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| Acute heart failure develops within. Signs of acute heart failure, how to help with attack and what are the symptoms before death. Heart defense mechanism |
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RCRZ (Republican Center for Health Development MD RK) Acute transmural myocardial infarction of other refined localizations (I21.2) Cardiology general informationShort descriptionApproved by the minutes of the meeting №13 of 28.06.2013 Acute heart failure (OSN) - Osn - clinical syndrome, characterized by the rapid appearance of symptoms that determine the impairment of systolic and / or diastolic function of the heart (reduced sv, insufficient fifuge of tissues, increased pressure in the lung capillaries, stagnation in tissues). I. Introductory part Protocol name: Protocol for the diagnosis and treatment of acute heart failure Protocol code: I50 - heart failure I50.0 - stagnant heart failure I50.1 - Left-deuded failure I50.9 - heart failure uncomfortable R57.0 - Cardiogenic shock I21.0 - acute transmural hearth miocardial infarction I21.00 - acute transmural infarction of the front wall of myocardium with hypertension I21.1 - acute transmural heart attack of the lower wall of myocardium I21.10 - acute transmural heart attack of myocardium with hypertension I21.2 - acute transmural myocardial infarction of other refined localizations I21.20 - acute transmural myocardial infarction of other refined localizations with hypertension I21.3 - acute transmural myocardial infarction of unspecified localization I21.30 - acute transmural myocardial infarction of unspecified localization with hypertension I21.4 - acute subgroundcardial myocardial infarction I21.40 - acute subgroundcardial myocardial infarction with hypertension I21.9 - acute myocardial infarction uncomputed I21.90 - acute myocardial infarction uncomputed with hypertension I22.0 - re-infarction of the front wall of myocardium I22.00 - re-infarction of the front wall of myocardium with hypertension I22.1 - re-infarction of the bottom wall of myocardium I22.10 - re-infarction of the lower wall of myocardium with hypertension I22.8 - Repeated myocardial infarction of other updated localization I22.80 - repeated myocardial infarction of other updated localization with hypertension I22.9 - repeated myocardial infarction of unspecified localization I22.90 - repeated myocardial infarction of unspecified localization with hypertension I23.0 - Hemopericard as the nearest complication of acute myocardial infarction I23.00 - Hemopericard as the nearest complication of acute myocardial infarction with hypertension I23.1 - Defect of the Interpidential Partition as the current complication of acute myocardial infarction I23.10 - Defect of the Interpidential Partition As the current complication of acute myocardial infarction with hypertension I23.2 - the interventricular septum defect as the current complication of acute myocardial infarction I23.20 - a defect of the interventricular partition as the current complication of acute myocardial infarction with hypertension I23.3 - Gap the heart wall without hemopericard as the current complication of acute myocardial infarction I23.30 - the gap of the heart wall without hemopericard as the current complication of acute myocardial infarction with hypertension I23.4 - Tono-Crude Chord Growth As the current complication of acute myocardial infarction I23.40 - te-referring chord as the current complication of acute myocardial infarction with hypertension I23.5 - Ripping muscle as a current complication of acute myocardial infarction I23.50 - Pospill muscle break as the current complication of acute myocardial infarction with hypertension I23.6 - atrium thrombosis, atrium ears and heart ventricle as the current complication of acute myocardial infarction I23.60 - atrium thrombosis and hearts and ventricle hearts as the current complication of acute myocardial infarction with hypertension I23.8 - Other current complications of acute myocardial infarction I23.80 - Other current complications of acute myocardial infarction with hypertension I24.1 - Dressler Syndrome I24.10 - Dressler syndrome with hypertension I24.8 - Other forms of acute ischemic heart disease I24.80 - Other forms of acute ischemic heart disease with hypertension I24.9 - acute ischemic heart disease unspecified I24.90 - acute ischemic heart disease unspecified AG - arterial hypertension Hell - blood pressure ACTV - Activated Partial Thromboplasty Time Bab - beta adrenoblays VACP - intra-aircraft counterploflsator Dzl - Pressure Pressure Pulmonary IAPF - an inhibitor of angiotensin glider enzyme IBS - Ischemic heart disease Im - myocardial infarction LH - left ventricle La - pulmonary artery CH - heart failure SV - Heart Emission Garden - systolic blood pressure C - Cardiac Index SPPD - Spontaneous Breathing with constant positive pressure NVPD - non-invasive ventilation with positive pressure MZP - interventricular partition IOC - minute volume of blood circulation Kag - Caanoanhibition OPS - general peripheral vascular resistance PZh - Right ventricle Tc- Heart transplantation TLT - thrombolytic therapy TELA - pulmonary artery thromboembolism CHF - chronic heart failure Heart rate - cardiac frequency CVD - central venous pressure ECG - electrocardiography Ex-electrocardiomulator ECMO - Extracorporal Membrane Oxygenation EchoCG - Echocardiography NYHA - New York Heart Association Cryman - Continuous Positive Airway Pressure NIPPV - NON-INVASIVE POSITIVE PRESSURE VENTILATION Table 1. Provoking factors and causes of acute heart failure Classification I. Acute decompensated heart failure (DE NOVO or as a decompensation of HSN) with characteristic complaints and symptoms of the OST, which is moderate and does not meet the criteria for cardiogenic shock, edema of the lungs or hypertensive crisis. IV. Cardiogenic shock - Extreme manifestation of land. It is a clinical syndrome in which along with a decrease in systolic blood pressure less than 90-100 mm Hg. There are signs of reduced perfusion organs and tissues (cold skin, oligognuria, lethargy and inhibition). At the same time, the cardiac index is reduced (usually 2.2 l / min per 1 m2) and the pressure of the sling of the pulmonary artery (\u003e 18-20 mm Hg) was increased. The latter features a cardiogenic shock from a similar state that occurs during hypovolemia. The main link of the pathogenesis of cardiogenic shock is a reduction in cardiac output, which cannot be compensated by peripheral vasoconstriction, which leads to a significant decrease in blood pressure and hypoperfusion. Accordingly, the main objectives of the treatment are the optimization of the pressure of filling the ventricles of the heart, the normalization of blood pressure and eliminate the causes underlying the reduction of cardiac output. V. CH with high cardiac emission It is characterized by elevated IOCs with usually increased heart rate (due to arrhythmias, thyrotoxicosis, anemia, diseases of the podget, yatrogenic and other mechanisms), warm limbs, stagnation in the lungs and sometimes reduced blood pressure (as under septic shock). Classification T. killip. (1967) is based on the accounting of clinical signs and radiographic results of the chest. Classification is used mainly for heart failure with myocardial infarction, but can be used in heart failure DE NOVO. stage I. - no signs of CH; stage II. - CH (wet wives in the lower half of the pulmonary fields, III tone, signs of venous hypertension in the lungs); stage III - heavy CN (explicit swelling of the lungs, wet wipes spread more than the lower half of the pulmonary fields); stage IV. - Cardiogenic shock (Garden of 90 mm Hg. Art. with signs of peripheral vasoconstrictions: oliguria, cyanosis, sweating). Classification J. S. Forrester (1977) based on clinical signs characterizing the severity of peripheral hypoperfusion, the presence of stagnation in the lung, reduced cardiac index (C) ≤ 2.2 l / min / m2 and increased pressure Enclosure in the pulmonary artery (ZLL)\u003e 18 mm RT. Art. After stabilization of the state of patients, the functional class of CH on NYHA is exhibited Diagnostics List of basic and additional diagnostic events Table 1 - List of basic and additional diagnostic events Complaints and history: Complaints are possible on short / suffocation, dry cough, hemoptysis, fear of death. With the development of edema of the lungs, cough with foamy sputter appears, often painted in pink color. The patient takes a forced position sitting. With a physical examination, special attention should be paid to the palpation and auscultation of the heart with the definition of the quality of heart tones, the presence of III and IV tones, noise and their character. It is important to systematically assess the state of peripheral circulation, temperature skin Pokrov, degree of filling of the ventricles of the heart. PJ filling pressure can be estimated with venous pressure measured in the upper vein floor. However, in the interpretation of the result, caution should be taken, since the increased central venous pressure (CVD) may be a consequence of the impaired stretchability of veins and PJ with inadequate filling of the latter. There is usually evidenced by the presence of wet wheels in auscultation of the lungs and / or signs of stagnation of blood in the lungs during chest radiography. However, in a rapidly changing situation, the clinical assessment of the degree of filling of the left heart departments may be erroneous. table 2 - Clinical and hemodynamic signs with different options Note: * The difference between the low-stroke syndrome from cardiogenic shock is subjective, when evaluating a particular patient, these classification items can partially coincide. ECG in 12 standard leads allows you to determine the rhythm of the heart and sometimes helps to clarify the etiology of the OSN. Radiography of the chest Radiography of the chest should be carried out as early as possible in all patients with the OSN to estimate the size and clarity of the shade of the heart, as well as the severity of blood stagnation in the lungs. This diagnostic study is used both to confirm the diagnosis and to assess the effectiveness of treatment. Radiography of the chest makes it possible to distinguish left-detecting deficiency from inflammatory disease lungs. It is important to take into account that the radiographic signs of stagnation in the lungs are not an accurate reflection of high pressure in pulmonary capillaries. They may not be absent with ZLL up to 25 mm RT. Art. And late react to favorable changes in hemodynamics associated with treatment (a delay of 12 hours is possible). Ehoche is necessary to identify structural and functional changes underlying the basis. It is used to assess and monitor the local and total function of the ventricles of the heart, the structure and functions of the valves, the pathologies of pericardia, mechanical complications of them, the volume formations of the heart. SV can be assessed by the speed of the contours of the aorta or la. Under the Doppler Research - to determine the pressure in LA (on a jet of tricuspid regurgitation) and monitor the preload of LV. However, the reliability of these measurements during the AUD was not verified by the catheterization of the right heads of the heart (Table 4). Table 4. - Typical disorders detected with echocardiography in patients with heart failure Expirate Echokg Cleaning echoch should not be considered as a routine diagnostic method; It is usually resorted only if there is a not enough clear image during transcular access, complicated by the valve lesion, suspicious of a mitral valve prosthetic malfunction, to eliminate the thrombosis of the left atrium, with a high risk of thromboembolism. Standard Halter Monitoring ECG has a diagnostic meaning only in the case of symptoms, probably associated with the presence of arrhythmias (subjective sensations of interruptions, accompanied by dizziness, fainting, syncopene in history, etc.). Magnetic resonance tomography (MRI) is the most accurate method with maximum reproducibility of calculations for calculating the volume of heart volumes, the thickness of its walls and the mass of the LV, which is superior to this parameter EchoCG and radioisotope angiography (RIA). In addition, the method allows you to identify the thickening of the pericardium, evaluate the length of myocardial necrosis, the condition of its blood supply and features of functioning. The diagnostic MRI is justified only in cases of insufficient informativeness of other visualizing techniques. Radionuclide ventriculography is considered a very precise method of determining the FV LV and most often performed when studying the myocardial perfusion to assess its viability and degree of ischemia. Indications for consultation of specialists: 1. Consultation of the arrhythmologist - the presence of violations of the rhythm of the heart (paroxysmal atrial tachycardia, fibrillation and fluttering of atrial, sinus-node weak syndrome), diagnosed clinically, according to ECG and HMEKG. 2. Consultation of the neurologist - the presence of episodes of convulsion, the presence of paresis, hemipresses and other neurological disorders. 3. Consultation of an infectious system - the presence of signs of infectious disease (pronounced catarrhal phenomena, diarrhea, vomiting, rash, changing biochemical blood indicators, positive results of IFA studies on intrauterine infections, hepatitis markers). 4. Consultation of the ENT doctor - nasal bleeding, signs of the upper infection respiratory tract, tonsillitis, sinusitis. 5. Consultation of the hematologist - the presence of anemia, thrombotosis, thrombocytopenia, disruption of coagulation, other deviations of hemostasis. 6. Consultation of the nephrologist - the presence of data for the ISP, signs of renal failure, reduced diuresis, proteinuria. 7. Consultation of the pulmonologist - the presence of concomitant pathology of the lungs, reducing the function of the lungs. 8. Consultation of an ophthalmologist is a planned inspection of the Eye DNA. Laboratory diagnosticsIn all cases, severe landing is needed invasive evaluation of the gas composition of arterial blood With the determination of the parameters characterizing it (PO2, PCO2, pH, deficiency of the base). At the same time, in patients of the elderly, these indicators are not studied enough, and with rapid development, their maintenance in the blood can remain normal when entering the hospital. In other cases, the normal content of BNP or NT-PROBNP allows you to exclude the presence of CH with high accuracy. Heart troponins It is important in determining the diagnosis and stratification of risk, as well as to ensure the possibility of carrying out the difference between them BP ST and unstable angina. Troponins are more specific and sensitive than traditional cardiospecific enzymes, such as creatinginase (CC), myocardial isoenzyme MB (MV-KK), and Mioglobin. Increasing the level of heart troponins reflects damage to the myocardial cells, which, with an ACS of ST, it may be the result of a distal embolization of platelet blood closures from the place of gap or a slope of plaques. Accordingly, troponin can be considered as a surrogate marker of active thrombosis. In the presence of signs of myocardial ischemia (chest pain, ecg changes or new wall movements), raising the level of troponin indicates them. In patients with them, the initial increase in the level of troponins occurs within ~ 4 hours from the moment of symptoms. Increased level of troponins can be maintained up to 2 weeks due to proteolysis of the contracting device. There are no significant differences between Troponin T and Troponin I No. Table 3. - Typical deviations from the norm of laboratory indicators in patients with heart failure
Differential diagnosis Table 5. - Differential diagnosis acute heart failure with other cardiological and non-cardiological diseases
Treatment purpose emergency treatment
- Fast stabilization of hemodynamics and a decrease in symptoms (shortness of breath and / or weakness). Improving the parameters of hemodynamics, first of all, CC and UO, ZLL and PP pressure. Table 6. - Targets of Treatment Tactics of treatment Osn is a life-threatening condition and requires urgent treatment. Below are the interventions shown by most patients with the OSN. Some of them can be performed quickly in any medical institution, others are available only to a limited number of patients and are usually carried out after initial clinical stabilization. 1) With the mainstream, the clinical situation requires urgent and effective interventions and can change rather quickly. Therefore, with a rare exception (nitroglycerin under the tongue or nitrates in the form of an aerosol), drugs should be entered into / in that in comparison with other methods provides the fastest, complete, predictable and controlled effect. 2) OSN leads to a progressive deterioration in blood oxygenation in lungs, arterial hypoxemia and hypoxia peripheral tissues. The most important task in the treatment of land is to ensure adequate oxygenation of tissues to prevent their dysfunction and the development of polyorgan deficiency. To do this, it is extremely important to maintain saturation capillary blood in normal limits (95-100%). Invasive respiratory support (IVL with tracheal intubation) should not be used to treat hypoxemia, which is possible to eliminate oxygen therapy and non-invasive methods of ventilation of lungs. Indications for IVL with tracheal intubation are as follows: Signs of the weakness of respiratory muscles - a decrease in the frequency of respiration in combination with the increase in hypercapinia and the oppression of consciousness; Severe respiratory impairment (in order to reduce respiratory operation); The need to protect the respiratory tract from the regurgitation of gastric content; Elimination of hypercaps and hypoxemia in patients unconscious after long resuscitation activities or drug administration; The need to rehabilitate the tracheobronchial tree to prevent the atelectasis and obturation of the bronchi. The need for immediate invasive ventilation may occur when the eats are eaten against the background of the OX. 3) It is necessary to normalize the blood pressure and eliminate disorders that can cause a decrease in myocardial reduction (hypoxia, myocardial ischemia, hyper-or hypoglycemia, electrolyte disorders, side effects or an overdose of drugs, etc.). The attitude to the early introduction of special means for the correction of acidosis (sodium bicarbonate, etc.) in recent years is quite restrained. Reducing the response to catecholamines in metabolic acidosis is questioned. Initially, it is important to maintain adequate ventilation of pulmonary alveoli and as soon as possible to restore sufficient perfusion of peripheral tissues; Further interventions may be required during long-term preservation. arterial hypotension and metabolic acidosis. To reduce the risk of iatrogenic alkalosis, it is recommended to avoid full correction of the base shortage. 4) in the presence of arterial hypotension, as well as before the appointment of vasodilators, it is necessary to make sure of hypovolemia. Hypovolemia leads to insufficient filling of the chambers of the heart, which in itself is the cause of reducing cardiac output, arterial hypotension and shock. A sign that low blood pressure is a consequence of the impaired pumping function of the heart, and not its insufficient filling, is a sufficient pressure filling of the left ventricle (the pressure of the slope of the pulmonary artery exceeding 18 mm Hg). When assessing the adequacy of the filling of the left ventricle in real clinical conditions, it is often necessary to focus on indirect indicators (physical signs of stagnation in the lungs, the degree of stretching of the veins of the neck, the data of the radiological study), but they react quickly enough to favorable hemodynamic changes due to treatment. The latter can lead to the use of unnecessarily high doses of medicines. 5) Effective aft to increase blood pressure, reduce post-loading of the left ventricle and increase the perfusion pressure in coronary arteries is an intra-roundal balloon counterpulcation (VBK). This allows you to improve the contractile ability of the left ventricle and reduce myocardial ischemia. In addition, PBC is effective in the presence of mitral regularity and defects of the interventricular partition. It is contraindicated in aortic regurgitation, aortic bundle and severe peripheral atherosclerosis. In contrast to drug treatment, it does not increase myocardial needs in oxygen (as positive inotropic agents), does not oppress myocardial reductions and does not reduce blood pressure (as drugs used to eliminate myocardium ischemia or reduction of post-loading). At the same time, this is a temporary measure that allows you to win time in cases where it is possible to eliminate the causes of the developed state (see below). In patients waiting surgical intervention, Other methods of mechanical support may be required (mechanical tools for bypassing left ventricle, etc.). 6) It is important to eliminate the reasons underlying the basis of a particular patient. Eliminate tachy - or bradycardia if they are causes of land or exacerbate it. If there are signs of a sharply arising persistent occlusion of a large epicardial coronary artery (the appearance of persistent lifts of ST segment per ECG), it is necessary to restore its permeability as soon as possible. There is evidence that when equipped with angioplasty / stenting (possibly, on the background of the IIB / IIIIA platelets glycoprotein plants, the surgery of coronary arteries (with the corresponding damage to the coronary arteries), more efficiently of thrombolytic therapy, especially with a cardiogenic shock. If there is an exacerbation of the IHD, when there are no signs of a rack of occlusion of a large epicardial coronary artery (unstable angina, including post-infarction, acute myocardial infarction, which is not accompanied by the Lifts of ST segment to the ECG), it is necessary to suppress myocardial ischemia as quickly as possible and prevent its re-occurrence. The symptoms of the OSN in such patients - the testimony to the maximum possible antithrombotic treatment (including a combination of acetylsalicylic acid, clopidogrel, heparin and in part of cases of the infusion of glycoprotein receptors of IIB / IIIA platelets) and as soon as possible performing coronary angiography with subsequent myocardial reversal (method Depends on coronary anatomy - percutaneous angioplasty / stenting or surgery of coronary arteries). At the same time, angioplasty / stenting of coronary arteries in the early periods of the disease should be carried out, without ceasing treatment with the combination of the above preparations. When it is possible to quickly perform the surgery of the coronary arteries, the purpose of clopidogrel is proposed to postpone until the results of coronary angiography are obtained; If it turns out that the patient needs coronary shunting and the operation is planned in the next 5-7 days, the drug should not be prescribed. If coronary shunting can be performed in the next 24 hours, it is recommended to use nephonic, and not low molecular weight heparin. Perform the most complete revascularization of myocardium in patients with chronic forms of IBS (especially effective in the presence of viable hibernated myocardium). Conduct surgical correction of intracardiac hemodynamic disorders (valve defects, defects of interpresentrial or interventricular partitions, etc.); If necessary, quickly eliminate sedzer tamponad. A number of patients are the only possible method of treatment is a heart transplant. At the same time, complex invasive diagnostic and therapeutic interventions are not considered justified in patients with the terminal stage of the concomitant disease, when the basis is based on the landslide, or when corrective interference or heart transplantation is impossible. 7) the diet of patients with the OSR (after stabilizing the state). The main positions are as follows: I functional class (FC) - not to use salted food (restriction of salt intake up to 3 g NaCl per day); II FC - do not direct food (up to 1.5 g NaCl per day); III FC - to eat products with reduced salt content and cooking without salt (<1,0 г NaCl в день). 2. When restricting the consumption of salt, the restriction of fluid consumption is relevant only in extreme situations: with a decomposed heavy course of CHSN, requiring C / in the introduction of diuretics. In conventional situations, it is not recommended to use a liquid volume of more than 2 l / day (maximum fluid intake - 1.5 l / day). 3. Food must be a calorie, easily absorbed, with sufficient content of vitamins, protein. 4. NB! Weight increase\u003e 2 kg in 1-3 days may indicate a fluid delay in the body and an increase in the risk of decompensation! 5. The presence of obesity or overweight worsens the prognosis of the patient and in all cases under the body mass index (BMI) more than 25 kg / m2 requires special measures and caloric content limitations. 8) Physical activity bed Physical rehabilitation is contraindicated with: Active myocarditis; Stenosis of valve holes; Cyanotic congenital vices; Violations of the rhythm of high gradations; Attimes of angina in patients with a low fraction of emissions (FV), left ventricle (LV). Medical treatment of chronic heart failure Major medicines, Used in the treatment of acute heart failure. Pressor (sympathomimetic) amines (Noraderenalin, dopamine and to a lesser degree of dobutamine) In addition to increasing myocardial contractility, it is capable of increasing peripheral vasoconstriction, which, along with an increase in the blood pressure, leads to a deterioration in the peripheral tissue oxygenation. Treatment is usually started with small doses, which, if necessary, gradually increase (titrate) until the optimal effect is obtained. In most cases, the selection of the dose requires invasive control of hemodynamic parameters with the definition of cardiac ejection and pressure of the slope of the pulmonary artery. The common drawback of drugs of this group is the ability to cause or exacerbate tachycardia (or bradycardia when using norepinephrine), heart rate disorders, myocardial ischemia, as well as nausea and vomiting. These effects of dose-dependent and often impede the further increase in the dose. Noraderenalin Causes peripheral vasoconstriction (including curls and kidney vessels) by stimulating α-adrenoreceptors. At the same time, cardiac emission can both increase and decrease depending on the initial peripheral vascular resistance, the functional state of the left ventricle and reflex effects mediated through carotid baroreceptors. It is shown in patients with severe arterial hypotension (systolic blood pressure below 70 mm Hg. Art.), With low peripheral vascular resistance. The usual initial dose of norepinerenaline is 0.5-1 μg / min; In the future, it is titrated until the effect is achieved and the refractory shock may be 8-30 μg / min. Phosphodiesterase III inhibitors (Amrinon, Milrinon) have positive inotropic and vasodilating properties, causing mainly ventilating and a decrease in the tone of pulmonary vessels. Also, like pressing amines, they are able to exacerbate myocardial ischemia and provoke ventricular violations of the heart rhythm. For their optimal use requires monitoring of hemodynamics parameters; The pressure of the pulmonary artery should not be below 16-18 mm Hg. The infusion of phosphodiesterase inhibitors III is commonly used in severe heart failure or cardiogenic shock, adequately not responding to standard treatment with pressor amines. Amrinon often causes thrombocytopenia, tachyphylaxia can be rapid to it. Recently it has been shown that the use of Millrinon during the weightlifting of chronic heart failure does not lead to an improvement in the clinical course of the disease, but is accompanied by an increase in the frequency of the pillar of arterial hypotension requiring treatment, and sufficiently valuable arrhythmias. Means that increase the affinity of contractual myofibrils of cardiomyocytes to calcium. The only drug of this group that came to the stage of wide clinical application With the land, is Levosimenan. Its positive inotropic effect is not accompanied by a tangible increase in the need of myocardium in oxygen and an increase in sympathetic effects on myocardium. Other possible mechanisms of action - selective oppression of phosphodiesterase III, activation of potassium channels. Levosimenan holds vasodilating and anti-host effect; Due to the presence of a long-acting active metabolite, the effect remains some time after the discontinuation of the drug. Digoxin has a limited value in the treatment of the OSN. The drug is distinguished by small therapeutic latter and is able to cause heavy ventricular arrhythmias, especially in the presence of hypokalemia. Its property slow down atrioventricular conductivity is used to reduce the frequency of ventricular cuts in patients with preserving fliccific arrhythmias or atrial trembles. 2) Vasodilators Capable to quickly reduce the pre- and postload due to the expansion of veins and arteriole, which leads to a decrease in pressure in the capillaries of the lungs, a decrease in peripheral vascular resistance and blood pressure. They cannot be used in arterial hypotension. Relax to a lesser extent than large arteries and veins. Nitroprusside sodium According to the effect on arterioles and veins, nitroglycerin is similar. It is usually introduced in doses of 0.1-5 μg / kg per min (in some cases up to 10 μg / kg per minute) and should not be in the light. It is used to treat urgent states arising from severe heart failure (especially associated with aortic or mitral regurgitation) and arterial hypertension. There is data on an increase in symptomatic efficiency (but not outcomes) in the treatment of states with low heart-emission and high peripheral resistance that do not respond to dopamine. Treatment is to immediately terminate the infusion of the drug, sodium thiosulfate is introduced in severe cases. 3) Morphine - Drug analgesic, which in addition to analgesic, sedative action and increasing the vagus tone causes ventilating. It is considered as a means of choosing to relieve pulmonary edema and eliminate pain in the chest associated with myocardial ischemia and not passing after re-taking nitroglycerin under the tongue. 4) Furosemid - loop diuretic with direct ventilating effect. The last effect occurs within the first 5 minutes after the Introduction, while the increase in the urine separation occurs later. The initial dose is 0.5-1 mg / kg in / c. If necessary, administration is usually repeated after 1-4 hours. 5) beta adrenoblays. 6) Anticoagulants. Anticoagulants are shown in patients with ox, flickering arrhythmia, artificial heart valves, deep vein thrombosis of the lower limbs and TEL. It is evidence that p / k administration of low molecular weight heparins (ENOCAPARIN 40 mg 1 time / day, Dalteparin 5000 me 1 time / day) can reduce the frequency of deep vein thrombosis in patients hospitalized with acute therapeutic disease, incl. Heavy CH Large studies comparing the prophylactic efficiency of low molecular weight heparins and an eneractic heparin (5000 units of 2-3 times / day) during the AUTN were not carried out. 7) fibrinolytic therapy. Patients with them with the element of the ST segment and the possibility of conducting the CCV requires mechanical (catheter) reperfusion (primary coronary intervention) within 60 minutes from the moment of appealing for help. In the absence of the possibility of carrying out the primary PCV, the reduction of blood flow in the infarction-dependent artery can be achieved by pharmacological reperfusion (fibrinolysis) within 30 minutes after the first contact with the patient. Despite the limited efficiency and high risk of bleeding, fibrinolysis on the pre-hospital stage should be considered as a priority treatment method, if there are all the conditions for its holding (trained personnel with the possibility decoding ECG). The bolus preparation (Tenctenise) has ease of administration and the best prognostic option with a smaller risk of bleeding. In the absence of contraindications, it is necessary to begin carrying out trobbolytic therapy (TLT) under the following conditions: If the time from the start of an angin attack is 4-6 hours, at least does not exceed 12 hours; The ECG is noted the rise of the ST\u003e 0, L MV segment, at least 2 consecutive breast leads or in 2 leads from the limbs or a new blockade of the left feet of the Gis beam (BLNPG) appears. The introduction of thrombolitics is justified for the same time as an ECG signs of the true rear. (High teeth R in the right precartial leads V1-V2 and the depression of ST segment in V1-V4 leads with award-up to teeth). Recombinant Fabric Activator Plasminogen (Alplaza)it is introduced in / in (pre-preparation is dissolved in 100-200 ml of distilled water or 0.9% sodium chloride solution) according to the "Bolox + infusion" scheme. Dose of the drug 1 mg / kg body weight (but not more than 100 mg): 15 mg is injected bolus; Subsequent infusion of 0.75 mg / kg body weight in 30 minutes (but not more than 50 mg), then 0.5 mg / kg (but not more than 35 mg) for 60 minutes (the total duration of the infusion is 1.5 hours). Tenctenise (Metalize) intravenously 30 mg for body weight<60 кг, 35 мг при 60-70 кг, 40 мг при 70-80 кг; 45 мг при 80-90 кг и 50 мг при массе тела >90 kg, the required dose is entered in the form of a bolus, within 5-10 seconds. For administration, an previously established venous catheter can be used, but only if it is filled with 0.9% solution of sodium chloride, after the introduction of metaly, it should be well washed (in order to complete and timely delivery of the drug in blood). Metalization is not compatible with dextrose solution, and should not be applied with a dropper containing dextrose. Any other medications It should not be added to the injection solution or in the mains for infusion. Given the longer period of half-life from the body, the drug is used in the form of a single bolus, which is especially convenient in the treatment at the prehospital stage. Absolute contraindications to fibrinolytic therapy: Previously suffered hemorrhagic stroke or violation brain circulation unknown origin. Ischemic stroke transferred over the past 6 months, with the exception of ischemic stroke, which occurred within 3 hours, which can be treated with thrombolytic. Recent extensive injury / operation / head damage (in the last 3 months). Brain tumor, primary or metastatic. Changes in the structure of cerebral vessels, the presence of arterio-venous malformation, arterial aneurysms. Suspicion of aortic aneurysm. Gastrointestinal bleeding over the past month. The presence of signs of bleeding or hemorrhagic diathesis (with the exception of menstruation). Puncture in places of non-compresses (for example, liver biopsy, lumbar puncture). Relative contraindications for fibrinolytic therapy: Transient ischemic attack in the last 6 months. Refractive arterial hypertension (systolic blood pressure ≥180 mm Hg and / or diastolic blood pressure ≥110 mm Hg). Reception of indirect anticoagulants (warfarin) (the higher many, the higher the risk of bleeding). State of pregnancy or within 1 week after delivery. Liver disease in the progressive stage. The aggravation of peptic ulcer or 12 pans. Infective endocarditis. Ineffectiveness of resuscitation activities. Traumatic or long-term (\u003e 10 min) Cardiovary resuscitation. For streptokinase - preceding use (\u003e 5 days ago and up to one year or more) or allergic reaction on her. Elimination of the causes of decompensation is the most important component of the treatment of the OSR and the prevention of its recurrence. Uncontrolled diseases may seriously complicate the forces of the OSN and make it difficult to make it. She is the most frequent cause The OSN, which can be represented by the left-chelochetic failure with low SV, left-detective failure with the symptoms of blood stagnation, as well as the right-hand deficiency. All patients with exacerbation of IBS shows the speedy execution of kag. Timely reperfusion with OIM with the approach of the ST segment on the ECG is able to prevent the OND or improve its flow. Preferably percutaneous coronary intervention, with appropriate testimony in patients with cardiogenic shock, emergency coronary shocking is justified. If invasive treatment is not available or associated with a significant loss of time, TLT should be held. Urgent myocardial revascularization is shown at the OSR complicated by them, without the lifting segment of ST on the ECG. and also with NA with expressed myocardial ischemia. The emergence of the OUND, reflex reactions, as well as violations of the rhythm of the heart and conductivity can be facilitated. Therefore, both adequate anesthesia and the rapid elimination of arrhythmia leading to the impaired hemodynamics are important. With a true cardiogenic shock of temporary stabilization, it can be achieved by maintaining the adequate filling of the chambers of the heart, the VACP, drug-based inotropic support and IVL. With bowls with symptoms of blood stagnation acute treatment The same as with other reasons for this option. Since inotropic agents can be dangerous, it is necessary to discuss the possibility of the VACP. Subsequently, along with the adequate revascularization of myocardium, β-adrenoblays and Raas inhibitors are shown. Read more Approaches to the treatment of OSN in exacerbation of the IBS are set out in the recommendations of the INC on the treatment of myocardial infarction with the stations of the ST segment to the ECG and OX without persistent lifting segment of the ST on the ECG (Cardiology. - 2004. -№ 4 (Appendix). - C. 1-28 ). Pathology of the valve apparatus of the heart The cause of the OSR may be the dysfunction of the heart valves in the exacerbation of the IBS (more often mitral failure), the acute mitral or aortic insufficiency of other etiology (endocarditis, injury), aortic or mitral stenosis, artificial valve thrombosis, aggravating aortic aneurysm. For infectious endocardite The main reason for the development of the OSR is the insufficiency of the heart valve. The severity of heart dysfunction can be aggravated by myocarditis. In addition to standard treatments, antibiotics should be assigned to the standard. For a quick diagnosis, a specialist consultation is shown. With pronounced acute mitral or aortic failure, urgent surgical treatment is required. With a long existing mitral regurgitation, in combination with a reduced SI and low FV, an emergency operation, as a rule, does not improve the forecast. In these cases, the preliminary stabilization of the state with the VACP can have a great value. Thrombosis of an artificial heart valve The ons of these patients often lead to death. In all patients with suspected thrombosis of the artificial valve, it is necessary to perform radiography of the chest and echoc. The question of optimal treatment remains unclear. When the valve thrombosis of the left side of the heart, the method of choice is operational intervention. The TLT is used in thrombosis of the valve of the right heart departments and in cases where surgery is associated with a high risk. A recombinant plasminogen tissue activator inhibitor is used for TLT (10 mg V / in a jet and subsequent infusion of 90 mg for 90 minutes) and streptokinase (250,000-500,000 me for 20 minutes with subsequent infusion 1 000 000-1.5 000 000 ME for 10h). After the injection of thrombolytic, it is necessary to begin in / in infusion of an unfractionated heparin in a dose that provides an increase in the AFTT 1.5-2 times from normal (control) values \u200b\u200bfor this laboratory. An alternative can be the purpose of the UrCinase in the dose of 4400 IU / (kg · h) without heparin for 12 hours or 2000 IU / (kg · h) in combination with an unfractionated heparin within 24 hours. The TLT is ineffective if there is an arrangement of fibrous tissue with small ignitions of secondary thrombosis. In patients with very large and / or mobile trom closures, TLT is associated with an increased risk of thromboembolic complications and stroke. In these cases, surgical treatment is possible. Pre-for refinement of the character of the damage of the valve is shown perchive echoch. After the TLT, repeated echoca is needed. The feasibility of operational intervention should be considered at the inability of the TLT to eliminate occlusion. An alternative way is to introduce additional trombolytic doses. Although mortality in emergency operation in patients with hemodynamicity instability III-IV FC, according to the classification of the New York Heart Association (NYHA) (Easy, arterial hypotension), high, TLT can lead to loss of time and increase the risk of surgical treatment in case Her unsuccessfulness. According to non-general studies, in less heavy patients, the long-term antithrombotic and / or TLT may not refresh surgical treatment. Aortic aneurysm agriculture The agricultural aortic aneurysm is accompanied by the OSN in the presence of GK, acute valve regurgitation, heart tamponades, myocardial ischemia. If aortic aortion, surgeon is needed to suspicion of an extensive aneurysm. The morphology and the function of the aortic valve, as well as the presence of fluid in the pericardia, is best evaluated at a perch-free echoc. Operational intervention is usually carried out according to life indications. Tamponade of the heart is a decompensated phase of its compression caused by the accumulation of fluid in the pericardia. With "surgical" tamponade (bleeding), intrapericardial pressure increases quickly - from a few minutes to hours, while at the "therapeutic" tamponade (inflammation) this process takes from several days to weeks. The impaired hemodynamics is an absolute reading to the pericardiocentsis. In patients with hypovolemia of temporary improvement, it can be achieved at the expense of a fluid in the introduction of a fluid, leading to an increase in the pressure of filling the ventricles of the heart. When wounds, breaking the aneurysm of the ventricular heart or hemopericade due to the bundle of the aorta, an operation is necessary to eliminate the source of bleeding. Always, when it is possible, you should treat the cause of the emission of pericarditis. Osn is one of the most frequent complications of hypertensive crises. Clinical signs of the OSN with a hypertonic crisis include only stagnation in lungs, which can be insignificant or heavy, up to a sudden elderish edema. In patients hospitalized with ethics on the background of a hypertensive crisis, often do not find significant changes in the systolic function of LV; more than half of the FV Lz\u003e 45%. Diastolic disorders are often observed, in which the processes of myocardial relaxation are worse. In / in the introduction of isosorbide of dinitrate, nitroglycerin or nitroprusside; In / in the introduction of loop diuretics, especially in patients with a fluid delay and a long history of CHF; Perhaps in / in the introduction of a long-acting dihydropyridine derivative (Nipage). However, with a hemodynamic action similar with nitrates, the drugs of this group are capable of causing hypersympathicotone (tachycardia), increase blood shunt in the lungs (hypoxemia), as well as to complicate from the central nervous system. A quick decrease in blood pressure can be achieved by receiving captopril under the tongue. Apparently, its use can be justified when it is impossible to / in the introduction of drugs, as well as inaccessibility or insufficient effectiveness of inhalation forms of nitrates. β-adrenoblockers under the elder edema should not be used, except in cases where the OSN is combined with tachycardia in patients without a serious impairment of the contractile ability of the LV, for example, with diastolic CH, mitral stenosis. Hypertensive crisis at the peuchromocytoma can be eliminated in / in the introduction of 5-15 mg of fantolamine with mandatory monitoring of blood pressure; Repeated administration is possible after 1-2 hours. Renal failure A minor and moderate change in the kidney function is usually asymptomatic and satisfactorily transferred to patients, nevertheless, even a slightly elevated content of creatinine in blood serum and / or a decrease in the SCF is independent FR adverse forecasts at the AUD. In the presence of acute renal failure, diagnosis and treatment of combined pathology are needed: anemia, electrolyte disorders and metabolic acidosis. Renal failure affects the effectiveness of CH's therapy, which involves the use of digoxin, IAPF, receptor blockers to angiotensule, spiroironolakton. An increase in the content of creatinine in blood serum by more than 25-30% and / or the achievement of a concentration exceeding 3.5 mg / dl (266 μmol / l) is a relative contraindication to the continuation of the IAP therapy. Renal insufficiency of the average and severe degree [Creatinine content in serum more than 2.5-3 mg / dL (190-226 μmol / l)] is conjugate with a decrease in the reaction to diuretics. These patients often have the need for a constant increase in the dose of loop diuretics and / or in the addition of a diuretic with another mechanism of action. This in turn can cause hypokalemia and even greater decrease in the SCF. The exception is thoramsmide, the pharmacological properties of which are practically independent of the impairment of the kidney function, since the drug is 80% metabolized in the liver. Patients with severe dysfunction of kidney and refractory fluid delay may be required continuous venous venous hemofiltration. The combination with inotropic means enhances the renal blood flow, improves the kidney function, restores the effectiveness of diuretics. In hyponatremia, acidosis and uncontrolled fluid delay, dialysis may be required. The choice between peritoneal dialysis, hemodialysis and ultrafiltration usually depends on the technical equipment of the hospital and the magnitude of the blood pressure. Light diseases and bronchopstructions When a combination of an axis with bronchological syndrome, it is necessary to use bronchodlators. Although the drugs of this group can improve the function of the heart, they should not be used to treat the OSN. Heart rhythm disorders can be the main cause of the asset in patients with both preserved and with impaired heart function, as well as to complicate the course of the already developed land. To prevent and successfully eliminate heart rhythm disorders, it is necessary to maintain a normal concentration of potassium and magnesium in the blood. Bradiarhythmia Treatment is usually started with in / in administration of 0.25-5 mg of atropine, if necessary, repeated to a maximum dose of 2 mg. In case of atrioventricular dissociation with a rare ventricular activity in patients without myocardial ischemia, it is possible to use in / in infusion of isoproterene in a dose of 2-20 μg / min. A low CSG at shimmer arrhythmia can be temporarily eliminated in / in the administration of theophylline at a rate of 0.2-0.4 mg / (kg · h) first with a bolus, then in the form of infusion. In the absence of a response to drug treatment, it is necessary to use an artificial driver of the heart rhythm. If there are myocardial ischemia, it should be eliminated as quickly as possible. Neckwarce Tahiaritimia Cleaning arrhythmia and fluttering atrial. It is necessary to control the heart rate, especially in the presence of myocardial diastolic dysfunction. However, when restrictive CH or Tamponade, hearts, with a rapid decrease in heart rate, the condition of the patients can suddenly deteriorate. Depending on the clinical situation, it is possible to maintain normosistol with continued arrhythmia or restoration and retention of sinus rhythm. If the violation of the rhythm is paroxysmal, after stabilization of the state, it should be considered the feasibility of drug or electrical cardioversion. With the duration of paroxysm, less than 48 hours, the use of anticoagulants is not necessary. If the arrhythmia lasts longer than 48 hours, it is necessary to use anticoagulants and for at least three weeks before cardioversion to maintain normistolis with appropriate drugs. In more severe cases: with arterial hypotension, expressed stomach in lungs - an emergency electric cardioversion is shown against the background of the administration of the therapeutic dose of heparin. The duration of the use of anticoagulants after successful cardioversion should be at least 4 weeks. In patients with persistent fliccific arrhythmias and atrial flutters, the feasibility of the use of anticoagulants depends on the degree of risk of arterial thromboembolism and is considered in the relevant guidelines. To reduce the heart rate and the prevention of recurrence of arrhythmias use β-adrenoblays. The possibility of fast digitalization should also be considered, especially when flickering arrhythmia is secondary to the OSN. Amiodarons are usually used for medication cardioversion and prevent recovery of arrhythmia. Patients with low FV should not use antiarrhythmic preparations of class I, verapamil and diltiazem. In rare cases, the possibility of assigning verapamil can be considered in patients without a significant reduction in the contractile ability of the LV to control the heart rate or eliminating the paroxysm of religorak tachycardia with narrow QRS complexes. Ventricular arrhythmias. Fibrillation of ventricles and stable ventricular tachycardia require immediate an email and, if necessary, respiratory support. Amiodaron and β-adrenoblays can prevent their reappearance. With recurrences of heavy ventricular arrhythmias and hemodynamic instability, it is necessary to immediately perform kag and electrophysiological research. Surgical intervention 1) emergency coronary It should be carried out as soon as possible patients with severe angina, deep or dynamic changes to ECG, severe arrhythmias or hemodynamic instability during admission or subsequently. These patients make up 2-15% of patients with a diagnosis of ACS ST. Table 8. - predictors of high thrombotic risk or high risk of developing myocardial infarction, which are an indication for emergency coronary frames 2) surgical treatment. In some diseases underlying the emergence of the OSN, urgent surgical intervention is able to improve the forecast (Table 9). Surgical treatment methods include the revascularization of myocardium, correction of anatomical heart defects, including prosthetics and reconstruction of valves, mechanical means of temporary support for blood circulation. The most important diagnostic method in determining the testimony to operation is ECCG. Table 9. - Heart disease with ASN, in need of surgical correction 3) Heart transplantation. The need for heart transplantation usually arises with severe acute myocardium, postpartum cardiomyopathy, extensive with a bad forecast after revascularization. 4) Mechanical ways to support blood circulation. Temporary mechanical support for blood circulation is shown by the patient with the OSN, which is not reacting to standard treatment, when it is possible to restore the myocardial function, showing surgical correction of existing disorders with a significant improvement in heart function or heart transplantation. LEVITRONIX devices - refers to devices providing hemodynamic support (from several days to several months), with minimal injury of cellular elements. Without exercise oxygenation. The VACP can significantly improve hemodynamics, but it should be performed when it is possible to eliminate the cause of the OSN - the myocardial referee, the prosthetics of the heart valve or heart transplantation, or its manifestations can regress spontaneously - stunning myocardium after OIM, operation on the open heart, myocarditis. Extracorporeal membrane oxygenation (ECMO) Implantation of VAD auxiliary devices: 5) Ultrafiltration Preventive actions: Emergency prevention - A complex of emergency measures to prevent the emergence of the emergency cardiological condition or its complications. Substantial benefit can bring the development of individual self-help physician for patients with cardiovascular diseases. The basis of emergency cardiological assistance is the elementary organization and equipment of the medical and diagnostic process, and most importantly, specialists who have clinical thinking, practical experience and dedication. Indicators of the effectiveness of the treatment and safety of diagnostic and treatment methods described in the Protocol Preparations (active substances) used in the treatment
The ardial structures perform the most important function - blood pumping, ensuring adequate gas exchange and tissue trophics. Outside the normal functional activity of the muscular organ of health and adequate state of the body there is no speech. Acute heart failure is a sudden impairment of the heart with a weakening of ventricular activities and the impossibility of providing organs and blood systems. Unlike chronic variety, this characterizes a momentum deflection, the body works about a third of its own capabilities. Hence the ischemia (oxygen starvation) both the myocardial himself and cerebral structures (brain), and other systems. Violation of the reduction of ventricles leads to a fatal outcome in 50-70% of fixed clinical situations. To restore life, the help of several specialists, both profile and resuscitative, are required. It's about urgent state, because only symptoms arise, you need to call an ambulance. Even in the case of spontaneous stabilization of the state, there is a high risk of severe consequences of the disabled genus: IBS, process chronicization. This is a direct path to a delayed fatal outcome. The essence of the pathological process is in violation of the reduction of cardiac structures. In the course of development, a deviation occurs in the work of the ventricles. There are two of them two. The left pumps blood in a large circle. He is responsible for providing the entire body with oxygen and nutrients. The right function is weaker, transports liquid connective tissue in small. Mainly provides gas exchange in pulmonary structures.
As part of acute heart failure, the reduction of tissues of cardiac structures is falling. Hence the impossibility of adequate nutrition of the body. Causes of this are different: hormonal failure, leaping blood pressure in critical limits, abuse of coffee or narcotic substances (the "street" heroin is especially dangerous. The development of the process is accompanied by generalized hypoxia and mass symptoms by organs and systems. ClassificationType the pathological process can be on the main basis. This is the localization of the pathogenic phenomenon. Accordingly, they are talking about such forms:
Oxygen and nutrients are not allowed all the fabrics, including the brain and the heart itself. The heart suffers first of all, everything can end the myocardial infarction and imminently fatal outcome. Recovery in case of timely assistance is probably important to skip the moment. The rehabilitation period lasts from 6 to 12 months, lifelong supporting therapy is required.
Accompanied by pulmonary deviations, gas exchange is violated to a lesser extent. Assistance is just as urgent, mortality is slightly lower. If, on the background of left-oscillatory failure, death occurs, about 30% of situations, this process ends fatally in 15% of cases
A generalized violation of all organs and systems is noted, without the possibility of recovery. Mortality maximum. According to medical calculations. The probability of death is approximately 95%. Resuscitation activities do not raise effect. Causes of acute left vehiclesThe factors for the development of the pathogenic process of this kind are diverse. These are mainly cardiac moments (about 98% of situations). Among possible pathologies:
Usually the regulation of the reduction of heart structures is disturbed. Especially often similar is observed at. Stroke prevention is the main method of prevention of heart failure of a neurogenic type.
Chaotic signals do not allow cardiac structures to work adequately. Treatment operational, radical. A frequent clinical option is hypercorticism, accompanied by the secondary disease of Isenko Cushing. It is a dangerous, severe condition, potentially lethal. The quality of life is reduced: the destruction of bones and the musculoskeletal system, obesity, hallucinatory syndromes, is just a part of possible manifestations.
Without treatment leads to cardiac dysfunction. Recovery is carried out under the control of the profile doctor. To eliminate problems, you need to normalize the work of the hematopoietic system. This can be done only by complex methods: medicines + vitamins and diet.
Causes of acute refereeA kind of variety is developing slightly. Factors of formation:
Causes are largely similar. You need to understand quickly, since there is no time for a complete study. Help urgent, urgent. In the intensive care unit. SymptomsProcess manifestations are developing rapidly, for 5 minutes - 2 hours. In extremely rare cases, there may be a gradual increase in signs, it gives some time on thinking. Act anyway need quickly. Leftvuel Osn.Acute cardiovascular lack of left ventricle manifests three syndromes: asthma, cardiogenic shock or pulmonary swelling. Among the characteristic moments:
Usually the symptoms of the acute heart failure of the left-sided plan are found in the system. Immediately everything. Their relief is great difficulties. Muslim Osn.The main phenomena of this variety of deviations are associated with blood stagnation in the system. Signs of acute heart failure of the right ventricle are as follows:
Symptoms of acute deficiency of right-sided type are stopped in resuscitation, which gives the best forecasts. Survival accomplishment reaches 50-70% in case of timely hospitalization. Algorithm of pretty aidRegardless of the qualifications, you need to call an ambulance. You can make at home very little, a specially equipped hospital is required. The approximate event scheme is as follows:
In the future, it is necessary to calm the alarming patient. Before the arrival of doctors can not do anything else. Attention: At the cooking stage, drugs can not be given, possibly a sharp aggravation of state and death. DiagnosticsCardiologists with emergency care doctors are engaged in patients in resuscitation doctors. For the time survey, there is extremely small, every minute in the account. Nevertheless, you need to carry out a minimum of events. But first partially stabilize the patient's condition. Approximate list of actions:
There is always data for organic pathology. But the elimination of the root cause is a secondary task. The main thing to stabilize the state. Then you can resort to a deeper diagnosis. Approximate list of activities:
It is possible to conduct invasive diagnostic methods. A set of measures is determined by doctors based on the intended pathological process. Load tests are never held. This is fraught with a heart stop and a fatal outcome. Urgent treatmentThe therapy is strictly medicated, in most cases surgical assistance does not make sense, at least at the first stage. Before stabilizing the state of speech on the operation does not go. An exemplary scheme is as follows:
These are the main directions of urgent treatment aimed at restoring and stabilizing cardiac activity. Supporting therapyAs part of the supporting therapy, such medicines are shown:
Possible consequencesProbable complications are understandable and without explanation. The most frequent options:
Mortality is nearing 100%. Even if the patient is getting out of the urgent state, the likelihood of death in the front of the nearest 2-3 years, perhaps less. Such patients need to be conducted under careful dynamic observation. Every 3 months you should visit the cardiologist.
Female outcome crowned heart failure. This is the most likely outcome outside competent aid. Prognostic estimatesForecasts are difficult to determine. It is necessary to take into account the mass of moments. Unfavorable factors:
Reverse signs are associated with a more or less normal forecast. If we talk more specifically, the median survival of patients is 3-5 years. Without medical care we are talking about 95% of mortality in the same perspective or less. Short-term phenomenon, like pathology, against the background of burns, pulmonary failure is eliminated easier if there are no accompanying complications, the forecast is good. Life expectancy is not limited to the framework of the disease. Attention: Nobody will predict an outcome in advance. To do this, you need to explore the history and history of the disease, look at the effectiveness of therapy and the general condition of the patient. FinallyThe acute form of heart failure is a significant reduction in the intensity of blood emissions. Restoration is unlikely, not counting rare cases. Alternating out of the state without serious consequences can only 10-15% of patients. The rest become disabled and take preparations constantly. It is also possible and even likely to death. The OSN may develop de novo, that is, in a person without heart dysfunction in history, or as an acute decompensation of the CHF. Causes of Osn: 1) leading to a rapid increase of symptoms: acute coronary syndrome (myocardial infarction or unstable angina, leading to ischemia and dysfunction of a significant zone of myocardium, mechanical complications of acute coronary syndrome, myocardial infarction of the right ventricular), hypertensive crisis, heart and conductivity rhythm violation, pulmonary thromboembolism Arteries, Tamponade Hearts, Building Aorts, Peripial Cardiomyopathy, Stress-induced Cardiomyopathy (Takotsubo), Complications of surgical interventions, tense pneumothorax; 2) leading to a slower increase of symptoms: infections (including myocarditis (except giant meal) and infectious endocarditis), metabolic and hormonal disorders (eg, thyroid dysfunction, feochromocytoma, ketoacidosis with diabetes mellitus), hypercitration, high syndrome Heart Emission (severe infection, especially sepsis, thyrotoxic crisis, anemia, arteriovenous fistulas, Pedge's disease). ASN, as a rule, develops due to the already existing damage to the heart. It is possible to allocate the options for the basis depending on the cause underlying it, or provoking factors, for example, the main artery for acute thromboembolism, the sharp decompression of the CHF. The most common cause, especially in old age, ischemic heart disease. Persons of younger age prevail: dilatation cardiomyopathy, heart rate disruption, congenital and acquired heart defects, myocarditis. Clinical picture and natural flow 1. Subjective and objective symptoms: 1) retrograde stagnation: a) in a large circle of blood circulation (right-hand deficiency) - peripheral swelling (swelling of the test consistency around the bones or the sacral zone; may not have time to appear), expanding the meropores and palpator pain in the epigastrium (due to the increase in the liver), sometimes - transdate in serous cavities ( pleural, abdominal, pericardial); b) in a small circle of blood circulation (left-deuded deficiency → Easy swelling) - shortness of breath, rapid breathing and shortness of breath in the sitting position, wet wilds over the pulmonary fields 2) reduction of cardiac output (peripheral hypoperfusion; there are rarely found, indicate the worst forecast) - fast fatigue, feeling of weakness, aimation, drowsiness; The skin is pale, cold, wet, sometimes peripheral cyanosis, threaded pulse, hypotension, oliguria; 3) the main disease that caused the OSN. According to ESC (2016) recommendations, it is recommended to apply the classification of patients based on T.N. Hemodynamic profile. The presence or exclusion of stagnation (stagnation \u003d wet profile without stagnation \u003d dry profile) and peripheral hypoperfusion(peripheral hypoperfusion \u003d cold profile VS Right peripheral perfusion \u003d warm profile), primarily on the basis of an objective examination (sometimes with additional laboratory studies), determines the diagnosis of 4 major patient profiles and makes it possible to develop further tactics (→). Attention: hypoperfusion is not synonymous with hypotension - in most patients with blood pressure within the normal range or increased. Figure 2.19-2.Algorithm for the treatment of patients with acute heart failure, depending on the clinical picture at an early stage of the disease (based on ESC 2016 Recommendations, modified) 2. The onset can flow as: 1) exacerbation or Decompensation of HSN- the symptoms of blood stagnation in the large and small circles of blood circulation; 2) swelling of the lungs; 3) - the subjective and objective symptoms of the CH are accompanied by high arterial pressure and, as a rule, stored systolic function of the left ventricle, signs of increased tone of the sympathetic nervous system, with tachycardia and spasm of blood vessels; The patient can be in a state of normopesia or only minor hyperhydration, often appear objective symptoms of pulmonary edema without symptoms of stagnation in a large circulation circle; 4) cardiogenic shock- Tissue hypoperfusion due to land, typical systolic blood pressure<90 мм рт. ст. или снижение среднего артериального давления на >30 mm RT. Art., Anuria or Oliguria, often - the rhythm of the heart; Symptoms of hypoperfusion of organs and pulmonary edema are developing rapidly; 5) isolated refereesmall emission syndrome without pulmonary edema, increase pressure in the jugular veins with an increase in liver or without; 6) OSN at ACS. Based on subjective and objective symptoms, as well as the results of additional research. Additional research methods 1. ECG: There are usually changes caused by the main disease of the heart, more often signs of myocardial ischemia, rhythm and conductivity disorders. 2 . RG chest:in addition to the symptoms of the main disease, it can reveal a stagnation in a small circulation circle, liquid in pleural cavities and an increase in heart chambers. 3. Echocardiography:receives functional disorders (systolic or diastolic dysfunction, valve dysfunction) or anatomical changes of the heart (eg, mechanical complications of myocardial infarction). 4. Ultrasound of the chest:makes it possible to visualize the intersecy edema of the lungs; Ultrasound of the abdominal cavity - are carried out in order to measure the width of the lower hollow vein and assessing ascites. 5. Laboratory studies:mandatory - general analysis of blood, concentration of creatinine, urea, potassium and sodium, glucose, heart troponins, liver enzyme activity, arterial blood gasometry (in patients with a slight breath, can be replaced with pulse oximetry, except for cases of shock with very low heart emissions and peripheral vazospasm). The determination of the brain sodium-formistic peptide (BNP / NT-PROBNP) will help in the differential diagnosis of cardiac (increasing concentration) and the extraimatic causes of shortness of breath; Remember that in patients with rapidly increasing swelling of lungs or acute mitral insufficiency of the concentration of peptides at the time of hospitalization can still be located within the normal range. The definition of the D-dimer is shown in patients with suspicion of the oral thromboembolism of the pulmonary artery. 6. Endomiocardial biopsy:indications →. Diagnostic tactics It follows quickly (max. For 120 minutes) to establish whether the main consequence of the disease in which specific actions are needed: coronorography and occasion. Revascularization in the case of an ox or cardiac surgery in the event of a myocardial rupture, aortic bundle, heart tumors, or dysfunction of a native or artificial valve. Differential diagnosis The reasons for the non-targeted edema of the lungs → (signs to help distinguish the non-mangy edema of the lungs from cardiogenic →), acute respiratory failure, interstitial lung diseases (with acute flow) →.
General principles 1. Hospitalization in the separation of intensive therapy(general or cardiological) patients who are present ≥1 from criteria: 1) the need for intubation; 2) SpO2.<90 % несмотря на оксигенотерапию; 3) respiratory frequency\u003e 25 / min; 4) Heart Rate Frequency<40 или >130 / min; 5) systolic blood pressure<90 мм рт. ст.; 2. Objectives of urgent treatment:control of subjective symptoms, first of all shortness of breath, and stabilization of hemodynamic states. 3. General diagram of therapeutic tactics at the basis depending on the presence of symptoms of hypoperfusion and / or stagnation →. 4. Etiotropic treatment:apply in each case. 5. Careful monitoring:breathing, heart rate frequency, ECG and blood pressure. Study Perform regularly (eg, every 5-10 min), and in unstable patients - constantly, until the stabilization of doses of LS and the patient's condition. If there are no strong vasospasm and significant tachycardia - measurement of blood pressure using non-invasive automatic devices are reliable. When the Rhythm monitoring and the ST on ECG segment is needed, especially if its cause is OCS or arrhythmia. In patients receiving oxygen, ensure monitoring SPO2 with a pulse oximeter (eg, every hour), and the best - constantly. Sometimes there may be invasive monitoring of hemodynamics, especially in the situation of coexistence of stagnation and hypoperfusion, as well as an unsatisfactory response to pharmacological treatment, since it helps in choosing proper treatment; It can be performed using: 1) Svana-Hansa catheter introduced into the pulmonary artery - to measure pressure in the upper hollow vein, the right of atrium, the right ventricle and the pulmonary artery, the pressure of the junction in the lung capillaries and the determination of cardiac output →, as well as saturation with oxygen mixed venous blood; 2) the catheter introduced into the central vein - to measure the central venous pressure (CVD) and saturation of hemoglobin oxygen in venous blood (SVO2) in the upper hollow vein or atrium right; 3) the catheter introduced into the peripheral artery (usually radiant) for permanent dimension of blood pressure. 4. Algorithm of actions, depending on the clinical form 1) exacerbation or decompensation of HSN →vasodilators + loop diuretics (in patients with impaired kidney function or long-receiving diuretics, consider the possibility of applying diuretics in large doses); Inotropic LS in the case of hypotension and symptoms of organic hypiperphus; 2) swelling of the lungs →;
Figure 2.19-3.Action algorithm for acute pulmonary edema (according to ESC 2016 Recommendations, modified) 3) High arterial pressure→ Vasodilators (careful monitoring is required); Small doses of diuretics in patients with hypershydration or pulmonary edema; 4) cardiogenic shock→ ; 5) isolated referee→ Support the level of intelligence of the right ventricle; Avoid, if possible, the use of vasodilators (opioids, nitrates, IAPF, BRA) and diuretics; Cautious infusion of solutions may be effective (with careful control of hemodynamic parameters), sometimes dopamine in a small dosage; 6) ASN, developed at ox→ To determine the cause of the OWN, perform echocardiography; in the case of stemi or NSTEMI → Coronaryography and endovascular intervention; In the case of mechanical complications of fresh myocardial infarction → Urgent cardiac surgery. Pharmacological treatment 1. Vasodilators:basically, they are shown to patients with symptoms of hypoperfusion and stagnation, without hypotension; Avoid patients with systolic arterial pressure<90 мм рт. ст. Уменьшают систолическое артериальное давление, давление наполнения левого и правого желудочков, а также периферическое сосудистое сопротивление; уменьшают одышку. Обязателен мониторинг артериального давления. Особенно осторожно назначайте пациентам с выраженным митральным или аортальным стенозом. 1) Nitroglycerin V / B - first 10-20 μg / min, if necessary, increase by 5-10 μg / min every 3-5 min to the maximum hemodynamically portable dose (max. 200 μg / min); Perhaps p / o or in an aerosol of 400 μg every 5-10 minutes; After 24-48 hours, tolerance is developing in high doses, so apply with interruptions. If the systolic blood pressure decreases<90 мм рт. ст. → уменьшите дозу, а если давление продолжает снижаться - прекратите инфузию. 2) Nitroprusside sodiumv / B - first 0.3 μg / kg / min, to max. 5 μg / kg / min; It is recommended to patients with severe landfills in arterial hypertension and the basis due to mitral insufficiency. Do not use when the ACS is based on an ACS, given the risk of the occurrence of the condemning effect; With long-term treatment, especially in patients with severe renal or hepatic insufficiency, symptoms of the toxic effect of its metabolites - thiocyanide and cyanide (abdominal pain, confusion, convulsions) may occur. 2. Diuretics: are represented mainly in patients with OSN with symptoms of hyperifolding - a stagnation in a small circle of blood circulation or peripheral edema. In high doses, can cause transient deterioration of the kidney function. Algorithm for treating diuretics in patients with Osn →, LS →. Applying diuretics: control the diuresis (it may require the installation of the blade of the blade) and select a dose taking into account the clinical response; Limit sodium use, control the concentration of creatinine, potassium and sodium in the blood serum every 1-2 days depending on the diuresis, adjust potassium and magnesium losses.
Figure 2.19-4.Algorithm for treating patients with diuretics with OSN (according to ESC 2008 Recommendations, modified) 3. Inotropic drugs: are represented mainly, with a row with peripheral hypiperphous and hypotension (systolic pressure of 90 mm Hg. Art.); Do not apply Routine if hypotension is a consequence of hypovolemia or other reversible cause; Conduct an ECG monitoring, given the high probability of tachycardia, the ischemia of the heart muscle and rhythm disorders. Preparations and dosage →. 4. Vazopressors: prescribe when preserving a resistant hypotension and hypoperfusion, despite the correct hydration. Preparations and dosage →.
Heart failure develops when the heart ceases to work normally and cannot pump the desired amount of blood. Against this, the blood circulation is worsening in all tissues and organs, and the body can no longer function properly. The problem often flows in a light form, but sometimes it can represent a completely real threat to life. Heart failure - classificationThere are different types of heart failure. One of the most common classifications is the one that depends on changes in the functional abilities of the ventricles. At the same time distinguish such types CH:
Why does heart failure arise? Causes of heart failure are different. Very often, the acute CH develops in people who have suffered a heart attack, myocarditis, heavy arrhythmias. Against the background of this, the amount of blood is sharply reduced, which enters the arterial system. In essence, cardiac acute insufficiency is very similar to the vascular, because specialists are often called her heart collapse. Chronic CH is characterized by pathological changes that develop in the heart for a long time, but compensate for its more intensive work:
Chronic heart failure develops against the background of various factors, it seems:
Chronic heart failureThe most common reason why stagnant heart failure appears -. In addition, the problem is often preceded by:
Other factors that can provoke HSN:
Acute heart failure To CH in acute form, all sorts of problems associated with the cardiovascular system, including cardiomyopathy, myocardial infarction, atherosclerosis of coronary vessels, heart defects, heart tamponades are given. Common reasons for which the lack of right-hand heart departments are developing, such as:
Factors due to which acute cardiovascular insufficiency in patients with compensated CH, which are:
Heart failure - symptomsIt is desirable to understand that there is a heart failure. This will help you to give a patient in time and perhaps will even save him life. The main signs of heart failure are:
Degree of heart failureMedicine allocates several basic stages CH:
Dyspnea with heart failureIt appears when the heart begins not to cope with the loads. The blood flow in the pulmonary system slows down, and the blood pressure increases. As a result, spasms are developing in branches of blood lines, which lead to a violation of gas exchange and accelerate the frequency of breathing. That is, the insufficiency of the heart valves leads to the fact that the brain comes a signal about hypoxia, and it causes the respiratory center to work more actively.  Recognize shortness of breath, which caused specifically CH, it is possible by such symptoms:
Candelle coughThis is a common symptom with a given diagnosis. The main reason for its appearance is the lack of left ventricle of the heart. It will not be difficult for specialists to distinguish a heart cough from the usual. It develops much longer than the cold. Left-deuded coronary heart failure is a process that takes several months. Only with heart attacks or serious toxic poisoning, the cardiac cough arises suddenly. The main difference of this symptom of CHA from colds cough spasms is not accompanied by a loss of nose, headaches. In addition, cough, which causes heart failure, remains dry and passes without a wet compartment, but as the main disease progresses, it can increase and complicate such phenomena as:
Swelling at heart failurePatients with heart failure with such a phenomenon from time to time also face. By the one where the swelling is located, the nature of the disease can be determined. For example, swelling in the field of lungs is a sign of incorrect work of the left ventricle. Feet with heart failure right-sided swell. At the initial stages, the problem is only closer towards the end of the day. When the patient's condition is aggravated, the edema become permanent and the usual rest with them can no longer work. How to understand the amateur that the accumulation of fluid began due to heart problems? There are several characteristic differences:
Methods of diagnosis of heart failure To diagnose, the doctor needs to thoroughly examine the patient, collect anamnesis and, if there is such a need to carry out some additional research. As a rule, diagnosis of cardiac insufficiency is carried out using such methods:
Heart failure - treatmentIn order not to face complications and return the patient to normal life as soon as possible, it is advisable for therapy to start promptly. Treatment of heart failure - the process is not easy, and engaged in its holding a specialist, but there are some nuances that you need to know and ordinary people in order to be able to provide first aid to a patient with an attack. First aid for acute heart failureFrom the on time and correctly, the first assistance in heart failure will be provided, all the following treatment depends. To make the chances of recovery to be the highest possible, you need to remember the simple algorithm:
The main task of treating CH is to prevent its transition to chronic stage. All the undertaken therapeutic measures should also help reduce the number of hospitalizations and fatal outcomes. In addition, with such a problem, as a heart failure, recommendations are aimed at:
Cardiac insufficiency treatment - drugsAll the necessary drugs in heart failure should be prescribed by a specialist who will actually appreciate the state of the patient's health and its prospects. In most cases, doctors appeal for help:
Among the most sought-after drugs in the heart failure can be allocated as follows:
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