edema, accumulation of fluid in the cavities (ascites, hydrothorax, hydropericardium, edema of the genitals). At this stage, cachexia occurs.
Diagnostics
Instrumental data
. ECG... you can identify signs of blockade of the left or right bundle branch of His, hypertrophy of the ventricles or atria, pathological Q waves (as a sign of a previous MI), arrhythmias. A normal ECG raises doubts about the diagnosis of chronic heart failure.
. Echocardiography allows you to clarify the etiology of chronic heart failure and assess the functions of the heart, the degree of their impairment (in particular, to determine the ejection fraction of the left ventricle). Typical manifestations of heart failure are expansion of the left ventricular cavity (as it progresses, expansion of other chambers of the heart), an increase in the end systolic and end diastolic dimensions of the left ventricle, and a decrease in its ejection fraction.
. X-ray examination.. It is possible to detect venous hypertension in the form of a redistribution of blood flow in favor of the upper lungs and an increase in the diameter of the vessels .. With congestion in the lungs, signs of interstitial edema (Curly lines in the phrenic sinuses) or signs of pulmonary edema are detected .. Hydrothorax is detected (more often right-sided) .. Cardiomegaly is diagnosed with an increase in the transverse size of the heart of more than 15.5 cm in men and more than 14.5 cm in women (or with a cardiothoracic index of more than 50%).
. Cardiac catheterization allows you to detect an increase in the pressure of pulmonary capillary wedging more than 18 mm Hg.
Diagnostic Criteria - The Framingham Criteria for the Diagnosis of Chronic Heart Failure, categorized as major and minor. Large criteria: paroxysmal nocturnal dyspnea (cardiac asthma) or orthopnea, swelling of the cervical veins, wheezing in the lungs, cardiomegaly, pulmonary edema, pathological III heart sound, increased CVP (more than 160 mm H2O), blood flow time more than 25 s, positive "Hepatojugular reflux". Small criteria: swelling of the legs, nocturnal cough, shortness of breath during exertion, enlarged liver, hydrothorax, tachycardia more than 120 per minute, decrease in VC by 1/3 of the maximum. To confirm the diagnosis of chronic heart failure, either 1 large or 2 small criteria are required. Signs to be identified must be associated with heart disease.
Differential diagnosis... Nephrotic syndrome - a history of edema, proteinuria, renal pathology. Cirrhosis of the liver. Occlusive lesions of the veins with the subsequent development of peripheral edema.
Treatment. It is necessary first of all to assess the possibility of influencing the cause of the insufficiency. In some cases, an effective etiological effect (for example, surgical correction of a heart defect, myocardial revascularization in IHD) can significantly reduce the severity of manifestations of chronic heart failure. In the treatment of chronic heart failure, non-drug and drug therapies are distinguished. It should be noted that both treatments must complement each other.
Drug-free treatment... Limiting the use of table salt to 5-6 g / day, liquid (up to 1-1.5 l / day). Optimization of physical activity .. Moderate physical activity is possible and even necessary (walking for at least 20-30 minutes 3-5 r / week) .. Complete physical rest should be observed when the condition worsens (at rest, the heart rate decreases and the work of the heart decreases).
Treatment
Drug therapy... The ultimate goal of chronic heart failure treatment is to improve the quality of life and increase its duration.
Diuretics When prescribing them, it should be borne in mind that the occurrence of edema in heart failure is associated with several reasons (narrowing of the renal vessels, increased secretion of aldosterone, increased venous pressure. Treatment only with diuretics is considered insufficient. In chronic heart failure, loop (furosemide) or thiazide (for example, hydrochlorothiazide) diuretics.In case of insufficient diuretic response, loop diuretics and thiazides are combined .. Thiazide diuretics. Usually hydrochlorothiazide is used in a dose of 25 to 100 mg / day.It should be remembered that when GFR of the kidneys is less than 30 ml / min, it is not advisable to use thiazides .. Loop diuretics begin to act faster, their diuretic effect is more pronounced, but less durable than that of thiazide diuretics.Apply furosemide at a dose of 20-200 mg / day intravenously, depending on the manifestations of edema and diuresis. 100 mg / day
ACE inhibitors cause hemodynamic unloading of the myocardium due to vasodilation, increased urine output, and decreased filling pressure of the left and right ventricles. Indications for the appointment of ACE inhibitors are clinical signs of heart failure, a decrease in the left ventricular ejection fraction of less than 40%. When prescribing ACE inhibitors, certain conditions must be observed according to the recommendations of the European Society of Cardiology (2001) .. It is necessary to stop taking diuretics 24 hours before taking ACE inhibitors .. Blood pressure should be monitored before and after taking ACE inhibitors .. Treatment begins with low doses with a gradual their increase .. It is necessary to monitor renal function (diuresis, relative density of urine) and the concentration of blood electrolytes (potassium ions, sodium) with increasing doses every 3-5 days, then every 3 and 6 months. can be prescribed only for hypokalemia) .. It is necessary to avoid the combined use of NSAIDs.
The first positive data were obtained on the beneficial effect of angiotensin II receptor blockers (in particular, losartan) on the course of chronic heart failure as an alternative to ACE inhibitors in case of their intolerance or contraindications to the appointment.
Cardiac glycosides have a positive inotropic (increase and shorten systole), negative chronotropic (decrease in heart rate), negative dromotropic (slowing down AV - conduction) effect. The optimal maintenance dose of digoxin is considered to be 0.25-0.375 mg / day (in elderly patients, 0.125-0.25 mg / day); the therapeutic concentration of digoxin in the blood serum is 0.5-1.5 mg / l. Indications for the appointment of cardiac glycosides are the tachysystolic form of atrial fibrillation, sinus tachycardia.
B - Adrenergic blockers .. The mechanism of favorable action of - adrenergic blockers in chronic heart failure is due to the following factors ... Direct protection of the myocardium from the adverse effects of catecholamines ... Protection against catecholamine-induced hypokalemia ... Improvement of blood flow in the coronary arteries due to a decrease in heart rate and an improvement in diastolic relaxation of the myocardium ... Reducing the effect of the vasoconstrictor systems (for example, due to a decrease in the secretion of renin) ... Potentiation of the vasodilating kallikrein - kinin system ... adrenergic blockers for the treatment of chronic heart failure are recommended for the use of carvedilol - b1 - and a1 - an adrenergic blocker with vasodilating properties. The initial dose of carvedilol is 3.125 mg 2 r / day, followed by an increase in the dose to 6.25 mg, 12.5 mg or 25 mg 2 r / day in the absence of side effects in the form of arterial hypotension, bradycardia, decreased left ventricular ejection fraction (according to Echocardiography) and other negative manifestations of the action of b - blockers. Also recommended are metoprolol, starting with a dose of 12.5 mg 2 r / day, bisoprolol at 1.25 mg 1 r / day under the control of ventricular ejection fractions with a gradual increase in dose after 1-2 weeks.
Spironolactone. It was found that the appointment of the aldosterone antagonist spironolactone at a dose of 25 mg 1-2 r / day (in the absence of contraindications) promotes an increase in the life expectancy of patients with heart failure.
Peripheral vasodilators are prescribed for chronic heart failure if there are contraindications or if ACE inhibitors are poorly tolerated. Of the peripheral vasodilators, hydralazine is used at a dose of up to 300 mg / day, isosorbide dinitrate at a dose of up to 160 mg / day.
. Other cardiotonic drugs... b - Adrenomimetics (dobutamine), phosphodiesterase inhibitors are usually prescribed for 1-2 weeks at the end stage of heart failure or with a sharp deterioration in the patient's condition.
Anticoagulants. Patients with chronic heart failure are at high risk of thromboembolic complications. Possible as PE due to venous thrombosis, and thromboembolism of the vessels of the systemic circulation, caused by intracardiac thrombi or atrial fibrillation. The appointment of indirect anticoagulants in patients with chronic heart failure is recommended in the presence of atrial fibrillation and a history of thrombosis.
Antiarrhythmic drugs. In the presence of indications for the appointment of antiarrhythmic drugs (atrial fibrillation, ventricular tachycardia), it is recommended to use amiodarone at a dose of 100-200 mg / day. This drug has a minimal negative inotropic effect, while most other drugs in this class reduce the left ventricular ejection fraction. In addition, the antiarrhythmic drugs themselves can provoke arrhythmias (proarrhythmic effect).
Surgery
The choice of the optimal surgical method depends on the underlying cause of the heart failure. So, in IHD in many cases, myocardial revascularization is feasible, in idiopathic subaortic hypertrophic stenosis - septal myoectomy, in valvular defects - prosthetics or reconstructive interventions on the valves, in bradyarrhythmias - implantation of pacemaker, etc.
In the case of refractoriness of heart failure to adequate therapy, heart transplantation is the main surgical method of treatment.
Methods of mechanical support of blood circulation (implantation of assistants, artificial ventricles and biomechanical pumps), previously proposed as temporary options before transplantation, have now acquired the status of independent interventions, the results of which are comparable to those of transplantation.
To prevent the progression of dilatation of the heart, devices are implanted in the form of a mesh, which prevents excessive expansion of the heart.
If pulmonary heart disease is tolerant to treatment, transplantation of the heart-lung complex seems to be a more appropriate intervention.
Forecast. In general, the 3-year survival rate of patients with chronic systolic heart failure is 50%. The death rate from chronic systolic heart failure is 19% per year.
Factors, the presence of which correlates with a poor prognosis in patients with heart failure .. Reduction of left ventricular ejection fraction less than 25% .. Inability to rise one floor and move at a normal pace for more than 3 minutes .. Reduction in the content of sodium ions in blood plasma less than 133 meq / l .. Decrease in the concentration of potassium ions in blood plasma less than 3 meq / l .. Increase in blood levels of norepinephrine .. Frequent ventricular premature beats with daily ECG monitoring.
The risk of sudden cardiac death in patients with heart failure is 5 times higher than in the general population. Most patients with chronic heart failure die suddenly, mainly from ventricular fibrillation. The prophylactic administration of antiarrhythmic drugs does not prevent this complication.
ICD-10. I50 Heart failure
Medicines and Medicines are used to treat and / or prevent "Chronic systolic heart failure".
Pharmacological group (s) of the drug.
Family doctor. Therapist (volume 2). Chronic renal failure mkb 10
Chronic renal failure
general information
There are various definitions of chronic renal failure (CRF), but the essence of any of them boils down to the development of a characteristic clinical and laboratory complex resulting from the progressive loss of all renal functions.
Chronic renal failure (CRF)- this is a loss of homeostatic functions of the kidneys against the background of renal disease for more than 3 months: a decrease in glomerular filtration and relative density (osmolarity), an increase in the concentration of creatinine, urea, potassium, phosphorus, magnesium and aluminum in blood serum, a decrease in blood calcium, alkaline balance (metabolic acidosis), the development of anemia and arterial hypertension.
Epidemiology
The problem of chronic renal failure has been actively developed for several decades, due to the significant prevalence of this complication. So, according to the literature, the number of patients with chronic renal failure in Europe, the USA and Japan ranges from 157 to 443 per 1 million population. The prevalence of this pathology in our country is 212 per 1 million of the population among patients over 15 years of age. Among the causes of mortality, chronic renal failure takes eleventh place.
Etiology
CRF is based on a single morphological equivalent - nephrosclerosis. There is no such form of kidney pathology that could potentially not lead to the development of nephrosclerosis, and, consequently, renal failure. Thus, CRF is the outcome of any chronic kidney disease.
Primary kidney disease can lead to chronic renal failure, as well as their secondary damage as a result of a long-term chronic disease of organs and systems. Direct damage to the parenchyma (primary or secondary), leading to chronic renal failure, is conventionally divided into diseases with a predominant lesion of the glomerular apparatus or tubular system, or a combination of both. Among glomerular nephropathies, the most common are chronic glomerulonephritis, diabetic nephropathy, amyloidosis, lupus nephritis. More rare causes of chronic renal failure with lesions of the glomerular apparatus are malaria, gout, prolonged septic endocarditis, myeloma. Primary damage to the tubular system is most often observed in most urological diseases accompanied by impaired urine outflow, congenital and acquired tubulopathies (renal diabetes insipidus, Albright's tubular acidosis, Fanconi syndrome, which occurs as an independent hereditary disease or accompanies various diseases), drug poisoning and toxic substances. Secondary damage to the renal parenchyma can lead to vascular diseases - damage to the renal arteries, essential hypertension (primary nephroangiosclerosis), malformations of the kidneys and urinary tract (polycystic, renal hypoplasia, neuromuscular dysplasia of the ureters, etc.). Chronic isolated damage to any part of the nephron is actually a triggering mechanism for the development of chronic renal failure, however, in clinical practice, late stages of chronic renal failure are characterized by dysfunction of both the glomerular and tubular apparatus.
Pathogenesis
Regardless of the etiological factor, the mechanism for the development of chronic renal failure is based on a decrease in the number of active nephrons, a significant decrease in the glomerular filtration rate in an individual nephron, and on a combination of these indicators. Complex mechanisms of kidney damage include many factors (violation of metabolic and biochemical processes, blood clotting, impaired urine passage, infection, abnormal immune processes), which, when interacting with other diseases, can lead to chronic renal failure. In the development of chronic renal failure, the most important point is the slow, latent impairment of all renal functions, which the patient is usually unaware of. However, modern examination methods make it possible to reveal the latent stage, since the changes that occur in the body when the functional ability of the kidneys is impaired are now well known. This is an important task of the clinician, which allows him to take preventive and therapeutic measures aimed at preventing the premature development of end-stage renal failure. The kidneys have significant reserve capacities, as evidenced by the preservation and maintenance of the body's life with the loss of 90% of the nephrons. The adaptation process is carried out by enhancing the function of the preserved nephrons and restructuring the whole organism. With the progressive death of nephrons, the rate of glomerular filtration decreases, the water-electrolyte balance is disturbed, there is a delay in the body of metabolic products, organic acids, phenolic compounds, some peptides and other substances that determine the clinical picture of chronic renal failure and the patient's condition. Thus, a violation of the excretory and secretory functions of the kidneys contributes to the development of pathological changes in the body, the severity of which depends on the intensity of nephron death and determines the progression of renal failure. With CRF, one of the most important functions of the kidneys is disturbed - maintaining the water-salt balance. Already in the early stages of chronic renal failure, especially due to diseases with a predominant lesion of the tubular apparatus, there is a violation of the concentration ability of the kidneys, which is manifested by polyuria, nocturia, a decrease in urine osmolarity to the level of osmotic concentration of blood plasma (isostenuria), and with far-reaching lesions, hypostenuria (osmotic concentration of urine lower osmotic concentration of blood plasma). Polyuria, which is persistent even with fluid restriction, can be due to both a direct decrease in tubular function and a change in osmotic diuresis. An important function of the kidney is to maintain electrolyte balance, especially ions such as sodium, potassium, calcium, phosphorus, etc. In chronic renal failure, sodium excretion in the urine can be increased or decreased. In a healthy person, 99% of sodium filtered through the glomeruli is reabsorbed in the tubules. Diseases with a predominant lesion of the tubular-interstitial system lead to a decrease in its reabsorption up to 80%, and, consequently, its increased excretion. Strengthening the excretion of sodium in the urine does not depend on its introduction into the body, which is especially dangerous when the patient is advised to limit salt intake in such situations. However, the predominant damage to the glomeruli, a decrease in the rate of glomerular filtration, especially with preserved tubular function, can lead to sodium retention, which entails the accumulation of fluid in the body, an increase in blood pressure. Up to 95% of the potassium introduced into the body is removed by the kidneys, which is achieved by its secretion in the distal tubule. With chronic renal failure, the regulation of the balance of potassium in the body is carried out by excreting it by the intestines. So, with a decrease in GFR to 5 ml / min, about 50% of the incoming potassium is excreted in the feces. An increase in plasma potassium can be observed in the oligoanuric phase of chronic renal failure, as well as with an exacerbation of the underlying disease, with increased catabolism. Since the main amount of potassium in the body is in the intracellular space (in plasma - about 5 mmol / l, in the intracellular fluid - about 150 mmol / l), in some situations (fever, surgery, etc.) against the background of chronic renal failure, hyperkalemia that threatens the patient's life. The state of hypokalemia in patients with chronic renal failure is observed much less frequently and may indicate a deficiency of total potassium in the body and a sharp violation of the secretory capacity of the distal tubule. Dysfunctions of the glomerular and tubular apparatus already in the early stages of chronic renal failure lead to hyperchloremic acidosis, hyperphosphatemia, a moderate increase in serum magnesium and hypocalcemia.
An increase in the blood concentration of urea, amino nitrogen, creatinine, uric acid, methylguanidine, phosphates, etc. An increase in the level of amino nitrogen may be associated with increased protein catabolism due to its excessive intake, or its sharp restriction during starvation.
Urea is the end product of protein metabolism, formed in the liver from the nitrogen of deaminated amino acids. In conditions of renal failure, not only the difficulty of its excretion is noted, but also, for still unknown reasons, an increase in its production by the liver.
Creatinine is formed in the muscles of the body from its precursor creatinine. The content of creatinine in the blood is quite stable, an increase in creatinemia in parallel with an increase in the level of urea in the blood occurs, as a rule, with a decrease in glomerular filtration to 20-30% of the normal level.
The overproduction of parathyroid hormone as a possible major toxin of uremia has attracted even more attention. This is confirmed by the effectiveness of at least partial parathyroidectomy. There are more and more facts indicating the toxicity of substances of unknown nature, the relative molecular weight of which is 100-2000, as a result of which they are called "average molecules". They are the ones that accumulate in the blood serum of patients with chronic renal failure. However, it is becoming more and more obvious that the syndrome of azotemia (uremia) is not caused by one or several toxins, but depends on the rearrangement of cells in all tissues and changes in the transmembrane potential. This occurs as a result of violations of both the function of the kidneys and the systems that regulate their activity.
Its causes are blood loss, shortening of the life span of erythrocytes due to a deficiency of protein and iron in the body, toxic effects of nitrogen metabolism products, hemolysis (deficiency of glucose-6-phosphate dehydrogenase, excess guanidine), decreased erythropoietin. The growth of medium molecules also inhibits erythropoiesis.
Osteodystrophy
Osteodystrophy caused by impaired calciferol metabolism. In the kidneys, an active metabolite of 1,25-dehydroxycalciferol is formed, which affects the transport of calcium by regulating the synthesis of specific proteins that bind it. With chronic renal failure, the conversion of calciferol into exchange-active forms is blocked. The water-electrolyte balance remains close to physiological for a long time, up to the terminal phase. Under conditions of impaired ion transport in the tubules, with tubular defects, the loss of sodium increases, which, if its replacement is insufficient, leads to the syndrome of hyponatremia. Hyperkalemia is regarded as the second most important sign of chronic renal failure. This is associated not only with the increasing catabolism characteristic of renal failure, but also with an increase in acidosis, and most importantly, with a change in the distribution of potassium outside and inside the cells.
The change in CBS occurs due to a violation of the "carbonic acid - bicarbonate" function. With various options for impaired renal function, depending on the nature of the process, one or another type of impairment of CBS may be observed. With glomerular - the possibility of acid valences entering the urine is limited, with tubular - the predominant inclusion of ammonio acidogenesis occurs.
Arterial hypertension
In its appearance, the role of inhibition of the production of vasodilators (kinins) is undoubted. The imbalance of vasoconstrictors and vasodilators in chronic renal failure is caused by the kidney's loss of the ability to control sodium levels and circulating blood volume in the body. In the terminal phase of chronic renal failure, a persistent hypertensive reaction can be adaptive, maintaining filtration pressure. In these cases, a sudden drop in blood pressure can be fatal.
According to ICD-10, chronic renal failure is classified as follows:
N18 Chronic renal failure.
N18.0 - Terminal stage of renal disease.
N18.8 - Other chronic renal failure
N18.9 - Chronic renal failure not specified.
N19 - Renal failure not specified.
Diagnostics
Diagnosis of chronic renal failure with known renal disease is not difficult. Its degree, and, consequently, its severity, is determined by an increase in serum creatinine concentration and a decrease in GFR. As it should be clear from the foregoing, it is very important to monitor the state of electrolyte, acid-base metabolism, to timely register violations of the activity of the heart and lungs.
Diagnosis of chronic renal failure is mainly laboratory. The first symptom is a decrease in the relative density of urine to 1.004-1.011, regardless of the amount of urine output. It should be borne in mind that the presence of sugar and protein in urine can increase the relative density of urine (each 1% sugar - by 0.004 and 3 g / l - by 0.01).
The study of electrolyte balance to establish the level of decreased renal function is of little information. The same can be said about the degree of anemia, and, moreover, the level of blood pressure.
Accurate assessment of kidney function, taking into account the state of other organs, the degree of dystrophic processes in the body when deciding on the prospects for kidney transplantation are becoming very important.
In general therapeutic practice, one can encounter creatininemia without a specific renal disease. This is observed with congestive heart failure. Usually creatininemia does not exceed 0.6-0.8 mmol / l. A more significant increase can be observed with a rapidly increasing decompensation of cardiac activity, for example, in patients with complicated myocardial infarction. A feature of such creatininemia is the unusual preservation of a sufficiently high urine density. Renal failure occurs when the "renal quota" of cardiac output is reduced to 7.8%. The deterioration of renal hemodynamics is associated with an increase in venous pressure, and the decrease in renal blood flow outstrips the reduction of glomerular filtration, so that the filtration fraction is usually increased. Deterioration of renal hemodynamics is accompanied by a redistribution of renal blood flow. The outer part of the cortical layer suffers most of all. The persistence of increased urine density is associated with a slowdown in blood flow, especially in the medulla.
Thus, “chronic” creatinemia, unusual for extrarenal causes, without the development of diffuse nephrosclerosis, not accompanied by isostenuria, which is usual for it, has a certain diagnostic and prognostic value for cardiac patients. Such renal failure does not require special treatment. Another feature of decreased kidney function in congestive heart failure is the appearance and increase of proteinuria. As a rule, blood plasma proteins are released, but the culprit is impaired tubular protein reabsorption. The histopathological picture of such a congested kidney reveals varicose veins. The glomeruli are enlarged, the capillary loops are wide, and contain erythrocytes. The stroma of the kidney is edematous, the tubules are somewhat dilated, their epithelium is in a state of dystrophy, and many of the tubules are showing signs of atrophy. Focal interstitial fibrosis and arteriosclerosis.
Clinical criteria
Main manifestations:
- symptoms of endogenous intoxication;
- oliguria;
- nausea;
- macrohematuria or microhematuria;
- violation of urination;
- itchy skin;
- bleeding.
Already the first communication with the patient and finding out such data from the anamnesis as the duration of a nephrological disease, the presence or absence of chronic glomerulo- or pyelonephritis, arterial hypertension, the duration of these diseases, the frequency of exacerbations of glomerulo- or pyelonephritis, the amount of urine excreted per day, as well as the identification of early symptoms of chronic renal failure, allow one to suspect renal failure and outline a plan for diagnostic and therapeutic measures.
An indication in the history of the duration of a nephrological disease of more than 5-10 years gives reason to suspect the presence of renal failure and perform all diagnostic studies that confirm or reject this diagnosis. The analysis of the studies showed that the total impairment of renal function and the identification of the stage of chronic renal failure are possible with the use of traditional methods of urine and blood examination.
Asthenic syndrome: weakness, fatigue, drowsiness, loss of hearing, taste.
Dystrophic syndrome: dryness and excruciating itching of the skin, traces of scratching on the skin, weight loss, real cachexia, muscle atrophy is possible.
Gastrointestinal Syndrome: dryness, bitterness and an unpleasant metallic taste in the mouth, lack of appetite, heaviness and pain in the epigastric region after eating, often - diarrhea, possibly an increase in gastric acidity (due to a decrease in the destruction of gastrin in the kidneys), in the later stages there may be gastrointestinal bleeding , stomatitis, mumps, enterocolitis, pancreatitis, liver dysfunction.
Cardiovascular syndrome: shortness of breath, pain in the heart, arterial hypertension, left ventricular myocardial hypertrophy, in severe cases - attacks of cardiac asthma, pulmonary edema; with advanced CRF - dry or exudative pericarditis, pulmonary edema.
Anemic-hemorrhagic syndrome: pallor of the skin, nasal, intestinal, gastric bleeding, skin hemorrhages, anemia.
Osteoarticular syndrome: pain in bones, joints, spine (due to osteoporosis and hyperuricemia).
Damage to the nervous system: uremic encephalopathy (headache, memory loss, psychosis with obsessive fears, hallucinations, seizures), polyneuropathy (paresthesia, itching, burning sensation and weakness in the arms and legs, decreased reflexes).
Urinary Syndrome: isohypostenuria, proteinuria, cylindruria, microhematuria.
Early clinical signs of CRF- polyuria and nocturia, hypoplastic anemia; then general symptoms join - weakness, drowsiness, fatigue, apathy, muscle weakness. Subsequently, with a delay in nitrogenous toxins, itching occurs (sometimes painful), nasal, gastrointestinal, uterine bleeding, subcutaneous hemorrhages; may develop "uremic gout" with pain in the joints, tofus. Uremia is characterized by dyspeptic syndrome - nausea, vomiting, hiccups, loss of appetite, up to aversion to food, diarrhea. The skin is pale yellowish (a combination of anemia and delayed urochromes). Skin - dry, with traces of scratching, bruises on the arms and legs; tongue - dry, brown. With the progression of chronic renal failure, the symptoms of uremia increase. Retention of sodium leads to hypertension, often with malignant features, retinopathy. Hypertension, anemia, and electrolyte changes can damage the heart. In the terminal stage, fibrinous or effusion pericarditis develops, indicating an unfavorable prognosis. As uremia progresses, neurological symptoms increase, convulsive twitching appears, encephalopathy intensifies, up to the development of uremic coma, with strong noisy acidotic breathing (Kussmaul breathing). The tendency of patients to infections is characteristic; pneumonia is often noted.
Laboratory criteria
Clinical analysis of urine- proteinuria, hypoisostenuria, cylindruria, possible abacterial leukocyturia, hematuria.
Blood test:
clinical- anemia, an increase in the erythrocyte sedimentation rate (ESR), moderate leukocytosis is possible, a shift of the leukocyte formula to the left, thrombocytopenia is possible;
biochemical- an increase in the levels of urea, creatinine, residual nitrogen in the blood, an increase in total lipids, B-lipoproteins, hyperkalemia, hypocoagulation, hypocalcemia, hyperphosphatemia, hypodysproteinemia, hypercholesterolemia is possible.
Laboratory diagnostics
- Clinical blood test, with the determination of platelets;
- biochemical blood test, with the determination of the level of creatinine, urea, cholesterol, proteinogram, electrolytes (potassium, calcium, phosphorus, sodium, chlorine);
- determination of daily protein excretion;
- determination of the functional state of the kidneys (glomerular filtration rate);
- acid-base state;
- ALT, AST;
- X-ray examination of the kidneys, bones, lungs.
Additional laboratory and instrumental studies
- Ferritin;
- percentage (%) of transferrin saturation;
- determination of parathyroid hormone;
- determination of urinary calcium excretion;
- determination of blood amylase;
- protein-sediment samples;
- determination of fibrin degradation products in blood serum;
- radionuclide studies (indirect renoangiography, dynamic and static renoscintigraphy);
- puncture biopsy of the kidney;
- functional studies of the bladder;
- echoencephalogram;
- echocardiography with an assessment of the functional state of the heart, vascular Doppler sonography.
Differential diagnosis
Diagnosis of chronic renal failure in clinicians does not cause any particular difficulties due to the characteristic clinical picture and laboratory changes in the blood and urine. The only thing that must always be remembered: such a clinic can be caused by an exacerbation of chronic renal failure as a result of an occlusive factor and the development of an acute inflammatory process in the upper or lower urinary tract. Under these conditions, the true stage of chronic renal failure can be established only after the restoration of the passage of urine and the elimination of the acute inflammatory process. For nephrologists, it is important to diagnose the early and pre-dialysis stages of chronic renal failure, which makes it possible to outline the treatment tactics and determine the prognosis of nephrological disease.
The detection of chronic renal failure, as a rule, is carried out in parallel with the diagnosis of nephrological disease and includes the history of the disease, clinical manifestations, changes in general blood and urine tests, as well as specific studies aimed at identifying the total function of the kidneys and methods that allow assessing the morphological and functional parameters of the kidneys.
Specialist consultations
- Oculist: fundus condition;
- neuropathologist: presence of uremic and hypertensive encephalopathy;
- gastroenterologist: the presence of complications from the gastrointestinal tract (gastritis, hepatitis, colitis, etc.);
- cardiologist: symptomatic arterial hypertension, hypertensive heart;
- cardiac surgeon: uremic pericarditis (puncture);
- urologist: presence of calculi in the calyx-pelvic region of the kidneys, ureters, etc.
Goals
Based on the classification, the treatment of CRF is indicated already with a glomerular filtration level of less than 60 ml / min, which corresponds to a creatinine level of 140 μmol / L for men and 105 μmol / L for women (renoprotection is indicated with a GFR level of about 90 ml / min). It is recommended to stabilize blood pressure to target numbers< 130/80 мм рт.ст. а при протеинурии – < 125/75 мм рт.ст.
Diagnostics and management of complications.
Treatment level
Outpatient: therapist, family doctor, cardiologist, gastroenterologist, etc.; stationary - indications for inpatient treatment.
Patients with chronic renal failure are subject to dispensary observation by a nephrologist, and in his absence - by a general practitioner at the place of residence.
Dispensary observation should include: examination of patients with chronic renal failure stage I 3 times a year, with chronic renal failure stage II - 6 times a year, and with chronic renal failure stage III - monthly, the appointment of an adequate regimen, employment and the choice of rational dietary and therapeutic measures; identification and elimination of factors that contribute to the progression of chronic renal failure. In the event of intercurrent diseases, patients are examined additionally. Patients with stage IV chronic renal failure should be treated with hemodialysis or peritoneal dialysis, or symptomatic therapy (if there are contraindications for renal replacement therapy (RRT) at the place of residence.
Treatment methods
Basic drug therapy(in accordance with international standards and protocols approved by the Ministry of Health of Ukraine: specifically the pharmacological group of drugs, dose, duration of the course) and additional.
Surgical treatment or other treatments (indications).
The main objectives of dietary treatment for CRF is to reduce the intake of protein with food - low protein diet (LBD); control of fluid intake; reducing the consumption of foods that contain Na +, K +, Mg2 +, Cl-, phosphates.
Limiting protein intake
A low protein diet (LBD) helps to inhibit the progression of chronic renal failure: intraglomerular hypertension and glomerular hypertrophy, proteinuria decrease, the incidence of secondary hyperparathyroidism decreases, and the level of nitrogen metabolism products decreases.
Correction of calcium phosphate disorders
Elevated serum phosphorus levels and the development of secondary hyperparathyroidism (SHPT) not only contribute to the development of osteopathy, but also affect the progression of chronic renal failure. With a GFR of 40-50 ml / min, the amount of phosphorus in the daily diet should not exceed 800-1000 mg. When GFR is below 40 ml / min, in addition to dietary restriction of phosphorus to 1 g / day, phosphate binders (FSP) are prescribed: phosphate binders.
Controlling blood pressure (BP) and proteinuria levels
ACE inhibitors (ACE inhibitors):
- enalapril - from 5 to 40 mg / day;
- perindopril - from 2 to 8 mg / day;
- quinapril - from 5 to 20 mg / day;
- moexipril - from 3.75 to 15 mg / day;
- ramipril - from 2.5 to 10 mg / day;
- spirapril - from 3 to 6 mg / day.
Angiotensin II receptor blockers (ARBs):
- valsartan - from 80 to 160 mg / day;
- losartan - from 25 to 100 mg / day;
- candesartan - from 8 to 32 mg / day;
- irbesartan - from 150 to 300 mg / day;
- Telmisartan - from 40 to 80 mg / day;
- eprosartan - from 400 to 1200 mg / day.
Calcium channel blockers:
- amlodipine - from 5 to 10 mg / day;
- lercanidipine - from 5 to 10 mg / day;
- diltiazem - from 30 to 90 mg / day three times;
- diltiazem retard - from 90 to 300 mg / day twice;
- verapamil - from 40 to 120 mg / day, 2 to 3 times a day;
- verapamil retard - from 240 to 480 mg / day.
ACE inhibitors (ACE inhibitors) and angiotensin II receptor blockers (ARBs) more significantly than diuretics, calcium antagonists and b-blockers, reduce proteinuria and microalbuminuria.
Calcium channel blockers... namely, the nifedipine group (dihydropyridine), effectively reduce blood pressure, but do not affect the level of proteinuria and the progression of chronic renal failure, which is associated with their property to dramatically reduce the tone of the afferent arteriole and increase hydraulic shock at high systemic blood pressure. On the contrary, nonhydropyridine calcium channel blockers (verapamil, diltiazem) practically do not affect the mechanism of renal autoregulation, help to reduce proteinuria, and inhibit glomerular fibrosis. Achievement of target blood pressure in chronic kidney disease occurs with the appointment of several drugs.
Correction of anemia
Iron saturation is controlled by target troughs of serum erythropoietin concentration above 100 ng / ml and transferrin saturation level> 20%. Iron preparations, if necessary, are prescribed in a dose of more than 200-300 mg of elemental iron per day. In parallel, other drugs are used that are mandatory in the treatment of anemia:
- folic acid - from 5 to 15 mg / day;
- pyridoxine (vitamin B6) - from 50 to 200 mg / day.
The main type of replacement therapy for erythropoietic deficiency anemia is the appointment of erythropoietin:
- eprex - from 20 to 100 U / kg three times a week;
- Recormon - from 20 to 100 U / kg three times a week.
Correction of hyperazotemia
In order to reduce the level of azotemia, the toxic load of uremia, drugs are used that enhance their excretion.
Hypoazotemic phytopreparations:
- Chophytol - from 2 to 3 tablets three times a day for 15 minutes. before meals or 2 ampoules twice a day intramuscularly or intravenously daily for 14-21 days;
- Lespenephril (Lespeflan) - from 3 to 6 teaspoons per day or intravenously at the rate of 1 ml / kg of the patient's weight.
Enterosorption with the use of enterosorbents - 1.5-2 hours before or after meals and medications:
- activated carbon - up to 5 g from 3 to 4 times / day;
- spherical carbonite - up to 5 g from 3 to 4 times / day;
- enterosgel - 1 tablespoon (15.0 g) 3 to 4 times / day;
- sorbigel - 1 tablespoon (15.0 g) 3 to 4 times / day;
- enterodesis - 5 ml per 1000 ml of water 3 to 4 times / day;
- polyphepan - 1 tablespoon (15.0 g) from 2 to 4 times / day or at the rate of 0.5 g / kg of weight / day.
Intestinal dialysis with the introduction into the large intestine through a probe from 8 to 10 liters of solution, which contains: sucrose - 90 g / l; glucose - 8 g / l, potassium chloride - 0.2 g / l, sodium bicarbonate - 1 g / l, sodium chloride –1 g / l.
Correction of dyslipidemia
Target LDL-C in Adults with Chronic Renal Disease< 2,6 ммоль/л; уровень ХС ЛПВП >1 mmol / L (40 mg / dL); TG< 2,3 ммоль/л.
Statins:
- lovastatin - from 10 to 80 mg / day;
- simvastatin - from 10 to 40 mg / day;
- pravastatin - from 10 to 40 mg / day;
- atorvastatin - from 10 to 40 mg / day;
- fluvastatin - from 10 to 40 mg / day.
Statins block a key enzyme of cholesterol synthesis in the liver and have a pronounced lipid-lowering effect. Desired LDL cholesterol level -< 2,6 ммоль/л.
Fibrates:
- gemfibrozil - 600 mg twice a day;
- fenofibrate - 200 mg / day.
Fibrates are prescribed at a TG level> 5.7 mmol / L (500 mg / dL), with a dose calculated according to renal function. The combination of fibrates and statins is not desirable as there is a high risk of developing rhabdomyolysis.
Indications for active treatment of chronic renal failure:
- serum creatinine level - above 0.528 mmol / l (with diabetic nephropathy - above 0.353 mmol / l), arteriovenous fistula is superimposed, with further increase in creatinine - "input" into hemodialysis;
- pericarditis, neuropathy, encephalopathy, hyperkalemia, high hypertension, impaired CBS in patients with chronic renal failure.
Today, the following active methods of treating CRF are used in Ukraine: chronic hemodialysis in combination with hemosorption and hemofiltration, peritoneal dialysis and kidney transplantation.
The prognosis is poor and improves with the use of renal replacement therapy (RRT) and kidney transplantation.
Prophylaxis
Timely detection and treatment of nephrological diseases leading to the development of chronic renal failure, such as acute glomerulo- and pyelonephritis, diabetic nephropathy.
Chronic heart failure. Definition. Classification. Clinic. Diagnostics. Treatment.
The urgency of the problem
The prevalence of clinically severe chronic heart failure (CHF) in the population is at least 1.5-3.0%. Among people over 65 years of age, the incidence of CHF increases to 6-10%, and decompensation becomes the most common cause of hospitalization in elderly patients. The number of patients with asymptomatic dysfunction of the left ventricle is at least 4 times higher than the number of patients with clinically severe CHF. Over 15 years, the number of hospitalizations diagnosed with CHF has tripled, and over 40 years has increased 6 times. The five-year survival rate of patients with CHF is still below 50%. The risk of sudden death is 5 times higher than in the population. In the United States, there are more than 2.5 million patients with CHF, about 200 thousand patients die every year, the 5-year survival rate after the onset of CHF signs is 50%.
Chronic heart failure (CHF) is a cardiac impairment of (pumping) function with corresponding symptoms, which consists in the inability of the circulatory system to deliver the amount of blood necessary for their normal functioning to organs and tissues. Thus, this is a disproportion between the state of blood circulation and metabolism, which grows with an increase in the activity of life processes; a pathophysiological condition in which dysfunction of the heart does not allow it to maintain the level of blood circulation necessary for metabolism in tissues.
CHF can develop against the background of almost any disease of the cardiovascular system, but the main three are the following nosological forms:
- Ischemic heart disease (CHD)
- Arterial hypertension
- Heart vices.
Ischemic heart disease. From the existing classification, acute myocardial infarction (AMI) and ischemic cardiomyopathy (ICMP is a nosological unit introduced into the clinical practice of ICD-10), especially often, lead to the development of CHF. The mechanisms of the onset and progression of CHF due to AMI are due to a change in the geometry and local contractility of the myocardium, called the term "remodeling of the left ventricle" (LV), with ICMP there is a decrease in total myocardial contractility, called the term "hibernation (" dormancy ") of the myocardium.
Arterial hypertension. Regardless of the etiology of hypertension, there is a structural reorganization of the myocardium, which has a specific name - "hypertensive heart". The mechanism of CHF in this case is due to the development of LV diastolic dysfunction.
Heart defects. Until now, Ukraine is characterized by the development of CHF due to acquired and uncorrected rheumatic defects.
A few words must be said about dilated cardiomyopathy (DCM) as the cause of CHF. DCM is a rather rare disease of unspecified etiology that develops at a relatively young age and quickly leads to cardiac decompensation.
Establishing the cause of CHF is necessary for the choice of treatment tactics for each particular patient.
Pathogenetic aspects of heart failure
From the point of view of modern theory, the main role in activating compensatory mechanisms (tachycardia, Frank-Starling mechanism, constriction of peripheral vessels) is played by hyperactivation of local or tissue neurohormones. This is mainly the sympathetic-adrenal system (SAS) and its effectors - norepinephrine and adrenaline and the renin-angiotensin-aldosterone system (RAAS) and its effectors - angiotensin II (A-II) and aldosterone, as well as the system of natriuretic factors. The problem is that the “triggered” mechanism of neurohormone hyperactivation is an irreversible physiological process. Over time, short-term compensatory activation of tissue neurohormonal systems turns into its opposite - chronic hyperactivation. The latter is accompanied by the development and progression of systolic and diastolic dysfunction of the left ventricle (remodeling).
If the heart is damaged, the stroke volume of the ventricle will decrease, and the end-diastolic volume and pressure in this chamber will increase. This increases the end-diastolic stretch of muscle fibers, which leads to greater systolic shortening (Starling's law). The Starling Mechanism helps maintain cardiac output. but the resulting chronic rise in diastolic pressure will be transmitted to the atria, pulmonary veins, or systemic circulation. The increasing capillary pressure is accompanied by extravasation of fluid with the development of edema. Reduced cardiac output, especially with a decrease in blood pressure, activates SAS, which stimulates myocardial contractions, heart rate, venous tone, and a decrease in renal perfusion leads to a decrease in the glomerular filtration rate, reabsorption of water and sodium chloride, and activation of the RAAS.
Tissue hypoxia in CHF is not only a resultant link in pathogenesis, but also a factor that has a direct provoking effect on its other leading components - a decrease in the pumping ability of the heart, preload, post-load and heart rate. Hypoxia is a complex multicomponent, multistage process. Direct primary effects of hypoxia are directed to targets localized at various levels: organismic, systemic, cellular and subcellular. At the subcellular level, hypoxia initiates the development of apoptosis.
The result of the described processes is an increase in peripheral vascular resistance and volume of circulating blood with a corresponding increase in afterload and preload.
Heart Failure Clinic
In most patients, left heart failure initially develops. The most common complaint is inspiratory dyspnea, initially associated with exercise and progressing to orthopnea, paroxysmal postural, and dyspnea at rest. Complaints of unproductive cough and nocturia are characteristic. Patients with CHF note weakness, fatigue, which are the result of reduced blood supply to skeletal muscles and the central nervous system.
With right ventricular failure, there are complaints of pain in the right hypochondrium due to stagnation in the liver, loss of appetite, nausea due to intestinal edema or decreased gastrointestinal perfusion, peripheral edema.
On examination, it can be noted that some patients, even with severe CHF, look good at rest, others have shortness of breath during conversation or minimal activity; patients with a long and severe course look cachectic, cyanotic.
In some patients, tachycardia, arterial hypotension, a drop in pulse pressure, cold extremities, sweating (signs of SAS activation) are found.
Examination of the heart reveals a cardiac impulse, an enlarged or elevating apical impulse (dilatation or hypertrophy of the ventricles), a weakening of the I tone, and a protodiastolic gallop rhythm.
With left ventricular failure, hard breathing, dry wheezing (congestive bronchitis), crepitus in the basal parts of the lungs, dullness in the basal parts (hydrothorax) can be determined.
With right ventricular heart failure, swollen jugular veins, enlarged liver are revealed; slight pressure on it can increase the swelling of the jugular veins - a positive hepato-jugular reflex. Ascites and anasarca appear in some patients.
Diagnosis of heart failure
The final clinical diagnosis of heart failure can be established only by taking into account instrumental data, primarily echocardiography, as well as radiography of the OGK, ECG, and data from laboratory research methods.
Echocardiography is used to assess: the condition of the valves, the presence of shunts, aneurysms, the state of the pericardium, the presence of a tumor or, thrombi, as well as the contractile function (diffuse changes or regional disorders, their quantitative assessment), the presence of myocardial hypertrophy, chamber dilatation, determine the global systolic function - PV.
An important role in the diagnosis of heart failure is played by the X-ray examination of the HHP: -estimation of the size of the heart (cardiothoracic index); -the presence and severity of stagnation in the lungs; -differential diagnostics with diseases of the respiratory system; -diagnostics and control of the effectiveness of treatment of complications of heart failure (pneumonia, hydrothorax, pulmonary embolism).
An indispensable component of the examination for HF syndrome is an ECG, which allows detecting hypertrophy, ischemia, focal changes, arrhythmias and blockades, and is also used to control therapy with B-blockers, diuretics, cardiac glycosides, amiodarone.
To determine the functional class (FC) in patients, a 6-minute walk test is used. This method has been widely used in the last 4-5 years in the USA, including in clinical trials. The condition of patients who are able to overcome from 426 to 550 m in 6 minutes corresponds to mild CHF; from 150 to 425 m - medium, and those who are not able to overcome even 150 m - severe decompensation. Thus, the functional classification of CHF reflects the ability of patients to perform physical activities and outlines the degree of changes in the functional reserves of the body. This is especially important when assessing the dynamics of the patient's condition.
Laboratory examination for heart failure includes a general blood test (hemoglobin, erythrocytes, leukocytes, platelets, hematocrit, ESR), a general urine test, a biochemical blood test (electrolytes -K +, Na +, creatinine, bilirubin, liver enzymes - ALT, AST, alkaline phosphatase , glucose).
SN classification
In Ukraine, the classification of the Ukrainian Association of Cardiologists of 2006 is used, according to which stages of heart failure are distinguished (based on the classification of V.Kh. Vasilenoko-N.D. Strazhesko), variants of dysfunction (according to EchoCG data) and functional classes (according to the NYHA classification)
The most convenient and meets the needs of practice is the functional classification of the New York Heart Association, which implies the allocation of four functional classes according to the ability of patients to endure physical activity. This classification is recommended for use by WHO. The principle underlying it is the assessment of the physical (functional) capabilities of the patient, which can be identified by the doctor with a purposeful, thorough and accurate collection of anamnesis, without the use of complex diagnostic techniques.
Four functional classes (FC) of CHF have been identified.
I FC. The patient has no limitations in physical activity. Normal exercise does not cause weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.
II FC. Moderate limitation of physical activity. The patient feels comfortable at rest, but doing normal physical activity causes weakness (lightheadedness), palpitations, shortness of breath, or anginal pain.
III FC. Pronounced limitation of physical activity. The patient feels comfortable only at rest, but less than usual physical activity leads to the development of weakness (lightheadedness), palpitations, shortness of breath or anginal pain.
IV FC. Inability to perform any load without discomfort. Symptoms of heart failure or angina syndrome may manifest at rest. When the minimum load is performed, discomfort increases.
It is the dynamics of PK during treatment that makes it possible to objectively decide whether our therapeutic measures are correct and successful. The studies carried out have also proved the fact that the determination of PK to a certain extent predetermines the possible prognosis of the disease.
In clinical practice, determining the variant of myocardial dysfunction is of decisive importance for a differentiated approach to treatment tactics. Clinically, both systolic and diastolic variants are manifested by the same type of symptoms - shortness of breath, cough, wheezing, orthopnea. In the absence of echocardiographic data, it is possible to try to determine the variant of dysfunction using clinical and radiological data, taking into account the etiology of heart failure, auscultatory data, determining the boundaries of the heart percussion and radiological, as well as ECG data (hypertrophy, dilatation, cicatricial changes, their localization, the presence of signs of heart aneurysm, etc. .).
CHF treatment.
The goals of HF treatment are:
Elimination or minimization of clinical symptoms of CHF - increased fatigue, palpitations, shortness of breath, edema;
Protection of target organs - blood vessels, heart, kidneys, brain (by analogy with hypertension therapy), as well as
· Prevention of the development of hypotrophy of the striated muscles;
Improving the quality of life,
Increase in life expectancy
· Decrease in the number of hospitalizations.
There are non-drug and medication methods of treatment.
Non-drug methods
Diet. The main principle is to limit the consumption of salt and, to a lesser extent, liquid. At any stage of CHF, the patient should take at least 750 ml of fluid per day. Restrictions on salt intake for patients with CHF I FC - less than 3 g per day, for patients with II-III FC - 1.2-1.8 g per day, for IV FC - less than 1 g per day.
Physical rehabilitation. Options are walking or an exercise bike for 20-30 minutes a day up to five times a week with self-monitoring of health, pulse (the load is considered effective when 75-80% of the patient's maximum heart rate is considered effective).
Medication for HF
The entire list of drugs used for the treatment of CHF is divided into three groups: main, additional, auxiliary.
The main group of drugs fully meet the criteria of "evidence medicine" and are recommended for use in all countries of the world: ACE inhibitors, diuretics, SG, ß-blockers (in addition to ACE inhibitors).
An additional group, the efficacy and safety of which has been proven by large studies, however, requires clarification (conducting a meta-analysis): aldosterone antagonists, angiotensin I receptor antagonists, CCCs of the latest generation.
Ancillary drugs, their use is dictated by certain clinical situations. These include peripheral vasodilators, antiarrhythmics, antiplatelet agents, direct anticoagulants, non-glycoside positive inotropic agents, corticosteroids, statins.
Despite the large selection of drugs, polypharmacy (unjustified prescription of a large number of drug groups) is unacceptable in the treatment of patients. At the same time, today, at the polyclinic level, the main group of drugs for the treatment of CHF does not always occupy a leading position, sometimes drugs of the second and third groups are preferred.
Principles of the combined use of essential drugs for the treatment of heart failure.
1. Monotherapy in the treatment of CHF is rarely used, and in this capacity only ACE inhibitors can be used in the initial stages of CHF.
2. Dual therapy ACE inhibitor + diuretic is optimal for patients with CHF P-Sh FC NYHA with sinus rhythm; the use of the diuretic + glycoside scheme, which was extremely popular in the 50-60s, is not currently used.
3. Triple therapy (ACE inhibitor + diuretic + glycoside) - was the standard in the treatment of CHF in the 80s, and now remains an effective scheme in the treatment of CHF, however, for patients with sinus rhythm, it is recommended to replace the glycoside with a β-blocker.
4. The gold standard from the beginning of the 90s to the present is a combination of four drugs - an ACE inhibitor + diuretic + glycoside + ß-blocker.
Acute vascular insufficiency
Under this term, several acute circulatory disorders are collected, which are not included in the concept of either circulatory arrest or shock. The border with the latter is so poorly delineated that one term is often used instead of another.
Collapse is a condition in which a disorder of peripheral circulation occurs as a result of a gross violation of the ratio between the capacity of the vascular bed and the volume of circulating blood.
This definition means damage to the body with intact defense mechanisms. The outcome of the collapse is difficult to predict. It can lead to death, recovery without consequences, or go into shock.
Pathological physiology
The main manifestation of the collapse is a drop in blood pressure, usually below 10.7 kPa (80 mm Hg) or 2/3 below the patient's usual blood pressure with the disappearance of the peripheral pulse. A characteristic feature of this hypotension is its sudden appearance due to poor adaptation of the body. This is one of the factors that distinguish it from shock, in which the activation of protective mechanisms leads to a delayed development of the pathological state of the present syndrome.
The absence of this "defense reaction" is characteristic of some tissues and systems:
Myocardium, where bradycardia of the heart originates during collapse;
Peripheral circulation (pale, cold, no cyanosis, marbled skin);
Venous circulation (venous pressure is low, veins do not fill under the tourniquet);
Cerebral circulation (frequent memory impairment, agitation and delirium, sometimes convulsions and even fainting);
Renal circulation (with collapse, there is almost always oligo- or anuria);
Neurovegetative system (increased sweating, pallor of the face, nausea).
The reasons for the collapse are numerous. It can result from:
a) acute hypovolemia due to bleeding, extracellular dehydration (in particular, with hyponatremia);
b) a decrease in cardiac output due to a violation of the heart rhythm in the direction of increased frequency (ventricular tachycardia, rotation of the apex of the heart) or its decrease (nodal or sinus bradycardia, atrioventricular block);
c) circulatory disorders due to difficulty in filling the cavities of the heart, for example, with cardiac tamponade;
d) a decrease in peripheral resistance due to a secondary reaction of the vasovasal reflex in a labile patient under emotional stress;
e) hyperventilation, which occurs with artificial ventilation in patients with pulmonary insufficiency with hypercapnia, as well as with the use of vasodilators.
These factors can be combined. It is this combination that is observed in collapse that appears in the initial stage of myocardial infarction (it should be distinguished from cardiogenic shock). As a result of barbiturate poisoning during collapse, fluid may accumulate in the splanchnicus zone; it is also characterized by the inhibitory effect of drugs on the myocardium.
The state of shock is characterized by a syndrome, the clinical essence of which is manifested by diffuse damage to brain cells and a secondary inadequacy of tissue blood supply to the needs of the body. It is sometimes fatal on its own. However, the stage of its irreversibility in humans has not yet been clearly defined.
Due to the difficulty of clinically defining "shock," numerous definitions have been proposed, of which Wilson's is the most widely accepted. According to him, a patient in a state of shock is characterized by the presence of three or more signs:
Systolic pressure equal to or less than 10.7 kPa (80 mm Hg);
Insufficient blood supply to tissues, which is manifested by moist, cold, cyanotic, marbled skin color or a decrease in the cardiac index below 2.5 L / min
Diuresis less than 25 ml / h;
Acidosis with a hydrocarbonate content of less than 21 mmol / l and lactacidemia of more than 15 mg per 100 ml.
Shock reasons
Maintaining adequate hemodynamics in the body is the result of a rational interaction between three main factors: BCC, cardiac output, and peripheral vascular resistance. A pronounced change in one of these factors can lead to a "state of shock".
Hypovolemic shock
Hypovolemic shock develops with a decrease in the volume of the BCC by 20%. Such an acute loss of volume can be the result of the following factors:
More or less significant external bleeding -
Internal bleeding that occurs in a cavity (abdominal cavity, alimentary canal) or tissue (hematoma). For example, a fracture of the femur is accompanied by blood loss up to 1000 ml, a fracture of the pelvic bones - from 1500 to 2000 ml;
Plasma loss (burns, pancreatitis);
Loss of water (electrolytes such as sodium)
Cardiogenic shock
The shock from heart failure can occur for two reasons.
Due to the failure of myocardial function and the development as a result of this critical decrease in cardiac output. Decompensation occurs with heart failure or disturbance of its rhythm (slow or frequent). Myocardial infarction resulting from one of these mechanisms is a fundamentally distant cause of cardiogenic shock.
Obstruction of contraction or systolic ejection results in underfilling or failure of a component of another mechanism that allows grouping of rather unrelated causes, such as pericardial tamponade, pulmonary embolism, aortic rupture, intracardiac thrombosis, and tumor.
Toxic-infectious shock
Toxic-infectious (bacterial) shock is, at least in the initial stage, a fairly common shock caused by impaired peripheral circulation.
Gram-negative organisms (enterobacteria and especially pseudomonas) usually cause shock, but septicemia caused by gram-positive organisms (especially staphylococci) can also cause bacterial shocks. This shock is often the first sign of a septic condition, but it can also appear during its development. In the pathogenesis, studied mainly in animals, a change in the mechanisms of microcirculation is noted. Peripheral vasoconstriction is followed by a stage of atony with the opening of arterioles and blockage of the veins. This leads to significant stasis, prevailing in the celiac zone, and, consequently, to hypovolemia, as a result of which there is a decrease in MOS. Direct damage to the myocardium by bacterial toxins can also contribute to this decrease in MOC. Bacterial endotoxins (staphylococcal exotoxins) act as a trigger for these disorders, releasing vasoactive substances such as histamine, kinins, and catecholamines.
Anaphylactic shock
Anaphylactic shock is the result of the interaction of circulating or tissue antigens with antibodies and develops according to a mechanism similar to bacterial shock.
Neurogenic shock
Under this term, disorders of various origins are combined that follow damage to the central nervous system or are the result of direct damage to the brain with damage to the brain substance or with pharmacological effects (ganglion blockers). Both of these reasons lead to a decrease in VD and a secondary fall in MOS, followed by a decrease in blood pressure. Inhibition of reflex vasoconstriction does not allow correcting these disorders.
There are also shock states, the mechanisms of which are more complex. This refers to shocks observed in massive barbiturate poisoning, where, in addition to the neurogenic cause of shock, there is a direct negative inotropic effect of the drug on the myocardium. The state of shock in a person with polytrauma occurs as a result of the appearance of two components: hypovolemia and neurovegetative reaction. Shock in pancreatitis is caused by hypovolemia, to which a toxic element is added, which, in all likelihood, causes vasoplegia.
CHRONIC HEART FAILURE
Chronic heart failure (CHF) - a disease with a complex of characteristic symptoms (shortness of breath, fatigue, decreased physical activity, edema, etc.) associated with inadequate perfusion of organs and tissues at rest or during exercise.
ICD-10 code
- I50.0 Congestive heart failure
CLASSIFICATION
Classification of CHF by the New York Heart Association by severity.
- I functional class. Normal exercise is not accompanied by fatigue, palpitations, shortness of breath, or angina. This functional class occurs in patients with heart disease that does not result in physical activity restriction.
- II functional class. Patients feel good at rest, but normal physical activity causes fatigue, shortness of breath, palpitations, or angina pectoris. This functional class occurs in patients with heart disease that causes a slight restriction in physical activity.
- III functional class. This functional class occurs in patients with heart disease that causes significant physical activity limitations. Patients feel good at rest, but light (less than normal) exertion causes fatigue, shortness of breath, palpitations, or angina pectoris.
- IV functional class. This functional class occurs in patients with heart disease, due to which they are unable to perform any kind of physical activity without discomfort. Symptoms of heart failure or angina occur at rest; with any physical exertion, these symptoms intensify.
The classification of CHF of the Society of Heart Failure Specialists (Russia, 2002) is presented in table. 1.
Table 1. Classification of CHF of the Society of Heart Failure Specialists (Russia, 2002)
CHF functional classes |
Characteristic |
There are no restrictions on physical activity: the usual physical activity is not accompanied by rapid fatigue, shortness of breath or palpitations. The patient suffers increased physical activity, but it may be accompanied by shortness of breath and / or slow recovery |
|
Slight limitation of physical activity: no symptoms at rest, habitual physical activity is accompanied by fatigue, shortness of breath or palpitations |
|
A noticeable limitation of physical activity: there are no symptoms at rest, physical activity of lower intensity compared to usual loads is accompanied by the appearance of symptoms of the disease |
|
Inability to perform any physical activity without discomfort; symptoms of the disease are present at rest and worsen with minimal physical activity |
|
CHF stages |
Characteristic |
The initial stage of heart disease (damage). Hemodynamics is not impaired. Latent heart failure. Asymptomatic left ventricular dysfunction |
|
Clinically expressed stage of heart disease (lesion). Disturbances of hemodynamics in one of the circles of blood circulation, expressed moderately. Adaptive remodeling of the heart and blood vessels |
|
Severe stage of heart disease (damage). Pronounced changes in hemodynamics in both circles of blood circulation. Maladaptive remodeling of the heart and blood vessels |
|
The final stage of heart damage. Pronounced changes in hemodynamics and severe (irreversible) structural changes in target organs (heart, lungs, blood vessels, brain, kidneys). The final stage of organ remodeling |
DIAGNOSTICS
ANAMNESIS AND PHYSICAL EXAMINATION
The most frequent complaints of patients with CHF (in descending order of frequency): shortness of breath, fatigue, palpitations, peripheral edema, cough, wheezing in the lungs, orthopnea, swollen jugular veins, hepatomegaly, cardiomegaly.
LABORATORY RESEARCH METHODS
- Complete blood count (determination of the level of hemoglobin, the number of erythrocytes, leukocytes and platelets).
- Biochemical blood test (study of the concentration of electrolytes, creatinine, glucose, activity of liver enzymes in the blood).
- General urine analysis.
INSTRUMENTAL RESEARCH METHODS
| Electrocardiography | All patients with suspected CHF should have a 12-lead ECG. Signs of previous myocardial infarction, left bundle branch block in IHD (as predictors of low left ventricular contractility) are most important for objectifying CHF. The diagnostic significance of ECG data increases in the presence of clinical signs of CHF. |
| Echocardiography | EchoCG is indicated for all patients with CHF, which is given a primary role in the diagnosis of CHF. Echocardiography allows you to solve the main diagnostic problem - to clarify the very fact of dysfunction and its nature, as well as to conduct a dynamic assessment of the state of the heart and hemodynamics. The criteria for diagnosing diastolic heart failure are given below (the first two criteria must be present).
|
| Chest X-ray | Chest X-ray is indicated for all patients with CHF. If CHF is suspected, the main focus should be on cardiomegaly (cardiothoracic index more than 50%) and pulmonary venous congestion. Cardiomegaly is a sign of the involvement of the heart in the pathological process. The presence of venous stasis and its dynamics can be used to characterize the severity of the disease, and also serve as an objective criterion for the effectiveness of therapy. |
| Magnetic resonance imaging of the heart | Magnetic resonance imaging (MRI) of the heart is the most accurate and reproducible imaging technique. Given the high cost and low availability, MRI is performed when other imaging methods are not fully informative. |
| Lung function assessment | This test is useful to rule out pulmonary pathology. |
| Load tests | The stress test is carried out to assess the functional status of the patient, to assess the degree of risk. In patients with CHF, it is possible to use various variants of the stress test: 6-minute walk test, bicycle ergometry, treadmill, including blood gas analysis. In routine practice, in the absence of special equipment for assessing physical tolerance and objectifying the functional status of patients, a walking test for 6 minutes can be used.
|
Table 2. Assessment parameters of the 6-minute walk test
Other studies
Other studies (daily ECG monitoring, determination of neurohormonal profile, radioisotope study) do not occupy an important place in the diagnosis of CHF. A test widely used in developed countries for diagnosing CHF - determining the level of brain sodium uretic peptide - is not yet available in the outpatient clinic in the Russian Federation.
INDICATIONS FOR CONSULTING OTHER SPECIALISTS
- Unknown etiology of heart failure.
- Systolic blood pressure less than 100 mm Hg.
- The content of creatinine in the blood is more than 150 μmol / l.
- The sodium content in the blood is less than 135 mmol / l.
- The potassium content in the blood is more than 6.0 mmol / l.
- Severe heart failure.
- Valvular heart disease as a cause of heart failure.
TREATMENT
| OBJECTIVES OF TREATMENT | The goals of treatment are achieved by carrying out the following activities. |
|
|
INDICATIONS FOR HOSPITALIZATION
- With the ineffectiveness of treatment on an outpatient basis in patients with functional class IV CHF, severe fatigue and decreased performance, as well as with ineffectiveness of diuretics.
- When planning parenteral administration of diuretics, vasodilators or LS with a positive inotropic effect under the control of hemodynamic parameters, requiring pulmonary artery catheterization.
- In patients with very low cardiac output who require therapy with positive inotropic drugs.
Hospitalization is necessary in the presence of life-threatening rhythm disturbances or arrhythmias that worsen the course of CHF.
- Persistent ventricular tachycardia, paroxysms of ventricular tachycardia, accompanied by a violation of the patient's condition, syncope, sudden cardiac death, supraventricular rhythm disturbances that worsen the course of CHF.
- Patients with life-threatening arrhythmias are hospitalized for electrophysiological examination in order to decide whether to install an implantable cardioverter defibrillator or to prescribe antiarrhythmic therapy.
- In patients with CHF and life-threatening rhythm disturbances, antiarrhythmic therapy should be limited to amiodarone or sotalol before implantation of a cardioverter-defibrillator.
NON-MEDICINAL TREATMENT
| Diet of patients with CHF |
|
| Alcohol | Alcohol is strictly prohibited for patients with alcoholic cardiomyopathy. In patients with ischemic CHF genesis, the use of up to 20 ml of ethanol per day can improve the prognosis. For all other patients with CHF, alcohol is limited in accordance with the usual recommendations. Drinking large amounts of alcoholic beverages (such as beer) should be limited. |
| Physical activity mode | Rest is not indicated for any patient with CHF. Physical rehabilitation is recommended for all patients with CHF. Physical rehabilitation is possible only with a stable course of CHF and is contraindicated in the following cases.
|
| General recommendations |
|
| Psychological rehabilitation | The main task of the doctor is to teach the patient and his immediate family to control the course of CHF, methods of self-help. It is also important to ensure the possibility of regular contact with the attending physician for the timely correction of the condition and prevention of emergency decompensations. |
DRUG THERAPY
All drugs for the treatment of CHF can be divided into three main categories: basic, additional and auxiliary (Table 3).
Table 3. Drugs for the treatment of chronic heart failure
Basic * |
Additional * * |
Auxiliary * * * |
|
|
|
* In the absence of absolute contraindications, each patient with CHF should be prescribed. |
||
ACE inhibitors
- ACE inhibitors are indicated for all patients with CHF (of any etiology and stage of the process, including asymptomatic left ventricular dysfunction).
- ACE inhibitors improve the clinical picture, quality of life, slow down the progression of the disease, reduce morbidity and improve the prognosis of patients with CHF, i.e. allow you to achieve all goals in the treatment of CHF.
- These drugs are considered the most reasonable way to treat CHF with preserved systolic heart function.
- The lack of prescription of ACE inhibitors cannot be considered justified and leads to a deliberate increase in the risk of death in patients with CHF.
Table 4 shows the doses of ACE inhibitors, most studied in the treatment and prevention of CHF, used in Russia.
Table 4. Angiotensin-converting enzyme inhibitors prescribed for the treatment of chronic heart failure
Medicine |
Initial dose |
Therapeutic dose |
Maximum dose |
Initial dose for arterial hypotension |
Enalapril |
2.5 mg 2 times a day |
10 mg 2 times a day |
20 mg 2 times a day |
1.25 mg 2 times a day |
Captopril |
6.25mg 2-3 times a day |
25 mg 2-3 times a day |
50 mg 3 times a day |
3.125 mg 2-3 times a day |
Fosinopril |
5 mg 1-2 times a day |
10-20 mg 1-2 times a day |
40 mg once a day |
2.5 mg 1-2 times a day |
Lisinopril |
2.5 mg once a day |
20 mg once a day |
40 mg once a day |
1.25 mg once a day |
Perindopril |
2 mg once a day |
4 mg once a day |
16 mg once a day |
1 mg once a day |
Ramipril |
2.5 mg 2 times a day |
5 mg 2 times a day |
5 mg 2 times a day |
1.25 mg 2 times a day |
Hinapril |
5 mg 1-2 times a day |
10-20 mg 1-2 times a day |
40 mg once a day |
2.5 mg 1-2 times a day |
Spirapril |
3 mg once a day |
3 mg once a day |
6 mg once a day |
1.5 mg once a day |
- The need for diuretics and vasodilators and their dosages should be assessed.
- Excessive diuresis should not be allowed before starting treatment; diuretics should be discontinued 24 hours before the first use of ACE inhibitors.
- Therapy should be started in the evening when the patient is in a horizontal position to minimize the risk of arterial hypotension.
- It is recommended to start treatment with low doses and increase them to maintenance levels.
- With a significant deterioration in renal function (an increase in the concentration of creatinine in the blood by more than 30% of the original), it is necessary to reduce the dose by half, and in the absence of improvement, cancel the ACE inhibitor.
- Avoid the appointment of potassium-sparing diuretics at the beginning of treatment, especially in patients with high levels of potassium in the blood (more than 5.0 mmol / l); however, this does not contradict the recommendations for the combined use of ACE inhibitors with high doses of spironolactone during the decompensation period and the combination of ACE inhibitors with low doses of aldosterone antagonists for long-term treatment of CHF.
- It is recommended to avoid the appointment of NSAIDs.
- It is necessary to control blood pressure and the content of electrolytes in the blood 1-2 weeks after each dose increase.
beta-blockers
- beta-blockers should be prescribed to all patients with CHF who do not have contraindications common to this group of drugs.
- beta-blockers should be used only in addition to ACE inhibitors.
- beta-blockers in addition to ACE inhibitors are indicated for all patients with asymptomatic left ventricular dysfunction after myocardial infarction.
- Beta-blockers should preferably be prescribed to patients who have achieved stabilization of the state (there are no signs of stagnation, there is no need for parenteral therapy).
- For the treatment of CHF, only four beta-blockers are recommended: bisoprolol, carvedilol, metoprolol succinate (sustained release) and nebivolol.
- Treatment with beta-blockers for CHF should be started with 12.5% of the therapeutic dose. Doses are increased slowly (no more than once every 2 weeks) until the optimum is achieved (Table 5).
- If heart failure worsens, arterial hypotension or bradycardia develops during dose titration, the following algorithm should be followed.
- When heart failure worsens, it is necessary first of all to increase the dose of diuretics and ACE inhibitors, if necessary, temporarily reduce the dose of the beta-blocker.
- With arterial hypotension, it is shown first of all to reduce the dose of vasodilators, if necessary, temporarily reduce the dose of beta-blocker.
- With bradycardia, the dose should be reduced or the drugs that slow the heart rate should be canceled, if necessary, the dose of the beta-blocker should be reduced or the latter should be canceled if there are clear indications.
- The possibility of re-prescribing a beta-blocker or increasing its dose after stabilization is always considered.
- If inotropic support is needed during circulatory decompensation in patients on continuous therapy with beta-blockers, the calcium sensitizer levosimendan is considered the drug of choice, since its hemodynamic effect does not depend on the degree of beta-adrenergic receptor blockade.
- Contraindications to the appointment of beta-blockers in CHF are severe bronchial asthma and / or chronic obstructive pulmonary disease, symptomatic bradycardia, arterial hypotension.
Table 5.beta-blockers for the treatment of chronic heart failure
Medicine |
Initial dose |
Therapeutic dose |
Maximum dose |
Bisoprolol |
1.25 mg once a day |
10 mg once a day |
10 mg once a day |
Carvedilol |
3, 125 mg 2 times a day |
25 mg 2 times a day |
25 mg 2 times a day |
Metoprolol succinate |
12.5 mg once a day |
100 mg once a day |
200 mg once a day |
Nebivolol |
1.25mg once a day |
10 mg once a day |
10 mg once a day |
Some patients may be on treatment with non-recommended beta-blockers (most often short-acting atenolol or metoprolol tartrate). Table 6 shows the scheme of conversion to recommended drugs.
Table 6. Scheme of transfer of patients with chronic heart failure from atenolol and metoprolol tartrate to the recommended beta-blockers
Drug being taken |
|||
Bisoprolol |
Metoprolol succinate |
Carvedilol |
|
Atenolol at a dose of less than 25 mg / day |
3.125 mg 2 times a day |
||
Atenolol at a dose of 25-75 mg / day |
6.25 mg 2 times a day |
||
Atenolol at a dose of 75 mg / day or more |
12.5 mg 2 times a day |
||
Metoprolol tartrate at a dose of less than 25 mg / day |
3.125 mg 2 times a day |
||
Metoprolol tartrate at a dose of 25-75 mg / day |
6.25 mg 2 times a day |
||
Metoprolol tartrate at a dose of 75 mg / day or more |
12.5 mg 2 times a day |
||
- CHF III-IV functional class.
- Heart failure of unknown etiology.
- The presence of relative contraindications: bradycardia, arterial hypotension, poor tolerance of low doses of beta-blockers, concomitant chronic obstructive pulmonary disease.
- Information about the cancellation of beta-blockers in the past due to adverse reactions or exacerbation of heart failure.
Aldosterone antagonists (spironolactone)
- Aldosterone antagonists are prescribed in addition to ACE inhibitors and beta-blockers for patients with CHF III-IV functional class.
- The recommended dose of spironolactone for chronic use in CHF is 25 mg / day.
- These drugs are indicated only for patients with III-IV functional class of CHF.
- Treatment should be started only if the level of potassium in the blood does not exceed 5.0 mmol / L, and the concentration of creatinine is less than 1.7 mg / dL.
- The recommended dosage of spironolactone for long-term use is 25 mg / day.
- Shown to monitor the content of potassium and creatinine in the blood every 4-6 weeks.
- If, after starting treatment, the level of potassium in the blood exceeds 5.0-5.5 mmol / L, the dose of spironolactone should be reduced by 50%, and if the level of potassium is more than 5.5 mmol / L, therapy with spironolactone should be discontinued.
- If, after a month of therapy, the symptoms of heart failure are still pronounced, the dose of spironolactone should be increased to 50 mg / day (subject to normokalemia). After increasing the dose of spironolactone, control of the concentration of potassium and creatinine in the blood is shown after 1 week.
Diuretics
- Diuretic treatment is started only with clinical signs of stagnation (stage II A, functional class II).
- It is advisable to start treatment with the constant use of thiazide diuretics, if they are ineffective, switch to loop diuretics (small doses, continuous use).
- Diuretics should always be combined with ACE inhibitors and beta-blockers.
- Thiazide diuretics should not be used if the glomerular filtration rate is less than 30 ml / min. Table 7 shows the diuretics prescribed in the treatment of CHF.
Table 7. Diuretics for chronic heart failure
Algorithm for prescribing diuretics depending on the severity of CHF
- I and II functional class without edema - no need to treat with diuretic drugs.
- II functional class (stagnation) - thiazide diuretics or loop diuretics (in small doses) are indicated.
- III functional class (decompensation) - prescribe loop diuretics (possibly a combination with thiazide) + aldosterone antagonists (at a dose of 100-300 mg / day).
- III functional class (supportive treatment) - loop diuretics (dose titration) + spironolactone (at a dose of 25-50 mg / day) are recommended.
- IV functional class - loop diuretics + thiazide diuretics + aldosterone antagonists are shown.
Cardiac glycosides
- Cardiac glycosides are indicated for atrial fibrillation and symptomatic heart failure, regardless of the degree of cardiac dysfunction.
- Cardiac glycosides do not improve the prognosis, but they do contribute to a decrease in the number of hospitalizations among patients with CHF and left ventricular systolic dysfunction with sinus rhythm.
- The main drug from the group of cardiac glycosides for the treatment of CHF is digoxin.
- The dose of digoxin for the treatment of CHF should not exceed 0.25 mg / day.
- A dose of digoxin 0.125-0.25 mg / day is taken in one dose daily, without gaps.
- A loading dose of digoxin is not recommended.
- The predictors of the success of glycoside treatment in patients with CHF are low left ventricular ejection fraction (less than 25%), cardiomegaly, and non-ischemic etiology of the disease.
- Angiotensin II receptor antagonists and ACE inhibitors are equally effective in reducing mortality and morbidity in CHF.
- Angiotensin II receptor antagonists should be used as an alternative to ACE inhibitors if the latter is intolerant.
- A triple combination (ACE inhibitor + beta-blocker + angiotensin II receptor antagonist) is not considered optimal. Only in case of intolerance to a beta-blocker should one switch to a combination of an ACE inhibitor + an angiotensin-II receptor antagonist.
- Indirect anticoagulants (warfarin) should be given to all patients with CHF and atrial fibrillation.
- Regardless of the heart rate, all patients with CHF who have had thromboembolic complications and / or with a floating thrombus in the left ventricular cavity should receive indirect anticoagulants.
- Indirect anticoagulants cannot be replaced with antiplatelet agents (acetylsalicylic acid, clopidogrel, ticlopidine) to reduce the risk of thromboembolic complications.
- For secondary prevention after myocardial infarction, either acetylsalicylic acid or indirect anticoagulants should be used (but not in combination due to the high risk of bleeding).
- Avoid the appointment of acetylsalicylic acid to patients with frequent repeated hospitalizations for worsening CHF.
- Indirect anticoagulant therapy should be carried out under close monitoring (1 time per month) of the International Normalized Ratio (INR). Safe and effective INR range of 2.0-3.0.
- It is recommended to prescribe nitrates in the presence of proven ischemic heart disease and angina pectoris, which is stopped precisely by nitrates.
- Calcium channel blockers (dihydropyridine series - amlodipine or felodipine) can be used in the following clinical situations: the presence of resistant angina pectoris, concomitant persistent arterial hypertension, pulmonary hypertension, severe valvular regurgitation.
- Only life-threatening and clinically manifested ventricular arrhythmias should be treated with CHF.
- Class I and IV antiarrhythmic drugs are contraindicated in patients with CHF.
- Beta-blockers are the drug of choice for antiarrhythmic treatment.
- With the ineffectiveness of beta-blockers, class III drugs (amiodarone, sotalol) are indicated.
- The means of choice for the treatment of ventricular arrhythmias in patients with moderate CHF (functional class I-II) is amiodarone.
- In patients with severe CHF (III-IV functional class), amiodarone should not be used.
- The most justified method of preventing sudden death in patients with CHF and life-threatening arrhythmias is the installation of an implantable cardioverter-defibrillator.
- In terms of the effect on mortality and morbidity, there is no difference between the tactics of maintaining sinus rhythm and the tactics of controlling the heart rate. The doctor determines the feasibility of restoring and maintaining sinus rhythm.
- Amiodarone is considered the most effective antiarrhythmic drug for maintaining sinus rhythm.
- To control heart rate in atrial fibrillation, the most effective combination is a beta-blocker + digoxin.
- NSAIDs.
- Tricyclic antidepressants.
- Class I and IV antiarrhythmic drugs.
- Calcium channel blockers (verapamil, diltiazem, short-acting dihydropyridine preparations).
- Glucocorticoids. They are prescribed for symptomatic indications in cases of persistent arterial hypotension and severe edema syndrome to facilitate the initiation of treatment with ACE inhibitors, diuretics and beta-blockers.
- How and when to take your medicine.
- A clear list of recommendations, including the name, dose and frequency of each drug.
- The most common side effects of drugs taken and the need to consult a doctor if they occur. Family members of patients with heart failure should be encouraged to learn cardiopulmonary resuscitation skills.
40-80 mg / day
* Effectiveness in influencing mortality and morbidity has been proven in large clinical trials.
Table 8 shows angiotensin II receptor antagonists for the treatment of CHF.
Antiplatelet and anticoagulants
Vasodilators
Antiarrhythmic drugs
Treatment of atrial fibrillation in patients with CHF
PATIENT TRAINING
Patients should be informed of the importance of monitoring body weight on a daily basis during the treatment of heart failure. The patient should be weighed daily and recorded. With an increase in body weight by more than 2 kg in 1-3 days, the patient should contact a doctor.
Patients should be encouraged to follow a low-salt diet and limit fluid intake. It is recommended to reduce the consumption of table salt to 3 g / day or less. In addition, you need to make sure that the patient fully understands all the details of his drug regimen.
The patient should be given the following information.
FORECAST
The mortality rate of patients with clinically severe heart failure within 1 year reaches 30%. The five-year survival rate of patients with CHF does not exceed 50%. The risk of sudden death in patients with CHF is 5 times higher than in the general population.
Cerebral ischemia is a type of cerebrovascular disease, a fairly common severe pathology. Dysciculatory encephalopathy is the name of a chronic ailment that is used in domestic medicine. What it is? Brain ischemia is an extremely topical neurological problem. This is a severe brain disorder. Nowadays, this diagnosis is very common in the opinions of professionals. Dysciculatory encephalopathy affects about 6% of the world's population. The number of such patients is constantly growing.
Etiology of disciculatory encephalopathy
The causes of ischemia are manifold. Various diseases lead to pathology. What is ischemic brain disease?
The following disorders are the causative factors of circulatory encephalopathy:
- vascular atherosclerosis;
- hypertension;
- atrial fibrillation;
- blood vessel disease;
- endocrine system damage;
- ailments of the spine;
- cervical pathology.
Blood flow in the brain tissue depends on the level of red blood cells. Improper diet is the cause of high cholesterol. There is a lesion of the vessels of the head. The age factor is of great importance. In adults, cerebral ischemia is often found. Young people suffer from this ailment less. Old age is a provoking factor.
Pathogenesis of disciculatory encephalopathy
The accumulation of cholesterol deposits in the blood vessels leads to pathology. Irreversible changes are taking place. An ischemic disorder of cerebral circulation develops. A vessel clogged with cholesterol plaque cannot perform its functions. If there is a blockage of the arteries, narrowing of their lumen, oxygen starvation of tissues develops. Brain cells damaged by nutritional deficiencies do not heal. Even one damaged vessel often leads to catastrophic consequences.
Classification of pathology
The ICD-10 includes cerebral ischemia as a chronic type of cerebral pathology. Symptoms and treatment of dysciculatory encephalopathy are in the competence of a neurologist. It is difficult and time-consuming to treat ischemia. A multifocal or diffuse lesion occurs, and ischemic brain disease develops. Cerebrovascular pathology is manifested by clinical, neurological, neuropsychological, mental disorders in the body.
Cerebral ischemia is diagnosed by a professional. The acute form of cerebrovascular pathology is a consequence of oxygen starvation. A sudden attack develops. The chronic form of pathology is formed gradually in conditions of impaired blood circulation in the vessels of the head.
Clinical picture
Signs of cerebral ischemia appear gradually or instantly.
Dysciculatory encephalopathy is manifested by the following symptoms:
- pain syndrome;
- frequent dizziness;
- constant noise in the head;
- gradual deterioration in memory performance;
- low level of attention, decreased performance;
- cognitive impairment.
At an early stage, cerebral ischemia is manifested by a dysfunction of the nervous system. There is a rapid, pronounced fatigue. Memory is severely impaired. This leads to a significant decrease in performance. However, people usually do not complain at this stage. Often, patients do not see a neurologist.
Dysciculatory encephalopathy - 1 degree brain damage. Neurasthenic syndrome develops. In general, the patient's state of health is normal, but the person may complain of mild malaise. The early stage of pathology is characterized by chills, sudden mood swings, irritability, nervous excitement, and sleep disturbance. If adequate treatment is not carried out, the patient's condition is aggravated.
Stage 2 of the disease develops. Gross neurological disorders occur. Pathological reflexes are noted. The patient is worried about numbness, a feeling of coldness in the feet and palms. This is a clear manifestation of pathology. Complaints about poor health are becoming more frequent. The gait is disturbed. Cerebellar disorders appear. The patient experiences constant drowsiness. The disease of the 2nd degree is characterized by a progressive loss of memory. All signs of the 1st degree of cerebral insufficiency are also preserved, but patients already notice these defects less. At stage 2, transient ischemic attacks are noted.
In the 3rd phase of tissue ischemia, memory deteriorates, dementia develops. The social and labor adaptation of the patient is impaired. Such a patient needs constant supervision and care. At stage 3, patients present with very few complaints. This is due to the fact that they have a reduced critical attitude towards their condition. In this phase, the headaches disappear. But the person's condition is grave. Patients often have severe strokes, vascular dementia, parkinsonism.
Diagnostic procedures
How can a correct diagnosis be made? The neurologist evaluates the painful symptoms and prescribes treatment when he hears the patient's complaints. If at least 2 of the characteristic symptoms have been manifested constantly over the past months, such complaints should be the reason for an in-depth examination of the cardiovascular system.
When signs of coronary artery disease of the cerebral vessels appear, laboratory blood tests are performed. Hardware studies include ultrasound, high-frequency ultrasound tomography, electroencephalography, brain Doppler, cardiography. The results of these studies can show the localization of the lesion.
Treatment tactics
If symptoms of cerebral ischemia appear, what should be done? How to cure a sick person? The most effective method of treatment is the use of special drugs, which are selected individually by the attending doctor. The main task of a specialist is the treatment of vascular pathology. With ischemia of cerebral vessels, treatment is required immediately.
It is important to reduce the symptoms of dysciculatory encephalopathy in order to improve the quality of life of patients. It is necessary to increase the blood supply to the inner ear, to reduce the activity of the vestibular centers. This will help relieve dizziness. Taking into account the patient's condition, the neurologist prescribes Piracetam, Betagistim, Gingko Biloba. Betahistim is the main drug indicated for use. It normalizes the electrical activity of the vestibular centers of the brain, peripheral receptors, and improves the blood supply to the inner ear.
Vestibo normalizes vestibular functions. This drug is necessarily included in the therapeutic course at 2 or 3 stages of cerebral ischemia. Vestibo, Actovegin significantly reduces tinnitus as it increases aerobic metabolism. Actovegin is a drug showing good results.
When using these drugs, processes of improving blood flow occur. The energy resources of the cells are increased. Oxygen transport is activated. Metabolic processes are improved. Neuroprotective agents prevent damage to neurons in the brain. Neuromodulatory drugs, vasoactive drugs, neurotrophic cerebroprotectors, neuropeptides are used.
Such medications neutralize the pathogenic factor, limit and stop damage to brain tissue. Cinnarizine, Vinpocetine, Nimodipine are calcium channel blockers. These drugs increase cerebral blood flow because they dilate the blood vessels in the brain. The doctor prescribes, according to the indications, Neuromedin, Pramipex, physiotherapy, therapeutic massage. Special vestibular gymnastics is performed. Spa treatment is effective. With signs of cerebral ischemia, symptoms, treatment is the competence of the doctor.
What are the complications of the disease? Dysciculatory encephalopathy can lead to stroke, heart attack. This often causes changes in body functions, daily activities. Patients with cerebral ischemia need complex treatment. Prevention of disciculatory encephalopathy is important. Prevention begins as early as possible. It is required to avoid stress in every possible way, control weight, exercise. The use of tobacco, hobby for alcoholic beverages is contraindicated. Cerebral ischemia is dangerous.
If the characteristic symptoms of cerebral ischemia occur, the patient should go to a neurologist. The patient should be shown to a specialist. Early detection of pathology, treatment of coronary artery disease helps to maintain a decent standard of living.
ICD code: 150
150.0 Congestive heart failure
150.1 Left ventricular failure
150.9 Heart failure, unspecified.
Heart failure is divided into acute and chronic, right and left ventricular. Currently, the term "heart failure" usually means chronic heart failure, more often - left ventricular (Table 32).
This classification combines the accepted Russian clinical classification of circulatory failure according to the stages of the disease N.D. Strazhesko and V.Kh. Vasilenko and the classification of chronic heart failure by functional classes, adopted in 1964 by the New York Heart Association (NYHA), establishing the severity of clinical symptoms. We present these classifications.
Table 32.
(edited by Yu.N. Belenkov, V.Yu. Mareev, F.T. Ageev, adopted by the Russian Society of Heart Failure Specialists in 2002)
Classification of circulatory failure N.D. Strazhesko and V.Kh. Vasilenko (1935)
Stage I. Initial latent circulatory insufficiency, manifested only during physical exertion, at rest these phenomena disappear, hemodynamics is not disturbed.
Stage II. Severe long-term circulatory failure, hemodynamic disturbances in the small and large circulatory circles are expressed at rest.
Period A. Signs of circulatory insufficiency are moderately expressed at rest, hemodynamic disturbances only in one of the parts of the cardiovascular system (in the large or small circle of blood circulation).
Period B. The end of a long stage, pronounced hemodynamic disturbances, in which the entire cardiovascular system is involved (both large and small circles of blood circulation).
Stage III. Ultimate dystrophic with severe hemodynamic disturbances, persistent metabolic changes and irreversible changes in the structure of organs and tissues.
New York Heart Association Classification of Heart Failure (1964)
Functional class I - no restrictions on physical activity, normal physical activity does not cause symptoms of heart failure.
Functional class II - mild limitation of physical activity, at rest the patients feel normal, but normal physical activity causes symptoms of heart failure.
Functional class III - a noticeable restriction of physical activity, at rest the patients' well-being is normal, however, physical activity less than usual, causes symptoms of heart failure.
Functional class IV - inability to endure physical activity without symptoms of heart failure, symptoms are present at rest and intensify with any physical activity.
To quantify the patient's tolerance to physical activity, a 6-minute walk test (the so-called Canadian classification) is used. Mild heart failure corresponds to the patient's ability to walk a distance from 426 to 550 m in 6 minutes, medium - from 150 to 425 m, severe - up to 150 m.
Pay attention: in the modern diagnosis, the term "heart failure" is used, not "circulatory failure". In addition, it is unacceptable to indicate simultaneously two stages of heart failure (as, for example, in the wording "stage III-III").
Framingham criteria for heart failure
Attacks of nocturnal shortness of breath Swelling of the cervical veins Moist wheezing in the lungs
X-ray cardiomegaly
Pulmonary edema
Gallop rhythm (III tone at the apex of the heart)
Increase in central venous pressure> 16 cm H2O
Blood circulation time> = 25 s Positive hepatojugular reflex
Pulmonary edema, congestive plethora, or cardiomegaly at autopsy
Weight loss? 4.5 kg in 5 days in response to heart failure treatment
Small criteria
Bilateral swelling of the legs
Night cough
Shortness of breath on normal exertion Liver enlargement Pleural effusion
Decreased vitality by one third of the maximum volume
Tachycardia (> = 120 beats per minute).
The diagnosis is established in the presence of two large or one large and two small criteria at the same time. Small criteria can be taken into account if they are not a manifestation of another non-cardiovascular disease.
By the nature of the violation of the function of the left ventricle, it stands out:
Systolic heart failure
Diastolic heart failure (Table 33-34)
Combined systolic and diastolic insufficiency.
The criterion for systolic failure is a decrease in the ejection fraction and cardiac output of the left ventricle. With systolic heart failure, the type is determined:
Low cardiac output (for most heart diseases such as heart defects, hypertension, coronary artery disease, cardiomyopathies, etc.)
With high cardiac output (with anemia, acquired and congenital arteriovenous fistulas, thyrotoxicosis, Paget's disease, beriberi, multiple myeloma, erythremia, carcinoid syndrome, acromegaly, fibrous dysplasia).
Table 33.
Note: HF - heart failure, * - chest X-ray, B-natriuretic peptide level, ** - determined by cardiac catheterization or Doppler echocardiography.
In the presence of diastolic insufficiency with Doppler echocardiography, its type is determined: impaired relaxation, pseudonormal, restrictive.
Table 34.
*
Notes: * - the assessment is carried out according to the study of blood flow during Doppler ultrasonography of the transmitral diastolic and pulmonary venous blood flow; Ye / Ya is the ratio of the maximum flow rates through the mitral valve, DT is the time of deceleration of the flow of early filling, IVRT is the time of isovolumetric relaxation of the left ventricle. Уs / Уd are the ratios of the maximum velocities of the systolic wave S and antegrade early diastolic wave D, D t PVag is the duration of the reverse wave Yag of the pulmonary venous flow, D t MUa is the duration of the atrial wave Ya of the transmitral flow.
Heart failure is always a complication of a particular heart disease. Code 150 is included in the "complications" heading of the statistical card of a patient who left the hospital if heart failure is considered the reason for the patient's hospitalization and, accordingly, a large share of the cost of the provided medical services falls on this condition. In the case when the diagnosis indicates hypertension with congestive heart failure, the code 111.0 is used.
Examples of the wording of the diagnosis for some rhythm disturbances are given in the previous sections.
Loading ...